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June 2011 Volume 97 Supplement I

heart
British Cardiovascular Society Annual Conference 13–15 June 2011 Manchester Central
heart.bmj.com www.bcs.com

Volume 97 Supplement I Pages A1–A104 HEART June 2011

Young Research Workers’ Prize
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ENDOTHELIAL CELL NITRIC OXIDE BIOAVAILABILITY AND INSULIN SENSITIVITY ARE REGULATED BY IGF-1 AND INSULIN RECEPTOR LEVELS
doi:10.1136/heartjnl-2011-300110.1 A Abbas, H Viswambharan, H Imrie, A Rajwani, M Kahn, M Gage, R Cubbon, J Surr, S Wheatcroft, M Kearney. Leeds Institute of Genetics Health and Therapeutics, Leeds, UK

Background In a similar manner to insulin, the growth promoting hormone Insulin-like Growth Factor-1 (IGF-1), may be an important regulator of endothelial nitric oxide (NO) bioavailability. We have previously reported evidence of increased basal NO production in the vasculature in two murine models of reduced IGF-1 receptor (global hemizygous knockout (IGFRKO) and endothelial cell specific IGF-1R knockout (ECIGFRKO)). Augmentation of this increase in NO is relative to progressive decrease in IGF-1R number (WT vs ECIGFRKO hemizygotes p¼0.01, WT vs ECIGFRKO homozygotes p¼0.001). Furthermore, by decreasing IGF-1R numbers in the insulin resistant hemizygous insulin receptor knockout (IRKO) model (IRKO 3 IGFRKO) we have shown insulin sensitivity in the vasculature can be restored. In this study, we have investigated further these receptor interactions with the generation of a mouse overexpressing the human IGF-1R specifically in the endothelium under control of the Tie-2 promoter-enhancer (hIGFREO), and by targeted knockdown of the IGF-1R in human umbilical vein endothelial cells (HUVECs). Methods Metabolic function was assessed in mice by tolerance tests using whole-blood micro-sampling after insulin or glucose intraperitoneal injection. Cardiovascular function was assessed by thoracic aortic vasomotion ex vivo in the organbath. Complimentary in vitro studies were conducted by siRNA mediated downregulation of the IGF-1 receptor in HUVECs with and wihout insulin stimulation. Nitric oxide synthase activity was measured using an assay measuring conversion of [14C]-L-arginine to [14 C]-L-citrulline. Results Glucose and insulin tolerance testing showed no difference between hIGFREO mice and wild-type (WT) littermates. Murine thoracic aorta from hIGFREO mice were hypercontractile to phenylepherine (PE) compared to WT (Emax hIGFREO¼ 0.9160.045 g; WT¼0.6260.045 g, p¼0.0036) with decreased response to LNMMA (Emax hIGFREO¼47.7069.87 g; WT¼106.1630.10 g, p¼0.048). These data indicate reduced endothelial NO bioavailability in hIGFREO mice compared to WT. HUVECs transfected with IGF1R-siRNA showed increased basal and insulin mediated eNOS phosphorylation in the presence of insulin (Ins: 16464.9% vs siRNA+Ins: 19260.7%, p<0.05). eNOS activity (L-arginine, L-citrulline assay) was enhanced upon trans-

Abstract A Figure 2

Abstract A Figure 3

Abstract A Figure 4

Abstract A Figure 1
Heart June 2011 Vol 97 Suppl 1

fection with IGF1R-siRNA (Scrambled siRNA: 95.7613.7% vs IGF1R-siRNA: 188.7648.3%, p<0.05). Implications These data demonstrate that increasing numbers of IGF-1R specifically in murine endothelium leads to reduced NO bioavailability. Complementary siRNA studies confirm results of previous murine studies that reducing IGF-1R numbers enhance NO bioavailability. Therefore this raises the intriguing possibility that manipulation of IGF-1R numbers may represent a novel therapeutic
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Young Research Workers’ Prize
intervention (PCI) were prospectively enrolled and underwent full 3-vessel VH-IVUS pre-PCI. Troponin-I (cTnI), IL-6, IL-18, hsCRP, neopterin, MCP-1 and sICAM-1 were measured pre-PCI and 24-h post-PCI. LTL was determined by qPCR. The combined primary endpoint (MACE) included unplanned revascularisation, myocardial infarction (MI) and death, with a secondary endpoint of post-PCI MI (MI 4a). Results 18 MACE occurred in 16 patients (median follow-up: 625 (463e990) days). 30 372 mm of VH-IVUS were analysed and 1106 plaques classified (Abstract B Figure 1) locally and via a core-lab. After multivariable regression:

Abstract A Figure 5

1. Total number of non-calcified VH-IVUS-identified thin capped fibroatheromata (VHTCFA) was the only factor independently associated with MACE (HR¼3.16, (95% CI¼1.16 to 8.64), p¼0.025). 2. Total VHTCFA number (OR¼1.26 (1.03 to 1.53) p¼0.021) and total stent length (OR¼1.04 (1.01 to 1.08), p¼0.01) were the only factors independently associated with MI 4a. 3. A novel 3-vessel vulnerability index (necrotic core: fibrous tissue ratio) and side branch loss were independently associated with stenting-related cTnI rise (standardised beta coefficient (sb)¼0.29, p¼0.004 and sb¼0.23, p¼0.019 respectively). 4. Necrotic core area at the minimum luminal area frame was the only factor independently associated with ACS presentation (OR¼1.59, p¼0.030). 5. Stented vessel VHTCFA number (OR¼1.75 (1.22 to 2.51), p¼0.002) was independently associated with the lower LTL tertile (DNA-based cardiovascular risk predictor). 6. Stenting-related IL-6 rise was the only biomarker independently associated with MACE (HR¼1.03 (1.01e1.05), p¼0.007).

Abstract A Figure 6

strategy by which to modify vascular NO bioavailability and endothelial cell insulin sensitivity.

Conclusion We present the first report of an association between VHTCFA and MACE. This provides novel evidence that VHTCFA definitions are important in their own right (rather than as analogues of histological TFCA definitions). We also present the first report of associations between VHTCFA and MI 4a as well as a novel vulnerability index that is association with stenting-related troponin rise. Finally, we report a novel association between VHTCFA and DNA-based cardiovascular risk prediction (LTL).

B

VH-IVUS FINDINGS PREDICT MAJOR ADVERSE CARDIOVASCULAR EVENTS. THE VIVA STUDY (VIRTUAL HISTOLOGY INTRAVASCULAR ULTRASOUND IN VULNERABLE ATHEROSCLEROSIS)
doi:10.1136/heartjnl-2011-300110.2

P A Calvert, 1D R Obaid, 2N E J West, 2L M Shapiro, 2D McNab, 2C G Densem, P M Schofield, 2D Braganza, 2S C Clarke, 2M O’Sullivan, 3K K Ray, 1M R Bennett. 1 University of Cambridge, Cambridge, UK; 2Papworth Hospital NHS Foundation Trust, Cambridge, UK; 3St George’s University of London, London, UK
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1

Background Identification of high-risk atherosclerotic plaques offers opportunities for risk stratification and targeted intensive treatment of patients with coronary artery disease. Virtual Histology intravascular ultrasound (VH-IVUS) has been validated in human atherectomy and post-mortem studies and can classify plaques into presumed high- and low-risk groups. However, VH-IVUS-defined plaques have not been shown to be associated with major adverse cardiovascular events (MACE), or biomarkers that confer increased cardiovascular risk, such as serum cytokines or shortened leukocyte telomere length (LTL). Methods 170 patients with stable angina or troponin-positive acute coronary syndrome (ACS), referred for percutaneous coronary
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Abstract B Figure 1
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Group 3: USPIO uptake in the aortic wall. Endothelial-regeneration following femoral artery wire-injury was also quantified at time intervals after denudation and following APC transfusion. Endothelial-regeneration of the femoral artery following denuding wire-injury was delayed in IRKO mice compared to WT (re-endothelialised area 35. with hyperinsulinaemia after a glucose challenge but a normal blood glucose response to a glucose tolerance test. J Surr. Defective endothelial-repair UPTAKE OF ULTRASMALL SUPERPARAMAGNETIC PARTICLES OF IRON OXIDE PREDICTS GROWTH IN ABDOMINAL AORTIC ANEURYSMS: A PILOT STUDY doi:10. is an important risk factor for the development of atherosclerotic cardiovascular disease. but not in bone-marrow or spleen. UK may be normalised by transfusion of APCs from insulin-sensitive animals but not from insulin-resistant animals. M Dweck. Using ultrasmall superparamagnetic particles of iron oxide (USPIO) and MRI. Methods and Results An image acquisition and data analysis algorithm for the detection of focal USPIO accumulation in tissues was developed.0e6. n¼7. *denotes p<0. N Yuldasheva. Group 2: USPIO uptake throughout the thrombus. p>0. consistent with reduced eNOS expression in bone marrow and impaired vascular eNOS activity. S Rashid. M T Kearney. R Cubbon. Research Design and Methods We quantified APCs and assessed APC-mobilisation and function in mice hemizygous for knockout of the insulin receptor (IRKO) and wild-type (WT) littermate controls. 0. S I Semple.Young Research Workers’ Prize C INSULIN RESISTANCE IMPAIRS ANGIOGENIC PROGENITOR CELL FUNCTION AND DELAYS ENDOTHELIAL REPAIR FOLLOWING VASCULAR INJURY doi:10. T J Mac Gillivray. D Introduction Insulin-resistance. J P Langrish. n¼9. UK Background Prediction of abdominal aortic aneurysm (AAA) expansion and rupture is challenging and currently relies on serial measurements of maximum aneurysm diameter.060. However.665.864.24 cm/yr) despite having similar aneurysm diameters (5. A Rajwani. p<0. S Wheatcroft. M Williams.002).5 and 5.1136/heartjnl-2011-300110. University of Edinburgh.6.2% at day 5 following injury and 35. Leeds University.8% vs 66.6 cm) were recruited from an outpatient surveillance programme and underwent 3T MRI before and 24e36 h after administration of USPIO. P<0. Histology of aortic wall tissue samples confirmed co-localisation and uptake of USPIO in areas with macrophage infiltration. p<0. M Gage.05) and patient characteristics (p>0. Paracrine-angiogenicactivity of APCs from IRKO mice was impaired compared to those from WT animals.4 J M J Richards. We set out to determine whether insulin-resistance per se adversely affects APCs and endothelialregeneration. we aimed to assess whether areas of cellular inflammation correlated with the rate of abdominal aortic aneurysm expansion. Transfusion of mononuclear-cells from WT mice normalised the impaired endothelial-regeneration in IRKO mice (5764% vs 2565%. USPIO uptake and inflammation extended beyond the aortic wall into surrounding tissues. Edinburgh. W Wallace.8% vs 59. The change in T2* value on T2*weighted imaging was used to detect accumulation of USPIO within the abdominal aortic aneurysm. transfusion of c-kit+ cells from IRKO mice was less effective at improving endothelial-repair (6262% vs 4564%. H Imrie.6% at day 7.66 cm/yr.1136/heartjnl-2011-300110.05) (Abstract C Figure 1A). aged 7065 years) with asymptomatic AAA (4.664. R T A Chalmers. 0. Results The metabolic phenotype of IRKO mice was consistent with compensated insulin resistance. p¼0. Heart June 2011 Vol 97 Suppl 1 Abstract D Figure 1 A3 . Conclusions Insulin-resistance impairs APC function and delays endothelial-regeneration following arterial injury. Defective VEGF-stimulated APC mobilisation was confirmed in IRKO mice. These data may have important implications for the development of therapeutic strategies for insulin-resistance associated cardiovascular disease.460. 0. This technique therefore holds major promise as a new method of risk-stratifying patients with AAA that extends beyond the simple anatomical measure of aneurysm diameter. D E Newby. O J Garden. Patients in group 3 with distinct mural uptake of USPIO had a threefold higher growth rate (n¼13.866. Group 1: periluminal USPIO uptake only.02) (Abstract C Figure 1B).020) than those with no (Group 1. the primary metabolic abnormality underpinning type-2-diabetes mellitus (T2DM) and obesity. 27 male. Type-2 diabetes is associated with fewer circulating APCs. p<0. Abstract C Figure 1 (A) Time-dependent endothelial regeneration following vascular injury (n=5 mice per group. G McKillop.5 cm respectively. Culture of mononuclear-cells demonstrated that IRKO mice had fewer APCs in peripheral-blood.05). Leeds. IRKO mice had fewer circulating Sca-1+/Flk-1+ APCs than WT mice at baseline.002). Circulating-angiogenic-progenitor-cells (APCs) participate in endothelial-repair following arterial injury. A Abbas. Patients were classified into one of three groups on the basis of imaging findings (Abstract D Figure 1).160. APC dysfunction and impaired endothelial-repair.22 cm/yr) or non-specific USPIO uptake (Group 2. Transfusion of c-kit+ bone-marrow cells from WT mice also restored endothelial-regeneration in IRKO mice (6262% vs 2565%. C Gray.05). 5. (B) Effects on endothelial regeneration 5 days after wire-injury of transfusion of spleenderived MNCs or BM-derived c-kit (CD117)+ve cells from WT or IRKO mice (n=4 mice per group).3 M B Kahn. These findings support the hypothesis that insulin-resistance per se is sufficient to jeopardise endogenous vascular repair. In one patient with an inflammatory aneurysm. Conclusion USPIO uptake in the aortic wall detects cellular inflammation in patients with AAA and appears to predict more rapidly progressive AAA expansion. H Viswambharan. suggestive of a mobilisation defect. Patients (n¼29.

Abstract D Figure 2 E INTEGRATIVE GENOMICS APPROACHES IDENTIFY NEW GENES CONTROLLING HEART RATE doi:10. 1T J Aitma. p<0.We have generated the first genomewide transcript expression profile of the SN. George’s University of London. We have translated these findings to humans using data from a genome-wide association study population. London.00005) that is equivalent to 5e9 bpm in humans. suggesting that the effect may be intrinsic to the heart. 6N S Peters. Methods Telemetric aortic pressure transducers were implanted into 226 animals from 33 rat strains: the Brown Norway. Abstract E Figure 2 (A) Interval mapping revealed a linkage peak on chr13. 1P J Muckett. 1S Wilkinson. with peak LOD score 6. which does not contain genes in pathways already known to determine HR. Statistical analyses were carried out using the R package. Mean nocturnal HR in strains carrying the SHR allele was 388. Manchester.7 (p>0. UK. the Spontaneously Hypertensive Rat. 3School of Medicine. Prague. Genes in the QTL that were expressed in the SN were resequenced to identify potential causative sequence variants. 6National Heart & Lung Institute. Conclusions We have identified a new genomic locus for HR. 2National Heart & Lung Institute. 4M Pravanec. Imperial College London. and quantitative trait loci (QTL) identified by linkage mapping using QTL Reaper.2S A Cook.0 ST microarray and analysed using Bioconductor.00005).Young Research Workers’ Prize (Abstract E Figure 2B) and potentially causative sequence variants in these 3 candidate genes have been identified. and is of prognostic and therapeutic significance. UK. Gene expression data were generated with the Affymetrix Rat Gene 1. Three genes at the new HR locus were enriched in the SN Abstract E Figure 1 Small (1 mm2) pieces of tissue were isolated from the rat SN and distant trabeculated RA and RNA extracted for gene expression profiling. rather than due to neurohumeral influences. The horizontal line approximates to genomewide significance. Differentially expressed genes were identified using SAM & Limma. Results Narrow sense heritability of HR in this population was 51%. 3H Dobrzynski. UK. 1MRC Clinical Sciences Centre. The sinus node (SN) and right atria (RA) of 20 rats were microdissected (Abstract E Figure 1). UK. corresponding to a decreased risk of cardiovascular death of 10%e29%. Imperial College London. Two independent approaches (linear regression modelling & correlation analysis) confirmed that this effect was independent of potential physiological covariates. We applied genetic and genomic approaches to identify new loci and genes controlling HR in a rat model that has previously been used to find human cardiovascular disease genes. (B) A volcano plot showing 3 genes significantly enriched in SN compared with RA. which may be targets for therapeutic modulation of HR in patients with heart disease. Imperial College London. We prioritised three candidate genes at the locus. Linkage mapping identified a region on rat chromosome 13 controlling HR.2 Introduction Heart rate (HR) is a fundamental measure of cardiac function. with a LOD score of 6.5 J S Ware. suggesting a large genetic contribution to HR. 5 Division of Clinical Developmental Sciences. 4Institute of Physiology. London. London. This QTL has not previously been identified in human. A4 Heart June 2011 Vol 97 Suppl 1 . Czech Academy of Science. UK.1136/heartjnl-2011-300110. and 31 strains from a recombinant inbred panel derived from these parental strains and HR was measured over several weeks. rat or mouse. Y Jamshidi. an allelic effect of 31bpm (8. University of Manchester. Potential covariates of HR were analysed in SPSS. Linkage was strongest for nocturnal HR.7%. UK 5 1. compared with 357 in BN-like strains. London. 1.7 (Abstract E Figure 2A). St.

National guidelines recommend “early” coronary angiography within 96 h of presentation.4% absolute.3% Transfer 6. Results 250/311 (80. the transfer group had significantly higher unadjusted mortality (2.27 Background Rapid delivery of reperfusion therapy with PPCI is the gold standard treatment in STEMI.7% absolute. has been investigated. Methods The study was performed in a single tertiary centre in North England. 58% relative increase (Abstract 1 table 2)). UK difference in outcome was noted by route of admission for either inhospital or 1-year events. or if patients arrive after 17:00 on the next available routine list. We have also compared the waiting time for angiography of pre-HAC-X and post-HAC-X groups. Despite this. Systems have been developed. Baseline clinical variables by route of admission were compared and unadjusted inhospital MACCE rates determined. M J Lovell.4) 367 (72.48 (1. London Chest Hospital.2) 177 (10. MA de Belder.5%) were treated with PPCI following transfer from a non-PCI capable centre. Analysis of baseline variables (Abstract 1 table 1) showed the transfer group were more likely to have an LAD occlusion treated.01) 1. R A Archbold. Results 2268 patients were included in the analysis.1 D Austin.74 0. and 311 patients treated via the novel pathway (Post-HACX).00 to 2. Methods A novel clinical care pathway for the management of NSTEMI. Data are collected routinely on all patients undergoing PPCI and include demographic.6%) were treated with coronary revascularisation (108 (75%) PCI and 36 (25%) CABG). There were 110 in-hospital MACCE events. A Mathur. Following angiography.58 (1.BCS Abstracts 2011 Abstracts 1 ROUTE OF ADMISSION IN STEMI: DO PATIENTS WHO PRESENT DIRECTLY TO A PCI-CAPABLE HOSPITAL DIFFER FROM INTER-HOSPITAL TRANSFERS? doi:10. This pathway identifies patients with NSTEMI by clinical assessment and rapid point-of-care troponin testing while in the emergency department (ED).28) 1. A G C Sutton.1) 225 (12.001 Introduction Patients with non-ST elevation myocardial infarctions (NSTEMI) are at high risk of further cardiac events. re-infarction or CVA) and mortality are collected providing relevant outcome measures.07) 1. Other baseline variables were statistically no different between groups. Despite shorter DTB times.39) 1. With the addition of call-to-balloon time. call-to-balloon time was added (models 2 and 4). D Jones.3) 188 (37.89) p 0. D F Muir. For stable patients.29) p 0.17 0. Most patients with NSTEMI present to their district general hospital (DGH).7% 4.61 0.7) 1331 (75. Systems of care should be designed to avoid admission of STEMI patients to non-PCI hospitals. Inhospital and 1-year outcomes were analysed after adjustment for factors known to be predictors of early mortality following STEMI (models 1 and 3).001 <0. We have undertaken a prospective observational study of post-HAC-X patients.2 S M Gallagher. James Cook University Hospital. known locally as the Heart Attack Centre-Extension or HAC-X.7) 28 (1. The study group consists of 775 patients divided into two groups.4) 630 (36. All unstable patients are taken straight to the cardiac catheterisation laboratory.001 64. After adjustment for relevant co-variates (models 1 and 3) route of admission remained a significant predictor of in-hospital and 1-year mortality. London.02 0.1) 35 (6.34 (0. and are transferred to the tertiary centre within 1 h without referral.1136/heartjnl-2011-300198.68 0.4%) of HACX patients underwent angiography.41 (0. a significant minority of patients are initially admitted to non-PCI capable hospitals. Middlesbrough. and await transfer to the regional cardiac centre for angiography. To determine the relative importance of delays in treatment.29 (0.6) 28 (1.0) 5 (1.64 (1. At 1 year. In-hospital MACCE (death. C Knight. assessing need for angiography and or revascularisation along with discharge diagnosis. suggesting that delays in treatment are critical.7% OR (±95% CI) 1.05 0.9) 154 (107e235) 34 (24e50) 0. M Awan. Logistic regression was used for the adjusted in-hospital outcomes. such as direct admission to a PCI-capable hospital. Adjustment for longer call-toballoon times attenuated the finding of poorer outcomes in these patients. and previous MI. One-year mortality by route of admission was calculated using the K-M product limit estimate. The transfer group had significantly higher unadjusted in-hospital MACCE rates (2. M Westwood.1136/heartjnl-2011-300198.001 0. coronary angiography is undertaken on the same day. Barts and the London NHS Trust. 464 patients treated before the instigation of the HAC-X pathway (Pre-HACX). S Antoniou.3 (12. A K Jain. 510 patients (22. 106/250 A5 Heart June 2011 Vol 97 Suppl 1 . S Mohiddin.87 to 1.0) 55 (10.3) p 0.9) 377 (73. the transfer group had a greater median CTB time (52 minutes longer) compared with direct admissions. R A Wright. The aim of this study was to determine whether patients differed in their characteristics.05 0.79 to 2.7) 102 (82e135) 44 (29e76) 13 (2. This care model has inherent time delays. Abstract 1 Table 2 Direct In-hospital MACCE Adjusted in-hospital MACCE (model 1) Adjusted in-hospital MACCE (model 2) Direct 1-year mortality Adjusted 1-year mortality (model 3) Adjusted 1-year mortality (model 4) 7% Transfer 9. patients who presented directly had superior in-hospital and 1-year outcomes compared with those who required transfer from other hospitals. and 168 deaths within 1-year follow-up. and outcome by route of admission.1) 249 (14. 48% relative increase (Abstract 1 table 2)). N M Swanson.03 0.99 to 2. clinical and procedural variables. time to PPCI. J A Hall. and delivery of early angiography is problematic.3) 812 (46.7) 1252 (71. 144/250 (57. UK Abstract 1 Table 1 Direct Age (years6SD) Male Diabetes Previous MI Treated vessel LMS LAD LCx RCA Graft Cardiogenic shock Smoking (ex/current) Call-to-balloon time Door-to-balloon time 24 (1.6) Transfer 63.04 to 2.5) 218 (42. to minimise the time from diagnosis to PPCI. J Shome. and Coxproportional regression for adjusted 1-year mortality. E Ferguson. and facilitate more rapid transfer of patients where this has not been possible.8) 89 (17.42 <0. J Carter. 2 A “DIRECT” TRANSFER PROTOCOL FOR PATIENTS WITH NON ST-ELEVATION MYOCARDIAL INFARCTION REDUCES TIME TO CORONARY ANGIOGRAPHY doi:10.9) 83 (16. Patients meeting criteria for urgent transfer receive evidence based medical therapy for NSTEMI (see Abstract 2 table 1) in the ED.20 Conclusion In this study. no significant HR (±95% CI) 1.06 to 2. Z Adam.9 (12.

6% had a non-cardiac diagnosis. Importantly. after adjusting for all the covariates.86 to 1. Leicester. To improve survival. the pathway allows accurate diagnosis of NSTEMI.5 mg Eptifibatide bolus (180 mg/kg) as long as no bleeding contraindications 1 SURVIVAL FOLLOWING ACUTE MYOCARDIAL INFARCTION IN PATIENTS OF SOUTH ASIAN AND WHITE EUROPEAN ETHNICITY IN THE UK doi:10. association of ethnicity with mortality became non-significant (HR 1. Heart June 2011 Vol 97 Suppl 1 . Dynamic T wave changes OR positive troponin I assay Exclusion criteria Unexplained anaemia (Hb<10) Hypoxia Acute renal failure Loss of consciousness Recent trauma Overt sepsis wait for transfer to tertiary centre was 4.05 to 1. Cox regression models were constructed to identify determinants of 30-days and 1year mortality.10 to 2. and inappropriate transfers are infrequent. Methods: We conducted a retrospective cohort study of total 4111 (SA 18%) consecutive patients with AMI admitted between October 2002 and September 2008.31. driven by higher prevalence of diabetes in the SA ethnic group. A6 Time from ED presentation to coronary Introduction Some UK studies have suggested higher case-fatality rates following acute myocardial infarction (AMI) in British South Asian (SA). 14. Similar associations were observed for 1-year mortality. 10% of patients had another cause for chest pain symptoms (including pericarditis and. K Khunti. On multivariate analysis (excluding antecedent diabetes and admission blood glucose) this association of SA ethnicity and mortality became significant (HR 1.23) and remained so when antecedent diabetes was added to the analysis (HR 1.9 % and 16.79 to 1. Baseline differences between the ethnic subgroups were examined using independent two-sample t tests for continuous and c2 tests for categorical variables. R L Mehta. However when admission blood glucose was added to the model. 3 Immediate medical therapy includes Aspirin 300 mg Clopidogrel 600 mg Fondaparinux 2.10) in this model. Median length of stay for HACX patients was 3 days. UK.004) or diabetes (40% vs 16%. Furthermore. p¼0.1136/heartjnl-2011-300198. In patients with AMI. Conclusions Despite higher prevalence of diabetes in SA patients.99). 2University of Leicester. UK 2 2 2 (42. Its introduction has resulted in a significant reduction in time to angiography for NSTEMI patients. The aim of this study was to compare survival rates following AMI in SA and WE patients drawn from a contemporary. and significant reductions in total hospital bed occupancy for patients with NSTEMI.005) at presentation compared to WE patients. All cause 30-day and 1-year mortality proportions were 10. multi-ethnic UK population. random admission blood glucose and antecedent diabetes individually and together along with other relevant variables.0 % and 15. NSTEACS (encompassing NSTEMI and unstable angina) was the discharge diagnosis for 75. p<0.2% in SA compared to respectively 9.4% of HACX patients.1 (64.7 % in WE patients. entering ethnicity. both prior diagnosis of diabetes as well as acutely elevated blood glucose regardless of diabetes status are associated with adverse outcomes.005) but more likely to have hypertension (55% vs 49%. For SA ethnicity.3 N N Gholap.005) and less likely to have smoked (16% vs 40%. 2I B Squire. p<0. T wave inversion in V1-4. their mortality post AMI was similar to WE patients. Results: SA patients were younger (62 vs 67 years.4 days per patient. the univariate HR of 30-day mortality was 1. Pre-HAC-X mean Abstract 2 Figure 1 angiography. Conversely each unit (mmol/l) increase in admission blood glucose was associated with 7% increase in mortality (HR 1. Leicester.7) days.56. Mean time from presentation to angiography was pre-HAC-X 7349 mins (66836) and post HAC-X 754 mins (6458) (p<0.10). M J Davies.13).30) compared to WE ethnicity. 1University Hospitals of Leicester. compared to white European (WE) people. admission hyperglycaemia more so than antecedent diabetes was an important predictor of increased mortality post AMI. myocarditis). regardless of their diabetes status or ethnicity. CI 1. p<0. CI 0.08. Conclusions This novel care pathway allows delivery of early angiography to NSTEMI patients in accordance with national guidance. However other studies have suggested similar or even better adjusted overall post-AMI survival for these ethnic groups.01 (95% CI 0.07. CI 1.04 to 1. Furthermore exclusion of ethnicity and antecedent diabetes from the model did not alter the predictive value of admission blood glucose (HR 1. CI 1.48. HAC-X has reduced wait for coronary angiography by 3. CI 1.BCS Abstracts 2011 Abstract 2 Table 1 Inclusion criteria Inclusion and exclusion criteria for HACX Symptoms suggestive of myocardial ischaemia With ECG changes including: ST depression.03 to 2. active management of admission hyperglycaemia should be considered in patients admitted with AMI.4%) of patients were treated with medical therapy alone.0001) (see Abstract figure 1).

Raised troponin without chest pain or dynamic ECG changes create diagnostic dilemmas.05 ng/ml or $0. it is unclear whether further reductions in the threshold of detection for plasma troponin concentrations impact on clinical outcomes in patients with suspected acute coronary syndrome. implementation phase) lowering the threshold of detection for myocardial necrosis from 0.84. A Anand. Clinical parameters guided investigations lead by two Consultant Cardiologists (KF. 0. aspirin and statins benefit both stroke and any coronary disease present.19 ng/ml were dead or had recurrent myocardial infarction at 1 year. increasing demand on cardiology services without increase in resources. OR 4.032e0. Royal Infirmary of Edinburgh.42. 2Edinburgh Heart Centre. p¼0.032 ng/l): 53 (22%) were “low” (0. Edinburgh University. 5 IMPLEMENTATION OF A SENSITIVE TROPONIN I ASSAY REDUCES DEATH AND RECURRENT MYOCARDIAL INFARCTION IN PATIENTS WITH SUSPECTED ACUTE CORONARY SYNDROME doi:10. seizure). Only 2 patients (3% of those with positive troponin) required percutaneous coronary intervention (PCI).3 and multiple cardiac risk factors. Five patients with “high” troponins had non-invasive stress testing (1 perfusion scan and 4 stress echos): all were negative. the result. M MacLeod. Royal Infirmary of Edinburgh. K F Fox.05 ng/ml with a sensitive troponin I assay were stratified into three groups: <0. 1A Shah.032e0.24 to 0. Introduction Although troponin assays have become increasingly more sensitive. Methods Consecutive HASU admissions over 6 months were assessed for measurement of troponin. 4Department of Clinical Biochemistry. A M D Churchhouse. During the validation phase.19 ng/ml in 170 (8%) and $0.3 ng/l).3 did not require PCIeall three had normal coronary arteries. We propose a pragmatic pathway for when troponin is performed as a routine test. lowering the diagnostic threshold to 0. Results 412 patients were admitted: 245 patients had a total of 435 troponin-I levels measured. UK Introduction Troponin is frequently measured on admission to hyperacute stroke units (HASUs). implementation of a sensitive troponin assay increases the diagnosis of myocardial infarction by a third. Wellcome Trust Clinical Research Facility. 3C Graham.05e0.20 ng/ml (p¼0. 1E Paterson. 1M A Denvir. whereas clinical outcomes were unchanged in patients with troponin concentrations <0. 39% of patients with undisclosed plasma troponin concentrations of 0. 67 had non-stroke (eg.05 ng/ml (p<0.05 ng/ml in 1340 (64%). J Barker. Without these. validation phase) and after (n¼1054. In contrast. Edinburgh.007) respectively. Management strategies were assessed with the introduction of the Imperial HASU covering North West London. an early invasive strategy confers no additional benefit over medical therapy. 237 had diagnoses readily available: 170 had stroke (ischaemic or haemorrhagic).05. and the cardiac investigations performed.20 ng/ml in 582 (28%) patients. N L Mills.0001). Imperial College Healthcare NHS Trust.20 ng/ml were reported to clinicians. p¼0.20 ng/ml (Abstract 5 figure 1). we caution against routine measurement of troponin in stroke.05e0. During the validation phase. 1K A A Fox. Conclusions Every positive troponin necessitated a review and additional tests. 70 (29%) patients had positive levels (>0. S Banerjee. 1D Gamble. non-invasive assessment and optimal medical therapy is sufficient in the majority.20 ng/ml. 6 patients had invasive coronary angiography: 3 “high” and 3 “low” troponin. The aim of this study was to determine whether lowering the diagnostic threshold for myocardial infarction with a sensitive troponin assay will improve clinical outcomes. compared to 7% and 24% of those with troponin concentrations <0.0e9.013). Edinburgh. London.1136/heartjnl-2011-300198. 1Centre for 1 1 1 Heart June 2011 Vol 97 Suppl 1 .4 S S Nijjer. 1D E Newby. UK. Edinburgh. Without chest pain or ECG changes. both had troponin >0. UK Cardiovascular Science. Troponin was more likely to be raised if stroke.05 ng/ml reduced 1-year death and recurrent myocardial infarction from 39% to 21% in patients with troponin concentrations of 0. S Connolly. Methods Consecutive patients admitted with suspected acute coronary syndrome before (n¼1038. A7 1 2 K K Lee. Lowering the diagnostic threshold of plasma troponin is associated with major reductions in morbidity and mortality.3 ng/l should be assessed for chest pain and ECG changes suggesting true myocardial infarction.05e0.19 ng/ml (OR 0.7. without chest pain or dynamic ischaemic ECG changes.001) or $0. Since this does not represent true acute coronary syndrome. Event-free survival (reinfarction and death) at 1 year were compared in patients grouped by plasma troponin concentrations.3 ng/l) represents myocytolysis: cerebral insular damage causes sympathoadrenal activation and patchy myocyte damage. SC) rather than strict research protocol. G Banerjee.5 Abstract 5 Figure 1 Conclusions In patients with suspected acute coronary syndrome. Raised troponins >0. Minor troponin rise (0. 0.19 and $0. Patients with troponin <0. 3Epidemiology and Statistics Core.1136/heartjnl-2011-300198. Modest elevations in stroke are common but whether patient management changes in response to the blood test is unclear. Results Plasma troponin concentrations were <0. 17 (7%) were “high” (>0.05e0. UK. Therefore. only concentrations above the original diagnostic threshold of $0. All positive troponins had echocardiography and cardiology review with no change in management in 91% of cases. 4S Walker. During the implementation phase.3 (2.3 ng/l). However only 2 patients required PCI with the majority medically managed. 95%CI 0. optimal medical management without further investigation is appropriate. Edinburgh. UK. The financial and medical implications of performing non-indicated tests in a routine manner when the result will be disregarded is significant. and identifies those at high-risk of reinfarction and death.20 to 0.BCS Abstracts 2011 4 A RATIONAL APPROACH TO RAISED TROPONINS ON A HYPERACUTE STROKE UNIT: COPING WITH THE IMPACT ON CARDIOLOGY SERVICES doi:10.

provides additional information to that gained from the GRACE clinical risk factor score. 5 (n¼134.37% 5.16 <0.07% 5. UK 2 2 1 Background Rapid assessment of patients with suspected acute coronary syndrome (ACS) allows the right patients to receive the right treatment at the right time. A score of 7 or 9 would merit admission to hospital. J H Barth. 7 (n¼110. In this study. 1Leeds Teaching Hospitals. troponin and highly sensitive CRP. Methods We studied 519 patients with suspected ACS admitted to a single UK Teaching Hospital. 2C Morrell.93% 18. are misdiagnosed as having noncardiac chest pain when in fact they are at high risk of cardiac events.1136/heartjnl-2011-300198. troponin Àve/H-FABP +ve 56. U M Sivananthan.1136/heartjnl-2011-300198.8%).2%). We hypothesise that a multi biomarker blood test incorporating troponin I.0001 or ACS 3. 1J H Barth. C Morrell. Introduction We have previously shown that heart-type fatty acid binding protein (H-FABP) has a role in predicting all-cause mortality after acute coronary syndromes (ACS) and after multivariable analysis.91 <0. 21. based on a negative 12-h troponin level.05% 18.0001 or CVA 3.6%). 2University of Leeds. for which 1-year mortality data was published in 2007. H-FABP is released into the circulation during myocardial ischaemia and after myocardial necrosis.4%). This group may benefit from an early invasive strategy. N Kilcullen.5%.28% 6. taken between 12 and 24 h after admission. taken on admission. Leeds. 25. UK.44% 22. It has been shown that the novel biomarker H-FABP can detect myocardial ischaemia even in the absence of myocyte necrosis.2%.11% 12. Mortality rate was independent of troponin status but strongly related to H-FABP status.81% 20. HEART-TYPE FATTY ACID BINDING PROTEIN IS A MORE ACCURATE PREDICTOR OF LONG TERM PROGNOSIS THAN TROPONIN doi:10. Leeds. H-FABP and CK-MB. and consideration of early cardiac catheterisation. Methods Six-year mortality data is now available for patients enrolled in the FAB 1 study. C P Gale. (ii) repeat acute coronary syndrome (ACS) (iii).77% 17. U M Sivananthan. Outcome measures up to 12 months were: (i) death from all causes. Discrimination of risk permits clinical triage into pathways of immediate inpatient or deferred outpatient care.9%.92% 6. A S Hall. it is likely that some ACS patients undergo angiography based on a false positive troponin level.81% 19. 1K Viswanathan. can accurately discriminate those patients with a non-cardiac cause of chest pain who are at low risk of cardiac morbidity or mortality. and who may benefit from invasive investigation. Abstract 7 Figure 1 A8 Heart June 2011 Vol 97 Suppl 1 . The addition of H-FABP measurement to the management of ACS could avoid this. Hypothesis Plasma H-FABP level.11% 5. have a very low rate of cardiovascular events. as measured on their admission blood sample. 1Leeds Teaching Hospitals.1%. K Viswanathan. 9 (n¼111. 1448 unselected patients admitted to hospital with ACS had serum H-FABP level measured in addition to usual care.6 I R Pearson. Abstract 6 Table 1 The cumulative incidence of events according to the Cardiac-Array Score Score 3 5 7 9 Ratio (9/3) p Value Death 0. Conclusion The current system of stratification of ACS patients for early invasive management if troponin positive will miss a cohort of patients who are at high risk of death despite being troponin negative. available for 1421 patients (98. (v) coronary revascularisation. Mortality was tracked by the UK Office of National Statistics. These were measured on a blood sample taken at the time of hospital admission. troponin +ve/H-FABP Àve 20. A risk scoring model was constructed based on tertile values for Randox Cardiac-Array measurement of troponin I.4%.23% 5. can identify troponin negative ACS patients who are at a high long term risk of death. If troponin Àve/H-FABP Àve mortality was 20. This tool could be used to safely triage patients towards early discharge and outpatient care. readmission for heart failure. The scores were then combined by summation resulting in an overall score of between 3 and 9.28 <0. C P Gale.21% 11. The cumulative incidence of events according to the Cardiac-Array score is shown in Abstract 6 table 1. We have also shown that there is a group of ACS patients who are at high risk of cardiac events and death despite normal troponin levels on admission.BCS Abstracts 2011 6 CARDIAC MORBIDITY AND MORTALITY CAN BE ACCURATELY PREDICTED IN PATIENTS PRESENTING WITH ACS USING MULTIPLE BIOMARKERS MEASURED ON AN ADMISSION BLOOD SAMPLE doi:10.7 I R Pearson. It is known that a significant proportion of the ACS patients sent home following an “MI screen”. CK-MB and H-FABP.08% 5. 21.11% 5. troponin +ve/H-FABP +ve 49. UK 1 1 1 1 2 2 1 1 2 7 IN ACUTE CORONARY SYNDROMES.29 <0. 31. (iv) readmission for cerebrovascular event (CVA). 1N Kilcullen.78% 16. 2University of Leeds.41% 24. Leeds.0001 or HF 3.1%). Conversely.0001 or Revasc 4.61% 3.08 <0. UK. based upon available resources. Leeds. in contrast to troponin which is released after myocardial necrosis only. A S Hall. Results The distribution of Cardio-Array scores was: 3 (n¼164.98% 21.0001 Conclusion Patients presenting with possible ACS who have a Cardiac-Array biomarker score of 3 or 5. The lowest two lower tertiles were each given a score of 1 and the top tertile a score of 3. Results At 6 years overall all-cause mortality. was 43.

99) and combined any mortality/morbidity (30% vs 32%.67.23. Melbourne.4%) 72 h (n[323) 64. A9 . Monash Medical Centre.14.0%) 21 (1.7 130 (12. W Y Shi.9 O Guttmann. 72 h. Barts and the London NHS trust. Monash University. Patients discharged at #48 h were significantly younger and had a lower incidence of multi-vessel disease than those discharged at 72 h (Abstract 9 table 1).5% vs 8062. UK 3. Propensity-adjusted multivariable regression did not show radial artery to be protective from 30-day mortality (p¼0.3e10). Abstract 9 Table 1 48 h (n[1079) Age Previous MI Previous CABG Previous PCI DM HTN Hchol 3 vessel disease 60. Methods A multicentre database was analysed.5569 0. We identified a higher risk subgroup (n¼3149) according to emergent status.7).20). We investigated the feasibility and safety of very early discharge (<48 h) coupled with regular outpatient support for lowrisk patients following PPCI.7858 0.3%) 448 (46. p<0.4G C Shardey.1% vs 8. D T Dinh. survival between radial and vein groups was similar (7962. Melbourne.1%.1136/heartjnl-2011-300198. 14% discharged at 72 h and the remainder discharged at a median of 6 days (4. 2231 (71%) received at least 1 radial artery graft in addition to a left internal thoracic artery (LITA).0001) female (22% vs 27%. or impairment of ventricular function are not disadvantaged in the early and midterm by use of a single arterial graft.78 to 1. p¼0. myocardial infarction (MI). K S Rathod.13). and >72 h. Despite this. encouraging clinical outcomes and low harvest site complication rates. 0.2% vs 7.h discharge (9. London. 3. 1C M Reid. University of Melbourne.48 to 1. p¼0. p>0. p<0. hospital readmissions (12% vs 12%. urgency of surgery. good or moderate left ventricular function. heart failure. p¼0.0%) 52 (16. or mid-term mortality (p¼0.55). Conclusions This multicentre analysis suggests that patients with the greatest coronary instability. Monash University. p¼0. resulting in shorter hospital stays.9%) 102 (9. out to 5 years of follow-up. myocardial infarction (1% vs 1%. p<0.7%. p<0. Discharge at 72 h in selected patients has been suggested. p¼0. ST segment resolution.8%) 124 (38. Melbourne. UK.51). UK. A K Jain. UK Abstract 9 Figure 1 MACE after primary PCI.74).2%) 29 (9. Patients with TIMI 3 flow. 8 and 52 weeks with a multidisciplinary team including rehabilitation.20).0 35 (10. p¼0.40 to 1. aortic counterpulsation or anticoagulant status.0112 9 EARLY HOSPITAL DISCHARGE AT 48 H FOLLOWING PRIMARY PCI FOR MYOCARDIAL INFARCTION IS BOTH SAFE AND FEASIBLE doi:10. 11 388 patients underwent isolated multivessel coronary surgery. S Mohiddin. HR 0.8007 0.6% vs 9%. E J Smith. coronary instability.19). p¼0.4%) 156 (14. 2Department of Cardiac Surgery.0002 0. stroke and target vessel revascularisation (TVR). A Mathur. Demographic and procedural data were documented at the time of intervention.79. and psychology. 0. Introduction Reperfusion therapy with primary PCI (PPCI) has reduced rates of recurrent ischaemia and arrhythmia following ST Heart June 2011 Vol 97 Suppl 1 Conclusion Early discharge at 48 h is feasible and appears to be safe for patients undergoing contemporary Primary PCI. P A Hayward. p¼0. elevation myocardial infarction (STEMI). M Akhtar.1%) 403 (37. radial: 66610 years vs vein: 71610. 548 patients in the radial group were propensity-score matched to 548 receiving LITA and veins. We sought to assess this by examining outcomes in higher risk subgroups. p¼0.8019 0. 1Department of Epidemiology and Preventative Medicine. D A Jones.4632 0.8 C H Yap. Austin Hospital.002). surgeons may utilise clinical judgement to select radial or venous conduits to supplement the LITA according to other patient factors or technical preference without prejudicing outcome. From 2001 to 2009.0001). Results 1079 patients (46. Monash University.8%) 7 (2.5%) were stratified to 48-h discharge. p¼0. UK.76. At 7 years.0001). This persisted out to 5 years (9. 30-day MACCE (p¼0.1136/heartjnl-2011-300198. return to theatre (5% vs 7%. A Wragg. C Knight. All-cause mortality data were provided by the Office of National Statistics via the BCIS CCAD national audit.4%) 156 (54. 4Department of Surgery.BCS Abstracts 2011 8 DOES THE ADDITION OF A RADIAL ARTERY GRAFT IMPROVE SURVIVAL AFTER HIGHER RISK CORONARY SURGERY? A PROPENSITY-SCORE ANALYSIS doi:10.002) or be of emergent status (11% vs 24%. Melbourne. At 30 days.9%) p Value 0. Remaining patients were discharged according to physician preference. p¼0. However it is not clear whether higher risk patients derive such benefits. A Ludman. Propensity-score matching and adjustment was performed to correct for group differences. stroke (1% vs 1%.2854 0.1%) 148 (45. Results Patients who did not receive a radial artery were more likely to be older (mean age.4 1 2 2 1 Introduction The use of the radial artery as a second arterial graft during coronary surgery has become popular due to high patency. Furthermore. Limitations include the inability to correct for unquantifiable variables retrospectively.4%) 455 (42. MACE at 3 years was similar between 48-h discharge patients and 72. left main stenosis (35% vs 41%.19). have poor left ventricular function (16% vs 23%.0001) and poorer 7-year survival (p<0. Monash Medical Centre. major adverse cardiac or cerebrovascular events (MACCE) (2% vs 4%. The remaining 918 (29%) received LITA and veins only. 3Department of Cardiothoracic Surgery and Surgery.97. J A Smith. Methods 2317 patients underwent PPCI for STEMI between October 2003 and May 2010 at a regional Heart Attack Centre (HAC). and no dysrhythmia were stratified to 48 h discharge.77). All patients were reviewed at 1.33). Outcomes were compared between those discharged at #48 h. OR 0. These patients experienced higher unadjusted 30-day mortality (2. low ejection fraction. Remaining baseline characteristics were similar.5%. there were comparable rates of mortality (radial: 2% vs vein: 3%. As expected patients with length of stays >72 h had significantly worse outcomes (Abstract 9 figure 1). 0. The primary endpoint was major adverse cardiac events (MACE) included death.0001). including those with complications.12). Among these. OR 0.

009) but NTproBNP did not (p¼0. when combined with NT-proBNP (0. Neither of these patients was found to have a 100% acute occlusion of a coronary artery.04 or Trop T<0.0 pmol/l and were significantly higher in those that reached the primary endpoint than the event free survivors. Edinburgh. UK 1 1 2 Background The Freeman Hospital (FRH) performs over 900 pPCI a year. NT-PROBNP DOES NOT doi:10. Aims We hypothesised that copeptin is an independent predictor of mortality following NSTEMI and.0005 respectively).1 or Trop T 0. J Struck. In a high volume Heart Attack Centre a nurse led triage is effective at discriminating patients with LBBB requiring immediate coronary intervention.4 p<0.01 (Normal) Trop I 0.008) whereas. 177 (16.7) respectively p<0.1e1. ROC curve c-statistics for GRACE-RS of 0. is a recognised prognostic marker in ST elevation myocardial infarction (STEMI) that is also useful to exclude MI as levels rise early after onset.3% p¼0.1136/heartjnl-2011-300198. 4 patients had unobstructed coronaries and were managed medically. Freeman Hospital. 2The Cardiothoracic Centre. University of Leicester.001. Copeptin has not been evaluated in a NSTEMI population to date. Re-classification analysis shows that copeptin improves accuracy of risk stratification when combined with the GRACE-RS as determined by net reclassification improvement (NRI 13.3 to 523. The sensitivity of detecting patients with an acutely occluded artery diagnosed at angiography is 100% with a specificity of 81%.1%) 1 (3.5%) were referred back to FRH for PCI. assess whether copeptin adds prognostic information to GRACE risk score (GRACE-RS). there remains considerable variation in the clinical utility of new or presumed new LBBB as a ST-elevation myocardial infarction (STEMI)-equivalent ECG diagnostic criterion. in accordance with AHA criteria for the evaluation of novel biomarkers. 1I B Squire. 1J E Davies.9% p¼0.1136/heartjnl-2011-300198. The sensitivity of the triage process in detecting patients with LBBB requiring urgent revascularisation is 75% and the specificity is 83%. which is triaged by experienced CCU nurses.11 O S Dhillon. median (IQR). Abstract 10 Table 1 Troponin levels in patients with LBBB referred for consideration of pPCI. GRACE-RS + copeptin and GRACE-RS + NTproBNP as covariates are shown in Abstract 11 figure 1. We use NT-proBNP for comparison. Kaplan-Meier analysis revealed that supramedian levels of copeptin were associated with increased mortality (log rank 28. median age 70613 years) within 36 h of symptoms. Abstract 10 Table 1 FRH Assessed Number of patients Number analysed 33 33 FRH Declined 144 132 (Biochemistry data not found for 12 patients) 84 (63. The major discriminators the triage staff use in this population are ECG findings and symptoms suggestive of AMI.0e16.802. On adjustment for baseline clinical and biochemical variables copeptin remained predictive (HR 3.4%) patients. 32. The relative utility for GRACE-RS + copeptin was consistently more than the relative utility for GRACE-RS + NTproBNP across a range of risks.0005 and HR 6.BCS Abstracts 2011 10 EVALUATING A NURSE LED TRIAGE PROCESS IN TREATING PATIENTS WITH LEFT BUNDLE BRANCH BLOCK (LBBB) REFERRED FOR PRIMARY PERCUTANEOUS CORONARY INTERVENTION (PPCI) doi:10.785).9%) 17 (12. Patients with suspected Acute Myocardial Infarction (AMI) are referred either by paramedics or networked hospitals for consideration of pPCI via a Telmed system. Median copeptin levels were 7. current tools are not fully discriminatory. The primary endpoint of all-cause mortality at 6 months was reached by 56 (7.03 p¼0. S Jamieson.0%) 11 (33.7) vs 7.70).0 (Moderately raised) Trop I or Trop T>1. 0. NTproBNP does not (NRI À4. Of those. 33 (18. Methods Consecutive patients referred to FRH with LBBB and suspected AMI from 1st August 2009 to 30th November 2009 were analysed by recording: 1) Peak Troponin Level 2) Angiographic findings 3) Revascularisation rates. Copeptin. UK 1 2 2 2 2 1 1 1 11 COPEPTIN IMPROVES EARLY RISK STRATIFICATION BY GRACE SCORE IN NON ST-ELEVATION MYOCARDIAL INFARCTION. B R Bawamia.3%) Conclusion Revascularisation was performed in only 6/33 (18.10 N V Joshi. Our aim was to evaluate outcomes in patients with LBBB accepted to FRH or referred to local hospitals for assessment.6%) of patients had new or presumed new LBBB.4%) were declined and referred to their local hospitals for assessment.2 (4.6%) patients were accepted by FRH and 144 patients (81. The relevant region was the region to the right of the sample risk for 6 months mortality. Abstract 11 Figure 1 A10 Heart June 2011 Vol 97 Suppl 1 . Newcastle Upon Tyne. UK.07 p<0. Troponin levels Trop I<0. 1L L Ng. Of the 132 patients declined for pPCI only 2 (1.6%) 2 (6.0 (12.0e88.835 when combined with copeptin (0. the stable 39 amino acid C-terminal portion of pro-vasopressin. However.074.98 p<0.01e0. Results 1069 patients were referred for consideration of pPCI.0 (High) 19 (57.2%) accepted for assessment and only 2/132 (1. Of the 33 patients admitted to FRH. for example at a risk threshold of 15% the additional utility of adding copeptin to the GRACE-RS was 0.001).5%) Background Risk stratification is vital to the optimal management of patients with non ST-elevation myocardial infarction (NSTEMI) however.9 range 0.9%) 6 (4. The University of Edinburgh.097 compared to 0.5%) were referred back to the centre for PCI. The pPCI Pathway can be activated in patients with LBBB suspected of having an AMI. H K Narayan.04e0. A Zaman. Only one patient had a 100% coronary occlusion believed to be an acute occlusion. UK. Leicester. The relative utilities for logistic regression models using GRACE-RS alone. 13 underwent inpatient angiography and 9 patients had significant coronary disease (coronary stenosis 70%e100% in at least one coronary artery). P A Quinn.1 (Mildly raised) Trop I or Trop T 0. 5 had PCI and 1 required urgent CABG.730) increased to 0. Centre for Cardiovascular Science. Hennigsdorf. 2Brahms. 26.21).799 increased to 0.009 for NTproBNP. R Edwards. Both copeptin and NT-proBNP were predictive of the primary endpoint on univariate Cox regression analysis (HR 5.6%) 25 (18.5% of patients with LBBB referred for consideration of pPCI had moderately to highly raised troponin. Methods and Results In this prospective observational study plasma copeptin and NT-proBNP was measured in 754 NSTEMI patients (519 men.

Massachusetts. (À25. 1J L Mckenzie. Neutrophil MPO content at the CA in patients with multiple complex plaques was similar to those with a single culprit however only in those with multiple complex plaques was a correlation between MPO content and CD11b (r¼À0. The addition of anxiety and depression contributed significantly to the reporting of lower physical health-related quality of life (PCS) at 6 months (ÄR2¼0. clinical and psychosocial variables.4 (SD 8.9).1). University of Manchester.02) shown.13 12 C J Marshall. Neutrophil MPO content was correlated with CD11b expression only at the culprit CA in STEMI (r¼À0.0 years (SD 11. USA) at the site of occlusion.1136/heartjnl-2011-300198. The clinical. n¼37). 3 Department of Cardiology.007) but no differences in LV function. after controlling for possible confounding factors. n¼31) (Abstract 13 figure 2). C Dickens.7. Boston Scientific Corporation. 2T Moccata.4.8) and 78% were male. 2CMFT. 1 3 13 NEUTROPHIL ACTIVATION AT THE CULPRIT LESION IN ACUTE ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION WITH MULTIPLE COMPLEX CORONARY PLAQUES doi:10. In order to identify variables at baseline that may contribute to SF-36 PCS at 6 months.03. p¼0. Abstract 13 Table 1 Variable Age (years) mean6SD Male (%) Culprit coronary artery lesion treated (%) Left anterior descending Diagonal Circumflex Right coronary Time to presentation (mins) mean6SD Baseline TIMI flow 0e1 STEMI (n[40) 62612 28 (70) 17 (42) 2 (5) 1 (3) 20 (50) 2226155 28 (70) Elective PCI (n[10) 6869. comorbidity-related. Results Baseline results revealed a small number significant differences between groups on a range of clinical variables. Neutrophil activation was measured by flow cytometry using neutrophil intracellular myeloperoxidase content (MPO Index) and the expression of the b2.2).1 7 (70) 5 (50) 1 (10) 2 (20) 2 (20) NA 0 p Value 0. H Iles-Smith. The results indicate that the assessment of psychological factors is important in both groups.0. there will always be a group of patients receiving lysis.001 (Abstract 13 figure 1). Methods We conducted a prospective cohort study of 385 postSTEMI patients who had undergone either lysis (183) or PPCI (202). Natick. MPO content was lower at the CA (À23. M Campbell. UKI. Patients were assessed on a range of demographic. and health-related quality of life (SF-36). University of Otago.integrin CD11b. 1C Rogers. such as depression and anxiety.9 1 0. we conducted a hierarchical multiple regression with four blocks of independent variablesddemographic.73 0. particularly in patients with multiple complex coronary plaques. The main outcome was the SF-36 Physical Component Score (PCS) at 6 months postSTEMI.1 0.15 <0.9). n¼30) and FA (À20. n¼37) compared to Ao (À22. Factors which contributed to the final model were cholesterol levels (p¼0. including measures of cardiac risk.1). Christchurch. Regarding psychological variables the total HADS score was significantly higher in the PPCI vs lysis group at baseline (means 13. Despite PPCI having improved clinical outcomes. New Zealand. the aorta at the coronary ostium (Ao).12. 2A J Kettle. (À24.4.001). Copeptin is also useful for rapid rule-out of MI and the current findings further support clinical uptake. 3J Blake. New Zealand THE RELATIONSHIP BETWEEN PSYCHOLOGICAL FACTORS AND IMPAIRED HEALTH-RELATED QUALITY OF LIFE POST ST-ELEVATION MYOCARDIAL INFARCTION doi:10. regardless of mode of treatment. The culprit lesion was sampled after passage of a guide wire across the lesion and use of a low profile sampling catheter (Multifunctional probing catheter. The mean age was 60. The aim of the study was to assess the contribution of anxiety and depression to HRQoL in post STEMI patients.037).4 to À13. demographic and angiographic characteristics of patients and controls are shown in Abstract 13 table 1. Ao and FA in STEMI compared to elective controls (p<0. Furthermore.BCS Abstracts 2011 Conclusions High plasma copeptin levels indicate a worse outcome in NSTEMI patients. 2F Fath-Ordoubadi. UK. Methods Forty STEMI patients having primary PCI were compared to 10 controls with chronic stable angina (CSA) undergoing elective PCI.199).001). 3C Frampton.8 to À16. and femoral artery (FA) prior to primary PCI. are independent risk factors for increased morbidity and mortality post ST-elevation myocardial infarction (STEMI). Conclusion The findings have shown that raised levels of depression and anxiety predicted impairment in health-related quality of life at 6 months post-STEMI. and that differences in activation may be detectable locally at the culprit lesion. As such it is important to assess anxiety and depression in post STEMI patients. illness perceptions (brief IPQ). CS (À20. clinical and psychological. the coronary sinus (CS). We have demonstrated that copeptin fulfils AHA criteria by improving risk stratification over established markers GRACE score and NT-proBNP. cardiac severity and comorbidity (Charlson Comorbidity Indexd CCI). Heart June 2011 Vol 97 Suppl 1 Introduction The activation of neutrophils at the culprit coronary lesion following acute plaque disruption has not been reported. Conclusion: In acute STEMI. A11 . In patients with multiple complex plaques. neutrophils are activated systemically.7 to À16. regionally and locally at the culprit coronary lesion. while anxiety and depression almost reached significance.035). (À24. a leukocyte adhesion and activation marker at the culprit coronary lesion (CA). n¼40). p¼0. including type of treatment. A lower MPO content indicates the depletion of intracellular MPO and cell activation. 2 Free Radical Research Group. Since improved treatments have increased survival rates post STEMI the emphasis has turned to more patient related outcome measures such as health-related quality of life (HRQoL). with raised anxiety and depression scores in the PPCI group. UK 2 1 1 Introduction Evidence suggests that psychological factors. prior to further mechanical intervention. p¼0. Lysis patients had more comorbid illness as measured by the CCI (p¼0.1. all p<0.6 to À17. We hypothesised that neutrophil activation occurs in ST elevation myocardial infarction (STEMI) prior to percutaneous intervention (PCI).2 (SD 7.5 0. p<0.6.9) and 11. 3D R Mcclean. Christchurch. (À24. 3M Nallaratnam.001 Results A marked decrease in MPO content occurred at the CA. Manchester.1136/heartjnl-2011-300198. including higher GRACE scores for PPCI group (p¼0. and to include these potentially modifiable factors in the design of suitable interventions for this patient group. Psychosocial assessment included anxiety and depression (Hospital Anxiety and Depression Scale). Christchurch Hospital. Manchester. Treatment group did not play a role (p¼0.01). M Richards. 1Sunderland Royal Hospital. there may be an extended local role for the activated neutrophil following acute plaque destabilisation. Sunderland.12 1 1 L McGowan.031) and depression (p<0.

N Karia. Department of Cardiology.1136/heartjnl-2011-300198. 3A P Banning. 3C Forfar.14 E Dall’Armellina. and 6 months (TP4). 3B Prendergast. We investigated changes in oedema and late gadolinium enhancement (LGE) with serial imaging early after acute A12 Abstract 14 Figure 2 Heart June 2011 Vol 97 Suppl 1 . USA. UK. UK 2 1 1 1 1 Introduction Changes in myocardial tissue in acute ischaemia are dynamic and complex and the characteristics of myocardial tissue on cardiovascular magnetic resonance (CMR) in the acute setting are not fully defined. All patients showed oedema at TP1. 1J M Francis. 3 R J Kharbanda. relating these to global and segmental myocardial function at 6 months. 14e17 days (TP3). University of Oxford. T D Karamitsos. 2NIH. 1S Neubauer. 1M D Robson. 1V Ferreira. 1R P Choudhury. Department of Cardiovascular Medicine. 5e7 days (TP2). Bethesda.BCS Abstracts 2011 Abstract 14 Figure 1 MI. 1K Channon. John Radcliffe Hospital. Oxford. 1NIHR Biomedical Research Centre. The mean volume of oedema (% LV) was 37616 at TP1 and 39617 at TP2 Abstract 13 Figure 1 Abstract 13 Figure 2 14 DYNAMIC CHANGES OF OEDEMA AND LATE GADOLINIUM ENHANCEMENT AFTER ACUTE MYOCARDIAL INFARCTION AND THEIR RELATIONSHIP TO FUNCTIONAL RECOVERY AND SALVAGE INDEX doi:10. Methods and Results CMR scans were performed on 30 patients with ST elevation MI (STEMI) treated by primary PCI at each of 4 time points: 12e48 h (TP1). P Kellman. 3NIHR Biomedical Research Centre. Oxford. A Lindsay.

Heart June 2011 Vol 97 Suppl 1 Discussion NSTEMI ACS treated with all the current evidencedbased therapies still has significant recurrent events. 28% prior MI.96) À4. Of segments showing LGE at 48 h. or for primary and secondary prevention have not primarily targeted inflammatory mechanisms. London.31 (0.BCS Abstracts 2011 with a reduction to 24613 (p<0. depending on the time point used. Enrolment completed in March 2010.19 to 1.00 1. S Mohiddin.8 0. 32% female. A Wragg.77) p 0. Injection site reactions reported as adverse events occurred in 14% of patients. The volume of LGE decreased significantly between TP1 and TP4 (27615% vs 22612%.14 (2. and the main secondary outcomes are AUC of troponin and safety and compliance of trial treatment. The primary outcome of the study was area under the curve (AUC) of high sensitivity CRP (hs-CRP) over the first 7 days of treatment.92 (1.54 0.35 (1. A Jain.01). (3) In 46% of patients.56 15.1136/heartjnl-2011-300198.08 (0.18 1.15 Results Five UK centres randomised 182 patients with non-ST elevation (NSTEMI) ACS to IL-1ra or placebo. Anakinra.61 0.75) 1.14 (1.86 0.001).35 0. (5) the reduction in LGE at the later time had a profound effect on the calculation of salvage index.44) 1. 2C Foley.79) 10 (0.34) 2.22 (0.56 44. the inflammatory driver for NSTEMI-ACS is not IL-1 mediated. C Knight.33 (0.32 to 1.01) than at TP1 (R2¼0.50 (1. (2) a large majority of segments that were positive for oedema also showed LGE.83 (2.32 (1.27 0. p¼0. UK 2 1 Abstract 15 Table 2 Event MACE at 30 days MACE at 3 months MACE at 1 year MI (%) Stroke (%) Death (%) CV hospitalisation (%) Revascularisation (%) Injection site reactions (%) Other SAE (%) MACE and other SAE Active (n (95% CI)) 6 (0. Amgen) which is licensed for the treatment of rheumatoid arthritis.56 (1.44 p 0. A Graham. p<0. 1J Gunn. 2M Flather. LGE present on early scans had diminished in size by 6 months.31 15 INVESTIGATION OF IL-1 INHIBITION IN PATIENTS PRESENTING WITH NON-ST ELEVATION MYOCARDIAL INFARCTION ACUTE CORONARY SYNDROMES (THE MRC ILA HEART STUDY) doi:10.31 0. p<0.82 0.16 E C Sammut. The data indicates that despite encouraging pre-clinical evidence. There was no significant difference in area under the curve for hsCRP between active and placebo groups.00 0. troponin.09 (1. The area of LGE measured at 6 months correlated more strongly with 48-h troponin (R2¼0.002). D A Jones. K Rathod.66 0.29 (0.01) and LGE (p<0. UK. the use of acute LGE may severely underestimate salvaged myocardium and should not be used to predict recovery of myocardial function. assessed at 12e48 h. placebo-controlled trial. and again at 2 weeks and 30 days. Compliance was good with 85% of patients receiving daily injections during the first 7 days. the proportion of segments with wall motion impairment increased in relation to the extent of both myocardial oedema (p<0. 1NIHR Cardiovascular Biomedical Research Unit. UK.69 0.54) 1. Patients were encouraged to self-administer trial treatment. Design and methods The UK MRC ILA-HEART study is an investigator-initiated.36 (0. phase 2.15) 1. B Lees.88) À3. London. UK Background Stent thrombosis (ST) is a recognised cause of ST Elevation Myocardial infarction (STEMI) in patients with previous A13 . 4Royal Infirmary of Edinburgh.92 (0. comparing the IL-1ra (100 mg) with matching placebo given as a single.22) 3.13 (0. 3 Academic Unit of Cardiovascular Medicine. MRC ILAHEART is the first study to evaluate the effects of the anti-inflammatory IL-1ra in ACS. multi-centre.03 (1.23 0.74 0.46) 1. von Willebrand factor and other biomarkers up to 7 days.43) 2. At TP1. p<0.09 4.01) by TP 3. Myocardial segments with oedema also had increased signal on LGE at TP1 (k¼0. non-industry sponsored.35) 0. Edinburgh. 1A Rothman.35 19. The difference in LGE between TP1 and TP4 had profound effects on the calculation of salvage index (26621% at TP1 vs 42623% at TP4.5).35) 0.02).31) À4.65 Background Inflammatory mechanisms are involved in both coronary atherogenesis and its presentation as acute coronary syndromes (ACS). Patients were followed up to 12 months for safety (Abstract 15 table 1). Leeds.42) 1.55 (1.56) 0.02) 0.35) 1.83 Placebo (n (95% CI)) 10 (1) 13 (1) 18 (1) 7.0001). IL-1 can be inhibited by IL-1 receptor antagonist (IL-1ra.028 0.73 (2.95 0. (6) From a clinical perspective. A Mathur. which varied by up to w60%.32 0.78 0 4.83 0. and 70% of patients were able to self-administer the injections.92) Placebo n 78 78 76 76 78 76 76 84 84 75 83 77 75 Placebo mean (SD) 3.86 69.51) 1.41) 0. Royal Brompton and Harefields NHS Trust. In segments with such a reduction in LGE. 3A Hall. 4K Fox. To date. 1D Crossman. 2CTEU.22 47. Conclusions (1) Myocardial oedema was unchanged over the first week but decreased by 15 days. The MACE and serious adverse event rates are shown in Abstract 15 table 2. daily subcutaneous injection over 2 weeks.77.28 (0. 3J P Greenwood. 15% diabetes. (4) resolution of LGE was associated with improvement in function. 90% were receiving a statin at the time of randomisation and 64% had early PCI or CABG.19 0. 65% also showed improved wall motion (p<0. Pre-clinical studies from our group have indicated that the pro-inflammatory cytokine IL-1 drives a number of vascular events relevant to coronary artery disease and ACS. UK.84) 20 (0.37 (0.32) 1.44 25 60 15.1136/heartjnl-2011-300198.30 0.74 (2. and underwent daily assessment of hs-CRP.46) 1. Mean age was 61 years.59 to 2.13) 1. A C Morton.62 (1. 16 ACUTE STENT THROMBOSIS RESULTING IN ST ELEVATION MYOCARDIAL INFARCTION (STEMI) IS ASSOCIATED WITH WORSE CLINICAL OUTCOMES THAN STEMI DUE TO NATIVE CORONARY THROMBOSIS doi:10. and to evaluate the safety and tolerability of treatment.35) À4. Abstract 15 Table 1 secondary outcomes Variable hsCRP AUC (days 1e7) hsCRP at day 7 hsCRP at day 14 hsCRP at day 30 Troponin AUC (days 1e7) Troponin at day 14 Troponin at day 30 vWF AUC (days 1e3) vWF at day 14 vWF at day 30 IL-6 AUC (days 1e3) IL-6 at day 14 IL-6 at day 30 Log transformed values for the primary and Active n 82 78 77 76 82 77 76 89 77 78 86 77 73 Active mean (SD) 3. drugs used at the time of ACS. Studies with aspirin and statin drugs indicate that anti-inflammatory properties of these compounds may contribute to their beneficial effects.26 1. Sheffield. The London Chest Hospital.51 (1. 50% showed resolution by 6 months. S May. Aims To investigate the effects of interleukin-1 receptor antagonist (IL-1ra) on inflammatory biomarkers in patients with ACS <48 h from symptom onset.89 (1.84.35) 0.91) 0.

UK 2 1 Abstract 16 Table 1 AST (n[180) Age Multi-vessel disease Previous MI Previous CABG Diabetes mellitus Hypertension Hypercholesterolaemia Cardiogenic shock 63. late (30 dayse1 year) in 22% (40/180) and very late (>1 year) in 42% (75/ 180) of pts.002 <0.001). Regression analysis demonstrated that a higher IMD is associated with increased mortality from CHD (r2¼0.2. Increased admission rates was not significantly associated with decreased mortality from CHD (r2¼0. Pts with STEMI due to ST had higher in-hospital MACE (11% vs 3%.0001) and death (18% vs 6%. UK.7%. p<0. particularly in economically developed countries such as the UK. MACE was driven by higher rates of MI (7% vs 2%. Conclusion Primary PCI for treatment of ST is less effective. Comparison with data from studies with strict clinico-pathological criteria showed this to be the age group in which official statistics were least accurate. diabetes or cardiogenic shock. 2D Watson.04 There was no difference in age.67%) No AST (n[2241) 62.0001).69. Brighton.74%) 246 (10.5 vs 2. JoinPoint regression analysis shows a constant rate of decline in mortality from 1993 to 2001 which then decreases faster between 2001 and 2006 before Abstract 16 Figure 1 Abstract 17 Figure 1 A14 Heart June 2011 Vol 97 Suppl 1 . Deprtment of Informatics. p<0.0001). p<0. p¼0. The incidence is increasing and to date outcomes are not well characterised. Methods Data from death certificates and studies with strict clinicopathological criteria on mortality from CHD were accessed.99. p<0. Results Between 1993 and 2008 deaths from CHD have fallen by over 50%. though there is a suggestion that there is a worse clinical outcome.4% in 2005 to 9. 1Brighton & Sussex Medical School.45%) 768 (34.004.8% vs 51. p¼0. Information was entered at the time of procedure.0001). ST occurred early (0e30 days) in 36% (65/180).8. Brighton. See Abstract 16 table 1. Results Stent thrombosis (ST) accounted for 7. See Abstract 16 figure 1. p¼0. revascularisation rates and index of multiple deprivation (IMD).0001 0.020 0.0001) and incidence of multi-vessel disease (59.93%) 9 (5. Infarct size based on peak enzyme markers was similar (2. p<0. deaths from CHD fell by over 50%.30%) 768 (34.3 to 2.4% (180/2421) of all STEMIs with a frequency that has increased over time (5.1. After adjusting for comorbidities. under-deployment of previous stent insertion (22%) and underlying prothrombotic conditions (eg. diagnosis of stent thrombosis made at the time by primary operator and outcome assessed by all-cause mortality information provided by the Office of National Statistics via the BCIS CCAD national audit. Pts with ST compared to native artery occlusion had higher rates of previous MI (53.02). this persisted up to 3 years (41% vs 12%.061 0.84%) 101 (56. Methods Clinical information was analysed from a prospective database on 2421 patients who underwent Primary PCI following STEMI between October 2003 and May 2010 at a London centre. Drug-eluting stents (DES) accounted for 48% of SToverall and 70% over the past 3 years. Trends in mortality overall and for different age groups were analysed over time to determine how the picture has changed and predict what may happen going into the future.045 <0. p¼0. Increased revascularisation was significantly associated with decreased mortality from CHD (r2¼0.0001). p<0.8% 2009). A range of statistical tests including. ANOVA and JoinPoint regression were employed. disability and economic impact: this should be looked at in the context of a disease that is preventable. p<0.76%) 96 (53. These were analysed in terms of hospital admissions.239). 17 SUDDEN CARDIAC DEATH AND ACUTE MYOCARDIAL INFARCTION: HOW HAS THE PICTURE CHANGED? doi:10. and these patients are at increased risk for in-hospital and long-term mortality compared with patients undergoing primary PCI due to de novo STEMI.67%) 108 (60.96%) 60 (2.BCS Abstracts 2011 percutaneous coronary interventions (PCI). MACE at 30 days (19% vs 6%. angiographic success (postprocedural Thrombolysis In Myocardial Infarction grade III flow) was worse than in patients with de novo STEMI (87. p¼0. Between 1980 and 2000. The mortality rates from the catchment area of the Royal Sussex County Hospital and York Hospital were analysed to assess reliability of official figures against strict clinico-pathological inclusion criteria.45). TVR (14% vs 3%. and have continued to fall. p¼0. linear regression. We therefore sought to compare STEMI caused by ST vs de novo coronary thrombosis to evaluate procedural risk and clinical outcome.0001). UK. The cost of CHD manifests itself in mortality.001). stent thrombosis was an independent predictor of long-term adverse outcome (OR¼2.0001 Introduction Coronary heart disease (CHD) is a major burden worldwide. Proposed mechanisms included premature discontinuation of anti-platelets (11%).406 0. p<0. Brighton. 3Brighton & Sussex University Hospital. The decline has been greater in older age groups particularly the 65e74 age group (the oldest age group analysed).67%) 407 (18. In patients with ST.74%) 108 (60.14%) 975 (43.7%. 3C Davidson. SLE) (6%).964 1011 (51.9% vs 11%.17 G Mole.2% vs 93.0001 <0. University of Sussex. 95% CI¼1.30%) Significance (p value) 0.06%) 46 (25.001).1136/heartjnl-2011-300198.9618 101 (59.

C Knight. aside from cardiogenic shock. p<0. J Behar. p¼0. A Jain. as a result a delay in mortality is presented as prevention of mortality from CHD. 19 TREATMENT OF MULTIVESSEL CORONARY ARTERY DISEASE IN PRIMARY PCI FOR ST ELEVATION MYOCARDIAL INFARCTION: CULPRIT ONLY REVASCULARISATION IS ASSOCIATED WITH HIGHER MACE RATES doi:10. E Sammut. D A Jones. UK 18 PATIENTS PRESENTING WITH ANAEMIA UNDERGOING PRIMARY PCI APPEAR AT SIGNIFICANTLY HIGHER RISK OF AN ADVERSE OUTCOME doi:10. Patients with baseline anaemia who received a blood transfusion were significantly more likely to suffer an adverse outcome than those that did not receive a transfusion (21% vs 6%.001). 23/263 (9%) patients in the CR group experienced at least one major adverse cardiac event (MACE).0001). Discussion There is a danger that previous successes are being offset by high rates in the younger cohorts. p¼0. UK Background Previous studies have demonstrated a relationship between pre-existing anaemia and inpatient mortality after percutaneous coronary intervention (PCI).0001). Barts and the London NHS trust. A Wragg. There were similar baseline characteristics between the 3 groups. hypercholesterolaemia (40 vs 30%. Methods Clinical information was analysed from a prospective database on 2357 STEMI patients who underwent Primary PCI between January 2004 and May 2010 at a London centre. See Abstract 19 table 1. A Graham.01). A Mathur. There is still work to be done in reducing risk factors and also applying treatments that have had a proven positive impact (such as revascularisation) more effectively. Conclusion Patients presenting with anaemia undergoing primary PCI appear at significantly higher risk of an adverse outcome. The primary end point used was major adverse cardiac events (MACE). Over a 3-year follow-up period there was significantly higher all cause mortality in the anaemic group compared to the normal Hb group (20. Future work This 10 000 word report formed the basis of a funding application to the British Heart Foundation for a follow-up to the United Kingdom Heart Attack Study.0001). S Gallagher. R Weerackody. After adjusting for comorbidities. B Rathod. anaemia remained an independent predictor of long-term adverse outcome (OR¼2. Information was entered at the time of procedure and outcome assessed by all-cause mortality information provided by the Office of National Statistics via the BCIS/ CCAD national audit.4% vs 13. staged revascularisation (SR group) and simultaneous treatment of non-IRA (CR group).2 vs 62. We therefore sought to clarify the outcome of patients with multi-vessel disease undergoing primary PCI dependent on management strategy.1136/heartjnl-2011-300198.0001). R Amersey. The anaemic cohort.7. p<0. Statistically significant changes in declining CHD mortality rates. A K Jain. previous PCI (13 vs 7%. L A McGill.1 to 3.4. p¼0.01. p¼0. p<0.19 Abstract 17 Figure 2 K S Rathod. Lastly the National figures on mortality from CHD are shown to be misleading as many people are still dying from CHD just when they have crossed the 75-year old exclusion criteria. There is limited data looking at the impact of baseline Haemoglobin and long term outcome after primary PCI.01). p<0. London Chest Hospital NHS Trust. 1 (1%) in the SR group and 35 (5%) in the COR group.18 K R Rathod. Patients were split into three different treatment groups: culprit vessel angioplasty-only (COR group). Results There were 963 (45%) consecutive patients with STEMI and multivessel CAD undergoing primary angioplasty. At 30-days of follow-up. hypertension (42 vs 35%. Abstract 18 Figure 1 All cause mortality after PCI for STEMI. and previous MI (23% vs 12%.1136/heartjnl-2011-300198. D A Jones. London. V S Rathod. had higher incidence of diabetes (27% vs 15%. 95% CI¼1.007). p<0.5%. C Knight.BCS Abstracts 2011 slowing dramatically from 2006 to 2008. See Abstract 18 Heart June 2011 Vol 97 Suppl 1 Background Multi-vessel disease occurs in 40%e65% of patients undergoing Primary PCI for STEMI and is associated with adverse prognosis. Results 471 (20%) patients were anaemic at presentation. p<0. A Mathur. JoinPoint regression analysis of different age groups demonstrates that the slower rate of decline from 2006 may be due to stubbornly high numbers of deaths in the 35e44 age group. Anaemia was defined according to WHO definition of Hb greater than or equal to 12 g/dl for females and 13 g/dl for males. which was significantly higher in the complete revascularisation group. figure 1. London. Contemporary guidelines recommend treating the infarct related artery alone (culprit) during the urgent procedure.0001).4. defined as death. were older (72. This trend continued A15 . There is limited data comparing outcomes of complete with infarct-related artery (IRA)-only revascularisation in primary PCI for STEMI with few studies including the option of later date elective procedures for the other lesions (staged revascularisation). and that the overall trend may be eventually be reversed. Patients with previous CABG were excluded. This risk increases further in population receiving RBC transfusions during index hospitalisation. Information was entered at the time of procedure and outcome assessed by all-cause mortality information provided by the Office of National Statistics via the BCIS/CCAD national audit. myocardial infarction (MI). stroke and target vessel revascularisation (TVR). There were similar incidences of three-vessel disease and cardiogenic shock. E Sammut. A Wragg. Methods Clinical information was analysed from a prospective data base on 2131 STEMI patients who underwent Primary PCI between January 2004 and May 2010 at a London centre.

1J Christie.20 Abstract 19 Table 1 COR N[638 Age Gender (female) Ethnicity (Caucasian) Previous MI Previous CABG Previous PCI Diabetes Mellitus Hypertension Hypercholestrolaemia GPIIb/IIIa Inhibitor Cardiogenic Shock 64. See Abstract figure 2. Southampton. might influence treatment decisions. Golden Jubilee National Hospital.0%) 93 (93. UK. these findings raise the question as to whether AAinduced clotting is an appropriate test of aspirin sensitivity.0511 0. Southampton.0114 0. 1H Gray. We investigated the effect of withdrawing clopidogrel in DES patients using a simple. Our results also confirm s-TEG as a plausible candidate for near-patient platelet function testing in this field. 1A Hobson. rapid.6%) 129 (19.7751 0. The aim of our study was to determine whether measurement of coronary pressure derived fractional flow reserve (FFR). UK. A16 Introduction Non-ST elevation acute myocardial infarction (NSTEMI) is the most common form of acute coronary syndrome and has a relatively poor prognosis. See Abstract figure 1. compared to coronary angiography alone. London.6%) 231 (89. However after 3 years MACE rates are significantly increased in the COR group (24%) but were similar in the CR (18%) and SR (17%) groups.6%) 312 (48.6%) 15 (2. 20 WHAT HAPPENS TO PLATELET FUNCTION AND VASCULAR INFLAMMATION WHEN CLOPIDOGREL IS WITHDRAWN? INSIGHTS USING SHORT THROMBELASTOGRAPHY doi:10.77 156 (23.0%) 40 (40. the aetiology of which is poorly understood.7%) 29 (4.0%) 2 (2.0001 N Sambu. platelet reactivity was determined using s-TEG and thromboxane (TX) B2.0%) 16 (16.8%) 91 (41.0%) 11 (11. Heart June 2011 Vol 97 Suppl 1 . 1N Curzen.0%) 109 (16.3%) 83 (12. 3The William Harvey Research Institute.0%) 5 (5. 48 h.5%) 572 (87. UK. and (ii) an unexpected and significant rise in AA-induced platelet aggregation.7%) 55 (20.0%) CR N[263 64. Abstract 19 Figure 1 disease.5%) 31 (12.5231 0.0%) 2 (2. S Corbett.0%) 79 (79.8%) 36 (13.7%) 441 (67. P Leadbeater. School of Medicine. UK Abstract 19 Figure 2 Breakdown of MACE at 5 years. Glasgow. 2J Norrie. As well as potentially helping to explain the observed clustering of ST events early after clopidogrel withdrawal.7%) SR N[100 61. 2Robertson Centre for Biostatistics.1%) 269 (41. 1F Foo. 1Southampton University Hospitals NHS Trust. 1C Berry. 2University of Southampton. in particular stent thrombosis (ST) has been observed following clopidogrel cessation 1-year after drug-eluting stenting (DES). Glasgow.1136/heartjnl-2011-300198.1136/heartjnl-2011-300198. 2 and 4 weeks post clopidogrel cessation.0%) 37 (37.26%) Significance 0.1724 p<0.9%) 185 (69. CD40 ligand and high sensitivity CRP were measured. Methods 33 patients on aspirin and due to stop clopidogrel at 1 year following DES were investigated. At all time-points. 1M Behan. 1I Simpson. N Englyst.BCS Abstracts 2011 up to 1-year of follow-up with the lowest rates of events in the SR group. Venesection was performed at (i) 4 weeks and 24 h pre clopidogrel cessation (ii) 24 h.031 0. MACE rates were driven mainly by death in the CR with high rates of TVR in the COR and SR groups.21 1 D Carrick. Results Clopidogrel cessation produced (i) a predictable increase in ADP-induced platelet aggregation. 1Department of Cardiology. 1A Calver. 1.2%) 92 (41.144 0. University of Glasgow.32 74 (27.1%) 23 (8.6%) 3 (1. T Warner. Abstract 20 Figure 1 Conclusion We have described for the first time an aspirin-independent increase in AA-induced clotting following clopidogrel withdrawal in DES patients. 1K Oldroyd. Conclusions Culprit vessel-only angioplasty was associated with the highest rate of long-term MACE compared with multivessel treatment. Patients scheduled for staged revascularisation experienced a similar rate of MACE to patients undergoing complete simultaneous treatment of non-IRA. H Dent. reproducible nearpatient platelet function test known as short Thrombelastography (s-TEG) that has been developed and validated by this group. Barts and the London School of Medicine and Dentistry. UK 1 1 2 3 2 3 Introduction A clustering of adverse events. Visual interpretation of the coronary angiogram is the standard approach to guide treatment decisions in patients with recent acute NSTEMI.1205 0. TXB2 was consistently suppressed confirming inhibition of COX by aspirin. Comparison of MACE between multivessel 21 INFLUENCE OF FRACTIONAL FLOW RESERVE MEASUREMENT ON TREATMENT-DECISIONS IN PATIENTS WITH RECENT ACUTE NON-ST ELEVATION MYOCARDIAL INFARCTION doi:10.2414 0.46 13 (13.5932 0. IL-6.

Methods We studied 94 patients with ACS admitted to a single UK Teaching Hospital for PCI. 2The Royal London Hospital. This approach should help to expedite early. The FFR results were then disclosed and the initial management decision was reviewed in light of the FFR result and changed as appropriate. Conclusion In our hospital about 1 in 20 NSTEMI had a coronary pressure wire study because of diagnostic uncertainty based on coronary angiography alone. and an impact on length of hospital stay is inevitable.1136/heartjnl-2011-300198. UK. 2M M Yaqoob. 15%.001). 50% and 62% of patients (p<0.1136/heartjnl-2011-300198. The proportion of patients allocated to each treatment group differed between the 2nd and 3rd Cardiologist (p¼0. 60%.22 A C Qureshi. UK. 7% and 5%. safe hospital discharge following PCI. 100 (6.05). 2Division of Biostatistics. R Rampat. PCI. Definitions The clinical indication for FFR measurement was the presence of an intermediate coronary stenosis (50%e75% of the reference vessel diameter) which resulted in diagnostic and treatment uncertainty. The London Chest Hospital. Contrast dose was similar in the CIN and non-CIN group (p¼0. M Roughton. UK 1 1 2 3 4 I R Pearson. FFR measurement was used to provide functional information on lesion severity and an FFR <0. the FFR resulted in a change in management in at least half of the patients. This occurs in approximately one third of procedures and has been shown to impact negatively on prognosis. U M Sivananthan. Results Baseline characteristics are summarised in table 1.80 was taken to represent a flow-limiting stenosis. or deferred management. UK 1 1 1 2 Background It is known that PCI can cause myocardial injury leading to the release of cardiac biomarkers into the circulation (procedural MI). Endpoint assessment consisted of one of the following three events (i) PC-induced MI (ii) readmission with MI by 6 months (iii) death by 6 months.8%) developed CIN. Of the new decisions made following FFR disclosure. C P Gale. Comparison of specificity and sensitivity of each biomarker for adverse cardiac events was made.249). Leeds. PCI 64%. 116 patients underwent coronary angiography and 92 underwent PCI. The treatment decisions for each cardiologist were: medical therapy 7%. CABG/MDT. University of Leeds. Abstract 22 Figure 1 23 SERUM NGAL IDENTIFIES CONTRAST NEPHROPATHY EARLY IN PATIENTS WITH DIABETES MELLITUS AND CHRONIC KIDNEY DISEASE UNDERGOING CORONARY ANGIOGRAPHY AND ANGIOPLASTY doi:10. Heart June 2011 Vol 97 Suppl 1 Background The incidence of contrast nephropathy (CIN) following coronary angiography or percutaneous coronary intervention (PCI) in patients with diabetes mellitus (DM) may be up to 30% and is associated with increased long term morbidity and mortality. 1%. In NSTEMI patients selected for FFR measurement. 70%. S M Harwood.23 22 COMPARISON OF 4-H HEART FATTY ACID BINDING PROTEIN WITH 12-H TROPONIN I TO ASSESS 6-MONTH RISK FOLLOWING PERCUTANEOUS CORONARY INTERVENTION IN ACUTE CORONARY SYNDROMES doi:10. whereas the proportion of patients allocated to deferred management or multivessel PCI decreased by 16%. Following FFR disclosure. The use of TnI to screen for procedural MI requires a wait of 12-h post procedure before the blood sample may be taken.BCS Abstracts 2011 Setting The cardiac catheterisation laboratory in a regional heart centre in the UK. although not yet standard practice.5 mmol/l. is increasingly undertaken as a measure of quality control. Methods We recruited 208 consecutive patients undergoing elective or urgent coronary angiography or PCI with known DM and chronic kidney disease (CKD) (defined as eGFR <60 ml/min). 1A S Hall. Results Of 1621 acute NSTEMI patients (January 2009eMarch 2010) in our hospital.02). Barts and The London NHS Trust. Hypothesis H-FABP at 4 h provides equivalent prognostic information to TnI at 12 h following PCI-induced myocardial injury. 8%. London. each cardiologist changed his/her treatment decision in 58%. London. 10%. the proportion of patients allocated to medical therapy increased by 26%. Barts and The London NHS Trust. These results support further studies of the clinical utility and prognostic implications of FFR measurement in patients with NSTEMI. 1Leeds Teaching Hospitals. Results The area under the receiver operator curve was 0. 8%.05).72 for TnI measured as 12 h.2%) had FFR recorded. 12%. made a decision for medical therapy. Heart-type Fatty Acid Binding Protein (H-FABP) is a small protein released rapidly and in large quantities from the myocardium into the circulation. J H Barth. respectively (all p<0. deferred management 16%. 3The William Harvey Research Institute. We evaluated serum and urine neutrophil gelatinase-associated lipocalin (NGAL) and albuminuria for additional information about CIN risk. Severity of coronary disease was assessed using the SYNTAX Score and risk of CIN using the Mehran risk score. The Mehran risk score was strongly A17 . 39 patients (18. UK. Methods The study involved three accredited interventional cardiologists and a study coordinator. and may be a factor when deciding time of discharge from hospital following the procedure. CABG/MDT 13%. 24% and by 5%. UK. both during ischaemia and following necrosis. N-acetylcysteine and intravenous hydration were given to all patients with eGFR <50 ml in accordance with local guidelines. Leeds. London. 19% and 29%. Monitoring for procedural MI. 24%). 4The Royal College of Physicians. The number of patients in whom the treatment decisions made by each cardiologist independently conformed (and so represented a consensus in at least 2 of the 3 decisions) increased from 74% to 92% as a result of FFR disclosure (p<0. 1A Kapur.73 for H-FABP measured at 4 h as compared to 0. CIN was defined as a post procedure rise in creatinine at day 3 of >25% from baseline or an absolute rise of 44. It allows detection of myocardial injury associated with PCI earlier than with TnI. London. FFR use increased the proportion of patients in whom treatment decisions conformed suggesting FFR use may also help to reduce the variation in treatment decisions using angiography alone. We used the Randox Cardiac-Array to measure H-FABP at 4 hrs after PCI and troponin I at 12 h after PCI. The cardiologists separately reviewed the coronary angiograms and together with the clinical history. Conclusion Early assessment of PCI-induced myocardial injury using the Randox Cardiac-Array to measure H-FABP is as sensitive and specific for adverse prognosis as is TnI measurement taken at 12 h post PCI.

076). Conclusion In selected patients Mitraclip edge-to-edge repair successfully reduces the severity of mitral regurgitation and improves symptoms.6) 84 (49.24 J Dungu. 10 patients (59%) had a reduction in MR to # grade 2+ and 8 patients (47%) had $2 grade reduction in MR (p¼0. (mean. NYHA class reduced significantly following intervention.8) 37 (97. The SYNTAX score did not differ between those who did or did not develop CIN (p¼0. SD) 70.75 0. Mitral regurgitation was graded by colour Doppler alone following intervention as standard quantitative analyses are not validated in the presence of a Mitraclip. Further studies are needed to examine whether these results are durable and associated with improved outcome.and 3-Dimensional TOE and fluoroscopic guidance.03) and this persisted at 4 h (p¼0. p¼0.2 (6. ischaemic MR in 7 patients (29%) and degenerative MR in 7 patients (29%).635) predicted development of CIN. Urine NGAL levels did not change significantly during the first 24 h. The reduction in MR grade remained significant for the 8 patients with echo data at 6-month follow-up (p¼0.6) 29. London.5) 19 (50.BCS Abstracts 2011 predictive of CIN development (p<0. p¼0.007) and 12e24 h (p¼0.7) 28. Hammersmith Hospital. Neither the SYNTAX score.038). The indication for intervention was functional MR in 10 patients (42%).54 Conclusions The current gold standard for measuring CIN is a rise in serum creatinine but this is of limited value as it does not increase until 48e72 h post renal injury.0) 7 (18.35 0. At 1-month A18 Abstract Figure 1 Change in MR grade post-Mitraclip. (mean. The Mitraclip device was deployed under 2. Imperial College London. Methods Patients were screened with transthoracic (TTE) and transoesophageal echocardiography (TOE). M F Bellamy. Twenty-four patients with $ grade 3+ symptomatic MR underwent percutaneous mitral valve repair under general anaesthesia between February 2009 and October 2010.78 0. There were no vascular complications or strokes. Results Mitraclip therapy was attempted in 24 patients aged 71611 years with an average Euroscore of 16%.1) 96 (55. All patients were discussed with the manufacturing company (Evalve) and in a multidisciplinary meeting including >2 cardiologists and 2 cardiothoracic surgeons with a special interest in mitral valve surgery prior to being accepted.5 (9.5) 155 (91.1136/heartjnl-2011-300198. There was no significant change in left ventricular size following intervention.8 (8.6 (5. Abstract Figure 2 Change in NYHA class post-Mitraclip.7) 165 (97.4) 15 (39.96 0. Abstract 23 Table 1 No CIN outcome (n[169) Age. UK Introduction Percutaneous mitral valve repair using the transcatheter Mitraclip device is a novel therapy for patients with severe mitral regurgitation (MR) who are too high risk for conventional surgery.4) CIN outcome (n[39) 71. SD) Hypertension (%) Hyperlipidaemia (%) Previous MI (%) Ex or current smoker (%) Heart failure (%) Valvular heart disease (%) Family history IHD (%) BMI.92 0. There was 1 procedural death due to leaflet tear in a patient with end-stage ischaemic cardiomyopathy and a grossly dilated left ventricle.1) 28 (16. 24 PERCUTANEOUS MITRAL VALVE REPAIR WITH THE MITRACLIP DEVICE: A TERTIARY CARDIAC UK EXPERIENCE doi:10.6) 66 (39. A rise in serum NGAL levels within the first 12 h following coronary angiography or PCI appears to be a very promising marker in the early diagnosis of CIN.149) or protein:creatinine ratio (p¼0.001).5) 33 (86. Fifteen patients (75%) had 2 clips deployed. 63% of patients were in NYHA class III/IV.102. We were unable to grasp the mitral valve leaflets in 2 patients due to an excessive coaptation gap. nor urinary albuminuria or proteinuria are predictive of CIN development.9) 32 (19. A significant rise in serum NGAL was seen as early as 2 h post procedure in the CIN arm (p¼0. One patient had persistent grade 3+ MR at 1-month follow-up due to late partial detachment of one of the 2 clips deployed. All patients (100%) treated with the Mitraclip had severe MR (grade 3 +/4+) prior to intervention. end systolic volume 92 vs 79 ml. although there was a trend towards reduced left ventricular volumes at 1-month follow-up (end diastolic volume 175 vs 160 ml.4) 7 (18. Neither albumin:creatinine ratio (p¼0.001).188).4) 20 (52. At 1-month follow-up postMitraclip only one patient (4%) was in NYHA class III (p¼0.64 0. We report the largest UK series to date. Heart June 2011 Vol 97 Suppl 1 . C S R Baker. Prior to Mitraclip.042) and 15 patients (83%) had at least 1 grade reduction in NYHA class. Mitral regurgitation was graded by British Society of Echocardiography criteria. follow-up to date.93 0.74 0.0015). Twenty patients had successful deployment of the Mitraclip device (83%).1) p Value 0.

6760.825 33.4%) 37 (52.9) 11 (15. J Cotton. Group 1 mortality was 30% and in group 2 was 17.778 0.9 days. with 10 (6.3%) 12 (12. Conclusions Overall TAVI operators are exposed to significantly higher radiation doses compared to PCI and ICD operators. The radiation dose TAVI operators are exposed to is not widely known.9 23. The six TAVI procedures performed via the transfemoral approach used only two operators.9%) 47 (48.2%) 46.5 16 (22.110 0.780 0. saphenous vein graft (SVG) to LAD (n¼1) and SVG to circumflex (n¼1).2 47.5 p Value <0. A Maher.8623. Results In total. Heart and Lung Centre.6%) 17 (17. Operator specific radiation doses were obtained from a central RRPPS Approved Dosimetry Service. UK. 1M Thomas. Wolverhampton.3% (p¼0. proximal left anterior descending artery (LAD) (n¼5). right finger (RF) and forehead.791 0. p¼0.09611.1614.95 0.5 27 (27.0%) undergoing PCI prior to their procedure.2%) p Value 0. subclavian TAVI operators have an unexpectedly higher dose (p¼0.6%) 12 (12. Method Ten TAVIs were performed.2 vs 4.7%. The end-point was all-cause mortality. There were no significant differences in either the baseline characteristics or access approach between the two groups (Abstract 26 tables 1 and 2). and percutaneous coronary intervention (PCI). Radiation protection was employed in all cases using standard lead skirts and screens. Introduction Patients undergoing surgical aortic valve replacement (sAVR) routinely undergo simultaneous coronary artery bypass grafting (CABG) for significant coronary artery disease (CAD) due to adverse prognostic impact.768. C Douglas-Hill.4 0.4627.0* 196.18 ±SD 1.9%) Group 2 No significant CAD (n[98) 81. TAVI and ICD operator doses were compared to the mean standardised PCI operator dose.1%) Group 2 No significant CAD (n[98) 29 (41. Additional radiation protection for TAVI operators is strongly advocated.03 0. 8 had single vessel intervention and 2 had PCI to 2 vessels. implantable cardiac defibrillators (ICD).14 p value Abstract 26 Table 2 Group 1 Significant CAD (n[70) Transfemoral 44 (44. 2H Haran.53 1. Despite the use of standard radiation protection measures. The third operator was a surgeon who was nearest to the x-ray images.01 PCI 3.67 2.96y ICD 3.20 18 (25.26 11. ySignificantly increased radiation exposure dose in TAVI procedures compared to ICD and PCI. 1S Redwood. Among those patients who underwent PCI in Group 1. During each procedure the radiation dose exposure was monitored for each operator using ThermoLuscent Dosemeters (TLD) on the left finger (LF). The target vessels were left main stem (LMS) (n¼2). using the same type of TLDs on LF and RF. 1K Wilson. 1J Hancock.658 0. R Singh. London. C Young. right coronary artery (RCA) (n¼2). Abstract 25 Table 2 Mean radiation dose (Gy/cmq) per operator Trans-femoral TAVI Subclavian TAVI ICD PCI 1.23 3.399 0. 1Guy’s & St. New Cross Hospital. the overall mortality was 22.5616.8611.008y Logistic Euroscore (%6SD) LV ejection fraction (%6SD) Aortic valve area (cm26SD) Previous CABG Previous PCI *Significantly increased radiation exposure time in TAVI procedures compared to ICD and PCI. Radiation exposure doses were also collected from ICD and PCI operators during the same period. S Khogali. They were divided into two groups according to the results of the pre-TAVI coronary angiogram: (Group 1) patients with $1 coronary stenosis of $70% severity and those without (Group 2).36 Transapical Transaortic Conclusion The presence of significant CAD had no significant impact upon the all-cause mortality of patients after TAVI in our Heart June 2011 Vol 97 Suppl 1 A19 .9 48.1 vs 12. in TAVI. London.4%) 48. While manufacturers advise percutaneous intervention (PCI) of significant CAD prior to transcatheter aortic valve implantation (TAVI) there is considerable variation among operators.25 M Drury-Smith.1136/heartjnl-2011-300198.5612. Thomas Hospital. circumflex (n¼1). 6 via the trans-femoral route and 4 via the subclavian approach.09 0.001* 0.7%) 16 (22.0369. Abstract 26 Table 1 Group 1 Significant CAD (n[70) Age (years6SD) Diabetes Mellitus Cerebrovascular disease Peripheral vascular disease Glomerular filtration rate 83.685 0.8613. We are currently evaluating the impact of using a RADPAD as additional protection during TAVI procedures. 1L Clack. 1K Macgillivray. 70 patients (41. UK 1 1 26 THE EFFECTS OF PRE-EXISTING SIGNIFICANT CORONARY ARTERY DISEASE UPON OUTCOME AFTER TRANSCATHETER AORTIC VALVE IMPLANTATION USING THE EDWARDS BIOPROSTHESIS doi:10.767. p¼0.928). 1V Bapat. PCI and ICD.6%. p¼0. the mean dose to operators undertaking TAVI was 6 times higher than the trans-femoral PCI operator (p¼0. but it is an important consideration in view of the increasing volume of procedures and the potential risks of over-exposure.BCS Abstracts 2011 25 TAVI OPERATOR RADIATION DOSE COMPARED TO PCI AND ICD OPERATORS: DO WE NEED ADDITIONAL RADIATION PROTECTION FOR TRANS-CATHETER STRUCTURAL HEART INTERVENTIONS doi:10.219 0. PCI was considered a standard trans-catheter procedure. Thomas’ Hospitals NHS Foundation Trust.03).9612.22 27 (27.03 0.6610.1 21. dose. London. The mean radiation exposure time of TAVI was seven times more than PCI. and individual operator dose. UK Introduction Trans-catheter cardiac aortic valve implantation (TAVI).256150. 2King’s College School Of Medicine & Dentristry. Although subclavian TAVI and ICD procedures were expected to be comparable with respect to operator dose.03 0.0%) 7 (7.766.7%) 15 (21.070 Abstract 25 Table 1 Variable Mean exposure Time (mins) Mean exposure Dose (Gy/cmq) 6 SD TAVI 27. 1I Nadra. Results The mean exposure times and doses for the different types of trans-catheter procedures performed are detailed in the tables below. Radiation dose exposure is cumulative and if above the recommended annual levels may have significant consequences for the operator. are common procedures associated with radiation exposure to the operator and the patient. Methods We performed a retrospective analysis of 168 patients who underwent TAVI using the Edwards bioprosthesis from March 2008 to October 2010 at St.7%) p value 0.1136/heartjnl-2011-300198. M Bhabra.3 0.008).112 0.492 0. Mortality in this sub-group was not significantly different from the CAD patients who did not receive PCI (50% vs 26.462) nor in the number of days to discharge (12. radiation exposure time.272). Our aim was to monitor and compare. while the subclavian approach involved three operators.7%) had significant CAD prior to TAVI.6360. At a mean follow-up of 3356277 days (mean6SD).9%) 4 (5.26 M Z Khawaja.124) (see Abstract 26 figure 1) There was no difference seen in the length of stay in the intensive care unit (2.

During coronary angioplasty 47% of radiation dose is related to screening at standard Heart June 2011 Vol 97 Suppl 1 . in conjunction with adhesion molecule expression. During ACS platelet and monocyte derived chemokines.8) compared with the stable angina patients (Mean (SD) 21.7 (5. PMAs correlate with measured microvascular dysfunction during PCI in stable angina and NSTEMI.3) p¼0. B Majumder.07). inflammation and microvascular dysfunction in coronary disease. promote the inflammatory process.4) p¼0.6)) compared with patients with stable angina (Mean (SD) 20. Activated platelets express p-selectin which binds to the pselectin glycoprotein ligand on the monocyte forming platelet monocyte aggregates (PMA). UK 1 1 2 1 Introduction Minimisation of radiation exposure during cardiac procedures is required by statute (IRMER 2000). Aim To investigate the relationship between microvascular dysfunction and PMA expression in patients with stable angina and non-ST elevation myocardial infarction (NSTEMI). in the presence of platelet activation. IMR was also higher in patients with NSTEMI (Mean (SD) 27. PMA expression is a sensitive marker of platelet activation and inflammation.28 S J Wilson. Exeter. O Gosling. UK.01) in NSTEMI but not in stable angina patients.02) Abstract 27 figure 1. PMAs were assessed using fluorescent monoclonal antibodies and flow cytometry. Blood samples were taken from the coronary artery (distal to the culprit lesion). CwP correlated positively with total PMA (p¼0. R D Rakhit. CD62+ PMAs were significantly higher in patients with NSTEMI (Mean (SD) 26.7 (5.1136/heartjnl-2011-300198. Royal Free Hospital.01). 27 PLATELET MONOCYTE AGGREGATES ARE DETERMINANTS OF MICROVASCULAR DYSFUNCTION DURING PERCUTANEOUS CORONARY INTERVENTION FOR STABLE ANGINA AND NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION doi:10. Microvascular dysfunction was assessed by measuring the coronary wedge pressure (CwP) and the index of Microvascular resistance (IMR) using a single pressure-temperature sensor-tipped coronary wire from the simultaneous measurement of distal coronary pressure and thermodilution derived mean transit time (Tmn) of a bolus of saline injected at room temperature into the coronary artery during maximum hyperaemia. A20 Abstract 27 Figure 2 Conclusions PMAs are elevated in stable coronary disease and ACS with elevated activated CD62+ PMA a hallmark of ACS. 2Royal Devon and Exeter Hospital. V Suresh. P Venables.27 Abstract 27 Figure 1 C A Mavroudis. As yet. the impact of PCI to significant CAD upon outcome after TAVI is not known and will be assessed in a prospective. UK. aorta and the right atrium for PMA estimation.BCS Abstracts 2011 Results As expected CwP was higher in patients with NSTEMI (46. London.1) p¼0.9 (4.8)) compared with stable angina (Mean (SD) 10.5 (SD) 18.2). Plymouth.1 (9. UK 1 1 2 1 Background Microvascular dysfunction is associated with adverse outcome in patients with acute coronary syndrome (ACS). 2Haematology Department. randomised controlled trial currently underway.08) Abstract 27 figure 2. Methods Six patients with stable angina undergoing elective PCI and six patients with NSTEMI undergoing non-elective PCI were recruited. London. 1South West Cardiothoracic Centre. M Lowdell. Royal Free Hospital.2)) compared with stable angina (Mean (SD) 13. activated (CD62+ PMA) may be directly involved in the pathophysiology of intracoronary inflammation and microvascular dysfunction in ACS. Although platelet monocyte interaction is a normal physiological process.9 (12. Total PMAs were calculated and expressed as a percentage of the total monocyte count. GIVES GOOD IMAGE QUALITY WITHOUT AFFECTING PATIENT OUTCOME doi:10. Activated CD62+ PMAs were expressed as a percentage of total PMAs.1136/heartjnl-2011-300198. Total PMAs were nonsignificantly higher in patients with NSTEMI (Mean (SD) 14 (4. 1Cardiology Department.6 (12. However. Abstract 26 Figure 1 study. IMR correlated positively with total PMAs in both stable angina (p¼0.3) p¼0. 28 LOW FRAME RATE SCREENING DURING PERCUTANEOUS CORONARY ANGIOPLASTY SIGNIFICANTLY REDUCES RADIATION EXPOSURE. This study supports the hypothesis that PMA formation may be important determinants of platelet activation.02) and NSTEMI (p¼0.

5 frames per second).01 Total DAP (mGycm2) 60746. < Age < Weight (Kg) < Height (cm) Radiation data: 29 < < < < Screening DAP (mGycm2) Total DAP (mGycm2) Total Fluoroscopy time (mm:ss) Number of acquisition runs Operator outcome: BIVALIRUDIN IN PATIENTS UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ACUTE ST-ELEVATION MYOCARDIAL INFARCTION: OUTCOMES IN A LARGE REAL-WORLD UK POPULATION doi:10. Additional heparin was not routinely given. The screening Abstract 28 Figure 1 Heart June 2011 Vol 97 Suppl 1 Background The HORIZONS-AMI trial demonstrated a significantly lower early and late mortality in patients undergoing primary PCI (PPCI) treated with bivalirudin compared to a Glycoprotein IIb/ IIIa inhibitor (GPI) + heparin. and GPI + heparin in 85 (8.5 frames per second) reduced radiation without affecting patient outcomes. See Abstract 28 table 1 and graph.3%). 1A Liu. review of hospital notes. 13. Bivalirudin was given in 882 patients (91. Cyprus < 30 day incidence of major adverse cardiovascular event (MACE): death. with no requirement for increased screening frame rate. Audit data from procedures performed at standard frame rate with the same inclusion criteria were used as a control group.5 fps) Mean DAP reduction Significance 28564. stroke. the apparently worse outcomes in the absence of additional pre-procedural heparin. Screening and Total DAPs (mean mGycm2) were 33% and 16% lower respectively in the low frame rate group. Weight was similar in both groups (83 kg vs 82 kg).4 À16% n/s Fluoro time (seconds) 770 800 e n/s Number of acquisitions 26. The frame rate could be increased at the operator’s request. but was favoured by some operators. However. 2Statistical service of Cyprus. 71. Leeds.3%) also received heparin (29 pre-PCI and 80 during) while bail-out GPI was used in 91 (10. This study assessed whether low frame rate screening (7. and the translation of trial results into a real-world population. 1S B Wheatcroft. We suggest that centres currently using 15 frames per second screening should undertake a similar assessment in order to minimise radiation. and telephone follow-up. We included elective. procedural.5 19248. non-fatal myocardial infarction or need for urgent revascularisation. with 2 MACE events (2%) in the control group.9% male. Nicosia. Results 55 consecutive studies were examined at low-frame rate and compared with the audit control group (n¼105). Demographic. All-cause mortality was 5. MACE (death. No safety concerns were reported. Statistical comparison was made with the Man-Whitney U-test. Primary endpoints were death. This showed a significant reduction in the Screening DAP (p#0. J M McLenachan. Phillips Allura flat plate XPER FD10 catheterisation equipment was used. In the screening group there was 1 MACE event at 30 days (2%). Data collection Patient data: times and number of acquisition runs were similar in each group. and stent thrombosis (ST) (ARC definition definite/probable) at 30-days follow-up. we now demonstrate that low frame rate screening coronary angioplasty is also safe. 1D Barmby.8%). 1 Leeds General Infirmary. Of bivalirudin-treated patients 100 (11. concerns remain regarding the increased incidence of acute stent thrombosis (ST) with bivalirudin. 1D J Blackman.1136/heartjnl-2011-300198. and low-dose infusion for 4 h post-PCI.29 1 1 < Need to increase screening frame rate Patient outcome: C Eftychiou. Bivalirudin was administered as a bolus.7 26. re-infarction. and 30day outcome data were obtained by abstraction from the ONS mortality database and BCIS PCI database.5613 years. 30-day incidence of major adverse cardiovascular events (MACE) was similar in both groups.0%. Methods All patients who underwent PPCI in Leeds General Infirmary from 1 January 2009 to 31 December 2009 were prospectively entered into a dedicated registry. Method We prospectively collected data from consecutive coronary angioplasty procedures performed at reduced screening frame rate (7.1%). Having shown that low frame rate screening for coronary angiography gives good imaging quality and is safe. high-dose intra-procedural infusion.2% in the bivalirudin treated patients. Low frame rate screening should be standard practice where modern facilities allow. In every case image quality was acceptable. Radiation exposure from screening is significantly reduced by 33% and total exposure is reduced by 16%. a median of 2 h post-PCI. and any safety concerns were reported immediately. unplanned target vessel revascularisation (TVR)). Acute SToccurred in 1. UK.8 e n/s frame rate (15 frames per second). Thirty-day outcomes are shown in Abstract 29 table 1. urgent and emergency procedures. Bail-out GPI was administered according to physician judgement. 1J M Blaxill.BCS Abstracts 2011 Abstract 28 Table 1 Screening DAP (mGycm2) Standard (15 fps) Low (7. 2L Makri. 1J P Greenwood.9 50953. Conclusions Low frame rate screening is a practical way of reducing radiation exposure in line with the ALARA “As Low As Reasonably Acheivable” principle.01) with low frame rate screening. 1R J Shelton. 1K Somers. Results 968 patients (age 63.5 À33% p<0. 1P Tooze. and within 6 h in 90%. Mortality in A21 . Mean age was 67 in the low screening rate group and 65 in the control group. Digital fluoroscopic technology has improved imaging making the use of lower frame rates feasible.2% diabetics) underwent PPCI. We evaluated the outcomes of patients undergoing PPCI with bivalirudin in a large all-comers UK setting.

53 respectively). 0. re-infarction. all other outcomes were similar.277 0.0%.4%) 100 (11.80. p¼0. MACE 14.1 1. We used Fisher9 s exact test to compare clinical outcomes between the groups. Grp 2.8%) Acute stent thrombosis 10 (1. Continuous data are presented as mean6 SD. UK Introduction Primary percutaneous coronary intervention (PPCI) has been established as a standard therapy for ST elevation myocardial infarction (STEMI).0% vs 5.2 6. The Essex Cardiothoracic Centre.8 3. Bivalirudin is shown to be superior to abciximab in reducing the net adverse clinical events and major bleeding in STEMI in the HORIZONS-AMI trial (Stone et al NEJM.4%) 14 (1. 2St Michaels Hospital. Abstract 30 Table 2 30 COMPARISON OF BIVALIRUDIN VS ABCIXIMAB VS “UNFRACTIONATED HEPARIN ONLY” FOR PRIMARY PERCUTANEOUS CORONARY INTERVENTION IN A HIGHVOLUME CENTRE doi:10. Canada Objective To assess the role of CMR in the treatment of true chronic total occlusions (CTO) with percutaneous coronary intervention (PCI) and drug eluting stent implantation.BCS Abstracts 2011 patients who suffered acute ST was 20%.8 1. Canada. Mortality data were obtained from the summary care record (SCR) database. Clinical outcomes are shown in Abstract 30 table 2.04).8%. J Davies.0%) 9 (1. 3University of Toronto. N Malik.5 4.Bivairudin+UFH and Grp 3. Ontorio.“UFH only”). p¼0.2 (30e96) 66. p¼0.4%) 2 (2. 3G A Wright. Patient demographics and procedural information are given in Abstract 30 table 1.6 0.1%) 54 (6.6%) 13 (1.7 12.9 89. p¼1.0% vs 10.4%) No.1 5. After excluding patients who had both bivalirudin and abciximab during their procedure (n¼15). The “UFH only” group had similar outcomes to both bivalirudin and abciximab.4 28 Bivalirudin + UFH (n[162) 65613. p¼0.2 6.6% vs none. p value: 0. thrombus burden in STEMI may require use of more potent antithrombotic agents. In addition to thrombectomy and unfractionated heparin (UFH).1%) 6 (7.8%. 2008).2 R Showkathali.7%) 16 (1.2%) 39 (4.8%) 882 46 (5. R Aggarwal.2% p¼0.4%) Conclusion Routine use of bivalirudin in a large UK all-comers primary PCI population was associated with excellent 30-day outcomes. Prospectively entered data were obtained from our dedicated cardiac service database system (Philips CVIS).4%) 2 (2.2 3. There was no difference in outcomes between bivalirudin treated patients who also received heparin compared to those who didn9 t (death 7.8 11. A22 Conclusion These “real-world” data do not show any significant difference in the clinical outcome for patients who had bivalirudin or abciximab.604 0.1 7.6% vs 3. Ontorio.1%.6% vs 0. However. our study is clearly limited by not being randomised and those patients treated with UFH alone may have been a lower risk group.2 0.5%) 2 (2. 1B H Strauss.8 Bivalirudin + UFH (n[162) 5.386 Age in yrs (range) Male (%) Diabetes (%) Pre-procedure cardiogenic shock (%) Drug eluting stent (at least one) (%) No of stents Single vessel PCI (%) Three vessel PCI (%) Radial procedure (%) Abciximab + UFH (n[346) 64614.9 91.2 56.61).5 1.460.645 0.31 1 G A Paul.8 4.3 2 31. 776 (77. There was no advantage seen with the more expensive agent (abciximab) in keeping with previous trial data. Methods Our PPCI service started in September 2009 and we included all patients undergoing PPCI between September 2009 and September 2010. Toronto. p: 0.8% vs 3. Both acute and 30 day stent thrombosis rates were also similar in the two groups (0. Basildon.2%) Subacute stent thrombosis 15 (1. stroke or TVR 110 (11. Results Of the 998 patients admitted with suspected STEMI to our unit during the study period.1%) Abstract 30 Table 1 0.4 2.1136/heartjnl-2011-300198.7%) 12 (1.0%) 1 (1.9%. Toronto.9 0. 2K Connelly.27).1%) 2 (2. despite the absence of routine additional heparin.Abciximab +UFH.3. Abstract 29 Table 1 Outcomes at 30 days All patients Bivalirudin GPI + heparin p value 85 6 (7. compared to 80% following subacute ST.450 0.5 0. Heart June 2011 Vol 97 Suppl 1 . In-hospital and 30-day mortality did not differ between patients who had bivalirudin vs abciximab (5.1 1. which suggests that this may be a viable alternative in its own right.4%) 45 (4. we divided the others (n¼761) into 3 groups according to the anti-thrombotic regime used (Grp 1.8% vs 5.7 53.5 UFH only (n[253) 67613.460.8 56.286 0.0 respectively). 1A J Dick. 31 ASSESSMENT OF LEFT VENTRICULAR FUNCTION WITH CARDIAC MRI AFTER PERCUTANEOUS CORONARY INTERVENTION FOR CHRONIC TOTAL OCCLUSION doi:10. Acute stent thrombosis was infrequent.2%) 56 (5.8 1. Ontorio. We aimed to carry out a “real world” comparison of different anti-thrombotic regimes in patients undergoing PPCI in our unit. The abciximab group had significantly higher major bleeding rates than the “UFH only” group (5.6 3. J Sayer.8% vs 2. of patients Death Cardiac death Re-infarction Unplanned TVR Stroke 968 52 (5.6%) 10 (1.4 7.3 1. This would have considerable economic benefits in the present situation.6 6. W Taggu.1 (25e99) 77.222 0.3%) 10 (11.9 26.8%) underwent PPCI. Canada.906 0.35 and 6. stent thromboses (acute and 30-day) and major bleeding.460. including all-cause and cardiac mortality. Even though the bleeding risk was higher in the abciximab group when compared with bivalirudin.4%.4 1. Toronto. There was also no difference in the outcomes between the bivalirudin and “UFH only” groups for mortality. this was not significant (5. 1Sunnybrook Health Sciences Centre.8 5. P Kelly.9 UFH only (n[253) 5.0 (31e94) 72.2 Death.1136/heartjnl-2011-300198.32.8 87 1. Therefore bivalirudin should be considered as a non-inferior alternative to abciximab. p value: 0.30 % In-hospital Mortality (including cardiogenic shock) 30 day Mortality (including cardiogenic shock) 30 day Mortality (excluding cardiogenic shock) Stent Thrombosis (within 30 days) Acute stent Thrombosis (24 h) # Major bleed requiring blood transfusion (non CABG related) Access related bleed requiring transfusion (includes IABP related) Abciximab + UFH (n[346) 3.2%.9 0 5. acute ST 0% vs 1.

0611. A23 . Technical success was defined as recanalisation of the occluded vessel and DES implantation with a final residual diameter stenosis <30%.8 6 19. n (%) RCA LAD LCx Prior MI. successful revascularisation was achieved.01) and with PCI-CTO failure (11.469. P H Loh. UK Abstract 31 Figure 1 Heart June 2011 Vol 97 Suppl 1 Introduction Chronic total occlusion (CTO) of coronary vessels is a relatively common finding on diagnostic angiography. can be used to help predict improvements in regional wall function. n (%) CCS Anginal Class LVEF/ % CTO duration.6 36.42 0. L Buchanan.89 0. CTO duration was greater in patients with failed revascularisation but other baseline demographics were well matched between groups (Abstract 31 table 1). Kingston upon Hull.001). Complete revascularisation was successfully achieved in 53. p<0. Results were analysed using SPSS statistics version 17.13 0.1 78.8 16 (53) 11 (37) 3 (10) 17 (59) 7 (23) 23 (77) CTO-PCI Success (n[19) 62.1.668.1360.8 619. Methods Thirty patients referred for PCI to a single vessel CTO underwent CMR examination prior to and 6 months after PCI. Mean duration of CTO was 29.1 7 (64) 4 (36) 0 6 (56) 2 (18) 9 (82) 0.5% (n¼177) patients.61 0. However.6 12.2160.32 N H Shah. Mean age was 56.35 DOES COMPLETE REVASCULARISATION CONFERS A LONG TERM SURVIVAL BENEFIT IN PATIENTS WITH CHRONICALLY OCCLUDED CORONARY VESSELS? doi:10.01 0. n (%) Hypertension 62. Methods We identified consecutive patients. Overall survival was relatively poor and emphasises the importance of optimal medical therapy in this cohort.3612. The transmural extent of infarction (TEI) was calculated by dividing the hyperenhanced area by the total area3100.1% vs 56. months Vessel. The TEI. while 46. PCI-CTO failure was not associated with increased MACE at medium-term follow-up. Results Technical success was achieved in 19 of the 30 patients (63%).5T GE MRI system.61 p value 0.2610.9670.6626. 32 Abstract 31 Table 1 Total (n[30) Age/ years Male. Both groups were age matched. on angiography performed between January 1999 and August 2000 in a single tertiary centre.09 0. p<0. J L Caplin.61 0. T Ungvari. Conclusion Complete revascularisation confers a significant long term survival in patients with CTO and underscores the importance of improved recanalisation rates when performing angioplasty in this patient group.3 years. Abstract 31 figure 1). LV function and infarct size were assessed using a 1.4 11 (100) 2.68 53. We used a dedicated database to record data on variables and used central National Health Service database to obtain survival data. Median follow-up duration was 10. Overall 10-year survival was 66.01. assessed with CMR.4 9 (47) 7 (37) 3 (16) 11 (58) 5 (26) 14 (74) CTO-PCI Failure (n[11) 61.1% were male and 21. long term survival data in this cohort is lacking. There were no episodes of MACE in either group at 21 months follow-up. There has been increasing interest in this clinically important area with development of technologies resulting in improved recanalisation rates.1136/heartjnl-2011-300198. p<0. Results We included 331 patients in the analysis. However most trials have included occlusions of short duration (less than 4 weeks).2 25 (83) 2. PCI-CTO success resulted in a significant increase in LVEF when compared to both baseline (50 6 13 vs 54 6 11.9 months and was only reliably estimated in 82.001.8 14 (74) 2. M F Alamgir.8% (n¼71) were diabetic.5%.8 years. In this study we assessed the impact of PCI on LV function in patients with true CTOs (TIMI flow grade 0 and greater than 12 weeks duration) using serial CMR imaging as well as the predictive value of late gadolinium enhancement when performed prior to revascularisation.63 50.BCS Abstracts 2011 Introduction Successful PCI for CTO may confer an improved prognosis and a reduction in major adverse cardiac events (MACE). 76.5% (n¼154) were either treated medically from the outset or had failed or incomplete revascularisation. R M Oliver.5% of cases.3 6 5. A Hoye. p<0. those with complete revascularisation had significantly improved survival over those with incomplete revascularisation or medical therapy (75. found to have CTO of at least one vessel of more than 1-month duration. S Thackray.8611. Segmental wall thickening (SWT) was measured within the perfusion territory of the CTO using the 16-segment model and segments were dysfunctional if the SWT was #45%. In dysfunctional but viable segments only PCI success conferred a significant improvement in SWT compared to baseline (26 6 6 vs 40 6 10.86101.0963. a score of #25% were considered viable.8 vs -2. Castle Hill Hospital.77 57. Abstract 31 figure 2).5625. n (%) Diabetes Mellitus.5%.060. Abstract 31 Figure 2 Conclusion PCI-CTO success of true CTOs can improve global LV function. In this study we looked at survival of patients in whom complete. M F Khan.

a modification of the Duke Jeopardy score to include LMS and CABG.00 to 1. Abstract 33 Table 2 Variables Cumulative survival according to Revascularisa- Univariate analysis HR (95% CI) 0.BCS Abstracts 2011 dysfunction.0001 0. A Kapur.20) 1.24 to 0.45 to 32.0001) (Abstract 33 table 2).661.78).002 0.26 (1.004 0.60 to 7.54).24 to 4.74 (1.08) 5.67) conferring a survival advantage in the medium term.33 K De Silva.33 to 6. B Clapp.14 to 1. Abstract 32 Figure 1 33 COMPLETENESS OF REVASCULARISATION PREDICTS MORTALITY FOLLOWING PERCUTANEOUS CORONARY INTERVENTION: UTILITY OF THE BCIS-1 JEOPARDY SCORE doi:10. is simple to use and overcomes many of these limitations.34 1 6 A Baumbach. Clinicians (who were blinded to clinical or outcome data) scored diagnostic and procedural coronary angiograms.81) 1.83 (0.30 (0. UK Introduction Many coronary-scoring systems are complicated to use on a day-to-day basis.34 to 3. We assessed the prognostic relevance of the BCIS-1 JS in patients undergoing percutaneous coronary intervention (PCI).39) 1.15 0.01 to 1.39 (0.69 to 11. D Perera. it can be used to assess the degree of revascularisation.58) 1.0 indicates full revascularisation and 0 indicates no revascularisation.0001 0. RI¼1.0001 Multivariate analysis HR (95% CI) 0.21 to 3. The primary end-point was all-cause mortality.54) 1.01 0. Over a follow-up period of 2. 2G Angelini.66) 2.10 Abstract 33 Table 1 Left Main Stem Disease classified Duke Jeopardy Score (Original) Syntax Score BCIS-1 JS x O O Patients with CABG classified x x O Ease of use O x O Relevance to contemporary PCI x O O Prognostic validation O O x Revascularisation Index (0.31 (1. 5R Hall. demonstrated that RI¼0.54) 1.88) 3. p¼0.25) p value 0. King’s College London. S Redwood.47 0.30) 14.51 (0.1136/heartjnl-2011-300198. S Kesavan.05 0.53 to 5. UK. a revascularisation index of $ 0.67 was associated with a survival advantage compared to a RI #0. p¼0.0001).82 (2.007 0. All-cause mortality was inversely related to baseline BCIS-1 JS (HR 2. Furthermore. Mortality data was captured by tracking the database of the UK Office of National statistics.78 (0.35 to 0. London.83 (0.97 (1. 44% presented as acute coronary syndromes with 41% having left ventricular A24 Conclusion The BCIS-1 Jeopardy Score predicts mortality following PCI.39) 1.002) and to post-PCI BCIS-1 JS (HR 3. with more complete revascularisation (RI$0.76 (2.1136/heartjnl-2011-300198. 1Bristol Heart Institute.33 to 0.14 (0.20 (1. have varying degrees of reproducibility and exclude important subsets of patients such as those with previous coronary artery bypass grafts (CABG) or left main stem (LMS) disease (Abstract 33 table 1).004) (Abstract 33 figure 1). Increasing degrees of revascularisation were associated with improved survival (Abstract 33 figure 1). Heart June 2011 Vol 97 Suppl 1 2 3 4 .88 to 3.0001 0. E Chong.82) p value 0. K Beatt. Abstract 33 Figure 1 tion Index (RI). St. 34 COMPARISON OF PCI VS CABG IN INSULIN TREATED AND NON-INSULIN TREATED DIABETIC PATIENTS IN THE CARDIA TRIAL doi:10. Results 660 patients were included (6869 years). Predictors of outcome were assessed by univariate and multivariate analyses. acuity of presentation.08) 3.0001 0.77 to 12.08 0.008 0.02) 1.24 to 0. P Sicard.62). UK.66 (HR 0.81. A multiple regression model. Bristol.24) 2.35 (1.23 to 1. p¼0. Patients were eligible if they had undergone assessment of left ventricular function before PCI and the sample was enriched for coronary artery bypass graft (CABG) cases by using the following weightingd1 CABG: 3 nonCABG.04 (1.65 to 2. A Indermeuhle.67e1 continued to be an independent predictor of survival (HR 0.0001 0.67e1) BCIS-1 JS pre PCI BCIS-1 JS post PCI LV impairment Age Renal dysfunction Acute coronary syndrome Cardiogenic shock Previous CABG Methods Consecutive patients undergoing PCI between 2005 and 2009 a single cardiac centre were screened.37) 1.04 (1. p¼0.56 (6. 4M Flather. M Thomas.48) 3.98 (2.0001 0.51 95% CI 0. The BCISd1 JS was recorded before and after PCI (range: 0 to 12) and a Revascularisation Index (RI) calculated as RI¼(JSPREdJSPOST)/JSPRE.35 (1. Thomas’ Hospital. The recently described BCIS-1 Myocardial Jeopardy score (BCIS-1 JS). E Cruddas.65 0.63 to 2.1 years there were 42 deaths. incorporating age. G Morton.93 to 3. Bristol.36 (0. 2Bristol Heart Institute.80 to 6. LV function and renal failure.

2 0. prior CABG 16. 36 IN-STENT RESTENOSIS PRESENTS AS AN ACUTE CORONARY SYNDROME (ACS) IN 40% OF CASES: NOT SIMPLY A BENIGN CLINICAL ENTITY doi:10.3 0.460. 6London Chest Hospital.6). 1C J Knight. L A McGill.760. risk factors for coronary artery disease appeared similar in the IT and NIT groups. Methods 508 patients with an established diagnosis of DM and de novo coronary artery disease were identified and randomised to CABG or PCI.5%) 416 (72.7%) 151 (26.35 J M Behar.1% (20) (p<0. Stroke.18 to 5.47 433 (75. 2Department of Cardiology. 35 SUCCESSFUL RECANALISATION OF CHRONIC TOTAL OCCLUSIONS IS ASSOCIATED WITH INCREASED LONG TERM SURVIVAL doi:10. Coronary stents were implanted in 96. perforation.51 to 2. UK. A Wragg. London.66 (0. Barts and the London NHS Trust.76 to 3. UK. but more patients in the IT group had a prior MI (30. The results suggest that IT patients may have a worse outcome with PCI compared to CABG.8%. UK Background In-stent restenosis (ISR) following stent implantation may occur in 20% to 40% of the cases according to patient and lesion complexity. Methods 6122 consecutive patients underwent elective PCI at a single centre (October 2003eMay 2010). clinical presentation. Conclusion Our data suggest that insulin treatment is a marker for higher risk for PCI when compared with CABG.9% (mean 2.001).5% vs 21.9%) 320 (63.8%) 193 (73. A Jain. Abstract 35 Table 1 Successful (n[572) Age Male Diabetes Hypertension Hypercholesterolaemia Previous MI Radial access Femoral access Dual site access (bilateral femoral or radial + femoral) 62.6 0.8%) 281 (56. stroke. K Rathod. (p<0.1%. Asian patients constituted one fifth of the total population with a slightly higher representation (24. Introduction Chronic total occlusion (CTO) remains a challenging lesion subset. 70% drug eluting). C Knight. For death.2 0.4% successful.6) and stratified according to successful or unsuccessful CTO recanalisation. MI. Demographics. MI.6%) in the NIT.1136/heartjnl-2011-300198. The clinical results of patients in the IT and NIT groups were compared.8%) p value 0. (p<0. 1The London Chest Hospital.6%) 160 (66.2%. stroke or death) was documented at discharge.8%). concomitant medications. access site (dissection.0001) but did not have an impact on in-hospital MACE (2% vs 1.41 (0. All cause mortality was 8% (21) in the unsuccessful group and 3% (17) in the successful group out to 4 years. The clinical severity of dyspnoea. 1D A Jones. 1A K Kapur. 5Imperial College. 1A Mathur. Despite advances in equipment and expertise. history. systolic and diastolic BP.1 stents per patient.0% vs 21. Demographic and procedural data were collected at the time of intervention (Abstract 35 table 1). heart rate. 1R Weerackody. Mortality following successful CTO-PCI was similar to that of the non-CTO elective PCI group (5.0001). London. 1K Rathod.01 (0. UK 3 to 4 years (mean 2. duration of DM and HBA1C were documented.7%) for CTO.7% vs 19.2%) 94 (36. The impact of insulin treatment on clinical outcomes after revascularisation is unclear. haematoma) were more frequent in unsuccessful cases (19% (52) vs 4.3 0.01). A Mathur. UK. A Wragg. For the comparison of CABG vs PCI for the primary outcome events the HR and 95% CI in the IT and NIT groups respectively were 1.0%) 174 (31. Barts and the London NHS Trust. London. 4Royal Brompton. Prior revascularisation was more frequent among patients with unsuccessful CTO-PCI than successful. Results There were 192 patients in the IT group (37. 1E J Smith. Although in the past ISR used to be seen as a “benign” A25 . haemodynamic parameters. (Abstract 35 figure 1).5 Results 572 (68. PCI 36.69 209 (79. 1A Jain.360.0001).004) and duration of diabetes was longer in the IT group (14 vs 6 yrs. p¼0.0%) Unsuccessful (n[264) 63. Connecticut. Yale University.1%) 18 (6. anti diabetic therapy. p¼0. USA 1 1 Abstract 35 Figure 1 All cause mortality after PCI for elective patients. London.BCS Abstracts 2011 Mayday University Hospital.20) in the ITand 1. Intra-procedural complications (coronary dissection. London. The secondary outcome events included death.6%. New Haven.71 to 2.4%) 47 (17. E Sammut. All cause mortality data was obtained from the Office of National Statistics via the BCIS/CCAD national audit out Heart June 2011 Vol 97 Suppl 1 Conclusion A successful angiographic outcome following CTO-PCI is associated with a survival advantage out to 4 years following intervention. In-hospital MACE (myocardial infarction. D A Jones. The aim of this study was to investigate the impact of procedural success on mortality following CTO-PCI in a large cohort of patients in the drug eluting stent era.47 (1. body mass index. p¼NS). Treatment with insulin rather than diabetic status alone should be considered when choosing the mode of revascularisation.6 0. UK. whereas no difference was found for NIT patients.5% unsuccessful vs 7. Baseline characteristics were otherwise similar (Abstract 35 table 1). 316 patients were treated with oral antidiabetic medication and the rest were treated with additional subcutaneous insulin injections.4%) CTO procedures were successful. stroke and myocardial infarction were classified as the primary outcome events.5 0.7%) 123 (21. Death. repeat revascularisation and TIMI major bleed. These data suggest that the adoption of new techniques and technologies to improve procedural success may improve prognosis. Of those.6%) 147 (61. urgent revascularisation.1136/heartjnl-2011-300198.36 H Abu-Own. many CTO patients may not be offered PCI as physicians perceive procedural success may be lower.2%) 74 (28. 2C A Thompson.57) in the NIT group.961. The present study is a sub group analysis of the CARDia trial comparing the cardiovascular outcomes at 12 months following revascularisation between the insulin treated (IT) and non-insulin treated (NIT) group.7%) 23 (4. and the anatomy is stable.1 0. repeat revascularisation they were 2. Aims The CARDia trial randomised diabetic patients to coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) and concluded that PCI is a potentially safe and feasible alternative to CABG in selected patients with diabetes mellitus (DM) and multivessel coronary artery disease. London. 836 (13.76) and 1. p<0.

See Abstract 36 figures 1 and 2. urgent revascularisation. Stent Thrombosis and Target Lesion / Vessel Re-Vascularisation. Manchester.49.4%). Demographic and procedural data were collected at the time of intervention (Abstract 36 table 1).5% were male in the BMS cohort vs 73. 2F Ordoubadi. 2M Mamas.4%) cases presenting with restenosis after previous PCI.05).76 9160 (97. Results Of the 1165 patients studied. Abstract 36 Table 1 Total Age Ethnicity (cau) Previous MI Previous CABG DM HTN Hchol Card Shock Restenosis n[922 63.09 683 (74. Cardiogenic shock was reported in 6 patients (0.1%) Sig e 0. DECREASE IN MACE RATES ASSOCIATED WITH DRUG ELUTING STENT USE IN PATIENTS WITH DIABETES UNDERGOING PCI IN LARGE DIAMETER CORONARY ARTERIES doi:10. a similar or even greater absolute reduction in MACE rates / restenosis risk is seen associated with DES use.8 years).02 to 2.36 10.04).1% in the DES cohort (p>0. 2C Deaton. Women had a higher incidence of unstable angina/nonSTEMI compared with men (32. there were similar rates of inhospital MACE in the 2 groups and over a 5year follow-up period. See Abstract 36 table 1.55).7%) Native disease n[13 523 63. hyerpcholesterolaemia) and higher rates of previous CABG and MI. In diabetic patients. 2Manchester Royal Infirmary.4% as stable angina.161. 2B Clarke.19.8611. Primary endpoint was defined as total mortality and secondary endpoint was major adverse cardiac event (MACE) defined as composite endpoint of Death.6% as unstable angina/Non-ST elevation MI and 9% with ST-elevation Myocardial Infarction. 170 had BMS and 995 had DES.37 A Dixit. p¼0. stroke or death) was documented at discharge. A total of 42/170 (24.7% at 5 years in patients with restenosis.27. UA/ NSTEMI/STEMI). 2D Fraser. p¼0.9%) 1986 (21.5%) and 91/995 in DES cohort (9.0%) 6 (0. All patients with restenosis presented with new or recurrent symptoms. nonselected patients and compare with native coronary disease.83 to 2. Drug-eluting stents with improved designs or drug elution systems that further decrease the incidence of ISR are needed.0001 p<0.7%) and 163/995 (16. 1.2 in BMS and 62. A26 Introduction Both large multi centre trials and registry studies have demonstrated that PCI with drug eluting stents (DES) is associated with reduced MACE and restenosis rates compared to bare metal stents (BMS) in native coronary vessels.2 years (mean 3.6%) 120 (13. Comparing the restenotic group with those undergoing PCI for de novo coronary artery disease.1%) but a lower incidence of STEMI (5% vs 10. 2P Williams. Baseline characteristics are listed in Abstract 36 table 1. Multivariate analysis Heart June 2011 Vol 97 Suppl 1 .0001 p<0.3%) MACE events were observed in the BMS and DES cohort respectively (HR 1. There were a total of 23/170 deaths in BMS cohort (13. Mean follow-up period was 43. more recent studies suggested that a reasonable amount of patients with ISR many develop ACS as the first manifestation of this adverse event. hypertension.38. R Khattar. Methods We therefore retrospectively studied 1165 consecutive diabetic patients with target vessel diameter $3 mm admitted to our centre for PCI from 2003 to 2009.0001 p<0. 1University Hospital Manchester MHC.9% at 1 year and 8. Manchester. MI.2339 Abstract 36 Figure 2 Comparison of mortality between restenosis and no restenosis in ACS. although it is unclear as to whether any benefit persists in those with larger diameter native coronary vessels. There was no difference in outcome of patients with restenosis vs de novo coronary artery disease regardless of presentation (angina.0001 p<0. Mean age was 62. 2A Wiper. 3. 30.0001 p<0. 2L Neyses. The aim of this study was to determine the different clinical presentations of ISR in a large cohort of consecutive.2%) 411 (44.1%) 648 (6. there was no difference in all cause mortality. Mortality rate was 0. although this benefit is less evident in those patients with a larger coronary vessel diameter and MACE rates may actually paradoxically increase in this cohort as observed in the BASKET trial.4 years old in DES (p¼0. 2M El-Omar. All cause mortality data was obtained from the Office of National Statistics via the BCIS/CCAD national audit out to 3.5%) 545 (59.98% at 30 days. In-hospital MACE (myocardial infarction.0%) 299 (32.3621. we identified 922 (6. 95% CI 0. Conclusions Clinical in-stent restenosis can frequently present as MI and such patients are more likely to have an aggressive angiographic pattern of restenosis.1136/heartjnl-2011-300198. there were similar ages and incidence of cardiogenic shock but the restenotic group had higher rates of baseline risk factors (diabetes.21). Other demographic parameters were similar in both groups.8 months).0868 p<0.5%) 3540 (37. Stroke. UK. Comparing outcome measures.1%) 544 (59. (HR 1. 2S Nair. Previous data derived from diabetic patients in large diameter native coronary vessels has come from registry studies in which numbers were either small (<200 patients) or were from highly selected patient sub groups excluding high-risk individuals (SCAAR registry).8%) 2160 (23.8 months (median 41. Methods 14 445 consecutive patients underwent PCI at a single centre (October 2003eMay 2010). 2V Mahadevan. 73. UK 2 1 Abstract 36 Figure 1 Comparison of mortality between restenosis and no restenosis in STABLE.8%) 100 (1.0001 0.65%). the largest series of its kind to date.BCS Abstracts 2011 event.1%).6% vs 29. There was also a higher proportion of South Asians in the restenotic group.2%) 4170 (44. 37 Results Restenosis presented in 60.

which is higher than the overall PPCI mortality of 6. However. R D Rakhit.BCS Abstracts 2011 illustrated that use of BMS was independently associated with increased risk of MACE (HR 1. Liverpool.0001) in our centre. hypertension.01 respectively). Robust pathways are required to minimise delay in further investigations and a need for risk stratification for a significant proportion who present with NSTEACS.7 months. UK 38 FALSE ACTIVATION FOR PRIMARY PERCUTANEOUS CORONARY INTERVENTION IS NOT A BENIGN PHENOMENON doi:10. Sixty-five (73%) had follow-up angiography (34 conv. LBBB in 19%. Trial was stopped prematurely following 18 months interim analysis which showed significant graft failure in the composite arm (40%). the composite surgical configuration could lead to preferential blood flow down one arm than the other (left internal mammary artery LIMA or radial artery RA) with its potential impact on graft patency. RBBB in 8% and other ECG abnormalities in 12%. The mean follow-up period was 18. Aim To investigate the impact of bypass graft configuration on short-term grafts patency and cardiac related quality of life.0% (including cardiogenic shock) (p¼0. Conclusions In our randomised trial.25. In A27 . but presented with breathlessness. This is in contrast to that of non-diabetic patients where the benefits of DES in large diameter coronary vessels are less evident. UK. fixed ST elevation or Q waves in 14%. Data on the outcome of this cohort of patients is limited. Liverpool Heart and Chest Hospital. pericarditis. Final Analysis was performed on intention to treat basis.1136/heartjnl-2011-300198.38 U Chaudhry. a gastric cause for presentation was diagnosed. Patients were allocated to conventional (conv n¼46) or composite (comp n¼43). Angina frequency. Data was collected via a “false activation” database together with retrospective review of case records. 95% CI 1. Methods and Results This is a single centre randomised. London. Musculoskeletal or non-cardiac chest pains were noted in 8% and 7% of the patients respectively. composite bypass graft surgery was associated with higher graft failure rate at 12e24 months after surgery compared to conventional type. false PPCI activation is not a benign phenomenon and masks underlying significant disease. 2% of the patients had pulmonary embolism and in 5%. 49% of deaths were cardiac (NSTEACS and CHF). Conclusion In conclusion. in one of the largest analyses of its kind. 93% of patients are direct access admissions by London Ambulance but a significant proportion (up to 20%) do not fulfil the diagnostic criteria for STEMI and are termed “false activations”.54. or quality of life between the two groups. repeat revascularisation procedures and myocardial infarction. sepsis in 19% and congestive heart failure (CHF) in 15%. UK Introduction Primary percutaneous coronary angioplasty (PPCI) is the preferred reperfusion strategy following an acute ST elevation myocardial infarction (STEMI). Quality of life). Royal Free Hospital.008) and 3. The ECG abnormality was non-specific ST-T changes in 22%. 25% (n¼11) died during the index admission and 33% (n¼15) died within 30 days of admission. Results Complete data was available in 165 cases. Aim To review the clinical outcome of patients presenting to our heart attack centre with false activation PPCI.03). critically for patients.5% of false PPCI activation admissions died (n¼45). The overall 30-day mortality for false activations was 7. Angina stability. Method From January 2008 until October 2010. This difference may be due to the composite conduit configuration. 39 A RANDOMISED CONTROLLED TRIAL COMPARING CONVENTIONAL CORONARY ARTERY BYPASS GRAFT SURGERY WITH A COMPOSITE ARTERIAL GRAFT TECHNIQUE doi:10. 2R A Perry. the traditional focus of clinical trialsdand. I Kemp. The two primary end points were graft patency defined as (Thrombolysis In Myocardial Infarction) TIMI III flow in distal anastomosis at angiography 12e24 months after surgery.1136/heartjnl-2011-300198.1136/heartjnl-2011-300198. There were no significant differences between the two groups in the percentage of improvement in these four domains (Physical limitation. 15% had other diagnoses.40 C Appleby. 29% sepsis and 22% other causes.001 respectively). R H Stables. Cardiology Department.39 1 A Alahmar. p¼0. use of DES in patients with diabetes in a real world setting undergoing PCI in large diameter coronary vessels ($3 mm) is safe and is independently associated with a reduction in MACE events. The final diagnosis was non-ST elevation acute coronary syndrome (NSTEACS) in 19%. and cardiac-related health status assesses by Seattle angina questionnaire (SAQ). Leicester. with total of 116 graft in conventional arm and 100 grafts in composite arm.3% (excluding shock) (p<0. 2Liverpool Heart and Chest Hospital. C Mavroudis. driven through an increase in revascularisation. 71% presented with chest pains and 29% had no chest pains. pericardial effusion and late presentation STEMI. All patients in both groups had LIMA graft to left anterior descending artery (LAD). The mean age for this cohort was 83. 2R H Stables. 31 comp). Further blood flow characteristics study in this configuration can help understand such an important finding and its implication on our clinical practice. left ventricular hypertrophy in 15%. early repolarisation changes in 10%. Heart June 2011 Vol 97 Suppl 1 Background Composite (Y/T) coronary artery bypass graft surgery (CABG) confers full arterial revascularisation. Baseline characteristics were similar between the two groups apart from diabetes where there were more diabetic patients in the composite arm than the conventional one (15(35%) vs 5(11%) p<0. dilated cardiomyopathy. UK Introduction The success of revascularisation therapies for coronary artery disease (CAD) must be measured by both an improvement in hard clinical endpointsdmortality. Graft patency rate was significantly higher in the conventional compared to composite arm (95(82%) vs 59(59%) p<0. 71% were male and 29% were female (mean age 67). the relief of angina symptoms. Despite the difference in graft patency there were no differences in physical limitation. angina frequency. angina stability. Stable angina was observed in 8% and syncope in 7%. palpitations or syncope. and “hands off ” aorta compared to conventional bypass graft surgery. Conclusion Patients presenting with false PPCI activation have a high observed mortality. Liverpool. controlled trial Between March 2006 and July 2007. 14% had other cardiac problems. although their use in cardiovascular trials is far from universal. including arrhythmia. 322 patients undergoing isolated bypass graft surgery at our institution were screened and 89 (27%) met the inclusion criteria and were randomised. This is probably due to significant associated comorbidities. The mean length of stay was 4 days (range 1e33).2%. we identified 209 false PPCI activations defined as patients with incomplete diagnostic criteria for acute STEMI: absence of chest pain and/or typical ECG features (ST elevation or new LBBB). Since 2005 24/7 primary PCI has been the first line treatment for an acute STEMI in our centre. including occult cardiac disease. 40 PATIENT VS PHYSICIAN REPORTED ANGINA BEFORE AND AFTER REVASCULARISATION OF CORONARY ARTERY DISEASE: EVIDENCE FROM A LARGE RANDOMISED CONTROLLED TRIAL (THE SOS TRIAL) doi:10.05 to 2. during which 21. Interest in patient reported outcomes (PROMs) has increased. Thus. Three main domains of the SAQs there was significant improvement between before and 6 months after surgery in both groups. 1Leicester University Hospital Glenfield.

Yet at follow-up. The published results of the SOS trial used doctor gradings to report freedom from angina at 1 year in 79% of CABG patients vs 66% of PCI patients (p<0. A28 Abstract 41 Figure 1 (A) shows aortic pressure traces taken at peak exertion with a reduction in pressure augmentation during Ex2. charting the patient score and. p<0. Thus there is little overall difference in mean CCS score (P 2. 2A Guilcher. 6 months and 12 months were available for 919. 41 REDUCED ARTERIAL WAVE REFLECTION AND ENHANCED LV RELAXATION CONTRIBUTE TO WARM-UP ANGINA doi:10.0001). 1D Perera. 1M Marber. doctors record freedom from angina (CCS¼0) in a more substantial proportion of the population. 3C Rolandi. the observed differenceddoctor (D) minus patient (P). If patient gradings are used instead these figures are reduced to 57% in CABG and 44 % in PCI (p<0. High quality data from the Stent or Surgery (SOS) trial allows such an analysis. The observed trend for doctors to insist that all patients must have some symptoms at baseline. Abstract 40 Figure 1 Difference between doctor and patient classification of Angina before revascularisation. preferring CCS grades 2 and 3. Results Paired CCS scores at baseline. 1Rayne Institute. considerably more so than patients self-report (p<0.41 1 2 T P E Lockie. 1S Redwood. to suggest that a greater proportion of patients have been rendered symptom free at follow-up (than is suggested by self-reported estimates) has important implications and may call into question our current understanding of the impact of revascularisation. rendering both treatment strategies significantly less effective at relieving angina from a patients perspective (p<0. Patterns of discordance change however between baseline and follow-up time points. and more importantly. 1R Williams. Heart June 2011 Vol 97 Suppl 1 . Methods The SoS trial was a large RCT (n¼988) comparing stentassisted percutaneous coronary intervention (PCI) with coronary artery bypass grafting (CABG) in patients with multivessel CAD. Participation in the SoS trial included an appraisal of angina symptoms by both patient and physician according to the Canadian Cardiovascular Society (CCS) Classification System prior to. Doctors are reluctant to record scores of 0 or 4.0001) (Abstract 40 figure 2). Abstract 40 Figure 2 Difference between doctor and patient classification of Angina at 12 m Fup. (B) shows WIA with an increase in the backward expansion. for each CCS grade. P Chowienczyk. or “sucking” wave originating from the microvasculature. 886 and 888 cases respectively. Abstract 40 table 1. St Thomas Hospital.0001). KCL. Abstract 40 Table 1 PCI (%) Doctor scoring CCS class 0 Patient scoring CCS class 0 66 44 CABG (%) 79 57 p <0. At baseline the overall level of agreement was good with >75% paired data sets demonstrating a difference of #61 CCS class. 3M Siebes.001).0001 <0.BCS Abstracts 2011 particular the differences between physician and patient reported outcomes has not been analysed.1136/heartjnl-2011-300198. In this study patient and doctor reported outcomes were compared systematically.0001 Conclusions This is the first randomised study to compare the improvement in angina status reported by patients and clinicians following revascularisation therapy for coronary artery disease. Abstract 40 figure 1 shows the paired scores at baseline.0001).5. and subsequently at 6 and 12 months following coronary intervention. 1K De Silva.2 vs D 2.

Only a small number of these patients have an additional clear indication for CABG over PCI. A 33% decline in aortic wave reflection (p<0. 3Department of Bio-Engineering. Throughout exertions. Papworth Hospital. Patients’ SYNTAX scores were calculated using pre-procedure angiograms.8 Referrals for CABG from within trust Referrals for CABG from outside trust 31. Methods We performed a retrospective analysis at the Freeman Hospital. The average SYNTAX score for CABG referrals from outside the trust was lower (25) than from within the trust (31). The recently reported SYNTAX study allows objective quantification of the degree of coronary disease and facilitates an evidence based decision between CABG and PCI.43 A J Brown. the latter was offset by reduced microvascular resistance (Pd/V). L). And this rises to almost one third in those patients referred from district general hospitals. IM) and $32.0 25.0 14. The SYNTAX score.0002. AMC. 2Clinical Pharmacology. Discussion The majority of patients undergoing PCI at the FRH have SYNTAX scores in the lowest tertile.8 84 84 84 % Patients with SYNTAX score % Patients with in middle third SYNTAX score in (23e32) higher third (>33) 11 12 10 5 4 6 Abstract 42 Table 2 % Patients with Average SYNTAX score SYNTAX in lower third score (0e22) All Referrals for CABG 28.0001). distal coronary pressure (Pd) and flow velocity (V) were recorded in the culprit vessel using a dual sensor coronary guide wire while aortic pressure was recorded using a second wire.1136/heartjnl-2011-300198. N E J West. However. Cambridge.003) and rate pressure product (RPP) was higher (p¼0. Furthermore we found that a significant proportion of these do not go through MDT planning.1136/heartjnl-2011-300198. There is no difference in the SYNTAX scores in patients having PCI from referral bases within the centre or from outside. Although the debate continues over a strategy of complete revascularisation (immediate or staged) vs culprit-only. University of Amsterdam. Patients are not routinely discussed at MDT but can be brought to the weekly meeting at the discretion of the referrer. At the Freeman Hospital (FRH). to date. Freeman Hospital.BCS Abstracts 2011 London. During cardiac catheterisation via radial access they performed 2 consecutive exertions (Ex1.9 Referrals for PCI from within trust Referrals for PCI from outside trust 15. The energy of the forward compression wave and overall coronary blood flow. Conclusions In patients with warm-up angina.025) confirming warm-up. R Edwards. ARE WE FOLLOWING BEST PRACTICE? doi:10. more patients are inappropriately having CABG than are inappropriately having PCI. This study compared changes in central haemodynamics. and enhanced left ventricular relaxation during Ex2 as suggested by a larger backwardtravelling suction wave (p¼0. UK. 84% of patients undergoing elective PCI had SYNTAX scores less than 22. This included 100 cases of CABG and 100 of PCI. Time to 1 mm ST depression was longer in Ex2 (p¼0. 22. London. the presence of diabetes mellitus.01) on wave intensity analysis (WIA) of the intra-coronary signals. Newcastle upon Tyne 43 Introduction Cardiologists are generally the gatekeepers of coronary artery disease and have been much criticised for not discussing all patients being considered for revascularisation therapy at an MDT (multi-disciplinary team) meeting or not referring patients with traditional “surgical disease” for CABG. Heart June 2011 Vol 97 Suppl 1 PROGNOSIS AFTER PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR STEMI: CAN THE SYNTAX SCORE HELP? doi:10. according to SYNTAX scoring. as measured by the velocity time integral. exercise induces changes in the aortic pressure waveform. These results may indicate that cardiologists are more likely to bring patients to MDT meetings than surgeons and. Amsterdam. St Thomas Hospital. 35% of all patients referred for elective CABG had scores greater than 33. UK Background Factors affecting prognosis after primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI) include age at presentation.3 yrs) with a positive exercise stress test and exertional angina completed the protocol. left ventricular function and/or cardiogenic shock. patients are typically referred for PCI or CABG by cardiologists working within the Newcastle upon Tyne Trust or from district general hospitals within the network. microvascular function and LV relaxation. are poorly understood. a large cardiothoracic unit in the North of England. Results 671 of 695 patients were included in the analysis with 24 being excluded owing to inability to score (previous CABG. did not change. Half of each were referrals from other hospitals. has been validated in unselected populations undergoing elective PCI. L M McCormick. These combine to reduce afterload without compromising myocardial diastolic blood flow thereby likely enabling improved performance on second exercise. peripheral wave reflection and patterns of coronary blood flow during serial exercise that may contribute.0 24 19 32 % Patients with SYNTAX score % Patients with in middle third SYNTAX score in (23e32) higher third (>33) 40 34 50 35 47 18 42 RETROSPECTIVE CALCULATION OF SYNTAX SCORE IN 200 PATIENTS UNDERGOING ELECTIVE CORONARY ARTERY BYPASS GRAFTING (CABG) AND PERCUTANEOUS CORONARY INTERVENTION (PCI). or warm-up angina. and patient data and outcome measures obtained by interrogation of local and national databases.5 (high. SYNTAX scoring was performed by a single trained operator blinded to patient details and outcome. compared to 29 for those undergoing CABG. MDT meeting records and patients’ notes were reviewed.5e32 (intermediate. 200 patients who had elective revascularisation between April 2009 and April 2010 were selected. images A29 . Ex2) using a supine cycle ergometer. KCL. The Netherlands Background The mechanisms of the clinically observed phenomenon of reduced angina on second exertion. Patients were split into 3 subgroups as in the SYNTAX trial (score #22 (low.0001) in Ex2 (see Abstract 41 figure 1A) coincided with a reduction in both tension time index and diastolic time index (p<0. See Abstract 41 figure 1B.42 L J Mullen. 6164. This gives us the opportunity to examine whether elective revascularisation is being performed appropriately at our institution. Methods and Results 16 patients (15 male. Scoring was validated by analysis of 3 separate cohorts by 2 other experienced operators. In total almost one quarter of all patients undergoing CABG have a SYNTAX score in the lowest tertile. H)). little is known about the impact of the extent of coronary disease at presentation on prognosis after PPCI. B Nyawo. p¼0. Abstract 42 Table 1 % Patients with Average SYNTAX score SYNTAX in lower third score (0e22) All Referrals for PCI 14. R Taylor. Based on this data in our institution discussing all patients at an MDTand the use of SYNTAX scoring at point of referral would be more likely to increase PCI revascularisation rates. no studies have assessed its utility in PPCI. designed to stratify outcomes in multivessel PCI and CABG. Methods Consecutive patients attending a single UK tertiary centre for PPCI between September 2008 and June 2010 (n¼695) were included. Results The average SYNTAX score for patients undergoing elective PCI was 15. UK.

88. UK. 100% of patients were prescribed clopidogrel.BCS Abstracts 2011 unavailable). provides important prognostic information regarding 1-year survival from death and revascularisation. heart rate <50 bpm. Similar results were obtained for freedom from death or unplanned revascularisation (p<0. systolic blood pressure <90 mm Hg. University Hospital Aintree NHS Foundation Trust. Quantitative prescribing of secondary prevention is excellent. Abstract 43 Figure 1 Conclusions The SYNTAX score. IM 88. Even in trials which claimed to have looked Heart June 2011 Vol 97 Suppl 1 . J Sayer. Reorientation is needed to focus on both quantity and quality. nor received instructions to escalate the dose (Abstract 44 figure 2). Contraindications and limits to dose escalation were noted (symptoms.8% aspirin.0001) and death or any revascularisation (p<0. Significant resources have been directed to achieving timely reperfusion throughout the UK. p<0. and 91. 95. Although there was no correlation between SYNTAX score and patient sex or diabetic status.03.44 Conclusion The national service framework and target driven initiatives such as advancing quality promote “tick box” medicine. Options include nurse or pharmacy led services and expansion of cardiac rehabilitation. M Nijjar. Liverpool. Myocardial infarction was diagnosed according to standard criteria. These findings may provide supporting evidence towards routine complete revascularisation of obstructive coronary artery disease after PPCI. Median scores in the 3 groups were: L 14. H 82. 2Liverpool Heart and Chest Hospital.6% b-blockers. maximum clinically tolerated doses. P Kelly.1136/heartjnl-2011-300198.45 Introduction Primary percutaneous intervention (PPCI) improves survival in patients with ST elevation myocardial infarction (STEMI). S Pettit. The case records of all patients were reviewed. UK Introduction Primary percutaneous coronary intervention (PPCI) has been established as standard therapy for ST elevation myocardial infarction (STEMI). Abstract 44 Figure 2 Outpatient titration of b-blocker and ACEI/ARB. IM 26. 1-year absolute survival (Abstract 43 figure 1B) followed SYNTAX score groups: L 94. G Clesham. Abstract 44 Figure 1 Inpatient titration of b-blocker and ACEI/ARB. and angiotensin II receptor blockers (ARB). with landmark clinical trials demonstrating unequivocal morbidity and mortality benefits from b-blockers. E Boston-Griffiths. when applied to an unselected population of patients undergoing PPCI for STEMI. J Davies.8% statin. 72% were male. On discharge. E Damm. Outpatient follow-up at a mean of 5.0002). Qualitative follow-up and titration is not. H 36 (Abstract 43 figure 1A). intensive medical therapy is of equal importance. However. R Perry. Frameworks to deliver titration of medical therapy must be explored. However. The majority of patients (83%) were neither receiving maximum tolerated doses of b-blocker or ACEI/ARB. Liverpool. R Aggarwal. Results Mean age was 62.0001).9 years. Very few trials have looked at the outcome of PPCI in elderly patients. the inpatient dose of b-blocker or ACEI/ARB was maximum or clinically limited in only 13% and 15% of patients respectively (Abstract 44 figure 1).1136/heartjnl-2011-300198. All trials employed rigorous titration to A30 R Showkathali. serum creatinine and potassium). 98. Medications and doses on admission.0001).0 months was equally concerning. Basildon. angiotensin-converting enzyme inhibitors (ACEI). Methods Consecutive patients with STEMI referred for PPCI to a large tertiary centre between 1st March and 1st August 2009 were included (n¼167). 45 J D Jones. 44 PRIMARY PERCUTANEOUS INTERVENTION: HAVE WE TAKEN OUR EYE OFF THE MEDICINE BALL? doi:10. The ability to allocate a SYNTAX tertile was reproducible between observers (r¼0. there was a linear relationship with patient age (r2¼0. N M Hawkins. UK 1 2 2 2 2 2 1 SHOULD PRIMARY PERCUTANEOUS CORONARY INTERVENTION BE THE ROUTINE REPERFUSION STRATEGY IN OCTOGENARIANS AND NON-AGENARIANS PRESENTING WITH ST ELEVATION MYOCARDIAL INFARCTION? doi:10. Whether suboptimal doses convey the mortality benefits observed in landmark clinical trials is unknown.0% ACEI/ARB. discharge and follow-up were recorded.0611.1% (p¼0.94).7%. The Essex Cardiothoracic Centre.7%. We examined whether medical therapy is being applied appropriately in patients referred for PPCI.

4% and left anterior descending in 37.2% of patients. Mortality data were obtained from the summary care record (SCR) database.25 to 74.7%) was similar to the subgroup analysis of the PPCI arm in similar SENIOR-PAMI patients (19%). 50e60. 1N Sheikh.3 26. The prevalence of coexisting risk factors (hypertension. There was a significant difference in the mortality between patients age <80 yrs and those $80 yrs (Abstract 45 figure 1). See Abstract 46 figure 1.BCS Abstracts 2011 at PPCI in elderly patients such as SENIOR PAMI (Grines.7% respectively. Ten patients (7. Prospectively entered data were obtained from our dedicated cardiac service database system (Philips CVIS). London. diabetes and cardiogenic shock renal function based on the GFR at admission remained a strong independent predictor of outcome. This risk increases linearly with declining eGFR. the thrombolytic group had a lower (16%) mortality. 63 female). Follow-up data were obtained from patients’ respective district general hospitals and general practitioners medical records. the mean age was 8563. A Mathur. Results Of the 998 patients who were admitted to our unit for primary PCI for suspected STEMI during the study period.1136/heartjnl-2011-300198. 2005) and TRIANA (Bueno. Our 30-day mortality outcome in patients $80 yrs (19. we included 132 (70. The London Chest Hospital. UK. previous MI. Heart June 2011 Vol 97 Suppl 1 S Ghani. Barts and the London NHS Trust. 1S Gati. 46 PROGNOSTIC VALUE OF BASELINE RENAL FUNCTION ON LONG TERM OUTCOME IN PATIENTS UNDERGOING PRIMARY PERCUTANEOUS CORONARY INTERVENTION FOR ST-ELEVATION MYOCARDIAL INFARCTION doi:10.3%) were $80 yrs of age. previous CABG and cardiogenic shock were higher among patients with reduced eGFR.37 (95% CI 72.9 ‡90 yrs (N[19) 26.1136/heartjnl-2011-300198.56) ml/min/1. 40e50. Information was entered at the time of procedure and outcome assessed by all-cause mortality information provided by the Office of National Statistics via the BCIS/CCAD national audit. B Rathod.5 Abstract 46 Figure 1 All MACE after PCI for STEMI. S Gallagher.40623.73 m2. Estimated glomerular filtration rate (eGFR) was calculated using the modified diet in renal disease equation and patients were divided into groups based on eGFR (<40. With an ageing population in the western world. K Rathod.94 to 7. A Kapur.47 Conclusion This study clearly demonstrates a significant mortality difference between patients aged <80 yrs and those $80 yrs treated with PPCI. >60 ml/min/1. 183 (18.2%) and 39 (29. Methods Our PPCI service was started in September 2009 and we analysed all the patients who were $80 yrs presenting to the PPCI service between September 2009 and September 2010 (13 months). E Wicks. however there is limited data assessing this relationship in the context of primary PCI and whether it exists with other major adverse cardiovascular events. Methods Clinical information was analysed from a prospective data base on 2310 STEMI patients who underwent primary PCI between January 2004 and May 2010 at a London centre.7 23. Results The average eGFR in all patients was 73. A Jain. Further studies are required to determine whether PPCI should be routinely used in very elderly patients presenting with STEMI.5%) had previous myocardial infarction. diabetes mellitus. 2J Somauroo.1%) patients for analysis. C Knight. 1A Zaidi. In the same analysis. UK Background Renal impairment is associated with increased cardiovascular mortality following acute coronary syndromes (ACS).7 14. 3S Kemp. 1H Raju. about 20% of patients admitted for suspected STEMI are $80 yrs. reinfarction. After adjustment for baseline characteristics including age. We evaluated the outcome of PPCI in patients $80 yrs who were admitted to our unit with STEMI. In patients $80 yrs. The infarct related vessel was the right coronary in 42. hypercholesterolaemia). 2009) the minimum age for inclusion was 70 yrs and 75 yrs respectively. Drug eluting stents were used in 40. for comparison between the highest and lowest eGFR groups). re-infarction and recurrent angina.5 2. A Wragg.9%) who did not undergo PPCI. Conclusion Baseline renal dysfunction in patients undergoing primary PCI is associated with an increased risk for combined death. After excluding 51 patients (27. In-hospital and 30-day mortality was 14.4% and 19.96.5 3. 2Countess of Chester Hospital. Abstract 45 Figure 1 Abstract 45 Table 1 % Inhospital mortality 30-day mortality 30-day MI 30-day CVA Major bleeding requiring blood transfusion 80e84 yrs (N[62) 9.6 1. 3-year composite of MACE (death. stroke and target vessel revascularisation) were compared between groups.6 85e89 yrs (N[51) 15. There was a progressive increase in MACE with declining eGFR (OR¼4. D A Jones. 95% CI 2. There were 20 diabetics (15. London. 1S Sharma.6%) were in cardiogenic shock on arrival of which 9 (90%) had an Intra aortic balloon pump (IABP).2 1.1%.95 yrs (range 80e99 yrs.73 m2). Of those who were included in the study (n¼132.84. 3Rugby Football Union (RFU) 1 1 Introduction Recent experience of pre-participation cardiovascular evaluation (PPCE) in Italian athletes demonstrates a significant A31 . 47 CARDIOVASCULAR EVALUATION OF ENGLISH PREMIERSHIP RUGBY PLAYERS doi:10. St Georges University London.3 0 0 10. mortality and bleeding risk increased markedly with advancing age (Abstract 45 table 1).46 O P Guttmann. median 85 yrs).0 0 3.

the state health system in the UK (and many other Western countries) does not support cardiovascular evaluation of athletes.161.760. We examined whether the erythropoietin analogue darbepoetin improves flow mediated dilatation (FMD). right bundle branch block (n¼3). left axis deviation (n¼17). At 24 h FMD was repeated after 20 min ischaemia-reperfusion of the upper limb. * p<0.463.6% were reassured after TTE. abnormal T wave inversion (n¼5) and prolonged QT (n¼1).4 31.1136/heartjnl-2011-300198. right ventricular hypertrophy (n¼1).9 Placebo 24 h 3.07 23. all receiving darbepoetin.9 years. CD34+/VEGFR2 +/133+ circulating EPC were enumerated by flow cytometry.160. Results Immunoreactive erythropoietin peaked at 24 h in the darbepoetin group (median value of 724 U/l (IQR 576e733 U/l). Conclusion Cardiovascular evaluation of British rugby players with a structured questionnaire and ECG resulted in clearance of 92.560.6 4.2 Darbepoetin Baseline 3. pulmonary stenosis (n¼1). Cardiovascular Division. range 15e37).8% were referred for further diagnostic evaluation.9 Placebo 72 h 2. 1.2 L M Tilling. ***p<0.6 17. and whether this is influenced by preceding ischaemia-reperfusion.4%) required TTE (35 (5.08%) due to family history of sudden death.8 20.6 17.964.001 Endothelial function and EPC Placebo Baseline 3.560.5 29. Abstract 48 Table 1 Endothelial function FMD% Progenitor cells CD133+/VEGFR2+ CD34+/VEGFR2+ CD133+/CD34+ Values are means6SE.63 101619 3. the International Olympic Committee and FIFA. King’s College London.6 Placebo 7d 3.4% of athletes required further investigation following initial ECG. suspicion of hypertrophic cardiomyopathy (n¼1) and QT prolongation on ECG (n¼1).460.05. UK Background Vasoprotective effects of erythropoietin in animal models are mediated by endothelium-derived nitric oxide (NO) and/ or mobilisation of endothelial progenitor cells (EPC) and may be Abstract 48 Figure 1 Change from baseline in FMD at 72 h.8% required further tests following TTE. whether they are present in humans is unknown. Methods 36 patients (50e75 years) with stable coronary artery disease were randomised to receive a single dose of darbepoetin 300 mg or saline placebo.364.960. Measurements were made immediately before darbepoetin/placebo and at 24 h. FMD did not differ significantly between groups at 24 h (before ischaemiareperfusion). and a low false positive rate.8* A32 Heart June 2011 Vol 97 Suppl 1 .75 123621 4. The reasons for these tests included possible arrhythmogenic right ventricular cardiomyopathy (n¼3).9*** 180611* 7. St Thomas’. ECG abnormalities warranting TTE included right axis deviation (n¼4).960.2P Chowienczyk. London.08%) due to symptoms). p<0.001).061. Trans-thoracic echocardiogram (TTE) and additional investigations were performed where indicated. requiring serial surveillance. 1British Heart Foundation Centre. (48 h after ischaemia-reperfusion) FMD increased from baseline in the darbepoetin group but not in the placebo group so that FMD (and change in FMD from baseline) was significantly greater in the darbepoetin group (change from baseline 1.61 182616* 13.664. and 1.7%) due to ECG abnormalities. 1. Although PPCE is endorsed by large medical and sporting organisations. 1. St Thomas’. A further group of 11 patients were studied according to the same protocol. London.660.163. 2Department of Clinical Pharmacology.92 146613 8. a measure of endothelium-derived NO. At 72 h.2B Clapp.73 117619 3. In 2010 the English Premier Rugby league introduced formal PPCE in all competing players. A w20% increase in CD133+/VEGFR2+ cells after darbepoetin was temporally dissociated with the increase in FMD.9 29. Overall 7.6* Darbepoetin 7d 3. Six of the 45 subjects demonstrated mild changes on TTE (markedly dilated LV cavity (n¼3). enhanced by ischaemia. mitral regurgitation (n¼1). with omission of forearm ischaemia-reperfusion at 24 h. Of these.BCS Abstracts 2011 reduction in mortality from cardiomyopathies and cardiac conduction disorders. 45 (7. 5 (0.48 1. compared to 12 U/l (IQR 9e21 U/l) in the placebo group) and remained elevated at approximately 500 fold baseline at 72 h. 72 h and 7 days. King’s College London. Immunoreactive erythropoietin was measured by an enzyme linked immunospecific assay. Results A total of 606 players were assessed (mean age 22. 48 h after ischaemia-reperfusion (+IR).5 17.01). Methods Athletes participating in the English Premiership Rugby underwent PPCE with a structured clinical questionnaire and 12lead ECG.80 110617.4 Darbepoetin 24 h 4. Certain elite sporting organisations in the UK mandate PPCE in all athletes prior to competition. FMD was measured at the brachial artery using high resolution ultrasound. UK.160. False positive rate was 5. possibly by increasing expression of the erythropoietin receptor and by a mechanism likely to involve Akt/NO rather than circulating EPC. Five demonstrated abnormalities on TTE and/or ECG that warranted referral for further evaluation including exercise stress test (n¼5).6%.460. and 5.260. Only 1% players required surveillance echocardiograms and 0. Conclusions Preceding ischaemia-reperfusion is required for darbepoetin to enhance endothelial function. None of the players exhibited a cardiac disorder that warranted disqualification from sport.6%. including the European Society of Sports Cardiology.The increase in FMD at 72 h after darbepoetin and ischaemia-reperfusion at 24 h was significantly greater than that without preceding ischaemia-reperfusion (p<0. 5 (0.763. 48 DARBEPOETIN ENHANCES ENDOTHELIAL-DEPENDENT VASOMOTOR FUNCTION IN PATIENTS WITH STABLE CORONARY ARTERY DISEASE ONLY AFTER PRECEDING ISCHAEMIA-REPERFUSION doi:10. dilated aortic root (n¼1)).763.2J Hunt.2A Donald. after placebo and darbepoetin (study 1) and after darbepoetin without preceding ischaemia-reperfusion (ÀIR.3% and À0. 1. The results indicate that PPCE carried out in an expert setting results in a relatively small number of athletes requiring further tests. False positive rate was 5.760.364* Darbepoetin 72 h 5.6% following initial tests.662.97 180613* 11. study 2).362.4% in darbepoetin and placebo groups respectively. 24-h ECG (n¼5) and cardiac MRI (n¼3).760.460.

UK 1 1 Background Studies in Caucasian (white) athletes indicate that a significant proportion exhibit an isolated prolonged corrected QT interval (QTc). E R Behr.9*62.9 64 (17. years Mean Heart Rate. No ethnic difference was observed in prevalence of QT prolongation. UK Abstract 50 Figure 2 Exercise tolerance test demonstrating dynamic Brugada ECG pattern. who were participating at national and international level in a variety of sporting disciplines.2%) 4 (0. ST segment elevation. N Chandra.001 white vs black athletes. Athletes diagnosed with structural heart disease or hypertension were excluded from analysis.0%) 7 (0.661. Methods We assessed 3035 elite athletes. Athletes were evaluated with ECG and 2D echocardiography. n (%) QTc >460 ms.3%) 204 (22.4*61. Results Thirty (9. obviating the need for ethnicity specific criteria for defining a long QTc. N Spath. 1St George’s University of London. Brugada type 1 pattern. Bivariate analysis revealed that none of T wave inversions. n (%) Mean QTc (Bazett’s).50 H Raju. E R Behr.2 2165 63610 84610 9.6%) 66* (4. Based on ESC Sports Consensus criteria.2 1864 5969 8869 7.4%) 407625 13 (10. raising concerns for potentially false diagnoses and disqualification from competitive sport. Methods Between 2006 and 2010.3%) 406 (24. An example of dynamic Brugada phenotype is given in Abstract 50 figure 2.49 H Raju. *p<0.6%) 20 (16. A Zaidi. n (%) 570 (63. S Sharma. or left ventricular wall thickness were associated with QTc. bpm 2265 61612 1764 56610 96610 9.8%) patients had an abnormality during ETT.2%) 412627 39 (10. Conclusion Despite demonstrating a higher prevalence of repolarisation changes and morphological left ventricular hypertrophy. 2S Basavarajaiah. details of which are summarised in Abstract 50 figure 1. No hypotensive BP response was seen. this ethnic group generally exhibits a high proportion of ECG repolarisation changes and increased left ventricular wall thickness. Aim We determined the diagnostic yield of exercise tolerance testing (ETT) in investigation of inherited cardiac conditions following familial premature SCD. aged 14e35 years. but QTc was similar among black and white female athletes. No patients with significant ST depression had evidence of coronary abnormalities on imaging. Results Demographic and cardiological results are summarised in Abstract 49 table 1. 2J Rawlins. Abstract 49 Table 1 Characteristics of athletes evaluated Black Male White Male Black Female White Female (n[901) (n[1652) (n[122) (n[360) Abstract 50 Figure 1 familial evaluation. ETTs were analysed for: QT prolongation. echocardiogram. as defined by ESC Sports Consensus criteria (male >440 ms. Individual pathological phenotypes were determined by a combination of 12-lead ECG. who completed at least 3 min of the Bruce protocol. CT coronary angiography and genetic mutation analysis. 1S Sharma. All ETTs with abnormal QT prolongation and dynamic Brugada pattern were associated with diagnoses of long QT syndrome and Brugada syndrome respectively.9%) 5 (1. multiple ventricular ectopics or arrhythmia. London. ms QTc >440 ms. UK. London. However. Stage 1 of Bruce protocol exercise (left) and postexercise recovery (right). female >460 ms).BCS Abstracts 2011 49 ETHNIC VARIATION IN QT INTERVAL AMONG HIGHLY TRAINED ATHLETES doi:10. Aim We aimed to assess the impact of ethnicity on QTc in young elite athletes. we evaluated 308 blood relatives of 148 SCD victims.4%) 404*620 49 (3. prevalence of a long QTc in black and white athletes is similar.6%) 1 (0. n (%) T wave inversions. Reliable diagnostic indicators include inappropriate QT prolongation and dynamic Brugada A33 Background Investigation of blood relatives for evidence of an inherited cardiac condition is advocated following an unexplained sudden cardiac death (SCD).261. Black male athletes exhibited shorter QTc than white male athletes. 50 DIAGNOSTIC ROLE OF EXERCISE TOLERANCE TESTING IN FAMILIAL PREMATURE SUDDEN CARDIAC DEATH doi:10. The prevalence of prolonged QTc interval in athletes of African/Afro-Caribbean (black) descent is unknown. London. as appropriate. M Papadakis. ms 88614 Mean LV wall thickness. mm 10.8%) Means presented as mean 6 SD. 24-h holter monitor.6%) 393626 20 (2. but exertional hypertension was associated with systemic hypertension. Ventricular ectopy was seen in 15 patients.4%) Mean QRS duration. ETT abnormalities and associated diagnoses at Mean Age. Heart June 2011 Vol 97 Suppl 1 . M Muggenthaler. 1M Papadakis. St George’s University of London. Conclusion The ETT is a useful diagnostic adjunct when evaluating relatives of victims of premature SCD. ST depression: blood pressure (BP) response.1136/heartjnl-2011-300198.8%) 15* (4.6 ST segment elevation. 2V Panoulas. with additional MRI. 2University Hospital Lewisham. that may impact on QTc. black athletes do not exhibit a longer QTc than white counterparts. R Bastiaenen. 1N Chandra. of whom 5 demonstrated phenotypic cardiomyopathy or channelopathy on further investigations.0%) 18 (14.1136/heartjnl-2011-300198.

saline/ischaemia ¼3. with no overlap in their 95% CI. saline/control ¼10. Therefore NaNO2 could potentially be an anti-ischaemic agent at much lower doses than those used historically. of DPSV/DHR were different in the saline/ischaemia group compared to the three other groups (ie. systemic hypotension and tachyphylaxis). hypertension. see Abstract 51 figure 1. 2Department of Cardiology. In addition. 1University of Dundee. Using placebo study data-set. see Abstract 51 figures 1 and 2. However. laboratory test data. Methods 500 patients with T2DM where studied with echocardiography between April 2002 and October 2003.1136/heartjnl-2011-300198. smoking status. 2C Williams. 1Cardiff University.52 B R Szwejkowski. After adjusting for confounding factors we have shown that for every 10-unit increase in BNP there is a 6% increased risk of death. Dundee. There appears to be a link between survival and BNP in T2DM. NO2-/ischaemia ¼8. walls were classified into tertiles: the lowest tertile of responders of PSV to an increase in heart rate (DHR) labelled ischaemia (n¼18) and the upper tertile control (n¼18). Transthoracic echocardiography was performed by one trained operator and left ventricular (LV) assessment was performed using modified biplane Simpson’s method over three cycles. Although more research is needed. Method A double-blind. We excluded individuals with EF of <55%. IHD.10) (p¼<0. placebo-controlled. saline/control and NO2-/control. p<0.06 (95% CI 1. repeated-measures ANOVA with Bonferroni post-test).01). Ventricular ectopy is non-specific. Recent in vitro evidence shows that nitrite (NO2-) exhibits an enhanced vasodilator effect in hypoxia. the effects were slow and unpredictable and so it fell out of favour as more potent and faster-acting agents became available. Cox proportional hazards model was used to examine the effects of BNP (bedside stick measurement) measure on all-cause mortality using age.to tissues in need only. D H J Elder. is unhelpful and should be viewed in the context of the patient’s cardiovascular risk profile. A Dawson. however. to mortality data. Data was divided into four groups according to the study-infusion received and the myocardial-wall examined: saline/ ischaemia. and be without the adverse side effects associated with organic nitrates (eg.51 1 1 T E Ingram. the linear regression gradient of the NO2-/ ischaemia group was similar to the saline/control and the NO2-/control gradient. 56 patients died over this time. (eg. Results Data from each stage of each DSE was plotted on a scatter plot graph with change in (DHR) on the x-axis and corresponding change in PSV (DPSV) on the y-axis (increase in both values compared to baseline). Outcome was all cause mortality. 2Royal Glamorgan Hospital.01. 1A G Fraser. duration of diabetes. Only three previous studies have specifically addressed the question as to whether BNP adds prognostic information in T2DM.1 cm/s/s. and prescribing via the community health index (CHI) number.5 mmol/min for 20 min. an environmental modification which encourages its reduction to nitric oxide (NO). as its stable chemical structure allowed for cheap preparation and easy storage. Linear regression analysis of the saline/ischaemia group was lower than the NO2-/ischaemia group. cross-over study was performed in 10 subjects with proven myocardial ischaemia documented by exercise tolerance testing and coronary angiography. NO2-/control ¼8.261. NO2-/ischaemia.1136/heartjnl-2011-300198. BNP may become an important tool in risk stratifying T2DM patients in the future. No difference was present between the three other groups.BCS Abstracts 2011 pattern.561. UK.6 cm/s/s.02 to 1. sex. Dundee. ST segment depression.9% saline and one with NaNO2. 2R A Bleasdale. and diabetic drug prescription as co-variants. UK 1 1 2 1 Abstract 51 Figure 1 A34 Introduction The use of brain naturetic peptide (BNP) to predict outcome in patients with normal ejection fractions (EF) and type 2 diabetes (T2DM) is understudied. Heart June 2011 Vol 97 Suppl 1 . Conclusions In patients with normal EF. HR 1.7 cm/s/s. Cardiff. We therefore studied the 5-year survival in a cohort of 500 T2DM patients prospectively phenotyped with echocardiography. organic nitrates). This dose of NaNO2 has previously been shown to be inert in normoxia but to vasodilate hypoxic tissue. Follow-up data was linked via the Health Informatics Centre (HIC). Two dobutamine stress echocardiography (DSE) studies were performed on each subject: one with 0. Dundee. Results In total we followed 316 patients over 8 years. UK Introduction Sodium nitrite (NaNO2) became a popular means of treating angina in the 19th century.760. BNP is an independent predictor of death in a cohort of T2DM patients. however these studies included small numbers of patients and did not fully exclude left ventricular systolic dysfunction (LVSD). see Abstract 51 figure 2. 51 LOW-DOSE SODIUM NITRITE RELIEVES MYOCARDIAL ISCHAEMIA IN PATIENTS WITH CORONARY ARTERY DISEASE: A TARGETED NO-DONOR EFFECT doi:10. Llantrisant. UK. This is the first study in patients to demonstrate a targeted vasodilator effect of NO2.460. 2C Templeton. but is associated with both cardiomyopathic and channelopathic processes in a significant minority. A D Struthers. P E James. Patients were recruited from the diabetes clinics at Ninewells Hospital. 1.0 cm/s/s. hospitalisation. Myocardial ischaemia was identified by the peak systolic velocity (PSV) response during DSE in a six basal-wall segment model of the left ventricle. 1A Margulescu. 52 BRAIN NATRIURETIC PEPTIDE PREDICTS ALL CAUSE MORTALITY IN PATIENTS WITH TYPE 2 DIABETES AND NORMAL EJECTION FRACTIONS doi:10. NHS Tayside. The peak-dose dobutamine values Abstract 51 Figure 2 Conclusions Low-dose NaNO2 delivers a therapeutic effect to ischaemic myocardial tissue in the absence of a vasodilator effect on normoxic tissue.

Framingham).1136/heartjnl-2011-300198. Faculty of Medicine and Health. 0. Leeds.53 1 1 A Nadir. 16. University of Dundee. a raised BNP is able to identify existing silent cardiac TOD of various subtypes particularly in males.62 (p¼0. After applying appropriate quality control filters. 18% LAE.002) among those with microalbuminuria than those without. Leeds. We measured BNP and calculated 10year global CV risk scores (based on Framingham.04. 1T M MacDonald. atrial fibrillation and renal impairment were excluded. Dundee. Conclusion Microalbuminuria is an independent predictor of silent “pancardiac” target organ damage in a non-diabetic primary prevention population. Results Out of 263 participants (Mean age 6466. Results One hundred and two (34%) patients (Mean age 6466.BCS Abstracts 2011 53 B-TYPE NATRIURETIC PEPTIDE PERFORMS BETTER THAN CURRENT CARDIOVASCULAR RISK SCORES IN IDENTIFYING SILENT “PANCARDIAC” TARGET ORGAN DAMAGE IN ALREADY TREATED PRIMARY PREVENTION PATIENTS doi:10.3% LVSD and 6. Results None of the analysed SNP-SNP interactions was statistically significant after correction for multiple testing (p¼7.8% LVSD and 6.7% LVH.1136/heartjnl-2011-300198. Glenfield Hospital.54 1 1 A Nadir.02) for QRISK. Leicester BRU.3e20.6160. University of Leeds. 2J Davidson. and left atrial volume while the presence of inducible ischaemia was assessed by dobutamine stress echocardiography or dipyridamole myocardial perfusion imaging.62 (p¼0.77 (p<0. Conclusion Silent cardiac TOD is highly prevalent (34%) in already treated primary prevention population but current CV risk estimation alone performs poorly in the detection of these silent cardiac abnormalities. The prevalence of cardiac TOD was significantly higher (53% vs 29%. The most significant interaction identified in this analysis was A35 . intermediate and high risk groups based on 10-year global CV risk.0001) in those with cardiac TOD compared to those without. 5A S Hall. The utility of UACR in discriminating between those with or without cardiac TOD was assessed by receiver operating characteristic analysis but the area under curve was only 0.7% LVH.0) pg/ml.6e40. However. left atrial enlargement (LAE) or silent myocardial ischaemia. UK. University of Sydney.1136/heartjnl-2011-300198.8310-10).4.0 years. In multivariate analysis adjusted for age. W Y S Wang. LV systolic and diastolic function. 2J Davidson.3% Ischaemia). UK Background Microalbuminuria is associated with increased cardiovascular mortality and is a marker of generalised vascular dysfuncHeart June 2011 Vol 97 Suppl 1 Background Only a small fraction of the heritability of coronary artery disease (CAD) has been explained by common variants identified by genome-wide association studies. become a new way to improve the primary prevention of CV events. 1T M MacDonald. One possible way to improve primary prevention of CV disease is to identify those patients who may already harbour silent pancardiac target organ damage in the form of left ventricular hypertrophy (LVH). A J Balmforth.2 to 4. BNP levels were significantly higher (median (IQR).1% LVDD.5) were included in pair-wise SNP-SNP interaction analysis using two complementary statistical approaches: logistic regression (PLINK and INTERSNP software packages) and Bayesian model (BEAM software). diastolic dysfunction (LVDD). 1Department of Cardiovascular Sciences. 1S Rekhraj. presence of microalbuminuria was an independent predictor of cardiac TOD with an adjusted HR of 2. S G Ball. UK.58 (p¼0. Patients were divided into low. p¼0.3% LVDD.3 years. Dundee. 5Division of Cardiovascular and Neuronal Remodelling. 1M Tomaszewski.54 (95% CI. Presence of microalbuminuria may help to identify those primary prevention patients who are at a particularly higher risk. We investigated whether interactions between common alleles in genes and pathways of known importance to cardiovascular regulation may contribute to the heritability of CAD. Methods Two hundred and sixty-three asymptomatic individuals without diabetes or previous cardiovascular disease on primary preventive therapy were prospectively recruited. UK 1 1 2 3 4 54 CAN MICROALBUMINURIA IDENTIFY SILENT “PANCARDIAC” TARGET ORGAN DAMAGE IN A NON-DIABETIC PRIMARY PREVENTION POPULATION? doi:10. 21. in the future. 1C C Lang. p¼0. We sought to investigate whether micoalbuminuria identified the presence of silent “pancardiac” target organ damage (TOD) ie. tion. Among the stones to be turned in the hunt for the missing heritability of CAD are genegene interactions. 1C C Lang. Methods We prospectively recruited 300 asymptomatic individuals without known cardiovascular disease already on primary prevention therapy.6 (13.001) for ASSIGN to detect presence of any form of TOD. 6. 3Division of Cardiovascular and Diabetes Research. p<0. systolic dysfunction (LVSD). systolic dysfunction (LVSD). gender. left atrial enlargement (LAE) or silent myocardial ischaemia in a non-diabetic primary prevention population. N J Samani. independent (r2 linkage disequilibrium coefficient of #0. Using BNP to identify silent cardiac TOD could.005).83 (p<0. hypertension and dyslipidemia. 17. 2Ninewells Hospital. QRISK and ASSIGN) in each participant. 1A D Struthers. 2School of Medical Sciences and Institute for Biomedical Research. LV systolic and diastolic function. 4LIGHT Research Institute.5 mg/mmol in males and $3. 2Ninewells Hospital. Dundee. University of Leicester. Microalbuminuria was defined as urinary albumin to creatinine ratio of $2. 11 332 common (minor allele frequency >10%). UK. left ventricular hypertrophy (LVH).001) for Framingham and 0. Patients with valvular heart disease. 7.5 mg/mmol in females. 1A D Struthers.8%) had evidence of silent cardiac TOD (29. 1S Rekhraj. Sydney. Methods 2101 CAD cases and 2426 controls of Caucasian origin recruited into Wellcome Trust Case Control Consortium were genotyped using 50 K IBC gene-centric array containing 45 707 single nucleotide polymorphisms (SNPs) of the highest biological relevance to cardiovascular system.7% LAE. However. Each participant underwent a comprehensive echocardiographic examination for the assessment of LV mass. and left atrial volume while the presence of inducible ischaemia was assessed by dobutamine stress echocardiography or dipyridamole myocardial perfusion imaging.55 M D Musameh. UK.0001) in males. 17. University of Leeds. discrimination power of CV risk scores was poor with area under curve of only 0.0) vs 11. Dundee Background Primary prevention needs to be improved because up to 70% of cardiovascular (CV) events occur outwith those classified as high risk by CV risk scores currently used in clinical practice (eg. diastolic dysfunction (LVDD). University of Leeds.4 (6. Leeds.1% Ischaemia). University of Dundee. 26%e33% in the intermediate risk and 36%e41% in the high risk groups based on three commonly used CV risk equations. Leicester. A spot urine sample was analysed for microalbuminuria and urinary creatinine by a trained laboratory technician blinded to clinical or echocardiographic data.0001) overall and 0. The prevalence of various cardiac TOD in each group was compared and ROC curves were constructed for BNP and for 10-year global CV risk scores to assess their ability to detect presence of silent cardiac TOD. Transthoracic echocardiography was used to assess LV mass. 55 GENE-GENE INTERACTIONS IN CORONARY ARTERY DISEASE doi:10. The prevalence of cardiac TOD ranged from 19 to 28% in the low risk. Australia. 58% males) had evidence of silent cardiac TOD (29. This could be achieved by reapplying traditional CV risk scores to primary prevention patients after they have been treated or by screening with a simple biomarker like B-type natriuretic peptide (BNP). UK.003. The AUC for BNP to identify any form of cardiac TOD was 0. 57% males) 89 (33. p¼0. 1.

average cost per patient would have been substantially higher at £838 (£362 per patient if likelihood <30%. An economic analysis of cost of investigation per patient was undertaken using current Payment by Results national tariffs. Overall this corresponds to a 60% increase in cost.464.9 Women 51 (48.01 3.0661.4) 40 (46. Average cost of investigation per patient was £528.9 Background The RACPC is a well-established “one-stop” service. K Al Fakih. with goal to identify patients with stable chest pain due to coronary artery disease (CAD) and quickly reassure those with non-cardiac pain.0612. As ICA is an expensive investigation.1 5.1136/heartjnl-2011-300198.90 / 1.7) 87 (52. S J Rooney. CT calcium scoring CT coronary angiography (CTCA) is recommended.46 29. T R Graham. 8.5) 53 (61.3860.86 / 1. In March 2010. Significantly. I C Wilson. NICE published a new guideline. Conclusion Our analysis suggests that common SNP-SNP interactions are unlikely to account for a large proportion of the missing heritability of CAD.9) 58 (34.3060.0 Men 86 (51.05) or molecular functionality (non-synonymous SNPs) did not contribute more significant findings than investigation of random set of SNPs.4% of patients were ultimately confirmed to have CAD on ICA. Relatively few patients would be eligible for CTCA. 49. UK Introduction There is limited data addressing the impact of preoperative renal dysfunction in type 2 diabetics (T2DM) undergoing firsttime coronary artery bypass surgery (CABG).7% of those with likelihood 30%e60% and 23. almost half of our patients would proceed to ICA as a first-line investigation.0 5.1% having a total of three or more RF.45310À8).3360. J Hodson. the guideline discourages the use of ETT to diagnose or exclude stable angina in patients without known CAD.4% had an estimated likelihood of 30%e60%.5) 47 (58. Conclusion The 2010 NICE guideline appears to significantly overestimate the true risk in our patient population.4) 72 (43. Methods 167 consecutive patients referred to RACPC between October 2009 and March 2010 were retrospectively assessed for likelihood of CAD according to the new NICE guideline. Methods We reviewed prospectively accrued data from 1/1/1999 to 31/12/2009. invasive coronary angiography (ICA) is recommended as the first-line diagnostic investigation. Consequently 23.0) 30 (37.BCS Abstracts 2011 between rs727139 (KCNH8) on chromosome 3 and rs11167496 (PDGFRB) on chromosome 5 (p¼2.1960.90 / 1. specifically exploring the influence of diabetic management (oral hypoglycaemic (OH) and insulin therapy (IN)).8 14 (17. but many of them would be found to have unobstructed coronary arteries. 27.06 3. Choice of investigations and eventual outcome (confirmed CAD vs no evidence of CAD) were compared between subgroups defined by estimated likelihood of CAD.761.0) 33 (40.43 30. gender.2360. 7. functional imaging is recommended.1460.3 15 (17.7) 137623 / 78610 5. £566 if likelihood 30%e60% and £1218 if likelihood >60%).04 3. D Pagano.5) 57.56 T Rogers. If estimated likelihood is 30%e60%. Were the NICE guideline strictly applied to our patient population. 14.4% had an estimated likelihood of >60%.8) 131618 / 80611 5. which advocates assessing likelihood of CAD based on age.2% of patients had an estimated likelihood of CAD of <30%.261.5) 55. We assessed the impact of preoperative renal status and diabetic management on the post operative renal status.3) 32 (39.166. University Hospital Birmingham. UK Abstract 56 Table 1 All Numbers (%) Age (mean 6 SD) Diabetes (%) Hypertension (%) Hypercholesterolaemia (%) Family history (%) Smoking (%) Systolic BP (mean 6 SD) / Diastolic BP (mean 6 SD) Fasting glucose (mean 6 SD) Total cholesterol (mean 6 SD) LDL (mean 6 SD) / HDL (mean 6 SD) BMI (mean 6 SD) 167 56. which correlated with pre-test estimated likelihood.2% of patients were lost to follow-up. 6% of patients with likelihood <30%.1136/heartjnl-2011-300198. A36 Abstract 56 Table 2 Average cost per patient prior to NICE guideline implementation Predicted likelihood <30% Predicted likelihood 30%e60% Predicted likelihood >60% OVERALL AVERAGE COST PER PATIENT £324 £467 £661 £528 Average cost per patient were NICE guideline strictly implemented £362 £566 £1218 £838 57 THE IMPACT OF PREOPERATIVE RENAL DYSFUNCTION AND THERAPY TYPE IN PATIENTS WITH TYPE 2 DIABETES UNDERGOING CORONARY ARTERY BYPASS SURGERY doi:10. A negative ETT resulted in average cost per patient of £347.0 5. Were the guideline strictly applied.1761. morbidity.2613. An inconclusive ETT resulted in higher cost (£728) as did inability to exercise (£435) due to the need for further investigations. University Hospital Lewisham.1) 100 (59. Pre and 4 to 5-day postoperative creatinine clearance Heart June 2011 Vol 97 Suppl 1 . this would inevitably result in a significant increase in average cost per patient.966.0611. 56 CLINICAL AND FINANCIAL REPERCUSSIONS OF THE MARCH 2010 NATIONAL INSTITUTE FOR HEALTH AND CLINICAL EXCELLENCE (NICE) GUIDELINE “CHEST PAIN OF RECENT ONSET” ON THE RAPID ACCESS CHEST PAIN CLINIC (RACPC) Abstract 56 Figure 1 doi:10. Birmingham. 30-day and long-term survival in T2DM-CABG.6 29 (17.57 A Menon.361. history and risk factors (RF).38 30. S Claridge. J Mascaro. R S Bonser.2961. Analysis of subsets of SNPs pre-selected based on their nominal association with CAD (p<0. A positive ETT resulted in average cost of £1174 due to the high cost of ICA.6) 54 (62. If estimated likelihood is <30%. If estimated likelihood is >60%. which is an excellent non-invasive “rule-out” test for CAD and relatively inexpensive compared with other investigations.6) 28 (32. Results Our patient population had a high prevalence of RF with 38. London.1) 134621 / 79611 5.2% of those with likelihood >60% were confirmed to have CAD.

C P G Gale. 0. UK 1 1 Introduction Offspring born to hypercholesterolaemic mothers have increased fatty streak formation in the fetal aorta. Renal dysfunction does not appear to affect hospital outcome or survival. p¼0. 18%.63.08%). COPD and mini-GRACE score.1136/heartjnl-2011-300198. STEMI. UK.411). revascularisation. However. IV 15e29. However.755) and LCOS (p¼0. p¼0. B L Lewin. Sex. York. 1. Similar percentages in each group had $1 grade deterioration of renal function postoperatively 19%. 58 TEMPORAL EVALUATION OF REFERRAL FOR AND LONGTERM SURVIVAL FROM CARDIAC REHABILITATION FOR ACUTE MYOCARDIAL INFARCTION doi:10. diabetes. Unadjusted survival for patients not referral for CR in 1995 was similar to that for patients referred for CR in 1995. II-584 (48%).48 to 0. 2Institute of Child Health. Overall 30-day mortality was 3. EMMACE risk score. Group I CrCl$90 ml/min. which persists into adolescence.34%) and was not different by group I-3. The Evaluation of the Management and Methods of Acute Coronary Events (EMMACE) 1 and 2 studies are 2 large prospective multi-centre registries of care of acute coronary syndromes (ACS) in Yorkshire undertaken in 1995 and 2003 in respectively.33% (CI 2.012 Spearman Rank).31. ablocker.04 to 1. p¼0.92 to 1. (Abstract 58 figure. This is despite the differences in patient and treatment factors between the 2 studies periods. S Neubauer. the Kruskal Wallis test was used for comparisons.09). p<0. Leeds. 95% CI) of CR referral was 0. 16% and 23% (grades IeIV respectively. Stroke (p¼1. anti-platelet agents and admitting cardiologist were regressed (backward logistic. regional aortic distensibility. Late KaplaneMeier survival data (compared by log rank method). KaplaneMeier (KM) curves compared unadjusted survival stratified by CR referral and EMMACE study. Unadjusted relative risk ratios (RRR) were calculated to assess mortality after referral for CR. 1J Diesch.001. III 4. 1J Francis.073.58 Abstract 58 Figure 1 KaplaneMeier survival estimates. p¼0.7%.8 to 9. the impact (HR.26%). reperfusion.0) vs OH 9. 1M Lazdam. Individuals exposed to maternal hypercholesterolaemia were excluded.96 to 1.8 vs 68. ACE-inhibitors.3 to 9. revascularisation. University College London. A Cox proportional model (Model 1: mini-GRACE score.57.32 to 4. bleeding (p¼0.6%) and Stage V 0% (CI 0 to 0.60 in 1995. 0. 2York St John University.001). 742 on OH and 472 on IN. Methods Baseline characteristics were described as numbers (%) or as means with IQRs.37% (CI 0. 36% of patients have CrCl <60 ml/min. 4University of Leeds. Even so. rate of referral for CR remain sub-optimal. IV-26(2%) and V (8(1%). age. 0. also has a long-term impact on the cardiovascular system we studied the vascular phenotype of adults in whom cholesterol levels were artificially elevated for a short period postnatally.4) years.6. University of Oxford.000). 2A Lucas. M B Bland. heart failure.54. admitting cardiologist) was used to compare the temporal long-term survival estimates (all cause mortality) by CR referral. York. UK 1 1 1 2 1 3 4 59 Background Cardiac rehabilitation (CR) is a cost-effective. Heart June 2011 Vol 97 Suppl 1 SHORT TERM ELEVATION OF CHOLESTEROL LEVEL IN NEONATAL LIFE AND LONG TERM CHANGES IN AORTIC STIFFNESS: INSIGHTS FROM USE OF INTRAVENOUS LIPIDS doi:10. II-2. 2A Singhal. reperfusion.101) or by therapy type. p<0. 0. (p¼0. Conclusions In T2DM-CABG. For those referred for CR. CR referral was 44% in 1995 and 59 % in 2003 (p<0. Leeds. the mean mini-GRACE score for CR referrals was lower in 2003 than 1995. University of York. the impact (HR. When examined as a continuous variable.1136/heartjnl-2011-300198. IN patients had shorter mean survival 8. Rates of uptake have and continue to vary despite recommendations from the NSF for CHD and NICE.59 A J Lewandowski. Aortic pulse wave velocity (aPWV). evidencebased approach to managing heart disease.55 to 0. Overall mean survival was 9 years (CI 8. higher preoperative CrCl correlated with a better postoperative improvement in CrCl (r¼0. Discrete variables were assessed by the c2 test. London.1(8. birthweight and gestational age with controls that did not receive IV lipids. P D Doherty. age.335) incidence were not different between therapy type.10 and goodness of fit with a group of 10) on CR referral and represented as 95% CI OR. Oxford. sex. Model 2: sex. censored at 1/10/2009 were obtained from the UK CCAD. II 60e89. UK. Patients were subgrouped into 5 grades based on preoperative CrCl. After adjustment using Model 2. anti-platelet agent. preoperative IN requirement increases the risk of renal dysfunction and is associated with worse longer-term survival. Methods We prospectively followed-up 102 subjects born premature now aged 23 to 28 years.2 years) and was not different by renal function grade (p¼0.001). UK. 1P Leeson. referral for CR increased and became a significantly important factor contributing to reduced mortality rates post-AMI. Results 4341 had AMI. UK. 1R Poole. Conclusion Between 1995 and 2003. p¼0.612). Surgical morbidity outcomes included re-exploration for bleeding.73 in 2003 and 1.1). 1E Davis. To understand whether exposure to elevated cholesterol in early life. left ventricular mass and ejection fraction were determined by cardiovascular A37 .76 to 7. Results 1215 patients (921 males) with a mean age of 64 years (31e89 years) underwent CABG. V <15 or haemodialysis. 1B Kelly. We studied the temporal changes in referral for and long-term survival from CR in patients who were admitted to hospital with an acute myocardial infarction (AMI). 3Yorkshire Heart Centre.92 to 5. C L Lewinter. 95%CI: 0. A S H Hall.09% (CI 0.3 vs 46.92 to 3.92% (CI 2.02. Higher CrCl protects against postoperative renal deterioration. IN patients had similar preoperative renal function (median CrCl 66.7 (8. heart failure.3 in 1995. independent of a maternal history of hypercholesterolaemia. After adjustment using the min-GRACE score (Model 1). statins. ACE-inhibitor. age.50 to 0. 0. but was not in 1995 (1. III-387(32%). COPD. 95% CI) of CR referral was 0.53 and 0.470). Preoperative renal status in the groups were Group I -209(17%). 1Cardiovascular Medicine. For Continuous variables.828) but a higher rate of postoperative renal deterioration (53. p<0.03.BCS Abstracts 2011 (CrCl) was calculated using Cockcroft-Gault formula.07. 0. III 30e59. Log rank tests compared the survival estimates. STEMI. CR referral was associated with reduced mortality in 2003 (RRR.4%.66 in 2003 and 1.82). IV 8% (CI 0 to 18.60).7 to 9.72. a-blockers. statins. stroke (type 1 deficit) and low cardiac output state (LCOS) requiring inotropes 6 intra-aortic balloon counterpulsation were compared using Fisher’s Exact tests. 18 received intravenous (IV) lipids during the first nine weeks of life and were matched 2:1 for pregnancy and early life complications. diabetes.

60 1 D Kotecha.56. University of Rennes.4%) WA (p<0. which we hypothesised could be used to risk-stratify cardiac patients (the Alternative Risk Markers in Coronary Artery Disease (ARM-CAD) study. 2F Carre. The greatest increase in stiffness was seen in the abdominal aorta. The association is graded depending on the degree of elevation of circulating cholesterol.61 60 ETHNIC DIFFERENCES IN REPOLARISATION PATTERNS AND LEFT VENTRICULAR REMODELLING IN HIGHLY TRAINED MALE ADOLESCENT (14e18 YEARS) ATHLETES doi:10. Dose given and number of days on IV lipids also associated with maximum cholesterol level during this period (r¼0. UK.003) and LVH (OR 3. 21% had diabetes. London. 3H Krum. regardless of comorbidity. 2Box Hill Hospital. London. These findings have important implications in the pre-participation screening era.001) were commoner in BA. p<0. Rennes. London. 1E Behr. 2G Kervio. 95% CI 1. mean blood pressure was 144/79 mm Hg (SD 21/10) and 16% had impaired left-ventricular function.71.56 to 8. Results Individuals that received IV lipids achieved significantly higher maximum cholesterol levels during the first 9 weeks of life than those that did not (mean6SD¼4. Melbourne.001).9164. The prevalence of ECG repolarisation changes and echocardiographic LVH in adolescent BA. respectively). UK.5% vs 14. In a stepwise regression model. p<0. ECG variables and medications. UK N Sheikh. Twave inversions and LVH were more prevalent in adolescent BA compared to WA.65 vs 3. with minor coronary irregularities 255 (400). 1St. is unknown. Abstract 60 Figure 1 Bar chart depicting the distribution of left ventricular wall thickness in black and white adolescent athletes. None of the athletes exhibited the broader phenotype of HCM on further investigation. 1R Bastiaenen. Twenty-three (10.461.6% of BA requiring further investigations for cardiac pathology. p<0. Patients with obstructive CAD had significantly reduced HRV. 3V Panoulas. black athletes (BA) demonstrate a high prevalence of ECG repolarisation changes and echocardiographic left ventricular hypertrophy (LVH) that may overlap with hypertrophic cardiomyopathy (HCM). UK.1136/heartjnl-2011-300198.001) and deep T wave inversions (11% vs 0. p<0.BCS Abstracts 2011 magnetic resonance.7464.557.596.001).584. solely derived from Caucasian cohorts.5%) BA exhibited a left ventricular wall thickness >12 mm vs only 6 (0. elite level.3%. 67% were male. There was a graded relation between the maximum elevation in circulating cholesterol postnatally and aortic stiffness (aPWV) in young adulthood (r¼0.006). Conclusions As with adult athletes.001). Methods Resting HRV prior to elective coronary angiography was analysed in 470 participants with predominantly normal cardiac rhythm. 61 FIVE-MIN HEART RATE VARIABILITY CAN PREDICT OBSTRUCTIVE ANGIOGRAPHIC CORONARY DISEASE doi:10. the group most vulnerable to exercise-related sudden death from HCM. 1S Sharma. Results ST segment elevation was common in both groups but more frequent in BA (63.78 mmol/ l. The presence of obstructive CAD ($50% stenosis) was regressed in a multivariate model including risk factors.5% vs 2. the median LF power (IQR) in patients with normal coronaries was 275 (612).17. H Raju.6 vs 9.001). 95% CI 1. p<0. 2French Institute of Health and Medical Research. Black athletes demonstrated greater left ventricular wall thickness (10. p<0.461. 3University Hospital Lewisham. Both T wave inversions (21. since extrapolation of ECG and echocardiographic criteria. UK 1 1 Purpose Studies in adult. 1J Rawlins. There were no differences between the groups in other vascular or left ventricular measures. In multivariable analysis black ethnicity was the strongest independent predictor for the presence of T wave inversions (OR 3. p¼0. 1Royal Brompton Hospital. Abstract 61 Figure 1 Heart June 2011 Vol 97 Suppl 1 . p¼0. France. inclusive) with 12-lead ECG and 2-D echocardiography.001 and r¼0.9%.1136/heartjnl-2011-300198. maximum cholesterol level achieved in the first few weeks of life was an independent predictor of aPWV in young adulthood (b¼0. There was a linear trend according to the severity of CAD. Athletes with T wave inversions and morphological LVH were invited for further investigation with exercise stress test. 3D Eccleston. High cholesterol exposure during sensitive periods of early postnatal life may have long term impacts on the cardiovascular system. p¼0. Conclusions Brief artificial elevation of cholesterol level in immediate postnatal life is associated with long term changes in aortic function independent of later cholesterol levels. 1M Papadakis.13.596.11/mm Hg3103. while ST segment depression was exceedingly rare. particularly in countries with a high proportion of BA competing at A38 Background Obstructive coronary artery disease (CAD) is evident in only half of patients referred for diagnostic coronary angiography. particularly in the low frequency (LF) range (median 180 vs 267 ms2 without CAD. p<0. would result in 25.012). p<0.2 mm.001) compared to WA. p<0.001).27 vs 12. George’s University of London. Methods This study evaluated 219 male adolescent BA (14e18 years.001) and accounted for 30.9% of the variance in hierarchical multiple regression (b¼0. p<0. Results Mean age was 65 years (SD 11). Metabolic parameters were measured multiple times per week for the first 9 weeks of life and again at follow-up visits. 24 h Holter and CMR.77 to 5. 1N Chandra. 2G New. p<0. Detailed lifestyle information and anthropometric measurements were collected during childhood and adolescence.9%.1260.3861. where distensibility was significantly reduced in the group that received IV lipids (mean6SD¼9.001). Five-minute heart rate variability (HRV) is a marker for autonomic control of the vasculature. Results were compared with 1440 male adolescent WA. Melbourne.001. 3Monash University.567. 1M Flather.

however. This audit shows that the rate of appropriate anti-coagulation among patients with AF is still low and could be improved further. Meta-analysis of anti-platelet therapy demonstrate a non-significant 19% reduction in the incidence of stroke. A39 .4%. London. occurring in 1%e2% of the general population. Only 57. Of the 125 selected case notes 114 arrived in time for analysis. CT calcium scoring should be offered. OAC instead of Aspirin or as first line antithrombotic therapy.0%).63 I U Haq.1136/heartjnl-2011-300198. were candidates for OAC. PCI or CABG were excluded. If the estimated likelihood of CAD is 61%e 90%. and if 10%e29%.0% vs 31. CHADS2 and CHA2DS2-VASc score.003. out of these 8 were excluded due to erroneous coding as AF. Abstract 62 Figure 1 Comparison CHADS2 & CHA2DS2-VASc scores. It will. Conclusions Application of NICE CG95 will change the investigation of patients with chest pain substantially. A random 10% of cases of patients discharged with a coding diagnosis of AF were selected (125 cases).3% vs 25. West Middlesex University Hospital. gender. The new ESC guidelines add to this challenge as significantly more patients will be considered for OAC therapy.0%. Royal Victoria Infirmary. correctly risk assessed. Recent guidelines have been published by the European Society of Cardiology (ESC) which focus on the most effective antithrombotic therapy in AF and propose a new risk scoring system. We determined the number and types of different investigations to diagnose coronary artery disease in patients referred with suspected cardiac pain before the publication of NCG 95 and compared this with the predicted investigations after the application of the guidelines. 62 WILL THE NEW EUROPEAN AF GUIDELINES LEAD TO MORE PATIENTS RECEIVING ORAL ANTICOAGULATION THERAPY? doi:10. A significant reallocation of resources will be required. ECG Q waves. The scoring systems were compared to identify patients in whom the ESC guidelines would change treatment―ie.6% vs 13. UK. functional imaging should be offered. UK Background The NICE clinical guideline for chest pain of recent onset (NCG 95) published in March 2010 recommends diagnosing angina based on clinical assessment and likelihood of coronary artery disease (CAD).46% (100) if CHA2DS2-VASc was applied.004) after adjusting for risk factors.22% (73) were high risk. diabetes and ST/T changes on ECG. prior cardiovascular disease or high-sensitivity CRP. Conclusion Low HRV is strongly predictive of angiographic coronary disease regardless of other comorbidities and is clinically useful as a risk predictor in patients with sinus rhythm. 73. 74. J S Skinner. Methods Data was collected prospectively in a bespoke database for patients referred to the Rapid Access Chest Pain Clinic. empower us to reassure almost a third of referrals that they do not have angina on clinical assessment alone. functional imaging tests and invasive coronary angiograms by pretest likelihood of coronary artery disease.0% vs 14. p-value for trend¼0. hyperlipidaemia. There was a similar reduction in LF power regardless of the anatomical location of coronary stenoses (see Abstract 61 figure 1). Invasive angiography will take on a more important role in the diagnosis of coronary artery disease. 95% CI 1. Patients with previous MI. type of chest pain (typical or atypical). In all cases the agent used for thromboprophylaxis was reviewed as to whether NICE recommendations had been met. The main outcome measures were actual and predicted future frequency of exercise tests. of whom 68. Patients with chest pain of suspected cardiac origin were referred from primary care between February 2002 and March 2010. They were risk assessed using the NICE 2006 stroke risk stratification. Heart June 2011 Vol 97 Suppl 1 IMPLICATIONS OF A LIKELIHOOD BASED APPROACH TO DIAGNOSTIC TESTING IN CORONARY ARTERY DISEASE: IMPACT OF THE NEW NICE GUIDELINES doi:10. In our institution the prescription and documentation of antithrombotic therapy in AF has been the focus of a previous audit that demonstrated poor compliance with the guidelines and documentation of decision making. this mostly comprised patients who were on Aspirin but. it is the most common sustained cardiac arrhythmia. the OR for obstructive CAD was 2.7%. Results The proportion of the study population before and after the guidelines undergoing exercise testing was 50. R Williams. Exercise testing will be replaced by anatomic or functional imaging. UK 63 Atrial fibrillation (AF) confers a 5-fold risk of stroke and the risk of death from AF-related stroke is doubled. P C Adams.04% (30) moderate and 2.0001). The analysis comprised 5598 men and women with no past history of coronary disease. 28. The focus of this audit was twofold: first to determine whether compliance with the guidelines and documentation had improved and second determine the effect of the new risk scoring system on prescription of OAC. CT coronary angiograms. S Khan. for whom OAC would be the recommended antithrombotic therapy (see Abstract 62 figure 1). CT coronary angiography will play an important role and replace functional imaging in some patients. smoking. Newcastle upon Tyne. In addition.BCS Abstracts 2011 single-vessel CAD 212 (396) and more severe disease 170 (327) ms2.77% (80) scored 2 or more points on the CHADS2 risk assessment―this number increased to 93.77% (45) of patients had no formal documentation why NICE guideline had not been followed. proving oral anticoagulation (OAC.1% vs 0. Comparing patients with LF<250 and $250 ms2. for functional imaging 25. No interactions were noted in sub-group analysis of age. If 30%e60%.8%. The proportion not requiring further testing was unchanged (30.80% (3) low risk according to NICE guidelines.50% or 61 patients were on the appropriate choice of thromboprophylaxis if the NICE guideline was used as risk assessment.1136/heartjnl-2011-300198. HRV added to risk prediction irrespective of baseline Framingham risk (p<0. coronary angiography should be offered. for calcium score/CT coronary angiography 0.62 T Kaier. medications and heart rate. the CHA2DS2-VASc score. Newcastle upon Tyne.38 (p¼0.33 to 4. and for invasive coronary angiography 15. 106 patients were risk stratified. 200 patients more per year would be considered high thromboembolic risk and hence appropriate for OAC. We extrapolate our findings to suggest that in an average sized DGH. sex. Likelihood of CAD was calculated by the Pryor equation using the variables age.42. diabetes. such as warfarin) to be far superior (64% relative risk reduction) in stroke prevention.

1West Midlands Deanery. preoperative renal dysfunction (OR 15. Methods Data for all patients undergoing cardiac surgery were collected prospectively in a registry. Conclusions In our population.19 vs ECG LRÀ ¼0. we found published studies regarding five different exercise testing modalities: treadmill ECG. bicycle ECG. we included 34 studies with 3352 participants.65 D A George. p¼0. However. is more useful at excluding CAD than confirming it. Retrospective analysis was carried using SPSS on data for 4901 patients operated on in the 6year period April 2004 to March 2010. p<0. Results During the study period. prevalence of CAD. treadmill echo. and modality of test used.1136/heartjnl-2011-300198. UK. Objectives To systematically review the literature to determine the diagnostic accuracy of exercise stress testing for coronary artery disease on angiography.38). We observed that the mortality rate in South Asian women undergoing cardiac surgery in our unit appeared to be relatively high.3. extra-cardiac arteriopathy (OR 4. but there is great scope for individualising the diagnosis of CAD using exercise testing. Clinicians have concentrated on individualising the treatment of CAD. South Asian ethnicity (OR 7.74) than in older patients (LR+ ¼2. p¼0. whether by echocardiography or ECG. A M Nevill.9% vs 4. p<0.005).8.3% in non-Asians (p¼0. diabetes (OR 7. sex and clinical characteristics of the patient.016).34) performed better than treadmill echo testing (LR+ ¼7. 16 were significantly associated with mortality.6%). Logistic regression showed the following to be independent predictors of postoperative mortality: urgency of operation (OR 32. bicycle echo and myocardial perfusion imaging. which outperformed both treadmill ECG and bicycle ECG. or patients without known coronary artery disease. Risk factors for inhospital mortality were subjected to univariate analysis.028). Birmingham. A Van den Bruel. p¼0.007).94) performed better than treadmill ECG testing (LR+ 3. Selection criteria We included prospective studies comparing exercise stress testing with a reference standard of coronary angiography in patients without known coronary artery disease. and a negative stress test may actually avoid angiography.BCS Abstracts 2011 64 DIAGNOSTIC ACCURACY OF EXERCISE STRESS TESTING IN INDIVIDUALS WITHOUT KNOWN CORONARY ARTERY DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS doi:10. Heart June 2011 Vol 97 Suppl 1 . 2Department of Primary Care. older age (OR 24.7%.1136/heartjnl-2011-300198. less expensive way of risk stratification prior to coronary angiography.2.64 A Banerjee. Results From 6055 records. C Heneghan. Oxford. Mortality in 113 South Asians was 8. Bicycle echo testing (LR+ ¼11.57) for ruling in CAD and ruling out CAD (echo LRÀ ¼0. Abstract 64 Figure 3 65 OUTCOMES AFTER CARDIAC SURGERY: ARE WOMEN OF SOUTH ASIAN ORIGIN AT INCREASED RISK? doi:10. Studies in larger populations are warranted. 1160 female patients underwent surgery with a mortality rate of 4. We investigated this observation further to determine whether ethnic origin was an independent risk factor for postoperative death in females. Categorical data associated with mortality were analysed using c2 tests.8. M Bhabra. Positive and negative likelihood ratios of stress testing increased in low prevalence settings. depending upon the age.8). UK 1 2 2 2 Background Exercise stress testing offers a non-invasive. 1New Cross Hospital.0. Overall. Wolverhampton. UK.001). previous meta-analyses have not included all exercise test modalities. D Newman.8. and those found to be significant were tested for independence using multivariate logistic regression. South Asian ethnicity appears to be an independent risk factor for mortality in females undergoing cardiac surgery. Treadmill echo testing (LR+ ¼7. p¼0. Exercise testing. UK 1 1 2 1 Abstract 64 Figure 1 A40 Objectives The population served by our centre has a relatively high proportion of people originating from the Indian subcontinent (“South Asians”) compared to the national average (14. Abstract 64 Figure 2 Probability of coronary artery disease. Wolverhampton. and an operation other than isolated CABG (OR 5. The prevalence of CAD ranged from 12% to 83%.3% vs 4. Search methods MEDLINE (January 1966eNovember 2009) and EMBASE (1980e2009) databases were searched for articles on diagnostic accuracy of exercise stress testing.001). University of Oxford. D Morrice. p<0.03).001). A positive exercise test is more helpful in younger patients (LR+ ¼4.94). 2University of Wolverhampton.8. Of 20 risk factors tested with univariate analysis. Conclusions The diagnostic accuracy of exercise testing varies.

1M A Mamas. LV dilatation and diastolic dysfunction similar to the clinical manifestations of diabetic cardiomyopathy. particularly in high-risk ethnic minority groups. GENA348 we demonstrate the development of a progressive cardiac phenotype including cardiac hypertrophy.3.0860. 1M Zi.4 to 6.960. Results In all. London. diastolic blood pressure and insulin resistance. including similar numbers of South Asian. GLK is the glucose sensor which regulates insulin secretion and GLK activity is reduced by 90% by the GENA348 point mutation resulting in severe hyperglycaemia.2 m/s (SD 0. 1S Prehar. characterised by an 8% increase in diastolic diameter (WT 4.8 mmol/l. 95%CI 0. 1Z Hegab. gender and allowed for clustering at school level. are apparent in childhood.475 mm (SD 0. oxford. 1400 children were invited to have measurements of cIMT (bilateral measurements were made with a Zonare ultrasound scanner). 2 Vascular Physiology Unit. 95%CI À0. South Asians have high risks of coronary heart disease and stroke while black African-Caribbeans have high risks of stroke and slightly low risks of coronary heart disease when compared with white Europeans. No significant changes in echocardiographic parameters were observed at 3 months.12. UK Heart failure (HF) is one of the commonest cardiovascular complications of Diabetes Mellitus (DM) with the prevalence of DM Heart June 2011 Vol 97 Suppl 1 Background Genome-wide association studies have been successful in identifying association between several common variants and coronary artery disease (CAD). suggesting a PI3K dependent signalling mechanism. A Rapala.035 mm). In contrast. 1M Tomaszewski. 2 MRC mammalian genetics unit. 2S G Ball. 2J E Deanfield.3 mmol/l vs HO 20. 1D G Cook.67 1 1 S M Gibbons.68 P Christofidou. HbA1c and triglyceride levels. 1C G Owen.1 to 5. E J Cartwright. 12 months-460%). London. A J Balmforth. 1A Donin.008 to 0. 1P S Braund. Following a baseline cardiovascular risk survey with measurements of body build. reported at around 30% in many pivotal heart failure studies. 6 and 12 months. UK. Because of the small number of observations for any given rare allele. 1R Debiec. AGE induced phosphorylation of Akt is inhibited in the presence of wortmannin. 6 months-140%.7 m/s). Leeds. C M Nightingale. markers of longterm cardiovascular risk. Serial echocardiography was performed. but little is known abut ethnic differences in vascular structure and function during childhood. UCL.1136/heartjnl-2011-300198. 95%CI 0. Systolic function was preserved although significant diastolic dysfunction was evident at 6 and 12 months with a 31% reduction in the E:A ratio. Leicester. insulin and HbA1c. Serum levels of advanced glycation end products (AGE) were also elevated by 86% (WT 2163. South Asian children had higher insulin. UK 2 1 67 SPONTANEOUS CARDIAC HYPERTROPHY AND ADVERSE LV REMODELLING IN A NOVEL HUMAN RELEVANT MOUSE MODEL OF DIABETES. South Asian children had similar cIMT to white Europeans but slightly higher PWV (% difference 2. 1L D S Bloomer. UK. black African-Caribbeans had higher cIMT (mean difference 0. However. Ethnic differences in cardiovascular risk factors are apparent in childhood. In conclusion. p<0. University of London. 2A E Donald.05). 939 children (67% response) had measurements of cIMT and 631 children (70% response) had measurements of PWV. at 3.021 mm) and PWV (% difference 3. 2A S Hall. common carotid intimal-medial thickness (cIMT) and carotidfemoral pulse wave velocity (PWV) in UK children from different ethnic groups. although by 6 months development of significant cardiac hypertrophy in HO mice was observed. identified through the MRC mouse mutagenesis programme with a point mutation in the pancreatic glucokinase (GLK) gene we investigate the molecular mechanisms that contribute to the HF phenotype in DM.660. A MECHANISTIC INSIGHT doi:10. St George’s. mean PWV was 5.no increase. Conclusions Ethnic differences in cIMT and PWV. fasting blood lipids.5%).66 1 2 P H Whincup. 1University of Leicester. D Joysurry. A subgroup of these children (n¼900) was also invited for PWV measurements. 1C P Nelson. made with a Vicorder device.5 ng/ml vs HO 3968. using the first human relevant mouse model of diabetes.001). 1N J Samani. These differences are not fully explained by the ethnic differences in established cardiovascular risk markers observed. It is becoming increasingly clear that the remainder of the “missing CAD heritability” could be explained by low frequency/rare alleles. We propose that the RAGE/PI3K/Akt pathway contributes to the molecular mechanisms associated with the cardiac phenotype.014 mm.1136/heartjnl-2011-300198. 2R D Cox. At 12 months of age left ventricular dilatation was evident. collectively these variants explain only a small proportion of CAD heritability. Mean random blood glucose was found to be increased in the GENA348 mutant (HO) mice compared to wild type (WT) littermates (WT 6.05) as was the protein expression level of the receptor for AGEs (RAGE). Methods We conducted a school-based study examining the cardiovascular risk profiles of 9e10 year-old UK children. Institute of Child Health.10 vs HO 4. black African-Caribbean and white European participants. All analyses were adjusted for age. however molecular mechanisms that contribute to HF development in the diabetic population are poorly understood.3 ng/ml. E Ellins.1136/heartjnl-2011-300198.2). 2M Prescott. Compared with white European children. In this study we have undertaken a novel statistical approach that combines information from all low frequency A41 . 2S Masi. Histological staining illustrated significant cellular hypertrophy with real time PCR data demonstrating a relative 150% increase in the hypertrophic marker BNP. 1A R Rudnicka.7. adjustment for these risk factors had little effect on the ethnic differences in cIMT and PWV observed. blood pressure. The results suggest that there may be important opportunities for prevention of cardiovascular disease before adult life. 1L Neyses. This was further confirmed in vivo where a bolus injection of wortmannin in 6-month old mutant mice returned Akt phosphorylation levels to those seen in WT mice. 1University of Manchester. 68 RARE ALLELES IN GENETIC PREDISPOSITION TO CORONARY ARTERY DISEASE: INSIGHTS FROM THE NOVEL ANALYSIS OF GENE-CENTRIC ARRAY doi:10. Black African-Caribbean children had lower LDL-cholesterol levels and higher insulin and HbA1c levels than white Europeans. UK.4160. the power to detect its association with a phenotype is a major limiting factor in genetic analysis. Similar mutations underlie Maturity Onset Diabetes of the Young Type 2 (MODY 2) in humans. However. PWV was positively associated with adiposity. cIMT was positively associated with systolic and diastolic blood pressure but not with other cardiovascular risk markers. We set out to measure two vascular markers of cardiovascular risk. DM is an independent predictor of mortality in patients with HF. Hypertrophic pathways were examined through western blot analysis revealing an age dependant increase in Akt phosphorylation (3 months.BCS Abstracts 2011 66 ETHNIC DIFFERENCES IN CAROTID INTIMAL MEDIAL THICKNESS AND CAROTID-FEMORAL PULSE WAVE VELOCITY ARE PRESENT IN UK CHILDREN doi:10. 1 Division of Population Health Sciences. Using a novel human relevant mouse model of DM (GENA348). In vitro cellular experiments also revealed AGEs directly activate Akt through phosphorylation and increase levels of the receptor RAGE. 2University of Leeds. p<0. 1T M A Mohammed. Mean cIMT was 0. UK 1 2 2 Introduction There are marked ethnic differences in cardiovascular disease risks in UK adults. Manchester. p<0.

The most significant over-representation of rare variants were identified at MMP23B (matrix metallopeptidase 23B gene.01). p¼6. the effects of the respective variants were independent of each other. The HumanMethylation27 chips interrogate 27 578 CpG sites spanning 14 495 genes with an average of 2 CpG sites per gene. 2Department of Medical Sciences.0% of the expression of these genes. Only one of the identified genes (LPAL2. University of Leicester. However. MTAP. We also found a correlation between methylation level and gene expression for a number of these genes. The number of analysed rare alleles at each of these loci ranged from 4 to 42. or differences according to genotype at CAD-associated SNPs. University of Leicester. ACD (p¼3. we examined the relationship of methylation level to transcript level in monocytes and macrophages on a gene by gene basis and identified several genes including GNAS and PCMT1 that showed significant correlations between gene expression and methylation.0310À64. Conclusions This pilot study has shown several significant differences in gene methylation patterns between CAD cases and controls. Results Global DNA methylation level was significantly higher in cases compared to controls (p¼9. Uppsala. 686 individual CpG sites. Pathway enrichment analysis of the differentially methylated genes using the DAVID bioinformatics resource identified a number of pathways that showed significant enrichment including the calcium signalling pathway (p¼3. Interestingly. the SNPs associated with CDKN2B and ANRIL expression were the same. ARF and MTAP in circulating monocytes from 422 healthy blood donors and 386 CAD cases and obtained genotypes for SNPs in the 9p21 region in the same subjects using genome-wide platforms. We compared expression quantitative trait loci (eQTL) associations for the genes with association findings for the same SNPs for CAD in the Wellcome Trust Case Control Consortium study. 70 1 1 GENE EXPRESSION AT THE 9p21 LOCUS AND CAD RISK doi:10. ranging in age from 40 to 57 years. To explore the potential funcA42 Background Human chromosome 9p21 harbours a locus that affects risk of coronary artery disease (CAD) through an unknown mechanism.69 K J Dick. tional importance of differences in methylation level in cases and controls for individual genes. Molecular Medicine. Results 5 candidate regions (MMP23B. Glenfield Hospital. these genes only explain part of the heritability. There is increasing evidence of the role of epigenetic regulation in complex diseases that may explain part of the missing heritability. PCMT1 (p¼7.94310À5). C P Nelson. Therefore we undertook an exploratory genome-wide screen to identify genes differentially methylated in CAD cases and controls. UK. ¨ Department of Cardiovascular Sciences.85310À7).0310À4). p¼1. We hypothesised that patients with CAD will show over-representation of rare alleles compared to controls. isolated from whole blood. P Lundmark. CDKN2B. Science for Life Laboratory. a gene previously unsuspected to play a major role in CAD and VEGFA (vascular endothelial growth factor A. A H Goodall. Methods We quantified transcript levels for CDKN2A.3310À38) and MTAP (p¼6. DNA methylation is an important epigenetic change that regulates gene expression. Uppsala University. Empirical p values were generated by permuting case-control status a predefined number of times and repeating the analysis for each replicate. The variants at the locus most strongly associated with CAD lie in non-coding regions suggesting that the affect on CAD risk may be mediated through regulation of gene expression.48310À4 part of the telosome/shelterin complex). Methods To examine associations between rare alleles and CAD. Differences in the proportion of cases and controls carrying rare “super loci” were tested by Pearson’s or Fisher’s exact test.BCS Abstracts 2011 (MAF<5%) SNPs at one locus in gene-centric analysis of CAD. the “missing heritability” of CAD. The mechanism by which the chromosome 9p21 locus affects CAD risk requires further elucidation. P S Braund.3/104). Any role of methylation in CAD is poorly understood. V Codd. We also quantified allelic expression (AE) for these genes and for ANRIL in 186 of the healthy blood donors. genomic DNA.1136/heartjnl-2011-300198.7310À3) lies within the locus that was previously shown to harbour rare variants associated with susceptibility to CAD.6310À3 and p¼0. which is involved in receptormediated signal transduction. explaining 17. spanning 633 genes showed statistically significant differences in methylation levels between cases and controls. Expression of CDKN2A and ARF was low but did not show any obvious eQTL effect. we have used data from 2119 CAD cases and 2440 healthy controls recruited to the Welcome Trust Case-Control Consortium (WTCCC) Study. All subjects were male. We investigated the association of single nucleotide polymorphisms (SNPs) across the locus with expression of genes in the locus and compared this with association of the same SNPs with CAD risk. we found strong cis eQTLs for both CDKN2B (p¼1. N J Samani. ATXN2 and APOA1 (p¼5. p¼2.94310À5).2310À12).6310À23). was bisulphite converted and run on Illumina HumanMethylation27 bead chips. Leicester. Results In the global gene expression analysis. Methods We characterised DNA methylation in 24 CAD patients with a documented history of MI and 24 matched controls from the Cardiogenics case-control cohort.70 C P Nelson. UK Background Using genome-wide association studies several genes have been identified that affect the risk of CAD. Association analysis was based on the CCRaVAT (Case-Control Rare Variant Analysis Tool) algorithm that maximises statistical power by combining all rare alleles within defined regions into a single “super locus”.5310À28). Significant signals after Bonferroni correction for multiple comparisons included GNAS (p¼7.1136/heartjnl-2011-300198. at least a proportion of. Furthermore. Sweden 2 1 1 69 GENOME WIDE METHYLATION ANALYSIS IN CORONARY ARTERY DISEASE doi:10. p¼1. A H Goodall.6310À4). VEGFA. Leicester. LPAL2) showed an over-accumulation of rare alleles in patients with CAD when compared to controls (FDR<50%). 1N J Samani. the SNPs showing e-QTL effects were distinct from SNPs that showed an association with CAD risk (p¼2. p¼1. However. Conclusions Our findings in monocytes do not support the hypothesis that the chromosome 9p21 locus mediates CAD risk by affecting expression of the genes at the locus. RIPK1. Even in the region with a physical overlap of variants affecting expression of CDKN2B/ANRIL and CAD risk. AE analysis confirmed these findings (CDKN2B. Conclusions Rare alleles are associated with predisposition to CAD and this gene-centric analysis combining information from lowfrequency variants of the same locus has a potential to uncover. While these findings require further validation they suggest that epigenetic changes may play an important role in the pathogenesis of CAD. For each subject. Heart June 2011 Vol 97 Suppl 1 . DVL1. 2A C Syvanen. DNA from each subject was genotyped for approximately 45 000 SNPs in more than 2000 genes/loci using 50K IBC array (version 1). Genes differentially methylated in CAD are significantly enriched for a number of pathways including the calcium signalling pathway.0% and 8.4310À38) and also showed a significant cis-eQTL effect on ANRIL expression (p¼3.

London.2D Das. a major risk factor for cardiovascular disease. 6M I McCarthy.1136/heartjnl-2011-300198.71 J Sehmi. P Muckett. UK. Cardiac troponin T2 knockdown prevented any cardiac contraction. Effect of troponin T knockdown on total vessel Conclusion Angiogenesis in response to hypoxic signalling is critically dependent upon haemodynamic force. 2Ealing Hospital NHS Trust. but embryos develop normally due to passive oxygen diffusion. Imperial College.1136/heartjnl-2011-300198. 2NIHR Cardiovascular Biomedical Research Unit. National University of Singapore. Cambridge University.7J Chambers. T2D is 2e4 fold more common among Indian Asians than Europeans. due to impaired HIF-1a degradation. loss of blood flow completely prevented excessive angiogenesis in vhl mutants (Abstract 72 figures 1D and 2). sodium nitroprusside (NO donor) (100mM) from 24-h post fertilisation (hpf) until imaging at 4dpf. we assessed whether NO contributed to angiogenesis in this model. Coding variant and eQTL studies at these loci identify genes closely involved in insulin secretion and signalling. 1. London. Sheffield. Physical forces exerted by blood flow have been shown to contribute to vascular remodelling. T J A Chico. London. Singapore. We used results from DIAGRAM+ to prioritise 19 loci for further testing in Indian Asians. However. F J van Eeden. In combined analysis of results from GWA and further testing. suggesting that the contribution of flow to excessive angiogenesis in response to upregulated hypoxic signalling is NO independent.2 3 4 5 Background Type-2 diabetes (T2D) is a major risk factor for cardiovascular disease. Imperial College London. Results There were two novel loci associated with T2D at p<10À6. Our observations provide new insights into the biological mechanisms underlying T2D. implying that both blood flow and hypoxic signalling are required for “pathological” angiogenesis but not developmental angiogenesis (vasculogenesis). Clinical Sciences Centre. Cambridge. compared with developmental vasculogenesis that can proceed in the absence of any blood flow. Oxford University. and a leading causing of mortality worldwide. PROMIS and SINDI cohorts. Results Imaging of the developing trunk vasculature revealed that vhl mutant embryos display excessive and aberrant angiogenesis from 3dpf (Abstract 72 figure 1A. 1MRC Centre for Developmental Biology and Genetics. and an additional 57 loci associated with T2D at p<10À4 in the GWA study. Oxford. Since NO has been shown to be both pro-angiogenic and released in response to haemodynamic force. University of Sheffield. haemodynamic flow and vascular development. 4E S Tai. UK Introduction Coronary flow reserve (CRF) is the ratio of peak coronary flow during maximal coronary artery dilatation to basal A43 . UK. and contributes to higher cardiovascular disease mortality in Asians. UK. London. NO synthase inhibition with L-NAME had no effect. UK 1 1 1 2 Introduction Hypoxia drives angiogenesis in a range of pathologies. Further testing of suggestive SNPs was carried out in independent cohorts of Indian Asian (12 K T2D cases and 25 K controls) and European ancestry (DIAGRAM+. 4Department of Medicine.72 O J Watson. GFP transgenic that expresses Green Fluorescent Protein (GFP) in the endothelium. UK. Methods Vhl mutant zebrafish were crossed with a fli1. D Salaheen. embryos were treated with either L-NAME (nitric oxide synthase inhibitor) (1mM) or Heart June 2011 Vol 97 Suppl 1 Abstract 72 Figure 2 length. 6Wellcome Trust for human Genetics. UK. 7Department of Epidemiology and biostatistics. 1National Heart and Lung Institute.73 R Ahmed. UK. Mutations in von hippel lindau protein (vhl) lead to excessive angiogenesis via upregulation of hypoxic signalling. W Zhang. We therefore used vhl mutant zebrafish to observe the interplay between hypoxic signalling. Methods We carried out a genome-wide association (GWA) study of T2D in 5561 Indian Asian cases and 14 458 controls from LOLIPOP. 3Department of Public Health and Primary care.2J Kooner. Whole genome scans were performed using the Illumina 317 k or 610 k arrays. Sheffield Teaching Hospitals NHS Foundation Trust.1136/heartjnl-2011-300198. Abstract 72 Figure 1 72 ANGIOGENESIS IN RESPONSE TO UPREGULATED HYPOXIC SIGNALLING IS DEPENDENT ON HAEMODYNAMIC FLOW doi:10. 2. B). To determine the role of blood flow in the angiogenic response. cardiac troponin t2 was knocked down by morpholino antisense injection. Little is known of the genetic basis of T2D in Indian Asians. Imperial College. C Gray. UK 3 1. Imperial College London. 1. Embryonic vascular development was observed in mutants and wild type siblings by confocal microscopy. 5Department of Epidemiology and biostatistics. To assess the contribution of nitric oxide. four loci now reached genome-wide significance (p<5310À8) among Indian Asians. S Cook. This indicates a different mechanism of development for hypoxia driven angiogenesis and vasculogenesis which may have important therapeutic implications. J Danesh. London. Y Yeo. 8 K T2D cases and 39 K controls).BCS Abstracts 2011 71 A GENOME-WIDE ASSOCIATION STUDY IN INDIAN ASIANS IDENTIFIES FOUR SUSCEPTIBILITY LOCI FOR TYPE-2 DIABETES doi:10. 73 HERITABILITY OF CORONARY FLOW RESERVE doi:10. Loss of blood flow did not alter normal intersegmental vessel patterning in either controls (Abstract 72 figure 1C) or vhl mutants (Abstract 72 figure 1D). Conclusion We identify four novel genetic loci associated with T2D in Indian Asians. Sheffield.

we will determine the quantitative trait loci and transcripts associated with CFR to improve our understanding of the genomic architecture of CFR. L Neyses.5 6 0.74 Z Hegab. 2) Heritability of CFR: Broad sense heritability (the proportion of total phenotypic variance attributable to total genetic variance) for CFR is 62% indicating a large and previously unrecognised genetic component of CFR. Manchester. the molecular mechanisms that underlie the pathophysiological contribution of AGEs to heart failure development are not yet fully understood. SHR¼1. A variety of environmental stimuli have been shown to affect CFR but little is known about the genetic component of CFR. 74 MECHANISTIC STUDY FOR THE ROLE OF ADVANCED GLYCATION END PRODUCTS IN THE DEVELOPMENT OF DIABETIC HEART FAILURE doi:10. However. Abstract 73 Figure 2 Correlation between BP and CFR. Results 1) CFR differs significantly between the two inbred parental rat strains.36. Brown Norway (BN) and Spontaneously Hypertensive Rat (SHR) which is a genetic model for hypertension and microvascular dysfunction.05) with subsequent nitrosylation of the Ryanodine receptor shown through immunofluoresence. Manchester University. Coexistence A44 Heart June 2011 Vol 97 Suppl 1 . p<0. Conclusions Our results demonstrate that CFR has a significant genetic component and is largely independent of BP effects. We demonstrated a 24% increase (p<0. r¼À0.1136/heartjnl-2011-300198.01) in the production of reactive oxygen species ROS in AGE treated cardiomyocytes mediated through increased NADPH oxidase activity (p<0.0001).6310À7.40. 4) Relationship between CF and myocardial relaxation (LV dP/dtmin): LV dP/dtmin correlated strongly with CF during all stages of the experiment (baseline CF. Methods Animals were anaesthetized using a mixture of Oxygen and Isoflurane. Changes in calcium transient were completely inhibited when we incubated the cardiomyocytes with inhibitors of NADPH oxidase. reperfusion CF.11. 3) Relationship between CFR and BP: We did not find statistically significant correlation between CFR and BP in the F2 intercross (r¼0. n¼16 each). Subsequent translocation of NF-KB. We then studied BP and coronary flow (CF) phenotypes in F1 and F2 crosses derived from BN and SHR to estimate the heritability of CFR and its relationship with BP.01) accompanied with 32% reduction in SR calcium content with no significant changes in the protein expression of calcium handling proteins. Standard molecular techniques were applied.05). UK Abstract 73 Figure 1 Coronary flow reserve. r¼À0. Furthermore we demonstrate a very significant relationship between CF and LV dP/dtmin indicating a link between LV diastolic dysfunction and impaired CF. The latter was associated with 10% increase in NO production (p<0. T M A Mohammed. A fluid filled balloon was placed in the left ventricular (LV) cavity to measure the pressure indices. BP was measured invasively by cannulation of carotid artery. Western blot showed that RAGE receptor is expressed in NRCM and adult mouse cardiomyocytes. n¼176). CF. p¼0. Following BP measurement hearts were excised and rapidly transferred to the ex vivo perfusion apparatus where retrograde perfusion was established using the Langendorff technique. LV developed pressure. The latter increased transcription of iNOS with increased NO production. We therefore investigated the effects and mechanisms of action of AGEs on isolated neonatal rat cardiomyocytes (NRCM).BCS Abstracts 2011 coronary flow and is an important predictor of coronary microvascular function. p¼2. a leading cause of morbidity and mortality in diabetic patients. Using 768 SNP genotyping assay for linkage mapping and gene expression analysis with Affymetrix rat gene chip.18. Advanced glycation end products (AGEs) are thought to play a crucial role in the development of diabetic complications including heart failure. M Mamas. during peak hyperaemia. To characterise the genetics of CFR we initially measured in vivo blood pressure (BP) and ex vivo cardiac phenotypes including CFR in two inbred rat strains. NOS or NF-KB prior to their incubation with AGEs. Hearts were perfused with Carbogen buffered Kreb9 s solution and paced constantly at 360 bpm. In conclusion.32. p<0.01).11.1 6 0. a transcriptional factor from the cytoplasm to the nucleus together with increased NF-KB activity resulted in a 56% increase in iNOS gene protein expression (p<0. a downstream target of NF-KB. regional ischaemia (induced by ligation of the proximal left anterior descending artery) and reperfusion. myocardial contractility (LV dP/dtmax) and myocardial relaxation (LV dP/dtmin) were recorded at baseline.0001. AGEs directly decline cardiomyocytes function through binding to their RAGE receptor leading to calcium handling impairment through increased ROS production inducing activation and translocation of NF-KB to the nucleus. (BN¼2. Incubation of NRCM for 24 h with AGEs showed a dose dependant reduction of calcium transient amplitude with a maximum of 52% at 1 g/l (p<0.

diamorphine. 2J Bell. Cardiff. 24-h Primary Angioplasty has been used for the treatment of ST segment elevation myocardial infarction (STEMI) since October 2008.2 mg/day Cardiac Glycoside: exemplar digoxin Frequency of use 43% Daily dose equivalent 83.1 mg/day ACE-I/ARB: exemplar lisinopril Frequency of use Daily dose equivalent 93% 11.75 1 S J Russell. A45 Heart June 2011 Vol 97 Suppl 1 . ACE-I/ARB. angiotensin converting enzyme inhibitors: ACE-I or angiotensin receptor blockers: ARB. We therefore conducted a retrospective analysis of our CRT database over a 9-month period to quantify the frequency of use. Total daily dose equivalences within each class of medication (bisoprolol for bB. UK. UK Introduction Cardiac resynchronisation therapy (CRT) is indicated in patients with left ventricular dysfunction (EF#35%). and loop diuretics) before and 6 months after CRT. A pathway was developed following consultation with the multidisciplinary team at an educational and mapping day. It was therefore agreed the point of contact and immediate decision making would lie with the Cardiac Care Unit (CCU) nurses. Conclusions The beneficial haemodynamic and pacing profiles provided by CRT offer important opportunities to further optimise heart failure medications after device implantation. UK Introduction In Brighton. 74 patients (age: 67611 yrs. and digoxin significantly increased.32 Methods The on-call cardiology team are non-resident out of hours. cannulation and venepuncture. we successfully initiated b blockers and digoxin in previously naive patients. aldosterone antagonists. while the dose of loop diuretics significantly reduced in the 6 months after CRT implantation. bB.4 mg/day <0.2 mg/day 93% 12. and follow-up components.963. defibrillation. and dose of HF medications (bblockers. Abstract 76 Table 1 % CTBT £150 mins Financial Year 2009e2010 Quarter 1 (AprileJune 2010) Quarter 2 (JulyeSeptember 2010) *p¼0.8 mg/day 28% 15. It was agreed that the ambulance crew would telephone the CCU nurse who would review the clinical history and the telemetry ECG. spironolactone for aldosterone antagonists. Pre-assessment and follow-up incorporate dedicated HF nurse clinics to support protocol-driven optimisation of medical therapies. and risks were addressed.76 S Young. The frequency of bB and digoxin use increased by 10% and 5% respectively. 86% male) underwent implantation of a CRT device. Cardiff.666. metoclopramide and clopidogrel were developed so that immediate treatment could be delivered by the CCU nurse without medical prescription before the cardiac catheter lab team arrived. UK.6 mg/day 100% 48.1136/heartjnl-2011-300198. In many cases target doses of HF medications prior to CRT are not achieved due to bradycardia and/or limiting hypotension. Nursing documentation was developed to prioritise the patient9 s emergency care. 4University Hospital Llandough.BCS Abstracts 2011 of ROS and NO favours the production of peroxynitrite that is capable of nitrosylation of key cellular proteins such as the Ryanodine receptor that has a crucial role in cardiac excitationcontraction coupling. with local patients being admitted via the Accident and Emergency (A&E) department. Cardiff. In addition. 3H Rose. and limiting heart failure (HF) symptoms despite optimal medical therapy. 4J Davies. Abstract 75 table 1 describes the frequency of use and daily dose equivalent of each class of medication used in the patients prior to and 6 months after device implantation. They would then make the decision to activate the catheter lab team. patients attended the pre and post CRT nurse clinic to optimise medical therapies and provide adjunctive HF support. Cardiff.02 Daily dose equivalent 5.864. CRT however provides bradycardia backup and improved haemodynamics. We conducted the present study to evaluate the potential to further optimise medical treatments in patients receiving CRT within the framework of nurse-led pre and post CRT clinics.4 mg/day Loop Diuretic: exemplar frusemide Frequency of use Daily dose equivalent 100% 63. and digoxin.8611.0013. ACE-I/ARB. while significantly reducing loop diuretic use in the 6 months after device implantation. UK.463. digoxin. Patient Group Directions for the administration of GTN. Results Between October 2009 and Jun 2010. In a dedicated nurse-led CRT follow-up clinic. The nurses were trained in their use and assessed as competent. 75 OPTIMISATION OF MEDICAL THERAPY AFTER CARDIAC RESYNCHRONISATION: A NURSING OPPORTUNITY NOT TO BE MISSED doi:10. Call to Balloon time (CTBT) <150 mins is a nationally recognised indicator measuring the time the patient first calls for professional help (usually the ambulance) to the opening of the coronary artery on the catheter lab Abstract 76 table 1.1136/heartjnl-2011-300198.5 mg/day Aldosterone Antagonist: exemplar spironolactone Frequency of use 32% Daily dose equivalent 16. 3University Hospital of Wales. 1Wales Heart Research Institute. Brighton. A de Belder. lisinopril for ACE-I/ARB.3 mg/day 48% 96. thus providing an opportunity to further optimise HF medical therapies known to confer substantial morbidity and mortality benefits. G Pretsell.01 <0.363. Methods Our unit operates an integrated CRT service with preassessment. All 76 EXPANDING THE ROLE OF CARDIAC CARE UNIT NURSES TO REDUCE TIME TO TREATMENT FOR PATIENTS REQUIRING PRIMARY ANGIOPLASTY doi:10.01 0. This study provides novel insights into the mechanisms of cardiac damage in diabetes that occur independent of vascular disease through AGEs.01 b-Blocker: exemplar bisoprolol Frequency of use 78% 88% 6. 3L Edmunds. Royal Sussex County Hospital.168. Nurses were already competent in ECG interpretation. 3Z R Yousef. 2Cardiff University. implantation. G Dixon. electromechanical dyssynchrony. and significantly uptitrated the doses of b blockers. A Gibbins.8 mg/day 0.567. and frusemide for loop diuretics) and titration protocols were based on National Institute of Clinical Excellence guidelines for HF (guideline 5). if required. With the publication of the National Infarct Angioplasty project report (DH 2008) it was evident that direct admission into the cardiac catheter lab from the ambulance could further reduce time to treatment. CTBT were monitored. UK.065. the dose of bB. 59/78 76%* 32/36 89% 44/45 98%* Median CTBT 125 mins 111 mins 99 mins Abstract 75 Table 1 Heart Failure nurse supervised use of medications before and 6 months After CRT Pre-CRT Post-CRT p Value <0.1613.

Along with the work of all members of the multi disciplinary team this has significantly reduced times to treatment for patients. Relatives domiciled outside UK were given our details with offers to support screening. Here we report our first year9 s experience of this facility. 77 SCREENING FIRST DEGREE RELATIVES FOR HYPERTROPHIC CARDIOMYOPATHY: 12-MONTH EXPERIENCE OF A CARDIOGENETICS NURSE SERVICE doi:10. The lounge is a day case unit that has no beds. we diagnosed 15 new cases of HCM. Methods We mapped the course of patients with suspected HCM referred to our tertiary heart muscle clinic which serves a population of 1.1136/heartjnl-2011-300198. K Khimdas. Of the 71 screened subjects. these 3 patients have received primary prevention defibrillators. Screening to identify at risk first degree relatives is therefore recommended. R Weerackody. They have said: Abstract 77 Table 1 Screening outcomes of 221 at risk subjects identified from 64 index cases of hypertrophic cardiomyopathy Number of Patients New screening initiated (local heart muscle clinic) New screening initiated (local paediatric clinic) New screening initiated (out of area service) Pre-existing screening in place Personal preference (declined screening) Awaiting response from subject (literature delivered) Complex family relationships (unable to deliver literature) Geographical/Logistical constraints Subject deceased (non-hypertrophic cardiomyopathy) Subject deceased (hypertrophic cardiomyopathy) 52 19 6 63 28 19 14 10 3 7 < < < < The process is quick which is good from their perspective They are fully informed The ambulance crews deal with them competently The lab staff are waiting for their arrival. UK 2 1 1 1 Introduction Hypertrophic cardiomyopathy (HCM) is an autosomally transmitted cardiomyopathy with an estimated gene prevalence of 1:500. 71 (19 through paediatrics) have undergone screening through clinical assessment at our unit with plans for long-term 2e5 yearly follow-up in view of variable gene penetrance. Pedigree analysis identified 221 first degree relatives at risk of carrying the HCM gene. UK Introduction The potential to achieve safe early mobilisation and same day discharge on a consistent basis after radial artery access has provided us with the opportunity to make a step change in the way we deliver elective care to patients undergoing percutaneous coronary procedures. 64 index HCM cases presented to our heart muscle clinic. Despite our approach. Of the 221 at risk subjects. After appropriate counselling. Our application for a nurse was successful and we present our 12-month experience of HCM screening. London Chest Hospital. Of 71 asymptomatic at risk subjects screened in our unit. A Archbold. N Cleary. Patients were suitable for the radial lounge if they were elective cases who had a satisfactory radial pulse and no pre-procedure contraindication to Heart June 2011 Vol 97 Suppl 1 . despite the challenges of working within the complex nature of traditional geographical referral patterns. Methods: The study population comprised all patients who attended the radial lounge between July 2009eJune 2010 for coronary angiography or percutaneous coronary intervention (PCI). Patients remain in their clothes throughout their hospital visit. and an important cause of sudden cardiac death. London. This is statistically significant when looking at Quarter 2 results from baseline.78 S Brewster. Conclusions The CCU nurses have embraced this development and expansion of their nursing practice. and 3 patients at high risk of sudden cardiac death who subsequently received primary prevention defibrillator implantation. Following phenotype confirmation. Cardiff. University Hospital of Wales. Conclusions Proactive screening for HCM can be effectively facilitated by cardio-genetic nurse services. The information pack included an open invitation (referral via primary care) to attend for screening. where we identified 3 patients at high risk ($2 conventional high sudden death risk factors). S Russell. Wales Heart Research Institute. Throughout. allowing major changes to be made to the Primary Angioplasty pathway within the existing infrastructure. a family tree and contact details from the index case were recorded by the cardiogenetic nurse. strict adherence to patient confidentiality was maintained. only chairs.77 1 2 S Finch.BCS Abstracts 2011 Results Following the implementation of the direct entry pathway in May 2010 the CTBT for all patients admitted direct to our hospital have reduced. Cardiff. Patients who were admitted directly have been asked about their experience and if anything could be done differently from their perspective. and televisions but no cardiac monitors.4million. Newly diagnosed HCM patients underwent further risk stratification for sudden cardiac death.4 (range 0e14 subjects). either due to complex family relationships (n¼14). Results Over 12 months. 15 were newly diagnosed with HCM. A Little. personal preference (n¼28) and/or geographical/logistical reasons (n¼10). The British Heart Foundation (BHF) recently funded nine Nationwide cardio-genetic nurses to support local initiatives.1136/heartjnl-2011-300198. 52 subjects remain unscreened (Abstract 77 table 1). UK. mean index-to-at RR: 1-to-3. We designed a dedicated “radial lounge” to accommodate patients before and after their procedure with the aim of minimising the feeling of “hospitalisation” that accompanies most encounters with health services. A Penswick. Z R Yousef. Each new index case generates 3e4 at risk relatives who require long-term surveillance. D Kumar. The index case was given literature to pass onto at risk relatives. A46 Abstract 77 Figure 1 78 FIRST YEAR EXPERIENCE OF A DEDICATED “RADIAL LOUNGE” FOR PATIENTS UNDERGOING ELECTIVE PERCUTANEOUS CORONARY PROCEDURES doi:10. For relatives residing outside our catchment area screening was arranged via links with the BHF cardio-genetic network and other health care providers. Patient safety has not been compromised. M Rothman.

Patients were excluded if they had any of the following: an unsuitable radial pulse. Of these. Having patients remain dressed did not reduce fluoroscopic image quality and there were no issues with infection. This demonstrated an average LOS of 4.3% vs 14. M Sinha. The average LOS for all PPCI patients (n¼274) decreased from 4.1136/heartjnl-2011-300198. prior coronary artery bypass surgery. a total of 274 patients were admitted with STEMI. and 439 underwent PCI. a retrospective baseline audit was conducted. or social reasons. and 8 (1. and the possibility of soiling the clothes with either blood or iodine. Salisbury. patients were then asked to fill in an anonymous questionnaire in which they were asked about their experience and whether not having to undress made them feel more relaxed. The other two patients felt that it made no difference. Femoral access is associated with a significantly greater requirement for overnight admission. haemodynamic instability. Of the 45 patients that had not had a previous DCA.8%) patients who had three vessels treated. 105 (23.7%) were discharged the same day. It was noted that introduction of the protocol also facilitated a structured approach to discharge for the medical team. Among the PCI patients.1% vs 2. After 5 months the audit was repeated to assess the average length of stay for patients presenting with STEMI.4 days to 2. Following the baseline audit.79 S Eve. 122 (45%) met the NLD criteria and were discharged by the ACS ANP. p<0.6 years. Results In the one year study period. 938 (84. This demonstrates part of the added value the advanced nurse practitioner brings to patient care and to tertiary centres that provide a 24/7 PPCI service. This is now standard at our Institution.8%. Conclusions/Implications In the current financial climate. Results 57 consecutive patients underwent (DCA) during this time period (100% uptake) with an average age of 68.0%) were discharged from the radial lounge on the same day as their procedure. A 48 h nurse led discharge (NLD) protocol was therefore developed and introduced by the acute coronary syndromes advanced nurse practitioner to streamline the patient journey. Conclusions A dedicated radial lounge free of cardiac monitors is a safe environment in which to manage most patients before and after elective coronary angiography and PCI. 71% were male and 21% (12/57) had undergone a DCA previously.4 days which is above the National Infarct Angioplasty Project 2008 average LOS of 3 days. a decrease in LOS can have a significant impact on any organisational resources thus increasing efficiency saving and patient throughput. data were electronically collected prospectively for 5 months. One of the many benefits claimed is reduced length of stay due to decreased morbidity (Zahn et al 2000.2%) of whom also had a pressure wire or intravascular ultrasound. T A Wells. 114 (10. ejection fraction <40%. This instructed the nurse and/or physician to ensure appropriate investigation and documentation was carried out in a timely manner to avoid unnecessary delays in patient discharge. 1109 patients underwent coronary angiography.2%. failure of radial access and the subsequent need for femoral access. 1548 patients were managed in the radial lounge. The only caveat stated was that female patients were not allowed to wear an underwire bra. This represented approximately 88% of our unit9 s elective angiograms and 60% of our elective PCIs. these 12 patients 92% (11/12) stated that not having to undress was a good idea while an identical number felt much more relaxed than their previous DCA experience. The PCI group included 326 (74. which included: absence of acute complications (eg. Salisbury District Hospital. ongoing chest pain.9%) who had two vessels or a bifurcation with a significant side branch treated. A47 . the average LOS decreased from 4.05) and PCI (21. Bristol. The remaining 152 (55%) were discharged by the medical physicians. Result Between 1st April 2010 and 31st August 2010. Method Suitability criteria for the 48-h NLD protocol were established.4 days to 3 days (30%).0 days (55%).1 6 9. or the requirement for an overnight hospital stay for planned complex/high risk PCI.80 V Oriolo.1136/heartjnl-2011-300198. p<0. J Tagney. It is therefore part of the cardiac catheter laboratory staff9 s role to reduce patient fears and hence improve their journey through the cardiac catheter laboratory. Following their DCA. patients undergoing radial DCA at Salisbury District Hospital were offered the option of remaining clothed for their procedure. Bristol Heart Institute University Hospital Bristol NHS FT. Conclusion Offering patients the option of having their radial DCA done without undressing is safe and helps to improve the patient journey through the cardiac catheter laboratory by making them feel more relaxed and less hospitalised. Requirement for overnight admission was significantly more common after femoral access compared with radial access for both angiography (4. appropriate support at discharge. respiratory compromise). Of Heart June 2011 Vol 97 Suppl 1 Introduction Primary Percutaneous Coronary Intervention (PPCI) is now considered the treatment of choice for patients experiencing ST Elevation Myocardial Infarction (STEMI) (European Society of Cardiology/European Association for Cardio-Thoracic Surgery 2010). between mid-August 2010 and the end of October 2010. 80 PPCI: IS THERE A ROLE FOR THE ACS ANP? doi:10. UK 79 REMAINING CLOTHED FOR RADIAL DIAGNOSTIC CORONARY ANGIOGRAPHY: AN IMPROVEMENT IN THE PATIENT JOURNEY doi:10. measuring date of admission to date of discharge to the usual place of residence. Methods Following infection control approval.: bleeding. The lack of monitoring necessitates patient selection but this does not prevent the lounge being suitable for the majority of elective patients. No patients required cross-over to femoral access and there were no blood or iodine stains on any clothes. Each patient was given an information leaflet included in which was explained possible downsides to being dressed including if CPR were needed then clothes would be cut. The final decision regarding route of arterial access was left to the operator. renal impairment. planned femoral access. For patients that were seen and discharged solely by the advanced nurse practitioner (n¼122). Kalla et al 2006). Several Cardiac centres have recently introduced radial lounges whereby patients feel less “hospitalised” by not needing to undress for their procedure. To assess performance of one English PPCI 24/7 provider organisation against the national average length of stay (LOS) for patients post PPCI. UK Background Patients undergoing invasive diagnostic coronary angiography (DCA) for the first time often display high levels of anxiety at the time of their procedure as they are unfamiliar with the cardiac catheter laboratory set up.5%) were performed radially and 1076 (97. 359 (81. 96% (43/45) stated that not having to undress was a good idea while 96% (43/45) felt that this had made them feel very relaxed during their pathway.8%) were performed radially and 372 (84.BCS Abstracts 2011 same day discharge.3%) patients who had a single vessel treated. Among the patients who underwent angiography.01). There were no deaths or arrhythmias in the radial lounge.

5 9.034 DR R/V SCREEN FOR ICD À8. E2 165 per year.0 0. Paediatric and multi-organ transplants were excluded from the transplant cohort.663.3 0.4 7. University of Birmingham. The software offered timing information to calculate SD and time delays for different motions.01 0.001 40. 8N R Banner.001).564. Patients who received prior short-term support (bridge to bridge) were excluded from the VAD group.on behalf of the UK VAD Forum and UKCTA Steering Group. ECG.059 in IVRT (8/mm) Conclusion Patients with HFNEF show a deterioration of basal rotation and a systolic and diastolic three plane dyssynchrony particularly on exercise.SaO2>93%) REG/SENIOR NURSE TO BOOK ECHO & TRANSFER TO WARD (IF APPLICABLE) Results As previously described apical rotation was reduced at rest and on exercise Basal rotation was comparable at rest but significantly reduced on exercise in patients. UK. Birmingham. University of Bristol.1 25. UK. R S Bonser.4 0. 5S Schueler.464.9 ml/min/kg). Stoke on Trent.7 21. 29 female. Method 72 Patients (age 7367 years.8 0. 4Cardiopulmonary Transplantation. 4S Tsui.NO NEW ECG CHANGES .1627.6614.9 <0. UK 7 1 Introduction Patients with advanced heart failure due to systolic ventricular dysfunction require “pump replacement” therapy. UK 1 2 3 3 Background The pathophysiology of heart failure with normal ejection fraction (HFNEF) is complex and not fully understood. UK. 5 Cardiopulmonary Transplantation.0 <0. Papworth Hospital NHS Foundation Trust. 2Institute for Science and Technology in Medicine. 3NHS Blood and Transplant. Cambridge. 2Clinical Trials and Evaluation Unit. IF PATIENT UNSTABLE AT ANY STAGE PLEASE D/W DR/ACS NURSE 82 Abstract 80 Figure 1 PPCI nurse LED discharge protocol. 7Cardiopulmonary Transplantation.1136/heartjnl-2011-300198. All underwent full Doppler 2D-echocardiography at rest and on supine exercise.7 3. 6Heart and Lung Transplantation.065. 3H L Thomas. J E Sanderson.011 19. Bristol. This might be a major contribution to their symptoms.565. Echo images were analysed off-line. too.9615. A Emin. Newcastle.063. longitudinal and radial displacement) was comparable at rest but on exercise controls showed a significantly reduced SD compared to patients showing a greater ability to synchronise motions.763. Bristol.82 81 DYSSYNCHRONOUS THREE PLANE MOTION AND IMPAIRED LEFT VENTRICULAR TWIST IN PATIENTS WITH HEART FAILURE AND NORMAL EJECTION FRACTION doi:10. We report UK activity.3651. Birmingham. REHAB TO SEE 48 HRS PATIENT STABLE* (AS ABOVE) BLOODS. Apical and basal rotation.38 Ratio Untwist/Extension 25.363. 75 (31%) also received a right VAD. longitudinal and radial displacement were measured by speckle tracking. MANAGEMENT OF ADVANCED HEART FAILURE IN THE UK: TRENDS IN HEART TRANSPLANTATION AND MECHANICAL CIRCULATORY SUPPORT doi:10.9 25. Methods Data were acquired from a comprehensive national database using 3 eras for analysis: E1: 5/2002e12/2004.4 Controls Rest Patients p value Exercise Controls Exercise p value EF≤ 39% 36 HRS PATIENT STABLE* (AS ABOVE) EF≥ 40% & KILLIP I Y N ARRANGE ASAP 13. trends and outcome for HTx and BTT VAD.1625. EF 6367%) with a normal exercise tolerance (VO2max 28. The software interpolated all curves and calculated twist as the difference of rotation at apex and at base. Keele. 3Department of Cardiovascular Medicine. UK. Keele University. Data were compared to 38 age-matched control subjects (age 7167 years.PAIN FREE . D/C LETTER.0 <0. F Leyva.966.676 18. 8Royal Brompton and Harefield NHS Trust . 24 HRS PATIENT STABLE * (AS ABOVE) Abstract 81 Table 1 DEMONITOR + ECHOCARDIOGRAM+ REHAB REFERRAL ECHO PERFORMED? Patients Rest Apical Rotation (8) Basal Rotation (8) Twist (8) 9. Queen Elizabeth Hospital. MINAP. The number of adult HTx fell from 132 per year in E1 to 94 per year in E3.464.001 À7. more patients require a ventricular assist device (VAD) as a bridge to transplant (BTT).064.001 12. London. Freeman Hospital. The SD for four different systolic peak motions (basal and apical rotation. Activity rose from 26 per year in E1 to 41 per year in E3.1 ml/min/kg). F W G Wenzelburger. All results are presented in Abstract 81 table 1. 1Department of Cardiovascular Medicine. E3 148 per year. COPY OF PROCEDURE.7 16. 6A Simon. E2: 1/2005e12/ 2007 & E3: 1/2008e6/2010.6632.81 Y T Tan. Previously. 239 patients needed left VAD support as BTT. UK. Middlesex. Speckle tracking pictures and colour TDI curves were loaded into custom made software. This might further contribute to the deterioration of early diastolic suction and therefore decrease stroke volume on exercise. heart transplantation (HTx) met this need but waiting times have increased due to shortage of donor hearts.363. 2C A Rogers. 1Clinical Effectiveness Unit. Results 1278 patients were listed for HTx over the 3 eras: E1 155 per year.964. The median waiting time for non-urgent HTx increased from 87 days in E1 (95%CI 55 to 119) to 321 days in E3 (95%CI 203 to 439) (p<0.01 TTA’S. UK. Furthermore a ratio of untwist during IVRT and longitudinal extension (Ratio Untwist /Extension in IVRT) showed a significant deeper slope on exercise for patients indicating a loss of synchrony in diastole.3 À8. Middlesex. MINAP TO BE SEEN BY ACS NURSE/DR HOME SD Systolic Motions (ms) 48.665. Royal Brompton and Harefield NHS Trust.763. 4J Parameshwar. University of Birmingham. Birmingham.1136/heartjnl-2011-300198.9 43. UK.1610. Device Heart June 2011 Vol 97 Suppl 1 A48 . UK. Consequently.BCS Abstracts 2011 PPCI NURSE LED DISCHARGE PROTOCOL PPCI -REPERFUSION TIME 0 CCU 12HRS PATIENT STABLE* (SYSTOLIC BP> 100 mmHg .7 0. 48 female) with breathlessness on exertion and normal EF (6067%) underwent cardiopulmonary exercise test to rule out alternative clinical reasons (VO2max 18.2 À9. 5G MacGowan.9 0. The Royal College of Surgeons of England. Whether a deterioration of basal rotation and a dyssynchrony of different three plane motions on exercise might contribute to symptoms in these patients is not known. VENFLON OUT. Recent publications showed a loss of apical rotation and longitudinal function particularly on exercise in these patients. UK.

While bridging appears to increase mortality early after HTx.160.3% (95%CI 88 to 92) respectively at 30-days (p<0. 2 patients were transplanted (at 3 and 241 days after implant) and 1 had recovery of LV function.961. E2 and E3 respectively.9% (95%CI 40 to 64) in E1 to 65.9 13963 p Value <0. All patients requiring right ventricular support were included (n¼24). p¼0.5 days (10e1917). cardiac output and sodium levels beyond 3 months of therapy. Median duration of support: 28 days (5e146). A McDiarmid. Method and Results We compared correlation coefficients of dyssynchrony indices with response markers. p¼0. 14(58. continuous flow LVADs: 60 HeartMate II.761. 2P Pabari.5%) patients were discharged from hospital after treatment. 3 underwent successful HTx. S Schueler. 18 male. Median duration of VAD support increased from 84 days (IQR 20e209) in E1 to 280 days (IQR 86e661) in E3 (p<0. G MacGowan.8 to 12. Imperial College Healthcare NHS Trust.7 to 12.3% (95%CI 82 to 87) respectively at 1-year (p<0. longer term survival is unaffected. 30-day/ 90-day/1-year survival: 79%/71%/60%. underwent implantation.10).85 Abstract 83 Table 1 Parameter NYHA functional class Mean PA pressure (mm Hg) Mean PW pressure (mm Hg) Transpulmonary gradient (mm Hg) Right atrial pressure (mm Hg) PA oxygen saturation (%) Cardiac Output (l/min) Sodium (mmol/l) Baseline 3. M Hedger. 7(29%) patients died during RV support.001 0. IS THE LEVITRONIX CENTRIMAG RIGHT HEART SUPPORT A SOLUTION? doi:10. 3Medtronic Bakken Research Center.01). total implantable. Of the 239 patients implanted. 18 of these remain alive & 2 died.8.3) or creatinine (122641 to 105638.5 days (10e219). London.8 13464 Follow-up 2.963.960. 4 recovered LV function and underwent successful LVAD explantation.BCS Abstracts 2011 choice has changed in favour of rotary pumps.5%) pts. UK.1136/heartjnl-2011-300198. Conclusion Levitronix CentriMag right ventricular support is an excellent option for post LVAD implantation treatment of refractory RV failure. 5174 total days of support). 84 TREATMENT OF REFRACTORY RIGHT HEART FAILURE AFTER IMPLANTATION OF A LEFT VENTRICULAR ASSIST DEVICE. AND ITS CLINICAL IMPLICATIONS doi:10. Heart June 2011 Vol 97 Suppl 1 Background It may be incorrect to believe that.2. Ongoing randomised clinical trials will establish the long-term outcome of this device. Post VAD survival has improved. A R Simon. The Netherlands. G Parry. 2Imperial College London. 90 days and 1 year. Maastricht.003 <0. upper panel). 5University of Birmingham. Results: 22/26 (85%) patients survived beyond 3 months. including survival at 30. A F Popov.360. age 37.161. 3(12. 3B Stegemann. Of these.660.1136/heartjnl-2011-300198. Royal Brompton&Harefield NHS Foundation Trust.4% (95%CI 71 to 88) & 90. UK 83 CLINICAL AND HAEMODYNAMIC STATUS BEYOND 3 MONTHS OF MECHANICAL SUPPORT WITH THE HEARTWARE VENTRICULAR ASSIST DEVICE doi:10. in extreme cases necessitating additional mechanical assist. 69% and 96% for E1.1136/heartjnl-2011-300198. 4Ospedale dei Pellegrini.02 0. p¼0.19). 2 stroke and 2 multi-organ failure) and 2 died after (mean survival 173 days. 19%.001 <0. N R Banner.08). Follow-up data is available for 14/20 survivors (mean 197 days from implant). 15(62. 1-year survival conditional on 30-day survival was similar with & without a pre-HTx VAD (93% vs 91%. It allows either bridging to transplantation or RV function improvement and provides an acceptable rate of survival. 4V Palmieri. 4 patients died before (mean survival 40 days. London. The resultant depression in r2 is calculated. Baseline and follow-up NYHA functional class. 83 (35%) have undergone HTx. Survival after HTx for patients with or without a pre-HTx VAD was 81. peak VO2 (bicycle exercise). The analysis included patient demographics as well as overall duration of support and outcome parameters. in externally monitored randomised controlled trials (EMRCTs) and highly skilled single centre studies (HSSCSs).6 2168 1065 963 564 6667 4.01) and 80. peripartum cardiomyopathy 1(4%). biochemistry and mortality outcome were compared using paired t test. UK Introduction Limited data exist on the longer term clinical and haemodynamic impact of the HeartWare left ventricular assist device (HVADÒ) when used as a bridge to heart transplantation. may reduce r2. 5N Freemantle.0% (95%CI 63 to 82) & 84. gender: M/F-15/9. N Wrightson.002 S S Nijjer. p¼0. DLVEF in CRT recipients comprises true CRT effect plus unpredictable spontaneous variability present in control patients (Abstract 85 figure 1. 1 stroke. R Hards. Naples. UK 1 1 Conclusions The HVADÒ results in significant improvement in functional class. Freeman hospital.7 years. 52 (22%) are alive on VAD support & 84 (35%) died on support. Conclusion Heart transplant activity has declined and waiting times have become prolonged leading to an increased need for bridging to transplantation. Twenty were explanted following myocardial recovery. months 3 and 4 and at 2 years). Methods 26 patients had a HVAD implanted from 07/2009 to 07/ 2010 (mean age 46. 3 remain on continuing LVAD support. 2A Hughes. 2D P Francis. for which the Levitronix CentriMag continuous flow. Variability between repeat echocardiographic measurements.001 0.006 0. and between successive dyssynchrony measurements.9613. with a good echocardiographic marker of mechanical dyssynchrony. UK. underlying disease: dilated cardiomyopathy 22 (92%). Median survival after procedure: 473.5 days (6e145)/78. viral myocarditis 1(4%). Birmingham. we determine this “contraction factor”. A Barsan.5%) underwent RVAD explantation. right heart haemodynamics. Overall survival to 1 year after VAD implant rose from 52. Harefield.83 B Gordon. underwent heart transplantation (HTx) on RV support. Results 24 pts. 1 right heart failure) discharge from hospital. Significant results are shown in the Abstract 83 table 1. Both will mandatorily limit the achievable r2.001 <0. HSSCSs overstate r2 between A49 . Introduction Right heart failure after left Ventricular Assist Device (LVAD) implantation is a severe complication.8 years. haemoglobin (12.4 3869 2565 1265 1166 5168 2. There was no significant change in peak VO2 (9. Newcastle upon Tyne. Median ITU/hospital stay: 19.01). There has been a shift from volume displacement VADs to rotary blood pumps and the duration of support has increased. Patients who had a device longer than 3 months were reviewed. Harefield Hospital. N Robinson. 25 Jarvik 2000 and 24 HeartWare.48). response to biventricular pacing (BVP) should be predictable with a high r2 value. 4 patients died after RVAD explantation (post explantation day 1. right heart haemodynamics. Material and Methods Between March 2001 and November 2010 109 patients underwent implantation of long term.84 B Zych. We present our institutional experience with the Levitronix CentriMag used for right ventricular support commencing LVAD implantation with refractory right ventricular failure.6% (95%CI 54 to 75) in E3 (p¼0. Italy. 85 PREDICTION OF RESPONSE TO BIVENTRICULAR PACING FROM DYSSYNCHRONY INDICES: THE ABSOLUTE LIMIT ON PREDICTABILITY. paracorporeal device was used.

7%). An “averaged” reported r2 between differing dyssynchrony markers to commonly used echocardiographic response markers is shown in Abstract 85 figure 1.0000000001). 87 OPTIMISATION OF VV DELAY OF CRT IS MORE REPRODUCIBLE USING PEAK VELOCITIES THAN USING VELOCITY TIME INTEGRAL. But surely VTI. whether response is LVEF (0. M S Virdee. Imperial College London. UK 1 1 1 1 1 2 Introduction A significant minority of patients do not experience clinical benefit following cardiac resynchronisation therapy (CRT).6) 1 (0. unrealistic. Data are presented as mean (SD). EDV (0. 0.6) AV Adjustment 29 (16. cardiac output was acutely augmented by 13. Haemodynamically-guided adjustment of the intervals between chambers paced (“optimisation” of atrio-ventricular (AV) and leftA50 Background It is not obvious which is a better echocardiographic marker for optimisation of AV or VV delay: stroke distance (VTI) or peak velocity.1) 89 (49.9) Data as N (%). we should choose measurements with the best signal-to-noise ratio and reproducibility. D P Francis.1%). Rationally. is more immune to disruption by spontaneous variability between beats.53 v 0.34). 29% of HSSCSs results do not. Methods Data were collected from 180 consecutive patients who underwent CRT followed by optimisation within 24 h. UK 86 HOW OFTEN IS IMPORTANT ADJUSTMENT OF PACING INTERVALS REQUIRED FOR OPTIMAL RESPONSE FOLLOWING CRT? doi:10.37. right ventricular (VV) delays) may be undertaken to improve the chance of response to CRT. reflect this reliably. 0. The final settings were compared with the pre-programmed settings for that device and the difference (AV or VV Adjustment) derived.4) VV Adjustment 50 (27.50). lower panel. AS WELL AS BEING QUICKER doi:10. being less susceptible to publication bias. Optimised CRT produced further improvement of cardiac output. Haemodynamic assessment was undertaken using either echocardiography or Non-Invasive Cardiac Output Measurement. Because optimisation of VV delay requires detection of persistent changes in cardiac function (“signal”). An alternative is peak velocity instead of VTI as the parameter to be measured. Dyssynchrony indices’ own 2 EMRCT data shows maximal r2 between dyssynchrony and variability further contracts observable r values (by x0. Frequent citation (without verification in independent cohorts) of the most exuberant values. A D Hughes. An AV or VV Adjustment of more than 40 ms was considered to be clinically significant.9 (32)% augmentation. 2D Begley.39 (DESV.1 (34)%. Results Optimal AV delay ranged from 60 to 200 ms (mean 124 ms (30)).54.01). Abstract 85 Figure 1 DLVEF is 0. Abstract 86 Table 1 optimisation of CRT 0 Adjustment of pacing intervals following 1e20 mS 21e40 mS 41e60 mS 61e80 mS 81e100 mS 22 (12.1) 7 (3. J Mayet. Natural variability forces observed correlation coefficients between dyssynchrony and response to be low.2) 53 (29. Optimisation of pacing intervals provides augmentation of cardiac output over and above the “out-of-the-box” settings.1136/heartjnl-2011-300198. or requiring only minor alteration in 120 (66. from HSSCSs creates mathematically unviable. The overall ceiling to r2 is between dyssynchrony and DLVEF is 0. L Ayers. A clinically significant alteration in AV delay was made in 40 (22. Cambridge.2%). F Z Khan.3) 32 (17. 0.6) 65 (35. only undertaking optimisation when clinical response is lacking. P J Pugh. M Moraldo. in VV delay in 12 (6. The findings suggest that optimisation is an important component of resynchronisation therapy. C Manisty.1136/heartjnl-2011-300198. taking into account the preset paced or sensed AV delay. All EMRCT r2 values obey these statistical limits.68).86 V Nayar. Heart June 2011 Vol 97 Suppl 1 .8) 11 (6. which is encompassing and cumulating more data. A Rawling. EMRCTs. ESV (0.26 vs 0. “Outof-the-box” settings were found to be optimal in 11 (6. Cambridge. London. which may be small in relation to beat-to-beat variability (“noise”).01). The standard echocardiographic method of choice for VV delay optimisation is to maximise left ventricular outflow tract velocity time integral (LVOT VTI).40 vs 0.9) 0 1 (0. Optimisation was performed with serial adjustment of AV and VV intervals. data to support this approach as standard management are lacking and many institutions programme CRT devices to deliver “out-of-the-box” intervals. DEDV. However. 1Addenbrooke’s Hospital. UK. We sought to determine how often the “out-of-the-box” settings are optimal or acceptable and how often CRT optimisation results in significant alteration of the pre-programmed pacing intervals. VV delay ranged from 0 to 100 ms (mean 23 ms (19)). 2Papworth Hospital.01). The optimal pacing intervals were considered to be those which resulted in greatest acute augmentation of cardiac output and the device was programmed accordingly.7%) or in either parameter in 49 (27.57 (DESV.87 P A Pabari. Simply searching for progressively more extreme correlations is therefore misguided. 0. Conclusions HSSCSs suggest dyssynchrony markers strongly predict response to BVP but EMRCTs cannot confirm this. DEDV. to 24. A Kyriacou.BCS Abstracts 2011 dyssynchrony and remodelling response in contrast to EMRCTs (p<0. Conclusions Significant adjustment of AV or VV delay is required in over a quarter of patients receiving CRT. The biggest problem is genuine physiological variability between beats. expectations. With the pre-set pacing parameters.2%). we should concentrate on improving testretest reproducibility of markers of dyssynchrony and of response. 1D P Dutka.

at a fixed heart rate. Scatter between replicate optimisations is reduced if.99 (p<0. Importantly. aortic flow velocity and myocardial oxygen consumption (MVO2) at four settings: 3 AV delays during biventricular (BiV) pacing (reference BiV-AV120 ms. P Kanagaratnam.99 (p<0. Abstract 87 Figure 1 88 EVALUATION OF THE IMPACT OF AV DELAY VARIATION ON THE ACUTE MECHANOENERGETIC EFFICIENCY OF CARDIAC RESYNCHRONISATION THERAPY AND ASSESSMENT OF PERFORMANCE OF NON-INVASIVE VS INVASIVE HAEMODYNAMIC OPTIMISATION doi:10. A51 . Abstract 88 Figure 1 The correlation of LV pulse pressure and aortic flow velocity during acute biventricular pacing. no different to LBBB (p¼NS). no different to LBBB (D¼0. MVO2 at At BiV-AV40 ms and LBBB was not significantly different (D463%. Dexternal work (Dpressure 3Dflow) correlated with D MVO2.01). R Baruah. for optimisation purposes it comparison of peak velocity between different settings is both faster and more reliable. Making replicate measurements further improves reproducibility.5 s for VTI (p<0. nor is known if non-invasive haemodynamic optimisation by blood pressure agrees with invasive haemodynamic measures during optimisation. individualised haemodynamic BiVAVoptimum).4%.00 (p<0. or triplicates (ANOVA p<0.860. While VTI measurement remains essential for assessing stroke volume and cardiac output. and identifies the VV optimum 3 times more confidently. Indeed.003). UK Background The impact of varying AV delay on the acute mechanoenergetic efficiency of cardiac resynchronisation therapy (CRT) is not known. in contemporary patients. (at three AV delays) and during LBBB. MVO2 increased from LBBB to BiV-AV120 ms by 964% (p¼0. with slope 1. at a fixed heart rate. r¼0. We also examine whether averaging multiple replicate measurements improves optimisation. and at intrinsic ventricular conduction (LBBB). Abstract 88 figure 1. significantly greater than 1.66 vs 0. We studied these invasively. The 4 pacing states lay on a straight line: for Dpressure against Dflow. At BiV-AV40 ms. we use pairs. Results LV pulse pressure rose from LBBB to BiV-AV120 ms by 1062% (p<0. ments of left ventricular (LV) pulse pressure (systolic minus diastolic). Time taken for acquisition and analysis of a single optimisation (6 settings) was 17. triplicate peak velocity assessment takes the same amount of time as a single VTI. QRS 154626 ms) underwent measureHeart June 2011 Vol 97 Suppl 1 Abstract 88 Figure 2 The correlation of cardiac work and myocardial oxygen consumption during acute biventricular pacing.6160. Peak velocity had a higher intraclass correlation coefficient (ICC) than VTI (0. aortic flow was.01).035) and to BiV-AVoptimum by 1263% (p¼0.001). 6 successive replicate optimisations were performed per patient at a single session. P Pabari.0001). measured at a fixed position throughout each individual’s study (ie. p¼0. with a single measurement for each.BCS Abstracts 2011 and therefore simply using peak velocity might give a less reliable optimum? Surely the time saved by using peak would have a price to pay in poorer reproducibility of the optimum? In this study. r¼0. Z Whinnett. Abstract 88 figure 2.17. we evaluate whether peak velocity is a suitable alternative to VTI.53. Perhaps guidelines should favour peak over VTI and mandate multi-replicate averaging? These data suggest a rare opportunity to reduce labour while increasing reliability of optimisation.88 A Kyriacou. Atrial pacing at 100 bpm ensured a fixed heart rate. Methods & Results VV optimisation was performed on 40 subjects with biventricular pacemakers using LVOT velocity (VTI or peak) as the echocardiographic marker being maximised. having regard to both time consumed and reproducibility. instead of single measurements.5 s for peak and 57.001) and 261% more (p<0. rose by 962% (p<0. D W Davies.002). pressure was 1062% worse than BiV-AV120 ms (p<0.0001).01) at BiV-AVoptimum. At BiV-AV40 ms. Methods Eleven patients with heart failure (EF 2968%) and left bundle branch block (LBBB. Scatter of apparent VV optimum between repeat optimisations was threefold smaller for peak than VTI (p<0.01) from LBBB to BiV-AV120 ms. BiV-AV40 ms. International Centre for Circulatory Health.05). p¼ns).1136/heartjnl-2011-300198. rising a further 361% (p<0. S Sayan. Invasive aortic flow velocity. D P Francis. p¼ns).03).001 among each).05) at the haemodynamic BiV-AVoptimum. J Mayet. London. cardiac output index). (at three AV delays) and during LBBB. This benefit occurs with both peak and VTI (p<0. Conclusions Doppler optimisation of VV delay using peak velocity rather than VTI is (as expected) quicker but (surprisingly) more accurate. K Willson. N S Peters.

it also increases the myocardial oxygen consumption. LV dP/dtmax was measured during different pacing modes. Patients with large SF had greater acute response to left ventricular (LV) and biventricular (BIV) pacing vs those with small/no SF (% increase dP/dt 28614% vs 11619% for LV pacing and 42628% vs 22621% for BIV pacing). 1Kings College London. 1A Shetty. 2S Kapetanakis. p<0. 1M Ginks. smallest and earliest at the superior part of the block (where area of block begins) with largest negative peak. as a result cardiac efficiency improves. Patients with large SF had areas of conduction block in noninfarcted regions whereas those with small or no SF did not (Abstract 89 figure 1). Functional conduction block has disappeared. Abstract 89 Figure 1 89 ELECTROMECHANICAL INTERACTION IN PATIENTS UNDERGOING CARDIAC RESYNCHRONISATION THERAPY: COMPARISON OF INTRACARDIAC ACTIVATION MAPS AND EARLY SEPTAL CONTRACTION IN LEFT BUNDLE BRANCH BLOCK doi:10. aortic flow velocity. There was a significant difference in the percentage rise in LV-dP/dtmax between the best and worst LV lead position (Abstract 90 figure 1).01. 3J S Gill. Bold white arrows on the electrogram indicate how the electrical activation spreads superiorly in a U-shape pattern leading to the development of split potentials. Methods 13 patients (63610 years. Methods 33 patients undergoing CRT (21 dilated & 12 ischaemic cardiomyopathy) were studied. RR was defined as reduction in LV end systolic volume (ESV) $15% at 6 months. 1M Sermesant. 3 C A Rinaldi. with the emergence of R-wave. A Pashaei. only 1% more energy is consumed per 1. at a fixed heart rate. UK.1136/heartjnl-2011-300198. Barcelona. E Cunliffe. When an AV delay improves external cardiac work. Multi-centre trials have shown echocardiographic techniques are poor at improving response rates. Unipolar isochronal map with NCM electrograms showing fragmented signals (development of split potentials) indicating a reduction of conduction and inability to cross throughout the inferior region. London.001)) with DDDLV pacing for the optimal LV lead position. 2B H Bijnens.81.01. 3Guy’s and St Thomas’ Hospital. However. 3J Bostock. UK 2 1 Introduction Cardiac resynchronisation therapy (CRT) reduces mortality and morbidity in heart failure patients. UK. London.8%) undergoing CRT underwent echocardiography and non-contact mapping (NCM) pre-implant. p<0. LV dP/dtmax.865. BIV pacing. 2Guy’s and St Thomas’ Hospital. Abstract 89 figure 1 Patient with a large SF. 1R S Razavi. London.68. 2S G Hamid. We evaluated the relationship between AHR and reverse remodelling (RR) in CRT. Row B. 1Kings College London. four small SF and four no SF. 2A F Frangi. r2¼0. r2¼0. Higher proportions do not remodel. Conclusions During acute biventricular pacing. We hypothesised that the degree of acute haemodynamic response (AHR) at implant can predict which patients remodel. compared to LBBB or a physiologically too short AV delay (eg. 1M Ginks.BCS Abstracts 2011 The correlations of optimal AV delays by non-invasive (Finometer) systolic blood pressure (SBP) vs invasive measures were as follows. 10 men) with severe heart failure (EF 22. Correction of SF corresponds with CRT response. Left ventricular (LV) volumes were assessed pre and post CRT. 2J Bostock. Results Five patients had a large SF. Row A. This should enable routine haemodynamic optimisation (easily automated) of CRT devices in clinical practice. 2C A Rinaldi. AV 40 ms). 2O Camara. We hypothesise that electromechanical interactions induced by SF are associated with functional changes in conductivity and a “U-shaped” activation pattern. 2G Carr-White. baseline with area of block and late anterior breakthrough. LVESV Heart June 2011 Vol 97 Suppl 1 .1136/heartjnl-2011-300198. p<0. Spain.90 S G Duckett. Abstract 89 figure 2 Activation maps of patient with a large SF. The lines of conduction block disappeared after LV and BIV pacing. Presence and extent of a SF was defined visually and with M-mode and fused with NCM bull9 s eye plots of endocardial activation patterns. The NCM mapping electrograms show the criteria used by Auricchio et al to define block. UK 2 1 Abstract 89 Figure 2 Introduction Early inward motion and thickening/thinning of the ventricular septum associated with left bundle branch block (LBBB) is known as the septal flash (SF).01. aortic SBP. London. 1R S Razavi. r2¼0. The LV lead was placed in potential target veins and the largest percentage rise in LV-dP/dtmax from baseline (AAI or RV pacing with atrial fibrillation) to DDDLV was used to determine optimal LV lead position. changing the AV delay affects the cardiac mechanoenergetics. 2J S Gill. Haemodynamic optimisation of AV delay can be achieved with high precision using non invasive beat-to-beat pressure measurements. Characterising the spatio-temporal relationship between electrical and mechanical events may explain why patients with a SF respond to CRT.96. however up to 30% of patients do not derive symptomatic benefit.6% more external work (pressure3flow) done. Row C. Results LV-dP/dtmax increased significantly from baseline (8016194 mm Hg/s to 9246203 mm Hg/s (p<0. 1P Chinchapatnam. 3G Carr-White. RV pacing showing the area of anterior block remains. AHR (LV-dP/dtmax) was assessed at implant using a pressure wire in the LV cavity. 90 INVASIVE ACUTE HAEMODYNAMIC RESPONSE TO GUIDE LV LEAD IMPLANTATION PREDICTS CHRONIC REMODELLING IN PATIENTS UNDERGOING CARDIAC RESYNCHRONISATION THERAPY doi:10. Correction of both mechanical synchrony and the functional conduction block by CRT may explain the large positive response in patients with a SF. 2UPF. while remaining present with RV pacing (Abstract 89 figure 2). A52 Conclusion A strong interaction exists between electrical activation and mechanical deformation of the septum.89 S G Duckett.

which provides a method of calculating a patient9 s predicted mean life expectancy using physiological variables. Ten patients (21%) met the primary end-point over a mean follow-up of 28. UK 1 1 91 RIGHT VENTRICULAR DYSFUNCTION IDENTIFIES CLINICAL OUTCOMES FOLLOWING CARDIAC RESYNCHRONISATION THERAPY doi:10. UK. HF was ischaemic in 42% of patients. GSF criteria were assessed by interviewing the specialist nurse responsible for each patient9 s care. UK. Imperial College.001) (Abstract 90 figure 2). There is much variation in the rise in LV-dP/dtmax depending on LV lead position.04. UK. University of Edinburgh. 1) all cause mortality. K K Haga. who were being managed in the specialist. University of Edinburgh. p<0.8. On time-to-event analysis. The primary end-point was a composite of all cause mortality (ACM) or unplanned cardiovascular hospitalisation. and the mean age was 77 years. A53 . Cardiovascular magnetic resonance (CMR) is an important tool in the assessment of HF and is considered the gold-standard in estimating RV function. CRT has not been investigated. 2S A Murray.5612. Clinical. 3J Reid. A similar relationship for AHR and RR in DCM and ICM (p¼0.BCS Abstracts 2011 decreased from 186668 ml to 157668 ml (p<0. 4D Yellowlees. Conclusions RV dysfunction is an independent predictor of adverse clinical outcomes following CRT.7 years. GSF criteria. biochemical. University of Edinburgh. NHS Lothian. Edinburgh. The mean LVEF estimated by CMR was 2768%. London. respectively).03 and 0. Atrial fibrillation/flutter was found in 27% of patients.80 per mm. 1M R Cowie. Methods Chronic heart failure patients. with the “Seattle Heart Failure (SHF) Model”. and 3) the sensitivity and specificity of the GSF and SHF to predict death at 1 year. Atrial fibrillation and low RVEF were the only independent predictors of mortality (p¼0. Methods We evaluated 48 consecutive patients attending a heart failure pacing clinic who had a CMR study within 6 months prior to CRT implantation. 2R Sharma.01 & p¼0. in NYHA class III or IV.96 per 1% EF. However. 2) place of death.066. 2T McDonagh.02) and RV dysfunction. Abstract 90 Figure 1 92 IDENTIFYING PATIENTS WITH CHRONIC HEART FAILURE: A COMPARISON OF THE GOLD STANDARDS FRAMEWORK WITH A CLINICAL PROGNOSTIC MODEL doi:10. a proportion of patients do not derive benefit post implantation of CRT.006) was seen. Patients were then followed up.6 months.001). reduced RVEF (HR 0. Edinburgh.01) were independent predictors of the primary end-point.1136/heartjnl-2011-300198. p¼0. The assessment of RV function may be considered in patient selection for CRT implantation. UK Background Cardiac resynchronisation therapy (CRT) is an established treatment for patients with advanced heart failure (HF). There was a significant relationship between percentage rise in LV-dP/dtmax and RR for DDDLV pacing (p<0. 3M O’Donnell. 1Royal Brompton Hospital.92 Abstract 90 Figure 2 Conclusions Acute haemodynamic response to LV pacing is useful for predicting which patients are likely to remodel in response to CRT both for DCM and ICM.01) or TAPSE (HR 0. 4University of Edinburgh. Edinburgh. The mean tricuspid annular plane systolic excursion (TAPSE) was 14. 2 Primary Palliative Care Research Group. only atrial fibrillation (HR 4. online databases and were used to estimate mean life expectancy and predicted mortality at 1 year. which were developed to determine the need for palliative care in non-cancer patients. Edinburgh. were identified from a clinical heart failure database. Using acute haemodynamic response measured with a pressure wire during CRT implant has the potential to guide LV lead positioning and improve response rates in the future. and the mean pulmonary artery pressure (on echocardiography) was 37 610 mm Hg. The aim of this study was to compare the “Gold Standards Framework” (GSF) criteria. Results The mean age was 64. while the median RVEF was 52% (IQR 35%e63%). 5M A Denvir. at 1 year. and 85% were in NYHA class III/IV at the time of implantation. 18 (56%) patients exhibited RR. ECG and imaging data were collected. p¼0. heart failure nursing service. UK. Biventricular function and myocardial scar were assessed by CMR including gadolinium enhancement. to evaluate. 3A Ness. 3 Heart Failure Nursing Service. the significance of RV dysfunction in gauging clinical benefit from Heart June 2011 Vol 97 Suppl 1 Introduction Heart failure has a worse survival rate than many common cancers. School of Medicine and Veterinary Medicine. Clinical data required for the SHF model were obtained from two. London.91 1 K Guha. Despite an established predictive role in HF. ie. 5Department of Cardiology. 2Royal Brompton Hospital.0 mm. School of Medicine and Veterinary Medicine. Results 138 NYHA III-IV patients were identified from a total of 368 patients currently managed within the specialist nurse service. 2S Prasad. Edinburgh. 2F Alpendurada.1136/heartjnl-2011-300198. We used this technique to assess the impact of RV dysfunction on clinical outcomes following CRT implantation. One of the main difficulties in providing palliative care for heart failure patients is the uncertainty around the course of the disease and the patient9 s life expectancy. UK. yet few patients receive any palliative care input during the course of their illness. 66% were male.

may remain unpredictable. the SHF model predicted that only 6/138 patients (4. protocol-guided optimisation of conventional HF therapies. and focus instead on a patient9 s increasing needs coupled with an understanding that death.7 41. Heart June 2011 Vol 97 Suppl 1 . and 18% of patients respectively (Abstract 93 table 1). aldosterone antagonists. the progress of palliative care in heart failure patients may require a shift away from the traditional “end of life” model developed in cancer treatment. Despite forced optimisation of medical therapy. Between the two clinic visits.6 Final Clinic Visit (post-optimisation) 67. H Llewellyn-Griffiths.369. 71 (41%) were in atrial fibrillation. 4Hywel Dda Health Board. Resting heart rate and blood pressure before and after optimisation of medical therapy are shown in Abstract 93 table 2. following an acute admission. UK. and the reasons for the inability to achieve target doses of bB. in this selected sample. tolerated in 92%.2 26.001 <0. 39% achieved the target maximal dose.0 67.8614.5 115. and as a disease modifying variable in patients with impaired left ventricular (LV) systolic function. 3University Hospital of Wales.2 1. Overall. The systolic heart failure (HF) treatment with If inhibitor ivabradine trial (SHIFT) for example recently demonstrated significantly improved outcomes in otherwise optimally treated HF patients following additional HR reduction with ivabradine. Overall. Camarthen.3%) had a predicted life expectancy of less than 1 year. patients underwent protocol-guided forced up-titration of standard neurohormonal HF therapies. 57% at least half target dose. Discussion Neither the GSF nor the SHF were very accurate in predicting which patients were in the last year of life. Despite the increasing drive towards palliation in heart failure. intractable lethargy (26%). Of these. ACE-I/ARB. and 4% less than half of the target dose of bB.1618. and cause (ischaemic vs non-ischaemic) were recorded. severity (ejection fraction>35% vs ejection fraction#35%). 78% had severe LV systolic dysfunction (Abstract 93 figure 1). 30%.038) than those patients that did not meet GSF criteria.4 p value <0. and hospitalisation with worsening airways disease (26%). Therefore. we collected data on patient’s resting pulse (absolute value and rhythm: sinus vs atrial fibrillation).7611.2610. However.1136/heartjnl-2011-300198. of these.3 83 92 30 18 10. ACE inhibitor (ACE-I) or angiotensin receptor blocker (ARB). In addition. 2University Hospital Llandough. 4A Raybould. At follow-up. Cardiff. The sensitivity and specificity for the GSF and SHF model were 22%/83% and 98%/12% respectively. w50% are in sinus rhythm with an ejection fraction #35%. (sensitivity/specificity¼82%/56%). 145 of 172 patients (83%) tolerated bB therapy. clinicians are still faced with a substantial prognostic barrier. 67% male).8 120619. 58% (25/43) died in hospital. Data on patient demographics and classification of HF including. 1Wales Heart Research Institute. Of the patients in sinus rhythm. Methods We performed a retrospective analysis from two HF clinics where patients are referred for nurse lead. 43/138 patients had died (31%).1 57 43 92. severe and limiting hypotension (48%).5 62. Reasons for failure to initiate bB (n¼27.BCS Abstracts 2011 identified 119/138 (86%) patients that met the minimum requirement for palliative care input. itself. We therefore estimated the number of patients who after optimisation of conventional HF medications may be suitable for additional HR reduction. Cardiff. M Oliver. 3 Z R Yousef. NYHA class).6 Patient Characteristics (n¼172) S Russell.93 Abstract 93 Figure 1 Heart Failure Patients Potentially Suitable for Additional Heart Rate Reduction After Optimisation of Standard Medical Therapy. We also collected data on the maximal tolerated doses of beta blocker (bB). UK. the patients renal function (eGFR<35 ml/min) was the best predictor of mortality. J Davies. 17%) included. Cardiff. Abstract 93 Table 1 NYHA Class (%) I II III IV HF aetiology (%) Ischaemic Non-ischaemic LV function (%) Ejection Fraction #35% Ejection Fraction >35% Cardiac rhythm (%) Sinus Atrial Fibrillation Medication use (%) b-blockers ACE-I/ARBs Aldosterone antagonists Digoxin 58. UK. and digoxin were A54 Abstract 93 Table 2 Haemodynamic profiles before and after optimisation of medication First Clinic Visit (pre-optimisation) Resting Heart Rate (beats/min) Systolic Blood Pressure (mm Hg) Diastolic Blood Pressure (mm Hg) 73. and blood pressure at the first and last clinic visits. half of these patients have a resting heart rate $70 beats/ minute.001) and had significantly lower predicted survival rates at 1 year (p¼0. Patients who met GSF criteria for palliative care had significantly more hospital admissions (p¼0. Results Of 172 consecutive patients referred for optimisation of HF therapies (age 71613 yrs. w1 in every 3 patients attending a heart failure clinic may be suitable for additional heart rate control. 2V Sim.6 71. 93 OPTIMAL MEDICAL THERAPY IN HEART FAILURE: IS THERE SPACE FOR ADDITIONAL HEART RATE CONTROL? doi:10. Overall.001 Conclusions Of 172 unselected patients attending HF clinics for optimisation of medical therapy. functional limitation (New York Heart Association.001 <0.4 7. UK 1 2 3 2 4 Introduction Current evidence suggests that heart rate (HR) may serve both as a modifiable risk factor. H Rose.

Cardiff.BCS Abstracts 2011 94 A COMPARISON OF FUNCTIONAL AND ECHOCARDIOGRAPHIC OUTCOMES IN NICE COMPLIANT AND NON-COMPLIANT PATIENTS UNDERGOING CRT IN THE REAL WORLD doi:10. but who do not meet NICE criteria). Cardiff. Several randomised clinical trials however have consistently reported beneficial effects of CRT in patients outside current NICE guidelines. cardiac surgeon and hospital manager.8 (4. Dilated cardiomyopathy is known to be associated with cardiac energy deficiency. 89 NICE:+ve and 50 NICE: Àve (Abstract 94 table 1).3 (4. Interrogation at high field strength improves signal to noise ratio. S Bowater. M Kuehl. ejection fraction (EF) and quality of life scores.68. LVEF was measured using biplane Simpson’s method.2 (5.1136/heartjnl-2011-300198. Cardiac energetic status is directly proportional to symptoms status and therefore any treatments targeted to improve cardiac energetics may improve patient symptoms in dilated cardiomyopathy. Guidelines should guide therapy but ultimately each therapy should be individualised and evidence based. L K Williams.5 (131.2) 158 (37) 46 R M Beadle.9 (25.001 216. The PCr/ATP ratio was correlated with NHYA class (r¼À0.4 (6. 1I Rees. This study involves a retrospective analysis of our CRT database and compares outcomes in NICE:+ve and NICE: Àve patients. 2F Leyva Leon.005). TA120) for CRT include: NYHA class III or IV symptoms despite optimal medical therapy.2) 24. 2Z R Yousef. M P Frenneaux. The energy status correlates strongly with symptom status but not with ejection fraction nor quality of life score.001 0.4) 185.5 (127.6) 40.5 (131. Methods 32 patients and 22 control subjects were studied using phosphorus-31 (31P) MRS and patients were classified to NYHA symptom class.1 (79. Compared to baseline. Follow-up at 3 and 6 months post CRT includes clinical evaluation. QRS <120 mS (n¼5). Results Between January 2007 and December 2009. In vivo energetics were measured using a commercially available Philips Achieva 3 Tesla scanner and dedicated 31P coil with ISIS volume selection. and follow-up components. Complete paired data comparing baseline and 6 month functional and echo data are available for 139 patients.001 13.02 0. device/medical optimisation. 2University Hospital of Wales.6) 177.1 (25. Pre-assessment includes clinical evaluation and baseline echo (EF: ejection fraction. Conclusions We observed significantly favourable and similar functional and echocardiographic responses to CRT in patients meeting and not meeting current NICE criteria for CRT.2 (67. Magnetic resonance spectroscopy (MRS) has been proposed as a non-invasive method of assessing cardiac energetics and as a method of measuring response to therapy. implantation.8) 291. Methods Our unit operates an integrated CRT service with preassessment.2) 135.4 (3. 1Wales Heart Research Institute.7 (10.001 208.2) 31.5 (31.0) <0. and to correlate the patient’s results to symptom status.31) compared with control subjects (1. all patients completed a Minnesota Living with Heart Failure (MLWHF) score and underwent echocardiography. and reassessment of echo and functional outcomes.40.5) <0. Furthermore. 253 patients received CRT. Conclusions This study confirms the presence of energy deficiency in dilated cardiomyopathy as measured by MRS at 3T.0005).3) 21. UK Introduction The National Institute for Clinical Excellence (NICE) define a population of patients that are most likely to respond to cardiac resynchronisation therapy (CRT) and have a favourable health economic profile.3560.94 1 S J Russell.64 <0. and ESV: left ventricular end-systolic volume) and func- tional characterisation: a) Minnesota quality of life score (QoL). interventional cardiologist.1) 30. sinus rhythm.24 <0. p<0. An additional 5 patients with right bundle branch block and otherwise NICE CRT compliance are analysed as NICE: Àve in this study.2 (23.baseline (SD) Ejection fraction.1) 164 (26) 57 Abstract 94 Table 2 patients Outcomes in NICE compliant and noncompliant p value (baseline v NICE:Lve 6 months) (n[50) 63.6 (73. pacemaker upgrades (n¼9).3) 144. 6-month outcomes were similar and significantly improved in both NICE:+ve and NICE: Àve groups (Abstract 94 table 2). b) 6 min walk test (6MWT).01 Introduction The aim was to measure the cardiac phosphocreatine to ATP (PCr/ATP) ratio non-invasively in patients with dilated cardiomyopathy and normal controls. Exclusions for the NICE: Àve patients included: atrial fibrillation (n¼19).01 12. and either QRS duration >150 mS alone or 120e149 mS together with echocardiographic (echo) evidence of mechanical dyssynchrony. 2P O’Callaghan.9060.5 (7.5) 0. 2University of Birmingham.4 (118.2 (57.2) 0.3) 324. This individualised and evidence based approach provides for a comparison of outcomes in NICE compliant (NICE:+ve) and NICE: Àve patients (patients with a clinical need and evidence base supporting CRT.1136/heartjnl-2011-300198.2) <0. No correlation was found with LVEF or MLWHF score. p<0. Heart June 2011 Vol 97 Suppl 1 A55 . and c) peak oxygen consumption on cardiopulmonary exercise test (VO2). UK.95 Abstract 94 Table 1 compliant patients Characteristics of NICE compliant and nonNICE:+ve NICE:Lve 66 (11) 90 24 (7.7) 38. n¼32.0) 12. Results The PCr/ATP ratio was significantly reduced in patients (1. 2K Abozguia. potential CRT patients are discussed at a multi-disciplinary team (MDT) meeting attended by a heart failure specialist. electrophysiologist.6) <0. 1University of Aberdeen. 95 IMPAIRED CARDIAC ENERGETICS IN DILATED CARDIOMYOPATHY: MAGNETIC RESONANCE SPECTROSCOPY AT 3T doi:10.6) 14.001 p value (baseline v 6 months) NICE:+ve (n[89) QOL (score): baseline (SD) QOL (score): 6 months (SD) 6MWT (m): baseline (SD) 6MWT (m): 6 months (SD) V02 (ml/kg/min): baseline (SD) V02 (ml/kg/min): 6 months (SD) Ejection fraction. CRT is offered where there is consensus agreement that the individual patient is likely to benefit. Current NICE criteria (technology appraisal. UK 1 1 2 2 2 Age: years (SD) Male: % Ejection fraction: % (SD) QRS duration: mS (SD) CRT-Defibrillator: % 65 (11) 83 22 (7.3 (7. UK. QRS 120e149 mS without mechanical dyssynchrony (n¼12). In our centre.6 months (SD) End-systolic volumebaseline /ml (SD) End-systolic volume6 months /ml (SD) 58. Java Magnetic Resonance User Interface (jMRUI) was used for analysis. Aberdeen. Birmingham. ejection fraction #35%.

1560.5.05) between RI and SE (mean6SD: 14. VO2peak was similar (p>0. Thirteen of these patients also performed RISE95 tests using slow (RI 3e8 W/ min.660. LT and VO2max were 9. at least in part. however. The sVO2/sTOI.05. may elicit a VO2peak lower than the maximum physiological limit (VO2max). the RISE95 protocol provides a robust measure of VO2max in CHF patients. There was no effect of ramp rate on VO2peak (p>0.663. the latter commonly “confirmed” using the secondary criterion of respiratory exchange ratio (RER) >1. VO2 kinetics remained slowed in 4 patients.1660.260. In CHF prior moderate-intensity exercise improved the dynamic matching of muscle oxygenation to its instantaneous requirement and speeded VO2 kinetics in all patients. however. was taken to reflect the relative matching of muscle oxygenation to its instantaneous requirement. and III: n¼1) initially performed a modified Bruce treadmill test. Both sVO2 (46620 vs 39618 s.exercise phases. Peak VO2 and RER were compared within-subjects. S R Murgatroyd.05) in treadmill and cycle exercise (mean6SD: 16. Thirteen CHF patients (NYHA class I: n¼3. As prior exercise is known to increase muscle blood flow in healthy individuals.1136/heartjnl-2011-300198.063. VO2 and RER were measured breath-by-breath by a mass spectrometer and turbine (MSX. p<0.2460. w10 min). although a lower sVO2 was typically reflected in a reduced kinetic index in bout 2. K K Witte. 5-min recovery (10 W). II: n¼9. These patients had a higher NYHA class (2. respectively).8 vs 2. n¼20. p<0. RER.05) than the others.7 (mean6SD) and 15.05) and slowed the rate of deoxygenation in the transient (sTOI: 1061 vs 21613 s.262.2 vs 14. University of Leeds. Heart June 2011 Vol 97 Suppl 1 . p<0. and III: n¼1) performed a ramp test on a cycle ergometer for estimation of lactate threshold (LT) and VO2max. and without the need for secondary criteria or incidence of false-positive. G Begg.5 vs 1. Therefore. the end-exercise RER was sensitive to both modality and ramp rate and provided a false-positive for VO2max attainment in every incidence. between RI and SE.2 ml/kg/min. n¼21). SE (95% of peak RI work rate). to a dynamic limitation in O2 delivery.05). was well tolerated by CHF patients: The SE phase was contraindicated in only 3 of the 47 tests. D T Cannon. Recent evidence in CHF of a transient overshoot in microvascular deoxygenation at exercise onset supports the latter. Japan). these findings suggest that an acute intervention to improve muscle oxygenation can increase aerobic energy provision on transition to exercise in CHF patients.05). NSpire.06). These VO2 kinetics. this approach revealed an apparent limitation in the control of muscle O2 consumption in the most severe patients.05) and the kinetic index (4. A VO2peak #14 (or 12 with b-blocker) ml/kg/min is associated with increased mortality and is a key criterion for cardiac transplant listing. However.09. H B Rossiter.BCS Abstracts 2011 (1. However. K K Witte. Measurements included breath-by-breath VO2 using a turbine and mass spectrometer (MSX. however. Nevertheless.9. despite RER being greater in cycling (1. however. H B Rossiter.1260.360.063. University of Leeds. determined if a ramp-incremental (RI) step-exercise (SE) (or RISE) test could determine VO2max in CHF patients without using RER. by satisfying the criterion that two different work rates are terminated at the same VO2peak.05 in the remaining 7 (1. and tissue oxygenation index (TOI) of the vastus lateralis by spatially resolved near-infrared spectroscopy (NIRO200.2 ml/kg/min.561. VO2peak was similar (p>0.97 T S Bowen. is sensitive to the test format. As a group. Twenty-one male CHF patients (NYHA class I: n¼3. by unpaired t test of the final 12 breaths of exercise. The single-visit RISE95 test incorporating incrementaland step. UK). Patients then completed a symptom-limited RISE95 cycle ergometer test in the format: RI (4e18 W/min. II: n¼16.05).963. bout 2) from rest to 90%LT. w15 min) and fast (RI 10e30 W/min.92) in bout 1.09) compared to the slow A56 Rapid adaptation of pulmonary oxygen uptake (VO2) at exercise onset reduces the reliance on limited anaerobic energy stores and is associated with increased exercise tolerance. p¼0.05). attenuated the transient overshoot in muscle deoxygenation by w50% (p<0. each to the volitional limit. A within-subject comparison. The RISE95 detected VO2max in 14 of 21 patients with a sensitivity of w10% (ie. This approach allowed VO2max and its associated 95% confidence limits to be estimated. w6 min) ramp rates.96 T S Bowen. we examined whether it could attenuate the fall in microvascular deoxygenation and speed VO2 kinetics on transition to moderate exercise in CHF patients. therefore.12 vs 1.05) were reduced following prior exercise. UK Abstract 95 Figure 2 96 A TEST TO CONFIRM MAXIMAL OXYGEN UPTAKE IN CHRONIC HEART FAILURE PATIENTS WITHOUT THE NEED FOR SECONDARY CRITERIA doi:10. UK). p<0.7 vs 15. or “kinetic index”. pathophysiology and prognosis in patients with chronic heart failure (CHF).6e3. D T Cannon.8 ml/kg/min). This could be due to limitations in the control of muscle O2 consumption and/or O2 delivery.961. Hamamatsu. however RER was greater (p<0. A symptom-limited exercise test.1136/heartjnl-2011-300198.06) and greater initial sVO2 (62617 vs 3369 s. similar to healthy subjects). This suggests that slow VO2 kinetics in CHF are due. V Baliga. We. despite RER being >1. which was only partly ameliorated by improving O2 delivery. Leeds. The exponential timeconstant (s) for TOI and phase II VO2 were estimated using nonlinear least-squares regression. to within an individuallydefined CI without dependence on secondary criteria.2 ml/kg/min.09).0860. respectively. UK Cardiopulmonary exercise testing for peak oxygen uptake (VO2peak) is widely used to evaluate severity. Abstract 95 Figure 1 97 INCREASING SKELETAL MUSCLE OXYGENATION BY PRIOR MODERATE-INTENSITY EXERCISE INCREASES AEROBIC ENERGY PROVISION IN CHRONIC HEART FAILURE doi:10. Leeds. sVO2 was well correlated to the kinetic index (R2¼0. Prior exercise increased resting TOI by 1063% (p<0. In contrast. separated by 6-min of rest. are slow in patients with chronic heart failure (CHF). Patients subsequently repeated two 6-min moderate-intensity exercise transitions (bout 1. NSpire. p<0.05) in the fast ramp (1. revealed that the VO2max criterion was met in 14 of 21 patients (measurement sensitivity range 0.

1136/heartjnl-2011-300198. 122:173).1% (278/427) of participants had valid data on previous diagnosis of HF.98 F Yousaf. 1A Kingston. A full cardiovascular and medical history.9% (n¼260) women) were visited in their usual place of residence. 60. NYHA 2.1% (n¼92/278) had no previous diagnosis of HF but had clinical evidence of HF and an additional 21. and achieved Vo2max of 16.0610. 37. 39. L B Tan. with those of healthy male volunteers with no known cardiovascular diseases (n¼101.BCS Abstracts 2011 98 HIGH PREVALENCE OF UNDIAGNOSED CARDIAC DYSFUNCTION IN THE OLDEST OLD: FINDINGS FROM THE NEWCASTLE 85+ STUDY doi:10. moderate or severe dysfunction) in 88. we cross-referenced our findings to preceding diagnoses present in general practice records. NYHA 2.1 (SD) years. Newcastle University.966.7 mls/kg/ min. p¼0. including current medication.6% (n¼60/278) had no previous diagnosis but evidence of pre-clinical HF (NYHA class I with systolic or moderate/severe diastolic dysfunction). 33. Leeds. and have generally been conducted in hospital-based settings. Institute of Ageing and Health. Of those with a previous diagnosis of HF. BMI 26.5 W.5% (n¼5/21) had no echocardiographic evidence of cardiac dysfunction.4% (n¼54/376) had isolated moderate or severe diastolic dysfunction.8.9 years. Methods We compared the cardiopulmonary exercise performance and non-invasive haemodynamics of overweight (BMI >34 kg/m2) and non-overweight (BMI #30) male heart failure patients in NYHA Classes II and III.864.6 mls/kg/min which was significantly lower than controls (37. We examined whether this variable is a good indicator of cardiac function in overweight heart failure (HF) patients. Newcastle upon Tyne.6 W.5% (82/278)) or isolated moderate or severe diastolic dysfunction (7. Their physical and cardiac functional reserves were measured during treadmill exercise testing with standard respiratory gas analyses and rebreathing method of non-invasively measuring cardiac outputs during peak exercise. 2 Freeman Hospital.1% (n¼167) men. 65. LV systolic and diastolic dysfunction were graded according to American Society of Echocardiography guidelines. However.51).7 W) of overweight HF patients were clearly above those of non-overweight (2. BMI 25. As shown in Abstract 99 figure 1.4% (104/278) had clinical evidence of HF. the uncorrected Vo2max were higher than those of non-overweight counterparts (Overweight: 25756748 vs 15946325 mls/min.4860. Newcastle upon Tyne. Conclusions Systolic and diastolic dysfunction and HF were commoner in our population than previous studies in the “younger old” have suggested. 3Institute of Human Genetics.50) managed to exercise to acceptable cardiopulmonary limits (peak RER¼1. Since in elderly people with multiple comorbidities. and 14.99 S Chinnappa. which was defined as NYHA class II. which was commoner in men (27. J Collerton. 23. Previous epidemiological studies of ventricular dysfunction and heart failure have included only small numbers of the “oldest old”. D Barker. Leeds Teaching Hospitals NHS Trust. UK.1% (n¼376). III. NYHA class and echocardiographic assessment of cardiac dysfunction.0019.2% of participants (n¼140/376) had normal cardiac function or isolated mild diastolic dysfunction. age 49615 years. T Kirkwood. 37.063. using a portable instrument (Vivid-I. potentially introducing ascertainment biases. UK 1 1 1 2 1 Background Heart failure prevalence increases sharply at older ages.5060. BMI 44.460. UK. Of these.9.0160.1136/heartjnl-2011-300198. Only 7. symptoms were graded using the NYHA classification. Methods Four hundred and twenty-seven individuals aged 86e89 years (mean age 87. including tissue Doppler measurements of LV long axis velocities. and its range of 1485e4210 mls/min overlapped with the range of 1244e5774 mls/min in controls. GE Healthcare).6 W. mild.6% (n¼78/398) had moderate or severe LV systolic dysfunction. Results Consecutive overweight HF were screened and 24 patients (age 4968(SD) years.1) as controls. heart failure may more frequently be incorrectly diagnosed.9% (22/278)) on echo.062. p<10À6). The peak cardiac power output (CPOmax. age 43. We conducted a community-based study of the oldest old using domiciliary echocardiography to estimate the prevalence of cardiac dysfunction and heart failure. Newcastle University.6% (21/278) had a previous diagnosis of HF. the overweight HF patients had Vo2max values which distributed around the 14 mls/kg/min cut-off value. 3B Keavney.7 mls/kg/min. The section of the population aged 85 and over represents the most rapidly increasing demographic worldwide. p<10À6) and also lower than those of 30 non-overweight HF counterparts (20. warranting consideration for transplantation (Circulation 2010.5%).4%) than women (14.12). 4. A Kenny. There are significant levels of both undiagnosed and misdiagnosed HF in this age group. Abstract 99 figure 2) and all above the transplant cut-off value of 1. UK Background Peak O2 consumption (Vo2max) of #14 ml/kg/min has been widely accepted as being indicative of poor cardiac function Heart June 2011 Vol 97 Suppl 1 Abstract 99 Figure 2 A57 . Abstract 99 Figure 1 99 IS VO2MAX/KG A RELIABLE INDICATOR OF CARDIAC DYSFUNCTION IN OVERWEIGHT HEART FAILURE PATIENTS? doi:10.063. and 9 of whom were indeed below this cut-off value. Newcastle upon Tyne. 19. was taken.561. N Lewis. 1C Jagger. Results LV systolic function could be quantified in 93.2% (n¼398) participants and diastolic function (classified as normal.2618. p<10À6. minimum 2. or IV symptoms with underlying systolic dysfunction (29. Previous diagnoses of heart failure (HF) were abstracted from the GP record. Participants underwent 2-D and Doppler echocardiography.

Mean RVSP was 43.001) and RVSP 51e106 mm Hg 1.4. In quartiles of RVSP. the practice of correcting Vo2max by body weight in cardiological practice would also require urgent reconsideration.BCS Abstracts 2011 Conclusion These results indicate that in principle Vo2max in ml/kg/min as an indirect indicator of cardiac function or for cardiac transplantation selection is unreliable when applied to overweight heart failure patients.0001).6 vs 2. R Baruah.7 mm Hg and median follow was 362 days (IQR 129e850 days). the HR after adjustment for confounding factors including LVSD and the presence of chronic obstructive pulmonary disease (COPD) were: RVSP 35e41 mm Hg.161. 1. p<0. Dundee. Signal-to-noise ratio was significantly better for pressure than flow (6.65 mm Hg/beat. 43 % male) met entry criteria. and blood pressure using continuous finger photoplethysmography.12 (95% CI 0. St. flow did not decline (p¼NS). For each 5 mm Hg stepwise increase in RVSP the HR for all cause mortality was 1. 2Department of Cardiology. Results 2910 patients (mean age. 2S D Pringle. It remains unclear the level at which pulmonary hypertension conveys a mortality risk in patients with LVSD. Patients were included in the analysis if they had LVSD and had a right ventricular systolic pressure (RVSP) measurement.363. Z I Whinnett. 1A M J Choy. Pressure changes are simpler to measure and easier to distinguish from random variation than Doppler measurements of flow. 1A D Struthers. p<0. r¼e0. Dundee Abstract 100 Figure 2 A58 Introduction The presence of pulmonary hypertension in left ventricular systolic dysfunction (LVSD) is an ominous sign. Conclusions Improving atrioventricular delay immediately increases blood pressure. but are best measured immediately.001). Datasets from HIC include mortality data and other health care activities linked anonymously by the community health index (CHI) number. p<0.07 to 1.38 to 1. Pressure showed a partial decline a few seconds later (average rate 0. The immediate pressure increment correlated strongly with the immediate flow increment (r¼0.07 (1.00001 within one heartbeat).175).1. p<0. Imperial College.3 6 12.101 Abstract 100 Figure 1 1 1 B R Szwejkowski.09. Abstract 101 figure 1 shows the Kaplan-Meier survival curves for all cause mortality for all patients expressed as different RVSP quartiles.95 to 1.1136/heartjnl-2011-300198.5611. RVSP 42e50 mm Hg. optimisation.1136/heartjnl-2011-300198. London. This is due to compensatory vasodilatation rather than a reduction in cardiac function. B Unsworth. NHS Tayside. 74.98.32. 1D H J Elder. however this effect decays slightly over the subsequent minute.0001).49. Heart June 2011 Vol 97 Suppl 1 . Abstract 100 figure 2. p¼0. J Mayet.0001).001).0001). the immediate increment in blood pressure seems to diminish somewhat in the initial minute: it is unclear whether this is due to an (undesirable) fall in stroke volume or a (desirable) compensatory reduction in peripheral resistance. during and after atrioventricular delay adjustment from 40 to 120 ms in 19 subjects with cardiac pacemakers. HR 1.100 C H Manisty. Cox proportional hazards regression analysis was used to examine the effects of different ranges of RVSP measures on all cause mortality. p<0. University of Dundee. P Pabari.4 years.74. Methods We performed a record-linkage study in Tayside. There was a significant correlation between RVSP and survival (p<0. 100 PRESSURE VS FLOW AS A GUIDE FOR PACEMAKER OPTIMISATION? THE ACUTE HAEMODYNAMIC EFFECTS OF CHANGES TO ATRIOVENTRICULAR DELAY doi:10.62 (1. 1C C Lang. However. UK (population approximately 400 000) utilising the Tayside echocardiogram database (>100 000 echo’s) maintained by the Health Informatics Centre (HIC). Methods and Results We studied this question by measuring beat-bybeat stroke volume (flow) using Doppler echocardiography. D P Francis. UK Background Non-invasive blood pressure monitoring by continuous finger photoplethysmography (Finometer) may have value in pacemaker 101 WHAT DEGREE OF PULMONARY HYPERTENSION PREDICTS POOR OUTCOME IN PATIENTS WITH LEFT VENTRICULAR SYSTOLIC DYSFUNCTION? A 10-YEAR FOLLOW-UP STUDY doi:10. Blood pressure and stroke volume (flow) both increased immediately (p<0. in contrast. p¼0.27 (1. before the vascular compensation. Marys Hospital. Extending this concept to the entire spectrum of body weights. Quintuplicate experimental runs were performed. UK. Abstract 100 figure 1.04 to 1.

41) years respectively. Twenty-five patients had a troponin T >0. 3C J Whelan. 3 National Amyloidosis Centre. 49 (89%) were male. London. respectively. In this study we aimed to compare parameters of macro. Royal Free Hospital. The diagnosis is often made after the onset of breathlessness. (ii) south Asian and (iii) African-Caribbean. Significant ethnic differences in endothelial function are present in patients with HF. Fifteen had had a coronary angiogram.05). 3S D J Gibbs. Results Compared to disease controls and healthy controls south Asian patients with HF had impaired microvascular response to acetylcholine (3906302%.864. This is finding is independent of LVSD and COPD.28). Patient survival was estimated using KaplaneMeier analysis. Blood results showed.24%) patients (p<0. 3N Wassef. UK. 1National Amyloidosis Centre and UCL Centre for Nephrology. UCL Division of Medicine. London. No ethnic differences were detected in pulse wave velocity. 3University of Birmingham Centre for Cardiovascular Science.41) and 4. but preserved arterial elastic properties. UK. Birmingham. and 4. Most patients are male but women can be affected.1) and ejection fraction was 45. 1University of Birmingham Centre for Cardiovascular Sciences.05). Twelve (21. HF patients of white origin had higher FMD than south Asian (4. London. Primary Care and Populational Sciences. UK. UK. 3 P N Hawkins. Royal Free Hospital.6 years) and 40 healthy controls (n¼40. E/E9 15. Arrhythmias were common. UCL Medical School.5%) and 39 (70.5%) from bladder. London. London.88%) and African-Caribbean (5. London.BCS Abstracts 2011 glyceryltrinitrate.1 years). 10 (18. Conclusion: South Asian patients with HF have impaired micro.7 (range 0. University of London.8%) patients had a history of ischaemic heart disease. Additionally.66%. 27 (49%) Twave changes. UCL Medical School. UK. 14 (25. 4.1136/heartjnl-2011-300198. 6.54e8. Clinical. data on ethnic differences in endothelial function in HF are scarce.4%) from GI tract.81 (range 7. USA). 2National Amyloidosis Centre. age 66. age 63. 4 National Amyloidosis Centre. ECG findings were. 103 SENILE SYSTEMIC AMYLOIDOSIS: A COMMON CAUSE OF HEART FAILURE IN THE ELDERLY? doi:10.5%) compared to white (258615.and micro-vascular endothelial function and arterial elasticity in HF age.3%) groups (p>0. 5496264%.4).03 (45%).and sodium nitroprusside-mediated (endothelialindependent) response was observed between study groups. The most common presentation was with breathlessness in 28 patients (51%). 3G Y H Lip. 20 patients (36.9%) patients between 2001e2003. 1 (1.8664. parameters of pulse wave velocity and augmentation index did not differ between those with HF and those in control groups.03 (range 0. 8 were reportedly normal and 7 required intervention.9) had pacemakers in situ. ECG and echocardiographic evaluation were performed at presentation to our centre. UK 1 Background Endothelial dysfunction is characteristic of patients with heart failure (HF) and is associated with an increased risk of future cardiovascular events.5%. Echocardiographic findings revealed the median IVSd was 1.5 (range 13e83)%.1136/heartjnl-2011-300198. respectively). 2P S Gill. UCL Division of Medicine. UCL Medical School.5e41.1 (range 5e2611) and troponin T 0. A history of carpal tunnel syndrome is common. our aim was to evaluate the natural history of the disease in the UK in a group of thoroughly characterised patients.9%) first degree block.8%) from carpal tunnel tissue were identified.6%) had prior carpal tunnel operations. 102 ETHNIC DIFFERENCES IN ENDOTHELIAL FUNCTION IN CHRONIC HEART FAILURE doi:10. London. Australia).9%) right bundle branch block.05) and reduced FMD (7.2%) left bundle and 6 (10.64%. median E/A ratio was 2. City Hospital.and macro-vascular endothelial function. Microvascular endothelial function was evaluated by laser Doppler flowmetry of forearm skin (DRT4. age 69. UK. Arterial stiffness was quantified by pulse wave velocity and augmentation index using (Sphygmocor.5) cm.6%) and African-Caribbean (286617. 2A Wechalekar. P Sattianayagam.1e2.1263. 3C A McCarthy. Conclusion An RVSP of greater than 42 mm Hg is predictive of increased mortality in heart failure. 24 (43. 2University of Birmingham.07e5. University of London. SA patients with systolic HF were compared to two matched control groups: (i) south Asian patients with coronary artery disease without HF(disease controls) and (ii) south Asian “healthy controls”. Twenty-four patients (43. Moor Instruments.5611.8%) from fat and 1 (1. The median age at diagnosis and death were 74 (range 66e89) and 79 (range 69e84) years respectively. 11 (20%) <5 mm complexes in all inferior leads.469.88%. p<0. Philips. However. Royal Free Hospital.2610. UK.58 (range 0.0610. white (n¼44. 2J D Gillmore.6%) had bence jones proteins.01e0. Ten patients (18%) had a detectable paraprotein and 2 (3. Survival from symptom onset and diagnosis was 7. In recent years more patients have been diagnosed with 2 (3.6%). Birmingham.04 (range 0.24 years).7 (range 1. biochemical.369. the median baseline NT-proBNP was 356. In south Asian subjects. 6National Amyloidosis Centre.79e5. SSA is present in >25% of the very elderly at post mortem but was rarely diagnosed during life. Macrovascular endothelial function was assessed as brachial artery flow mediated dilation in response to hyperaemia (FMD) and glyceryltrinitrate were assessed by vascular ultrasonography (iE33.103 Abstract 101 Figure 1 Survival of RVSP quartile. 14 (25. HF patients of south Asian origin had impaired microvascular endothelial function (response to acetylcholine123695. UK) after iontophoresis of acetylcholine and sodium nitroprusside. 6 (10.3663. Birmingham.4 years) and African-Caribbean (n¼21. Methods We recruited 186 age/sex-matched patients with HF (ejection fraction <40%) of SA (n¼43. 3 (5. 55 patients with histologically proven SSA. age 68. as well as 36 disease controls (age 64. No difference in Heart June 2011 Vol 97 Suppl 1 Senile systemic amyloidosis (SSA) is a rare cause of heart failure due to the deposition of wildtype transthyretin.7J Dungu.6%) in AF. 2004e2006 and 2007e2009 respectively. and 123695. 5The Heart Hospital. It is becoming more frequently recognised perhaps due to widespread use of cardiac MRI. 2H J Lachmann.5S M Banypersad. UK 3 1 E Shantsila. 36 (65.102 J H Pinney. 7St George’s Hospital. UK.8664.and sex-matched patients of different ethnic origin: (i) white European. Systolic and diastolic dysfunction A59 . The clinical features and outcome are ill defined. 11. The series included all cases of biopsy proven transthyretin (TTR) amyloidosis with wildtype TTR gene sequencing who were prospectively followed up between January 2001 and May 2010.5%) from cardiac.3%) had a history of atrial fibrillation and 6 (10.3 years) origin.

With supportive management medium term outcomes are good.2M Thomas. 65 (46%) were male. aortic stenosis and left ventricular systolic dysfunction. p<0. mean serum creatinine 117 mmol/l (2. WITH LEVELS OF EACH RELATED TO MARKERS OF SEVERITY doi:10. a and b are gender-specific constants) from their ideal PV ((c 3 weight). 2K K Witte. UK. Leeds. G A Begg.2S Aggarwal. Incidental paraproteins are prevalent in up to 8% of this population and it is important to obtain a tissue diagnosis to rule out AL amyloidosis. 1. left ventricular systolic dysfunction. However. UK. 1.2.106 Abstract 104 Figure 1 1 2 Conclusions Calculating plasma volume status in CHF patients appears prognostically useful and suggests that dehydration is better tolerated than volume excess in these individuals and that targeting therapy to achieve a plasma volume status #178 ml might increment survival. median vitamin D levels (IQR) 30 (20e43) nmol/l (normal for skeletal health>75 nmol/l) and median parathyroid levels 8.104 H Z Ling. However. A Hunter. reduced tricuspid annular plane systolic excursion (p¼0.5 pmol/l).1136/heartjnl-2011-300198. aortic stenosis. PV status was calculated (Hakim RM. 1. UK. plasma NT pro-BNP and transthoracic echocardiographic parameters were studied in 140 patients with stable COPD attending a respiratory outpatient clinic. c¼gender-specific constant). J Watson. 6M Pye. 38 (27%) were prescribed diuretics and 15 (11%) had a left ventricular ejection fraction <45%. UK. University of Leeds. 95% CI 0. Department of Respiratory Medicine. p¼0. Results Median (6IQR) PV status wasd2616550 ml with 78% and 21% of patients having PV contraction and expansion. A positive troponin is a common finding with a subsequent normal coronary angiogram. LVEF 2868%). UK 105 CLINICAL AND ECHOCARDIOGRAPHIC DETERMINANTS OF N-TERMINAL PRO B-TYPE NATRIURETIC PEPTIDE LEVEL IN PATIENTS WITH STABLE CHRONIC OBSTRUCTIVE AIRWAYS DISEASE: A PROSPECTIVE OBSERVATIONAL STUDY OF 140 PATIENTS doi:10.37. 5I R Pearson.BCS Abstracts 2011 can be seen on echocardiogram. R Cubbon. J Mayet. Method Arterial blood gases.017) and higher pulmonary artery systolic pressures (p¼0. LVEF. right ventricular impairment.4).68.105 1 6 C P Gale. PV status predicted mortality (HR 1. Department of Echocardiography. Concentrations were significantly higher in those with a dilated left atrium. Significant predictors of NT pro-BNP were a dilated left atrium. London.001 to 1. 106 CHF PATIENTS ARE VITAMIN D DEFICIENT AND HYPERPARATHYROID. 1L Kearney.90).001. 2 2 3 4 Background The vitamin D-parathyroid (PTH) axis is increasingly recognised as potentially being involved with many of the features of the syndrome of CHF. haematocrit and creatinine.0007) and conferred a 75% reduced hazard for death (HR 0. for example.2A Cheng. 6Department of Cardiology. 2J Barth. Leeds.2S Weissert.16. 2The Heart Hospital. weight. 4NHLI Imperial College London. 1Leeds General Infirmary. The prognostic utility of such formulas in chronic heart failure (CHF) is unknown.8 (6. London. UK. We wanted to explore the relationship between vitamin D and PTH levels in a group of CHF patients and relate these to markers of severity. Methods We analysed serum 25(OH) vitamin D3 levels in 406 consecutive attendees of the Leeds Advanced Heart Failure clinic (310 men) and correlated these to clinical markers of severity.07 to 0.01). et al) by subtracting the patients actual PV ((1-haematocrit) 3 (a + (b 3 weight)). J White. Imperial College London.1136/heartjnl-2011-300198. Leeds. 1University College London Hospital. 2M T Kearney. UK. London. likely due to right ventricular strain. UK. atrial fibrillation and those prescribed diuretics and ACE inhibitors. 3D P Francis. 115 (82%) were current smokers. 1R Byrom. 2University of Leeds.2e13.2S Woldman. The median (IQR) NT pro-BNP concentration was 16. 1. UK 3 1 Background Plasma volume (PV) expansion is a hallmark feature of worsening heart failure that is notoriously underestimated by clinical examination. Leeds. several other clinical variables also associated with increased NT pro-BNP concentrations are prevalent in this population.0001. York Hospitals NHS Foundation Trust. York. 5Leeds Teaching Hospitals. 1S Barnes.002. NT Pro-BNP was an excellent discriminator of RV impairment (C statistic¼0.001).5) pmol/l (normal<6. Patients with cor pulmonale (n¼6) were more likely to have left ventricular systolic dysfunction (p<0. NHLI. York. Background Brain natriuretic peptides have been shown to be reliable indicators of left ventricular failure and markers of risk in cardiac disease. 2A C Wheatcroft. 1J Gierula.4D O Okonko. York Hospitals NHS Foundation Trust. mean left ventricular ejection fraction (LVEF) 31 (2)%. 1Division of Biostatistics. Over a median follow-up of 13616 months. York Hospitals NHS Foundation Trust. York Hospitals NHS Foundation Trust. 4 Department of Biochemistry. it has been suggested that it could be used to guide the initiation of non-invasive ventilation. Results Of the 140 patients. J Owen. The aim of this study was to identify clinical and echocardiographic determinants of the polypeptide N-terminal proBrain Natriuretic Peptide (NT pro-BNP) in patients with stable COPD. A PV status #À178 ml optimally predicted survival (ROC AUC 0. numerous haemodialysis-based equations also exist for its estimation. 1. This has been shown to have prognostic value and has a potential role in the management of the condition. 36 (15%) patients died. Abstract 104 figure 1B). UK. 1. Patients with PV excess had significantly higher creatinine and lower albumin levels. UK. While radioisotope assays optimally quantify PV status. Conclusions NT pro-BNP readily identifies patients with stable COPD who have right ventricular dysfunction. respectively. UK 3 2 104 PROGNOSTIC UTILITY OF CALCULATED PLASMA VOLUME STATUS IN CHRONIC HEART FAILURE doi:10. 1. 26 (19%) received home oxygen therapy. 4I Holbrook.2J Flint. p¼0.2 (25.001) in a graded fashion (Abstract 104 figure 1A) and did so independently of NYHA class. 95% CI 1. NYHA class 261. London.1136/heartjnl-2011-300198. 3International Center for Circulatory Health.4) pmol/l. Results Mean age (SE) was 69 (3) years. 1N Aung. York. patients with chronic obstructive pulmonary disease (COPD) are also known to have elevated concentrations of brain natriuretic peptides in the absence of overt cardiac disease. This is likely to confound clinical decision making. Aetiology was ischaemic Heart June 2011 Vol 97 Suppl 1 A60 . Methods We analysed the relation between estimated PV status and mortality in 246 outpatients with CHF (mean (6SD) age 67613 years. York. N Durham.

2S Weissert. iron deficiency (ID)) that may drive chronic heart failure (CHF) progression. UK.BCS Abstracts 2011 heart disease in 63% and 23% had diabetes mellitus. London. Although there was no relationship between vitamin D levels and baseline LVEF. LVEF 2868%. 3J Mayet. a fall in Hb. creatinine or CRP. and no differences between those patients taking and those not taking b-blockers and ACE inhibitors.001) and there was a negative correlation between vitamin D and fasting glucose levels (r¼0. The combination of a rising RDW and a falling mean cell volume (MCV) identified evolving ID. p<0. p<0. a higher RDW independently predicted increased mortality (HR 1. UK. 88% on ACE inhibitors.89.05). Over time.21. there was a positive relationship between pVo2 and vitamin D (Abstract 106 figure 4).2S Aggarwal. London.1136/heartjnl-2011-300198. placebo-controlled study in CHF patients with efficacy and mechanistic outcomes. and 46% on spironolactone). Hb<12. On Cox proportional hazards analyses.5) ml/kg/ min). UK. While an elevated RDW and iron deficiency at baseline predict mortality in CHF. in a subgroup of 150 patients followed up one year after titration to optimal CHF therapy. p¼0.0001. p¼0. UK 3 1 Abstract 106 Figure 1 Abstract 106 Figure 2 Heart June 2011 Vol 97 Suppl 1 Background Red cell distribution width (RDW) is a surrogate of many aberrations (inflammation. using a dose of vitamin D capable of normalising both vitamin D and PTH levels. Patients were optimally treated (84% on b-blockers. Conclusions The vitamin D-PTH axis is abnormal in CHF. calcium. A61 . 1. Whether vitamin D deficiency is causally related to CHF remains unknown and requires a long-term.13. 51%. 46%. an RDW >15%. London. p¼0.0001). Over a median (6IQR) follow-up of 15617 months. 40%. Results On initial consultation. London. D P Francis. respectively. A rising RDW predicted death (HR 1. Evolving ID was also associated with poorer survival (HR 2. Patients with worse symptoms as measured by NYHA status had lower vitamin D levels and higher PTH levels (Abstract 106 figures 1 and 2).6 (0. and MCV <80 fl were evident in 41%. and 23% of patients had a rise in RDW. 1. there was a significant positive relationship between change in LV dimensions and vitamin D levels at the time of the baseline scan (p<0. Abstract 106 Figure 3 Abstract 106 Figure 4 107 EXPANSION OF THE RED CELL DISTRIBUTION WIDTH AND EVOLVING IRON DEFICIENCY AS PREDICTORS OF POOR OUTCOME IN CHRONIC HEART FAILURE doi:10. 1University College London Hospital. and 8% of patients.62.2A Cheng.4D O Okonko. 2The Heart Hospital.107 N Aung.2M Thomas. a fall in MCV. related to the severity of the condition. 1.18. 60 (22%) patients died. 1H Z Ling. 1T Richards. little is known about the prognostic implications of their temporal trends. The mean daily dose of furosemide was 60 (3) mg. Patients with diabetes had lower vitamin D levels than non-diabetics (p<0. 4NHLI Imperial College. and evolving ID.2.002) independently of baseline RDWs and changes in Hb. Abstract 107 figure 1B). Very few patients (5%) were sufficient in vitamin D. 3International Center for Circulatory Health.02). 1.05). with an absolute increase >1% conferring a twofold escalated risk of mortality (Abstract 107 figure 1A). There was no relationship between vitamin D levels and age. randomised. NYHA class 261. Our data suggest that reverse remodelling in response to optimal drug titration is greater in those with higher vitamin D levels. 1. 58%. There was also a negative relationship between furosemide dose and vitamin D (Abstract 106 figure 3) and. malnutrition. in an unselected subset of 160 patients (mean peak oxygen uptake (pVo2) 16.2J Flint. 54% ischaemic). NHLI Imperial College London. Methods We analysed the relation of red cell indices on first consultation and over time with mortality in 274 outpatients with CHF (mean (6SD) age 70614 years. 1.5 g/dl. In 8 unselected patients we found a negative relationship between tumour necrosis factor-alpha (TNF-a) levels and vitamin D (r¼0.

H Watt. Oxford. I Kylintireas. University of Oxford. or to late complications after aortic dissection.54 N/m2 in healthy controls). J M Lee. and was rated as normal or abnormal.BCS Abstracts 2011 Results Significant vortical flow in any segment (defined as flow disturbance occupying more than one half of the aortic lumen) was present in all patients with MFS. Type B: flow disturbance confined to the proximal descending aorta. Prior repaired aortic dissection was associated with marked abnormalities of blood flow (Abstract 108 figure 1C). Oxford. 1 for controls. 4Nuffield Department of Medicine. MRI may be able to detect features of atherosclerotic plaque rupture that have been associated with an increased risk of recurrent atherothrombosis. using a time-resolved 3-dimensional flow technique.9 N/m2. aneurysm formation and aortic dissection.0005). Oxford. Oxford. B. but in only 7/18 controls (p<0. C. There was marked regional variation in the prevalence of major flow disturbance (Abstract 108 figure 2). S Neubauer. A Handa. 1S N Neubauer. Methods 18 patients with MFS (3 with a prior history of aortic dissection and aortic root surgery. Conclusion Patients with MFS commonly show aortic flow disturbance. Flow visualisation in a healthy volunteer. therefore current angiographic imaging techniques cannot reliably determine which patients are most likely to suffer future ischaemic events. Abstract 107 Figure 1 Conclusions An expanding RDW and evolving iron deficiency over time predict an amplified risk of death in CHF and could be utilised for risk stratification or therapeutically targeted to improve outcomes. L Biasiolli. UK 5 1 1 1 1 Background Marfan syndrome (MFS) commonly leads to progressive aortic dilation. Each segment was visualised using streamlines (Abstract 108 figure 1B) and particle traces. London. UK. University of Oxford. A62 Introduction Luminal stenosis is a poor predictor of the risk posed by any given atherosclerotic plaque. p<0. The aorta was segmented into regions on the basis of anatomic features (Abstract 108 figure 1A). 2Department of Cardiovascular Medicine. UK. M D Robson. Oxford. The severity of flow disturbance was greater in MFS patients than controls (median severity score 3 for Marfan patients. extent of abnormality was classified on a 4-point scale determined by the extent of radial involvement of the aortic lumen. Type C: flow disturbance in both the sinuses of Valsalva and the proximal descending aorta. R P Choudhury. 109 3T MRI OF ACUTE ATHEROSCLEROTIC PLAQUE RUPTURE AND DOWNSTREAM EMBOLIC INJURY doi:10.1136/heartjnl-2011-300198. UK. (defined as the presence of turbulent flow vortices) and. with corresponding increases in axial WSS within the true lumen of the dissected aorta (typical axial WSS in the dissected ascending aorta was +0. J M Francis. J Suttie. Wall shear stress (WSS) quantification was undertaken at predefined aortic locations (Abstract 108 figure 1A). 1Oxford Centre for Clinical Magnetic Resonance Imaging. Abnormal aortic blood flow patterns may contribute to the enlargement and dissection of an inherently weak aorta. Abstract 108 Figure 2 Prevalence of vortical flow disturbance occupying >50% luminal diameter for each aortic region for Marfan patients and controls. sex and height underwent CMR at 3T. 5John Radcliffe Hospital.108 A Pitcher.109 A C Lindsay. and descending thoracic aorta (w30% of dissections). J Kennedy. and we anticipate that flow abnormalities within a segment will predict progressive aortic dilation and dissection in an ongoing follow-up study. UK. 7Centre for Advanced Cardiovascular Imaging. particularly at the aortic sinuses (w60% of dissections). However. 108 4D-FLOW CMR DEMONSTRATES THE REGIONAL DISTRIBUTION OF AORTIC FLOW DISTURBANCE IN MARFAN SYNDROME doi:10. The sinuses of Valsalva and proximal descending aorta are most frequently affected. William Harvey Research Institute. 15 with no such history) and 18 healthy volunteers matched for age. Germany. J C Forfar. T E Cassar. compared to +0. Oxford. 7S E Petersen. UK. 6M Markl. UK Abstract 108 Figure 1 A. Planes for aortic segmentation and WSS quantification. 2P Leeson. 3Department of Clinical Genetics. Heart June 2011 Vol 97 Suppl 1 . 3E Blair. W Kuker. where abnormal. Flow visualisation in a patient with prior aortic dissection fulfilling the Ghent Criteria for Marfan syndrome. University of Oxford. 6University Hospital.1136/heartjnl-2011-300198.0005). Freiburg. Flow disturbance can be categorised into one of three categories. with the sinuses of Valsalva and proximal descending aorta being most frequently affected. Aortic flow disturbance in MFS was of one of three types: Type A: flow disturbance confined to the sinuses of Valsalva. 4B P Wordsworth. Churchill Hospital.

All patients underwent T1. without overt cardiovascular risk factors.17e7. E Davis. Statistical analysis was performed using the Wilcoxon sign rank test and Fisher9 s exact test to compare plaques. p¼0. Results AHA type VI (ruptured) plaque was seen in 22/41(54%) in the symptomatic group vs 8/41(20%) in the asymptomatic group (p<0. is being increasingly used to evaluate patients with chest pain and exclude coronary artery disease (CAD). Calcification of the coronary arteries is an excellent marker of underlying atherosclerosis. J Suttie. age. Peak mid-ventricular myocardial circumferential systolic strain and left ventricular mass adjusted for body surface area (LVM) were assessed by CMR. If physically able. triglycerides.9%) patients had normal coronary arteries. Total cholesterol level and waist to hip ratio were both significantly associated with reduced myocardial strain. with associations that extend to those in the normal range of cardiovascular risk. S Neubauer. or luminal thrombus (7% vs 0%. dual source CT coronary angiography (CTCA― Siemens Flash). Increased LVM. 42/116 (36%) patients had incidental findings on A63 . evidence of cerebral injury on DWI imaging was seen in 32/41 patients. Objectives (1) To evaluate the probability of CAD in patients with a CAC score of zero. UK Background In the elderly. but a zero CAC score does not completely exclude the diagnosis as potentially significant non-calcified plaques will not be detected by CAC scoring. respectively.1136/heartjnl-2011-300198. 41 presented acutely with TIA or minor stroke and 40 asymptomatic patients acted as the control group.5%) patients had nonobstructive CAD (stenosis <50%).1 days (range 0. 4 (6. Methods 116 symptomatic patients undergoing cardiac CT to exclude CAD from November 2009 to October 2010 were prospectively enrolled. p¼0. body mass index and waist to hip ratio. Results 62/116 patients had a CAC score of zero. as well as reduced high-density lipoprotein.068 mm vs 0. 54/116 had non-zero CAC scores. (2) To determine the incidence of non-cardiac incidental findings on cardiac CT and to quantify resulting investigations. however the presence of plaque surface rupture independently predicted a higher number of DWI lesions. T2 and proton densityweighted turbo spin echo MRI to 10 mm either side of the carotid. there was already evidence of early changes in systolic function related to subclinical atherosclerosis. 128-slice. R Banerjee. reduced left ventricular function is related to elevated carotid intima media thickness (IMT). incorporating coronary artery calcium (CAC) scoring and angiography. Scans were dual-reported by a cardiac radiologist and a cardiologist. We therefore sought to determine if in young adults. D R Obaid.24. In particular. patients underwent follow-up scanning a minimum of six weeks later. J Diesch. central and peripheral systolic blood pressure.1136/heartjnl-2011-300198. independent of the degree of luminal stenosis caused. Methods We studied 81 individuals (44 females.111 A J Shah. This study further establishes the ability of CMR to detect early changes in cardiovascular disease development. Statistical analysis was performed using GraphPadPrism.042 mm. Of these.01). Abstract 109 figure 1A). J Babar. Abstract 109 figure 1B). 17/30 (57%) cases of AHA VI (ruptured) plaque were seen to cause <70% stenosis―the current cut-off for surgical treatment. As part of a combined scan protocol. Plaques were graded according to the MRI modified American Heart Association (AHA) system by two independent reviewers blinded to the clinical status of the patient.03. surface rupture (24% vs 5%. CT imaging may also identify non-cardiac incidental findings that can lead to further downstream testing and medical expense. p<0. LVM as well as peripheral and central blood pressure measures.08. D Gopalan. as recommended in the recent NICE guidelines.392. No significant associations were noted between AHA plaque type and downstream cerebral injury.6%) had significant obstructive CAD (stenosis>50%).4265. Results Individuals with reduced peak myocardial circumferential systolic strain had higher carotid IMT (r¼0.4760. either due to intra-plaque haemorrhage (34% vs 18%. Of these. University of Oxford. the median number of lesions per patient was 7 and the median total lesion volume was 10. Conclusions We have shown for the first time that subclinical changes in cardiac function and subclinical atherosclerosis are closely interrelated in young adults. p¼0. P Leeson. Addenbrooke’s Hospital. a higher total DWI burden at presentation. and higher total cerebral FLAIR signal at follow-up when compared to all other plaque types (p<0. At follow-up scanning a minimum of 6 weeks later. Of the 41 patients in the acute group. R Poole. 111 SINGLE CENTRE PROSPECTIVE CARDIAC CT STUDY TO DETERMINE THE PREVALENCE OF PATIENTS WITH CORONARY ARTERY DISEASE WITH A ZERO CORONARY ARTERY CALCIUM SCORE AND ASSOCIATED NON-CARDIAC INCIDENTAL FINDINGS doi:10. Heart June 2011 Vol 97 Suppl 1 Introduction Cardiac CT. Males also had higher carotid IMT than females (mean6SD ¼ 0.05). in addition to the Mann Whitney U test to compare cerebral injury. Methods 81 patients with carotid artery disease were recruited.BCS Abstracts 2011 Hypothesis 3T MRI of the carotid artery can identify atherosclerotic plaque rupture in patients presenting with TIA or minor stroke. peripheral pulse pressure. 37 males) without cardiovascular risk factors and with a mean age of 28. J Francis. p<0. a well-established subclinical marker of atherosclerosis.62 ml (range 0e522 ml). Cambridge. This patient with obstructive CAD had a high grade lesion in the proximal left anterior descending artery that required intervention. Median time from symptom onset to MRI in the symptomatic group was 2. Carotid IMT was measured as a marker of subclinical atherosclerosis using ultrasound. Demographic and anthropometric characteristics were measured as well as metabolic parameters and peripheral and central blood pressure. Of particular note. Abstract 109 figure 1C).05). The association between carotid IMTand peak myocardial circumferential systolic strain was independent of gender. Cardiovascular Medicine. 57 (91.001). Patients underwent CAC scoring and had contrastenhanced. Cardiovascular magnetic resonance (CMR) allows for precise quantification of changes in myocardial structure and function. UK Abstract 109 Figure 1 Conclusion Acute atherosclerotic plaque rupture can be visualised using 3T MRI.5460. smoking. M Lazdam. 13 (24%) had obstructive CAD and 41 (76%) nonobstructive CAD.110 A J Lewandowski. J H F Rudd. Oxford.001). and 1 patient (1.0).36 years (mean6SD). 110 MYOCARDIAL SYSTOLIC STRAIN AND SUBCLINICAL ATHEROSCLEROSIS IN YOUNG ADULT LIFE doi:10. only two cases of AHA VI plaque showed evidence of full healing. glucose. were all significantly associated with increased carotid IMT (p<0. MRI can provide detailed information on plaque morphology that can predict downstream embolic injury. study participants then underwent diffusion-weighted imaging (DWI) and Fluid-Attenuated Inversion Recovery (FLAIR) imaging of the brain to assess acute and chronic injury. D Augustine.

positive and negative predictive values of 71%. 8% of this group had evidence of non-calcified plaque. Cambridge. The mean radiation dose (6 SEM) for subsequent CTCA was 2. Because patients are often asymptomatic. and 92% respectively. A G Mitchell. 83 (92%) out of 90 patients who responded to a patient survey preferred CTA to ICA as a screening test for CAV. The mean radiation dose (6 SEM) for CAC scoring was 0. The Agatston calcium score (CS) was calculated for all patients.6160. These incidental findings resulted in further investigations. UK. D Gopalan. T K Mittal. None of the 61 patients with completely normal CTA had CAV on ICA.50 mSv in prospective mode (n¼64) and 17. 113 DUAL ENERGY CT IMPROVES DIFFERENTIATION OF CORONARY ATHEROSCLEROTIC PLAQUE COMPONENTS COMPARED TO CONVENTIONAL SINGLE ENERGY CT doi:10.113 D R Obaid. Despite a mean resting heart rate of 82 bpm SD613 and body mass index of 27 kg/m2 SD 65. with one patient having obstructive CAD that required intervention. One has to exercise caution in just using CS in these patients as significant CAV can be missed out. 1 to 24 years post transplant (mean¼12 years SD6 6) underwent CT coronary artery calcification (CTCAC) followed by retrospective ECG gated coronary angiogram on a 64slice scanner without the use of any b-blockers. UK Abdomen (n¼7) Diaphragm (n¼5) Vasculature (n¼11) Aorta Renal Coeliac Abstract 111 Table 2 Cardiac CT Investigation Bone scintigraphy Chest clinic referral CT chest DMSA MR adrenals MRA renal Nephrology clinic referral Pleural fluid aspiration Ultrasound kidneys Ultrasound liver Further investigation of incidental findings on n 1 2 4 1 1 1 1 1 1 3 Abstract 111 Table 3 incidental findings Investigations or referrals Bone scintigraphy Chest clinic referral CT chest DMSA MR adrenals MR cardiac MRA renal Nephrology clinic referral Pleural fluid aspiration Ultrasound kidneys Ultrasound liver Investigations and referrals generated by Number 1 2 4 1 1 2 1 1 1 1 3 Objective To evaluate ComputedTomographic Coronary Angiography (CTA) as an alternative to Invasive Coronary Angiography (ICA) for the detection of Cardiac Allograft Vasculopathy (CAV). Further research is needed to evaluate the added cost. For all the 1755 segments assessed by CTA irrespective of the image quality. Out of 77 patients with absent CS. N R Banner.1136/heartjnl-2011-300198.03 mSv. specificity. if strong clinical suspicion remains in patients with a CAC score of zero further coronary investigation may be warranted. Conclusion The study shows that CTA compares favourably with ICA in detecting CAV in heart transplant recipients. documented in Abstract 111 table 2. 5.66 6 0. Majority (89%) of patients had CTA within 24 h before ICA. We conclude that A64 Introduction Vulnerable plaques have a relatively high necrotic core area and low fibrous tissue content. surveillance ICA is performed in our institution. CTA is effective for the diagnosis of coronary disease in non-transplant patients.68 mSv in the retrospective mode (n¼25). and may be a preferable screening technique because of its non-invasive nature. 94%. 72% and 78% respectively for the detection of any CAV found by ICA. specificity. 81% of the CTA images were graded as excellent or satisfactory. Methods 117 HT patients. The CTA images were systematically analysed for image quality and the presence of CAV (graded as significant if >50% luminal stenosis) using a fifteen coronary segments model by an independent investigator blinded to the results of ICA. Background CAV is an important cause of late mortality after heart transplantation (HT). 79%. UK 1 1 1 2 Conclusions Despite 62 patients having a reassuring CAC score of zero. clinical benefits and radiation exposure created by investigation of such incidental findings in the context of cardiac CT.32 mSv in high pitch “flash” mode (n¼27). 1University of Cambridge. P A Calvert. 79%. 1M R Bennett. Harefield. Incidental findings are common. patient preference and yield of additional information. Results CS ranged from 0 to 1681 (Mean¼91.BCS Abstracts 2011 cardiac CT that are summarised in Abstract 111 table 1.1561. Abstract 111 Table 1 Area Chest (n¼27) Incidental findings on cardiac CT Structure Lung parenchyma Incidental Finding Nodule <1 cm Emphysema Atelectasis Fibrosis Tumour recurrence Bronchiectasis Pleura Lymph node Liver Adernal Effusion Calcification Adenopathy Cyst/Nodules Adenoma/metastasis Hiatus Hernia Dilatation Aneurysm Stenosis Stenosis n 5 3 6 4 1 2 2 2 2 6 1 5 8 1 1 1 112 COMPUTED TOMOGRAPHIC CORONARY ANGIOGRAPHY TO SCREEN FOR ALLOGRAFT VASCULOPATHY AFTER HEART TRANSPLANTATION doi:10. On a patient basis. but few studies have been done after HT.1136/heartjnl-2011-300198. and can result in multiple further investigations for patients. Although CT can identify plaque components on the basis of their x-ray attenuation. Non-coronary cardiac and non-cardiac abnormalities were identified in 18% and 14% patients respectively. positive and negative predictive values of 74%. CTA had sensitivity.8660. Cambridge. J H F Rudd. there is Heart June 2011 Vol 97 Suppl 1 . 2Papworth Hospital NHS Trust. Harefield Hospital.112 M G Panicker. 3 had significant CAV on ICA.76275). CTA best performed in diagnosing CAV of more than 25% with sensitivity.

6 Dual Energy Index (mean) 0.51) 84.34) 582.9 128. Results Attenuation values for 1088 ROIs were measured from 70 paired data sets at 100 kV and 140 kV creating 70 DEIs (12 necrotic core.57 63. We therefore examined whether DECT was better than single energy CT in determining plaque components defined by virtual histology IVUS. Plymouth. ROI densities were measured (in Hounsfield Units) and assigned to the plaque component. Abstract 113 Table 1 Plaque Component Necrotic Core Fibrous Plaque Calcified Plaque Lumen 100 kV mean HU (SD) 57. UK.27) 140 kV mean HU (SD) 42. DECT may allow better differentiation of necrotic core and fibrous plaque. UK 1 1 1 1 1 Abstract 113 Figure 1 Demonstration of plaque co-registration between VH-IUS and 140kV/100kV CT data sets. S Iyengar.69 150. DEI derived from both energy Heart June 2011 Vol 97 Suppl 1 Background CT coronary angiography CTCA now has an established role in the investigation of patients with chest pain. with the change in attenuation of plaque components to different energies depending upon their material composition.26 (42. Previous publications have used a chest conversion factor to calculate the effective dose (mSv) from CTCA. pre-EP studies and problem solving. VHIVUS images were co-registered and orientated with the corresponding CT images using distance from coronary ostia and fiduciary markers (Abstract 113 figure 1).BCS Abstracts 2011 significant overlap between their attenuation ranges. 114 RADIATION DOSES TRENDS FROM CARDIAC CT USING A CARDIAC SPECIFIC CONVERSION FACTOR: SYSTEM UNDERSTANDING & AN OPTIMISATION STRATEGY SIGNIFICANTLY REDUCES THE DOSE TO THE PATIENTS IN A CLINICAL SERVICE doi:10.1136/heartjnl-2011-300198.0283 0.028 mSv (mGy. UK. Exeter.114 O E Gosling. R Loader. a weakness of conventional cardiac CT. data sets permitted resolution of necrotic core and fibrous plaque without overlap (Abstract 113 figure 2B). We aimed to investigate what impact the implementation of new technologies has had on the radiation dose of CTCA. CT scanning A65 . 3C Roobottom. CABG assessment.93) Mean Difference (100e140 kV) 14. Cross section taken through this plaque (blue arrow) and following orientation with VH-IVUS cross section HU region of interest sampling is performed in calcified plaque. Scan indication included: rule out coronary artery disease. 52 plaques were chosen with either homogenous fibrous plaque or confluent areas of calcified plaque or necrotic core as defined by VH-IVUS. calcified plaque is distinguishable from all others but necrotic core and fibrous plaque overlap. 2W D Strain. allowing for more accurate non-invasive identification of vulnerable plaques. Our department follows the ALARP ethos and has implemented new technologies together with physician training to reduce the radiation dose from CTCA. In particular.0450 0. Recently introduced dual energy CT (DECT) permits acquisition of 2 different energy data sets simultaneously.47) 733. Under the IRMER regulations radiation doses to patients should be kept as low as reasonably practical (ALARP). Plymouth. 3Peninsula College of Medicine and Dentistry. A dual energy index (DEI) was created for each component. In DECT. Plymouth Hospitals NHS Trust. 29 calcified plaques and 18 lumen). most crucially between necrotic core and fibrous plaque. lumen (iodinated contrast) showed the greatest change in attenuation and hence had the highest DEI. CT data was obtained at peak voltages of 100 kV and 140 kV. 11 fibrous plaque. (B) The use of dual energy index from the attenuation data at 2 energies (100/140kV) allows significant separation of necrotic core and fibrous plaque (p<0. G Morgan-Hughes.30 (49.7) 411. Multiple regions of interest (ROI) were placed within the plaque components or in lumen on cross sectional CT images pre-classified by VH-IVUS (Abstract 113 figure 1). Calcified plaque is identified 5mm from side branch adjacent to characteristic calcification (yellow line). defined as the ratio of the difference in attenuation at 2 different energies / sum of attenuation with 1000 added to each attenuation value to avoid negatives.0071 0.90 (55. Methods 20 patients underwent DECT and 3-vessel VH-IVUS.10 (226. Method All patients who were coded as attending for a cardiac CT scan on the PACS and CRIS systems were included in the analysis.05) (Tukeys multiple comparison test). 2Peninsula College of Medicine and Dentistry.0483 Conclusions The additional attenuation data provided by DECT improves the differentiation of plaque components when compared to conventional single energy CT. We have previously demonstrated that chest conversion factors significantly under-estimate the effective dose to the patient when applied to CTCA and have calculated a cardiac specific conversion factor of 0.20 (194.05). Necrotic core had the lowest DEI and could be distinguished from all other components (p<000.69 (31. Abstract 113 Figure 2 (A) Defined CT attenuation spectra of plaque components using a single energy (140kV). Values obtained using a single energy data set showed good differentiation between calcified plaque and all others (p<0. in contrast to the single energy data.cm)-1.9) 282.60 (30.1) Importantly. but considerable overlap between necrotic core and fibrous plaque (p¼ns) (Abstract 113 figure 2A) (Abstract 113 table 1).5 (82.20) 148.

using the accepted conversion factor at the time the mean dose was 14.BCS Abstracts 2011 between September 2007 and August 2010 was included. Patients with AHREs had significantly larger indexed LAV (p¼0. were analysed by ELISA. D P Francis. As CTCA programmes become established in hospitals around the UK it is important that clinicians have the appropriate training and experience to keep the radiation dose to the patients as low as reasonably practical. Methods In total. Conclusion Cumulative Vp and increased LAV are associated with the development of AHRE. p<0.74 0. This study suggests AHREs and AFB have dissimilar pathophysiologic associations with left atrium and ventricle remodelling. Birmingham. G Y H Lip.661.4 27.962.5 Zero paddingd 100 kV 636 7.4 55. Results Baseline characteristics and comorbidities were comparable between groups (Abstract 115 table 1).6 14.012).612.23 0. retrospective. septal A9 were independently associated with AFB (all p<0. G Dwivedi.0e99. 115 ATRIAL HIGH RATE EPISODES AND ATRIAL FIBRILLATION BURDEN: DO THEY HAVE SIMILAR ASSOCIATION WITH CARDIAC REMODELLING? doi:10.869.6 mSv.0611.01). Abstract 114 Table 1 Retrospective Gatingddose modulation 150 29.4 14.561. LV systolic and diastolic parameters were comparable between groups.014) which significantly underestimates the effective dose from CTCA.6 (41. Scans were performed on a Lightspeed VCT or HD750 (GE Healthcare).766. B Unsworth. 87 patients with dual-chamber pacemaker underwent two-dimension (2D) and tissue Doppler imaging (TDI) echocardiography.464.011) and higher cumulative Vp (p¼0. For each analysis period all scans were included.060.6 6.9 mSv. p¼0.467. For the final 6 months the mean radiation dose for a cardiac scan was 5. high definition scanning and retrospective ECG gating for a variety of differing clinical scenarios. A.163. UK Background and Objectives Contemporary pacemaker devices allow quantification of atrial high-rate episodes (AHREs) and atrial fibrillation burden (AFB) accurately. In patients with AHREs. this Abstract 114 figure 1 incorporates scans performed with standard filtered back projection.8 27. N Sutaria.4 8 6.8 Final 6 months 461 5. but AFB is independently associated with changes in LA function and LV diastolic function. University Department of Medicine Centre for Cardiovascular Sciences.3 116 Scanning protocol Number of Patients Mean Effective Dose (mSv) CIs (99%) (mSv) CRT OPTIMISATION: IMPROVING ECHOCARDIOGRAPHIC TECHNIQUES BY ACCOMMODATING BIOLOGICAL VARIABILITY WITHIN DIFFERENT ECHOCARDIOGRAPHIC PARAMETERS doi:10. matrix metalloproteinases-1 (MMP1) and tissue inhibitors of metalloproteinases-1 (TIMP1).966. In March 2009 the scanner parameters was set to zero padding and 100 KV reducing the dose to 7.7 34.4 0.5 98. A. and inversely correlated with late acceleration velocity (A) (r¼À0. S Krishnamoorthy.2 21.4 mSv. Results In the 3-year period 1736 scans were performed.001). LA volume (LAV) was evaluated by area-length method and indexed to body surface area.5 5. Cumulative ventricular pacing (Vp) is associated with development of atrial fibrillation. this resulted in a halving of the mean radiation dose to 13.6 Prospective gating 489 13. London.9) p Value 0. A D Hughes.9 mSv.116 P A Pabari. Septal A9 was used to measured regional LA function.0) Conclusion The introduction of dose saving strategies and appropriate physician training has lead to a significant reduction in the radiation dose from cardiac CT.664. H S Lim.38 0. Plasma markers. low kV and zero padding. A cardiac specific conversion factor was used rather than a chest conversion factor (0.468. Data was transformed and expressed as a geometric mean with 99% CI. UK Background In optimisation of CRT (and even selection for implantation) we may have underestimated the impact of beat-to-beat Heart June 2011 Vol 97 Suppl 1 A66 . A Kyriacou. To calculate the effective dose a conversion factor was applied to the dose length product of each examination. City Hospital. The mean radiation dose in the first 6 months of the study (retrospective gating) was 29.2 1. The presence of AHREs (defined by atrial-rate $220 beats/min and $5 minutes) and AFB were derived from pacemaker diagnostics.2 8.8e99. the AFB ranged from 0 to 99% and correlated with E/A (r¼0. In March 2008 prospective ECG gating was installed.01 0.962. Age (years) Body mass index (kg/m2) Indexed LA volume (ml/m2) LV ejection fraction (%) E/A Septal A’ (cm/s) Septal S’ (cm/s) Septal E/E’ Percentage Vp 71.115 C W Khoo. iterative reconstruction.9 12. Imperial College London. E/A.6 7.9 52. LV systolic and diastolic parameters were evaluated by mitral inflow velocity (E.9 (1.1136/heartjnl-2011-300198.169. The DLP is the radiation dose in one CT slice multiplied by the length of the scan. LV ejection fraction (biplane Simpson’s) and septal TDI velocity. the total dose for the whole examination is used including the scout and nonenhanced scan (calcium score). On linear regression analysis.16 0.71 0. B Balakrishnan. prospective. Plasma markers of remodelling.1136/heartjnl-2011-300198. E/A).860. J Mayet.8611.8 13.009).6 26.6 mSv.2 6. but it is not clear if AHREs and AFB share similar pathophysiologic associations with left atrium (LA) and ventricle (LV) function and remodelling. Abstract 115 Table 1 No AHRE (n[70) AHRE (n[17) 75.9 0. but this was not associated with elevation of MMP1 and TIMP1.1 0.9 6.01 Abstract 114 Figure 1 Effective dose (mSv) by protocol period.6 33 26. M Moraldo.

046). and of far more replicate measurements than is current practice. area and height were measured at 6 points of the cardiac cycle adapting commercially available software designed for assessing the mitral valve (MVQ.19. USA). are to be developed. 21 ms to 16 ms (LVOT VTI) and 14 ms to 10 ms QRS duration (p¼0. 0. Papworth Hospital NHS Foundation Trust. the TVA dilates in a septo-lateral direction.63. Smoothing biological variation by averaging multiple measurements allows the full potential of echocardiographic optimisation to be achieved and improves the consistency of optimisation. p¼0. resulting in a more circular orifice. requires a greater number of measurements. Methods and Results In this large study of biological variability.55 respectively. was similarly low. For single measurements at each setting. The dynamics of the normal TVA has not been described in any significant detail.54 and 0.001) when averages of paired measurements were used. as seen in Abstract 116 figure 1. and is incompletely understood. 54% for LVOT VTI and 58% for QRS width. 117 TRICUSPID VALVE ANNULAR DYNAMICS IN NORMAL VS DILATED RIGHT HEARTS. A67 Heart June 2011 Vol 97 Suppl 1 .66 (p¼0. and is greatest in mid-diastole. This study was designed to assess the feasibility of assessing the TVA throughout the cardiac cycle using 3D transoesophageal echo (TOE). Antero-posterior (AP) diameter. nor has the impact of abnormal right hearts on the TVA been described. To optimise within 20 ms or 10 ms of the true optimum. 0. Agreement between one method and another. The area is significantly larger in the abnormal group (mean 1795 mm2 abnormal vs 1204 mm2 normal. replicate measurements at a series of interventricular delays of each potential optimisation modality at rest. reaching significance at end systole (6. (ii) aortic preejection time.0002). resulting in a circular orifice and lower eccentricity ratio throughout the cycle (mean 0. if reliable predictors of which patients will benefit from CRT.91 abnormal v 1. 28 ms to 22 ms (IVMD). Phillips). A 3D TOE STUDY doi:10.1136/heartjnl-2011-300198.42.01). 3D zoom images of the TVA were acquired using an iE33 imaging platform and X7-2t transducer (Phillips. using single replicates. This can be quantified most clearly in the optimisation process. Abstract 117 Figure 1 Eccentricity ratio of the tricuspid valve annulus during the cardiac cycle: normal vs dilated rated hearts. These observations may also cast light on to why attempts to identify future responders from CRT has not e when tested in externally monitored randomised trialsdbeen fruitful: dyssynchrony assessment to select patients for implantation may need averaging too. The eccentricity ratio was calculated as AP/SL. (iv) LVOT VTI and (v) QRS width. This included (i) 3D systolic dyssynchrony index.30. dependant on the intraclass correlation coefficient. Cambridge. B Rana.11. 14 ms to 10 ms (aortic pre-ejection time). divided into 2 groups: normal right hearts (n¼10). we performed over 2000 echocardigraphic measurements in 12 patients. The SL diameter increased more in the abnormal group.BCS Abstracts 2011 variation on echocardiographic measurements. 0.22 normal.117 L Ring. 41% for aortic pre-ejection time. The equivalent of 31 optimisations per patient were performed.9 mm. This pilot study suggests that 3D TOE provides insight into understanding tricuspid annular dynamics.51. 0. see graph). 32% for IVMD. Abstract 116 Figure 1 Conclusions Because of beat-to-beat variability. R A Rusk. UK Background The tricuspid valve annulus (TVA) is a complex three dimensional structure that is non-planar. (iii) interventricular mechanical delay.01. Massachusetts. and dilated right hearts (n¼10). Conclusions In patients with abnormal right hearts. Andover. Trying to save time by performing inadequate numbers of replicates is a false economy and leads to optimisation being a form of randomisation. at 39% for SDI. We performed separate. Methods 20 patients were included. in which genuine small changes in cardiac function (signal) must be detected among potentially large beat-to-beat variation (noise). agreement between successive optimisations was low.50 and 0. 0. Integration of this biological insight into technological achievements of clinical imaging is necessary. septo-lateral (SL) diameter. with the average agreement between optima by two methods being only 18% similar to pure guesswork. The intraclass correlation coefficient was low for all methods at 0. The dynamic changes of the TVA are similar in dilated vs normal right hearts.7 mm vs 4. p<0. The scatter of optima obtained reduced (improved) significantly when using averaged pairs of measurements compared to single measurements from 23 ms to 18 ms (3D SDI). 0. VV delay optimisation by any of the echocardiographic techniques is not realistic unless multiple replicates are performed and averaged. with the exception of annular height. p<0. Annular height is similar in both groups but has an upward trend in systole in normals and reduces in abnormals. Results TVA area decreases during systole in both groups. The intraclass correlation coefficients improved to 0.

BCS Abstracts 2011
118
HIGH-RESOLUTION CARDIAC MAGNETIC RESONANCE PERFUSION IMAGING VS POSITRON EMISSION TOMOGRAPHY FOR THE DETECTION AND LOCALISATION OF CORONARY ARTERY DISEASE
doi:10.1136/heartjnl-2011-300198.118 G D J Morton, M Ishida, A Chiribiri, A Schuster, S Baker, S Hussain, D Perera, M O’Doherty, S Barrington, E Nagel. King’s College London, London, UK

supplied by stenotic arteries by PET and 76% by CMR. Remote ischaemia was detected in 24% of territories by PET and 16% by CMR.

Abstract 118 Table 1
Characteristic Male Number (percentage) of affected patients 25 (81%) 12 (39%) 10 (32%) 22 (71%)

Background Non-invasive imaging has a key role in the detection of coronary artery disease (CAD). Its importance has been affirmed by recent National Institute of Clinical Excellence (NICE) guidelines. Localisation of ischaemia to a coronary territory is also important in patient management. Cardiac Magnetic Resonance (CMR) perfusion imaging is a well-established and radiation-free test for these purposes. However, there are few data comparing perfusion CMR with Positron Emission Tomography (PET), which is widely regarded as the non-invasive gold standard. Furthermore novel CMR methods, including those based on k-t acceleration techniques, allow myocardial perfusion imaging with unprecedented spatial resolution. Methods 31 patients with known or suspected CAD referred for diagnostic x-ray coronary angiography (XCA) underwent both CMR and PET examinations. Both PET and CMR protocols included adenosine stress and rest perfusion imaging. CMR perfusion imaging was performed at 1.5T with a k-t-accelerated steady-state free-precession sequence. PET imaging was performed with 13NAmmonia. The Abstract 118 figure 1 shows an example. Experts blinded to the clinical data analysed the imaging data and experts blinded to the imaging results visually analysed the XCA data. A significant coronary artery stenosis was defined as $70% reduction in diameter or a fractional flow reserve <0.8 where available. Sensitivity and specificity for PET and CMR vs invasive angiography were calculated. Localisation of ischaemia was assessed in patients with CAD by classifying myocardial territories as either supplied by, or remote from, a stenotic artery.

Diabetes Previous PCI Hypertension

Conclusions CMR is at least as accurate as PET for the diagnosis of CAD and also for the localisation of ischaemia to coronary territories. Relatively low numbers mean that CIs are wide and further work is required. Using an anatomic test as the reference-standard for functional tests has well-described limitations. Remote ischaemia is likely to occur for several reasons including underestimation of disease severity at XCA, microvascular disease and also false positive results.

119

CARDIOVASCULAR MAGNETIC RESONANCE IMAGING (CMR) DETECTS SUBCLINICAL CARDIOMYOPATHY IN ASYMPTOMATIC PATIENTS WITH LEFT BUNDLE BRANCH BLOCK (LBBB) AND NORMAL ECHOCARDIOGRAPHY
doi:10.1136/heartjnl-2011-300198.119

M Mahmod, T D Karamitsos, J J Suttie, S G Myerson, S Neubauer, J M Francis. University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Oxford, UK

Abstract 118 Figure 1
Results Patient characteristics are shown in the Abstract 118 table 1. Mean age 6 SD was 6469 years. One CMR examination was nondiagnostic. The interval between PET and CMR was 266 days (77% same day), between PET and XCA 22628 days and between CMR and XCA 22629 days. The prevalence of CAD was 81%. For the detection of CAD PET sensitivity was 80% (95% CI 59% to 92%) and specificity was 67% (24% to 94%). CMR sensitivity was 83% (95% CI 62 to 95%) and specificity was also 83% (36% to 99%). In patients with CAD ischaemia was localised to 63% of the territories
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Introduction Asymptomatic left bundle branch block (LBBB) is a common indication for referral for cardiovascular magnetic resonance (CMR) imaging. However, it is not known whether referral for LBBB returns a high diagnostic yield. We evaluated the diagnostic value of CMR in these patients. Methods All clinical CMR referrals for LBBB from January 2005 to November 2010 were reviewed by two independent investigators. Only patients with asymptomatic LBBB and normal echocardiograms (echos) who underwent complete CMR evaluation were included in the study. Patients were excluded if they had cardiac symptoms or known coronary artery disease. Anthropometric data, pre-existing conditions, medications, smoking status, family history and echocardiographic data were recorded. Results From January 2005 to November 2010, 63 asymptomatic patients with LBBB were referred to our institution for CMR from a total of 3596 CMR referrals. Of these, 34 had normal echos; 20 subjects who had abnormal echos and 9 who had no echos at presentation were excluded from further analysis. Mean age of the 34 patients with normal echos was 5469 years, and 19 (56%) were men. Demographic data and left ventricular (LV) measurements are presented in the Abstract 119 table 1. The most common associated medical conditions were hypertension (11 patientsd33%) and hyperlipidaemia (8 patientsd24%). Ten subjects (30%) had a family history of heart disease. Nine (27%) patients underwent coronary angiography which was normal. Of the 34 patients, 14 (41%) were found to have pathological findings on CMR. The commonest abnormalities were dilated cardiomyopathy (DCM) (23%), followed by LV hypertrophy (LVHddefined as LV wall thickness >13 mm) (9%), arrhythmogenic right ventricular cardiomyopathy (ARVC) (6%) and Ebstein anomaly (3%). Two patients (6%) had mid wall late gadolinium enhancement. In the remaining 20 (59%) patients, no abnormalities on CMR were detected.
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BCS Abstracts 2011
Abstract 119 Table 1
All patients Normal CMR Abnormal CMR (n[34) (n[20) (n[14) p value Age (years (median, IQR)) Male gender (no, %) BMI (mean, kg/m2) LVEDV (ml (median, IQR)) LVESV (ml (median, IQR)) LVEF (ml (mean, SD)) 54.368.9* 19 (55.8%) 57.5 (19.7) 11 (55.0%) 48.5 (17.0) 8 (57.1%) 29.366.5 182.5 (60.5) 71.5 (39.5) 55.7613.6 12.5 (9.4) 83.0 (14.5) 0.6 0.59 0.37 0.012 0.005 0.004 0.059 0.001

28.365.6 27.664.9 155.0 (58.0) 133.0 (41.5) 51.0 (26.0) 60.6613.9 48.0 (12.5) 66.165.5

LV thickness (mm (median, IQR)) 11.0 (7.4) 9.0 (6.1) LVMI (g/m2 (median, IQR)) 72.5618.1* 64.0 (15.0) *mean, SD. IQR.

Conclusions There is a high rate of sub-clinical cardiomyopathy (41%) detected by CMR in asymptomatic patients with LBBB despite normal echocardiograms. These findings support the claim that CMR is a valuable adjunct to conventional investigations in asymptomatic LBBB. Further studies are needed to evaluate the prognostic implications of CMR abnormalities in this cohort of patients.

The MBH SR curves were filtered with a moving average (MA) to reduce noise sensitivity, results from a sample width of three and five were examined. Differences between SBH and MBH were assessed using Wilcoxon signed-rank test as not all measures were normally distributed. Reproducibility assessments were carried out on all techniques. Results PeakEcc was significantly higher with MBH vs SBH, but reproducibility was slightly worse. Results are summarised in Abstract 120 table 1. Systolic SR was approximately equal with all techniques although MBH using MA of five led to a borderline significant reduction. Diastolic SR was higher when measured with MBH although only significant using MA of three. Systolic and diastolic SR measures were more reproducible with MBH compared with SBH, except for the diastolic SR using MA of three, which was substantially worse. Strain and SR curves for the same patient are shown in Abstract 120 figure 1.

Abstract 120 Table 1
Peak systolic strain (%) SBH MBH (MA of three) e13.762.4 e15.163.1 (p¼0.023 vs SBH) MBH (MA of five) e15.163.1 (p¼0.023 vs SBH) SBH reproducibility 0.5061.52; 11.1%; (MD6SD; CoV; B-A) e2.5 to 3.5 Peak systolic strain rate (1/s) e0.7460.15 e0.7360.11 (p¼0.877 vs SBH) e0.6960.10 (p¼0.049 vs SBH) e0.0160.13; 18.1%; e0.26 to 0.28 Peak diastolic strain rate (1/s) 0.7560.27 1.1260.54 (p¼0.017 vs SBH) 0.9160.36 (p¼0.535 vs SBH) e0.0460.16; 21.0%; e0.36 to 0.27 e0.1360.44; 39.0%; e1.00 to 0.75 0.0960.15; 16.9%; e0.39 to 0.22

Abstract 119 Figure 1 CMR findings in asymptomatic patients with LBBB and normal echocardiogram.

MBH reproducibility (MA of three) (MD6SD; CoV; B-A) MBH reproducibility (MA of five) (MD6SD; CoV; B-A) MD6SD¼mean difference 6 SD

1.1362.23; 14.7%; 0.0660.04; 5.3%; e3.3 to 5.6 e0.02 to 0.14 1.1362.23; 14.7%; 0.0460.05; 7.8%; e3.3 to 5.6 e0.07 to 0.15 CoV¼coefficient of variation BeA¼BlandeAltman 95% limits of agreement

120

COMPARISON AND REPRODUCIBILITY OF STANDARD AND HIGH TEMPORAL RESOLUTION MYOCARDIAL TISSUE TAGGING IN PATIENTS WITH SEVERE AORTIC STENOSIS
doi:10.1136/heartjnl-2011-300198.120

C D Steadman, 2N A Razvi, 1K I E Snell, 3J P A Kuijer, 3A C van Rossum, G P McCann. 1Leicester Cardiovascular Biomedical Research Unit, Leicester, UK; 2 Department of Cardiovascular Sciences, University Hospitals of Leicester, Leicester, UK; 3Department of Physics and Medical Technology, ICaR-VU, VU University Medical Center, Amsterdam, The Netherlands; 4University Hospitals of Leicester, Leicester, UK
4

1

Objectives The aim of this study was to compare and assess the reproducibility of left ventricular (LV) circumferential peak systolic strain (PeakEcc) and strain rate (SR) measurements using standard and high temporal resolution myocardial tissue tagging in patients with severe aortic stenosis (AS). Background Myocardial tissue tagging with cardiac magnetic resonance (CMR) can be used to quantify strain and SR, however, there are little data on the reproducibility. Diastolic SR may be of particular interest as it may be the most sensitive marker of diastolic dysfunction often occurring early in the course of disease. Methods Eight patients with isolated severe AS without obstructive coronary artery disease were prospectively enrolled. They underwent CMR in a 1.5T scanner (Siemens Avanto) on two separate occasions, median interval 12 days. Complementary tagged (CSPAMM) images were acquired with both a single breath-hold (SBH: temporal resolution 42 ms), and a multiple brief expiration breath-hold (MBH: high temporal resolution 17 ms) sequence. Midwall PeakEcc was measured in the LV at mid-ventricular level with HARP Version 2.7 (Diagnosoft, USA). SR was calculated from the strain data; SR¼Ecc2-Ecc1/Time2-Time1. PeakEcc, peak systolic and diastolic SR were read from curves of strain and SR against time.
Heart June 2011 Vol 97 Suppl 1

Abstract 120 Figure 1
Conclusions It is likely than SBH may be adequate or even superior to MBH for assessment of PeakEcc. The increased temporal resolution of MBH may be advantageous for examining systolic and diastolic SR; a MA of five for diastolic SR may be the preferred method for quantification given the improved reproducibility of this measure.
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BCS Abstracts 2011
121
INCIDENTAL EXTRA-CARDIAC FINDINGS ON CLINICAL CMR; A COMPARISON OF 3 HASTE TECHNIQUES
doi:10.1136/heartjnl-2011-300198.121 R B Irwin, 2T Newton, 3C Peebles, 4A Borg, 5D Clark, 4C Miller, 6N Abidin, M Greaves, 4M Schmitt. 1Wythenshawe Hospital, Manchester, UK; 2Royal Blackburn Infirmary, Blackburn, UK; 3Southampton General Hospital, Southampton, UK; 4 Wythenshawe Hospital, University Hospitals of South Manchester NHS Trust, Manchester, UK; 5Alliance Medical, Wythenshawe Hospital CME unit, Manchester, UK; 6Salford Royal Hospital, Salford, UK
4 1

Introduction Cardiac magnetic resonance (CMR) is an increasingly important imaging modality, which by necessity incorporates a large field of view. Both “localiser ” and multiple slice half-fourier spin echo (eg, HASTE) sequences provide coverage of the thorax and upper abdomen. Such imaging may reveal hitherto unexpected incidental extra-cardiac findings (IEF). First we sought to assess the frequency of IEF found on clinically indicated CMR scans. Second we compared the 3 clinically used HASTE acquisition protocols in this context. Lastly we determined the impact of the 3 different protocols on acquisition time and image quality. Methods Three subsequent groups of 238 patients (714 patients in total), all referred for clinically indicated CMR, were scanned with either breath-hold (BH) HASTE (Group 1), free breathing (FB) HASTE (Group 2) or diaphragmatic navigated (NAV) HASTE (Group 3). Additionally “localiser” sequences performed in 3 orthogonal planes were analysed. All 714 clinical reports were reviewed regarding the presence of IEF. These were categorised as either minor, or major if recommendations for further investigation, follow-up, and/or clinical correlation were made. Finally, to determine the impact of each HASTE protocol on acquisition time and image quality, an additional cohort of 15 patients underwent 3 protocols back to back in a random fashion. The length of each acquisition was timed and image quality was reviewed and scored externally. Results A total of 180 IEF were found in 162 (22.7%) out of 714 patients. There was no significant difference in frequency of IEF between the 3 HASTE groups. Out of 180 IEF, 88 were considered minor and 92 major findings. Of the latter, 8 (1.1%) were considered highly significant. These included one bronchoalveolar carcinoma stage 1B requiring lobectomy, 2 cases of florid sarcoidosis in patients presenting with VT and “structurally normal hearts” on echocardiography, one case of pulmonary aspergillosis, 2 cases of advanced pulmonary fibrosis, one ascending thoracic aortic aneurysm and a case of iatrogenic liver haemorrhage following placement of a pericardial drain. FB HASTE acquisition (6962.5 s) was significantly faster than BH (10563.8 s) and NAV (12162.7 s), p<0.001, but also produced the lowest image quality on a 5 point scale; 3.5 (FB) vs 3.9 (BH) vs 3.8 (NAV), p¼0.08. Conclusion Overall, IEF are common and lead to follow on investigations in a substantial minority of cases. However, the overall incidence of highly significant findings in the current study was low (w1%). There was no difference in the frequency of incidental extracardiac findings between the 3 HASTE protocols. While the free breathing HASTE technique is statistically significantly faster than breath hold and navigated HASTE, the absolute time saving is small and probably out-weighted by lesser image quality.

sclerosis via a direct paracrine or vasocrine route. Excess adipose tissue accumulation leads to adipose tissue dysfunction characterised by a pro-inflammatory and potentially pro-atherogenic pattern of adipokine secretion. We used MRI for PVAT imaging and quantification and evaluated the effects of obesity and increased perivascular adiposity on the relationship of PVATwith the function and structure of the underlying vessels. Methods We measured peri-aortic fat, aortic stiffness and atheroma burden by MRI in 128 cardiovascular patients and in 18 healthy lean subjects at baseline and in 22 healthy obese subjects (before and after weight loss intervention (diet or bariatric surgery). Fat around the brachial artery and FMD of the brachial artery was measured among 75 cardiovascular patients. Results There was good inter-observer and intra-observer reproducibility (coefficient of variance (CV) <6% and<5%) and inter-scan repeatability (CV<8%) of the measurement of PVAT. After adjustment for anthropometric indices, demographics and cardiovascular risk factors as appropriate: I) A positive independent association between PVAT and aortic atheroma was detected among obese participants (BMI$30 kg/m2)(p<0.005) but not among individuals with intermediate (BMI<30 and $26) and low BMI (BMI<26). II) Perivascular fat was independently, inversely associated with aortic stiffness among lean patients (p<0.0005) while the association was independent and positive for obese participants (p<0.05). III) An independent, negative linear correlation between peri-brachial fat and FMD was noted among overweight and obese subjects (BMI$26) (p<0.001), but not among normal weight participants (BMI<26). IV) PVAT was an independent negative predictor of aortic elasticity among healthy obese individuals (BMI$30) (p<0.01) while it was positively and independently associated with aortic elasticity among lean healthy controls (BMI#18) (p<0.05). V) Following weight loss intervention, PVAT reduction was an independent predictor of aortic elasticity improvement in the obese group (p<0.05). Conclusions Our results suggest an influence of both generalised and regional excess adiposity on the functional state and the effects of perivascular adipose tissue on dysfunction and remodelling of the underlying vessels.

123

CARDIOVASCULAR RISK IN ASYMPTOMATIC POTENTIAL SIMULTANEOUS PANCREAS-KIDNEY TRANSPLANT RECIPIENTS IS DETERMINED BY MYOCARDIAL PERFUSION SCINTIGRAPHY
doi:10.1136/heartjnl-2011-300198.123

V M S Stoll, N S Sabharwal, O O Ormerod. The John Radcliffe Hospital, Oxford, UK

122

OBESITY AND PERIVASCULAR ADIPOSITY IN ATHEROSCLEROSIS
doi:10.1136/heartjnl-2011-300198.122

I Kylintireas, C Shirodaria, O Rider, J M Lee, I Bechar, J Digby, M D Robson, S Neubuer, R P Choudhury. University of Oxford, Oxford, UK

Introduction It has been proposed that perivascular adipose tissue (PVAT) contributes to inflammation and advancement of atheroA70

Introduction More than 50% of renal transplant recipients will die as a consequence of cardiovascular disease (CVD). Type I diabetics undergoing simultaneous pancreas-kidney transplantation (SPK) are at an even greater risk of CVD. Optimising a patient9 s cardiovascular status is necessary before SPK transplant surgery. Patients can remain on transplant waiting lists for years. There is little evidence as to how frequently repeat cardiovascular risk assessments are required in asymptomatic patients. Myocardial perfusion scintigraphy is used in SPK patients to detect any asymptomatic myocardial ischaemia or abnormal left ventricular function. This study analyses data from a SPK transplant centre with an annual surveillance programme to aim to establish the suitable frequency of MPS. Methods Potential SPK transplant recipients who had undergone two perfusion scans were included for analysis. An abnormal MPS was defined as either showing a regional wall motion abnormality, inducible ischaemia, or impaired left ventricular function. The scan results were both documented and compared. Angiography results from the study period were also recorded. Results 99 out of 130 patients on the SPK waiting list in November 2009 had undergone two perfusion scans as part of their
Heart June 2011 Vol 97 Suppl 1

As expected.5T (40 patients) or 3T (20 patients).4 yrs (range 0. There was no difference between 3T and 1. London.and epicardial sub-segments. Of the remaining 16 patients. the correlation is imperfect which is likely to be a result of difficulty predicting haemodynamic effects of angiographically moderate disease.124 G D J Morton. The BCIS JS was calculated from visual analysis of the coronary angiogram. with 41% female and a median time between scans of 1.87 (95% CI 0. Area under the receiver-operating characteristic curve for BCIS JS to detect $10% myocardial ischaemic burden was 0. 16% of patients with a normal 1st scan developed an abnormal 2nd scan within a median period of 1. The median age was 45 yrs (range 26e63). p<0. microvascular disease and limitations of CMR imaging. CMR perfusion and scar data were segmented according to the standard 17-segment model excluding the apex. A BCIS JS $6 predicts the prognostically important ischaemic threshold of 10% with high specificity. Conclusions 40% of SPK patients on the waiting list have an abnormal MPS.75. 2 patients were excluded (1 claustrophobia. 1M Ishida. 1E Nagel.0). non-invasive means by which to monitor patients at very high risk of asymptomatic cardiovascular disease while awaiting a SPK transplant. Of the 59 patients with two normal scans. The BCIS JS was also correlated with the combined burden of scar and ischaemia: r ¼ 0. Advantages include ease of use and universal applicability including classification of left main stem disease and CABG. 2Guy’s and St Thomas’ NHS Foundation Trust. 1 died before angiography and the other 15 patients were treated with medical therapy. Therefore a near annual MPS is a useful. The current screening interval is successfully monitoring changes in the patients’ cardiovascular status with only one patient requiring an intervention which was not predicted by MPS. BCIS JS $6 predicted $10% myocardial ischaemic burden with sensitivity 68% and specificity 90%. Of the patients with normal scans 5% required an angiogram because of new symptoms with only 2% requiring revascularisation. Segments were subdivided into equal endo. Abstract 124 Figure 1 Results Patient characteristics are summarised in the Abstract 124 table 1.BCS Abstracts 2011 pre-transplant assessment. p<0. Correlation between myocardial ischemic Conclusions The BCIS JS correlated well with ischaemic burden on CMR. London. Mean interval 6 SD between CMR and coronary angiography was 40647 days. CMR included standard functional and scar imaging and also high-resolution k-t accelerated adenosine stress and rest perfusion imaging at 1. 124 VALIDATION OF THE BCIS-1 MYOCARDIAL JEOPARDY SCORE USING CARDIAC MRI doi:10. Heart June 2011 Vol 97 Suppl 1 A71 . which are important for management and prognosis. Expert observers blinded to the clinical data analysed the angiographic and CMR data. 2K De Silva. 1A Schuster. 1D Perera. UK.00001 (Abstract 124 figure 2). 2 had minor plaque disease. 13 patients (22%) with no history of myocardial infarction had CMR evidence of prior infarction. 28 (70%) of the patients with an abnormal MPS underwent angiography.6e3. 1 incomplete imaging data). Cardiac magnetic resonance (CMR) imaging allows reliable assessments of myocardial ischaemia and scar in a single examination and was used to examine the functional relevance of the BCIS JS. Methods 60 consecutive patients with angina and known or suspected CAD referred for diagnostic x-ray coronary angiography underwent CMR examination at a single UK centre. do not incorporate myocardial ischaemia and scar.77 to 0. 1 of these patients required revascularisation after presenting with an ACS. each assigned 3% of the total myocardial volume and classified as normal. 1King’s College London. including the BCIS JS.97). 1A Chiribiri.00001. UK 2 1 Introduction The recently described angiographic BCIS-1 Myocardial Jeopardy Score (BCIS JS) was designed to classify the extent of coronary artery disease (CAD). However anatomic tests.1136/heartjnl-2011-300198. 12¼maximum jeopardy). 59 patients (60%) had two consecutive normal scans. The remaining 40 patients had at least one abnormal scan. It provides a semi quantitative estimate of the amount of myocardium at risk as a result of severe coronary stenoses (0¼no jeopardy. Abstract 124 Figure 2 burden and BCIS JS. There was a strong correlation between the BCIS JS and myocardial ischaemic burden: Pearson’s r¼0. 3 underwent angiography during the study period (for new symptoms). S Redwood. Of the patients undergoing angiography driven by MPS 43% subsequently underwent revascularisation. Myocardial ischaemia and scar burden were calculated and correlated with the BCIS JS individually and as a combined score (Abstract 124 figure 1).5T CMR imaging. 1A Indermuhle.77.4 years. ischaemia or scar. of these 12 required revascularisation (either PCI or CABG).

BCS Abstracts 2011
Abstract 124 Table 1
Characteristic Age (mean6SD) Left ventricular ejection fraction (mean6standard deviation) Male Diabetes Previous CABG Previous percutaneous coronary intervention Previous MI Hypertension Number of patients 65610 59614% 48 (83%) 17 (29%) 13 (22%) 22 (38%) 10 (17%) 38 (66%)

125

ASSESSING PATIENT BENEFIT FROM THE REVASCULARISATION OF CHRONICALLY OCCLUDED CORONARY ARTERIES BY ADVANCED CARDIOVASCULAR MRI TECHNIQUES
doi:10.1136/heartjnl-2011-300198.125

PCI and 3 with CABG). In those with successful revascularisation by PCI LV volumes reduced (EDV 185 (54) vs 174 (50) p<0.05; ESV 85(60) vs 77(58) p<0.001) and the left ventricular ejection fraction improved (56.5(12)% vs 58.9(12)% p¼0.01). During adenosine stress imaging there was a significant improvement in absolute myocardial blood flow in the revascularised segments (from 1.87(0.51) to 3.77 (0.67) ml/g/min p<0.001) but not in the remote regions (from 3.76 (0.52) to 3.95(0.58) ml/g/min p¼ns). LGE was only present in 25 (20%) revascularised segments. In these segments there was a strong inverse correlation between the extent of scar and improvement in segmental systolic thickening (r¼À0.736, p<0.001). There was a weaker association between the segmental response to low dose dobutamine and the degree of functional improvement following successful revascularisation (Pearson r¼0.249, p<0.01). Conclusion Following revascularisation of CTO, myocardial perfusion increases and both regional and global systolic function improves. While the majority of subjects in this study had no scar on LGE imaging, when segments are scarred there is a negative correlation with improvement in regional systolic thickening.

N J Artis, 2A Crean, 1A Zaman, 1S Sorbron, 1A N Mather, 1S G Ball, 1S Plein, J P Greenwood. 1University of Leeds, Leeds, UK; 2Toronto General Hospital, Toronto, Canada
1

1

Background Cardiovascular magnetic resonance (CMR) imaging can provide an array of information about cardiac function and anatomy. The utility of CMR in the setting of coronary artery chronic total occlusion (CTO) has not been fully investigated. We set out to examine the ability of CMR to show regional improvements in left ventricular (LV) function and perfusion and to investigate if any features were able to predict those that benefit from revascularisation. Methods Twenty-seven patients with single vessel CTO were recruited from clinical waiting lists and underwent a comprehensive CMR assessment prior to and 6 months following attempted CTO revascularisation. A multi-parametric CMR protocol was performed which included cine imaging to assess regional wall thickness/ thickening and global LV function, rest and adenosine stress perfusion imaging (Fermi model), low dose dobutamine stress to assess inotropic reserve, and late gadolinium enhancement (LGE) imaging to determine scar location and extent. Using the AHA 16 segment model only segments supplied by the CTO artery were studied for functional improvement. Data are presented as mean (SD). Results Procedural success in terms of revascularisation of the occluded artery was achieved in 23 of the 27 patients (85%, 20 with

Abstract 125 Figure 2 Relationship of improvement in segmental systolic thickening against segmental scar (top panel) and change in thickening with low dose dobutamine (bottom panel).

126

THE IMPACT OF NICE GUIDELINES FOR THE INVESTIGATION OF CHEST PAIN ON OUTPATIENT CARDIOLOGY SERVICES IN THE UK
doi:10.1136/heartjnl-2011-300198.126

Abstract 125 Figure 1 Changes observed in the CTO and a remote territory following attempted revascularisation. (non-revascularisedd black lines). Adenosine stress increases perfusion only in the CTO territory with no change in resting perfusion.
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1 C Patterson, 2E Nicol, 3L Bryan, 4T Woodcock, 1S Padley, 1D Bell. 1Imperial College, London, UK; 2Royal Brompton Hospital, London, UK; 3Chelsea and Westminster Hospital, London, UK; 4NIHR CLAHRC for Northwest London, London, UK

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BCS Abstracts 2011
Introduction The National Institute for Health and Clinical Excellence (NICE) have released guidelines for the investigation of chest pain of recent onset (1). There is concern that the guidelines will increase the burden on cardiac imaging, requiring service reconfiguration and investment (2, 3). This study was performed to assess the impact of the guidelines on outpatient cardiology services in the UK. Methods 595 consecutive patients attending chest pain clinics at two hospitals over six months preceding release of the NICE guidelines (51% male; median age 55 yrs (range 22e94 yrs)) were risk stratified using NICE criteria. Preliminary cardiac investigations recommended by NICE were compared with existing clinical practice and the relative costs calculated. Results NICE would have recommended 443 patients (74%) for discharge without cardiac investigation, 10 (2%) for cardiac computed tomography (CCT), 69 (12%) for functional cardiac imaging and 73 (12%) for invasive coronary angiography (ICA). Relative to existing practice there would have been a trend towards reduced functional cardiac imaging (À24%; p¼0.06) and increased CCT (+43%; p¼0.436) but a significant increase in ICA (+508%; p<0.001). The cost of investigations recommended by NICE would have been £15 881 greater than existing practice. Conclusions This study suggests implementation of the NICE guidelines will require investment in cardiology services, particularly ICA. It will be necessary to establish and maintain CCT for relatively few patients; also to establish and maintain functional cardiac imaging even though referrals are likely to decline. Individual hospitals should assess their local populations prior to service reconfiguration. acquired at “1 week” were better predictors of LVEF and infarct size at “3 months” than data collected at “day 2”. Conclusions The extent of myocardial oedema and infarct size decrease significantly during the first week after reperfusion for AMI and these changes are associated with a significant improvement in LVEF over the same interval. These findings have implications for the timing of CMR studies in the early post-infarct period. We found that the percentage myocardial salvage index did not change significantly between “day 2” and “1 week”. Therefore, accurate assessment of the efficacy of reperfusion therapy can be made up to one week after revascularization. In addition, CMR data acquired at “1 week” were better predictors of CMR endpoints measured at “3 months”. Thus, we conclude that the optimal time point to image patients post-reperfusion therapy for AMI is at 1 week.

128

BRIGHT BLOOD T2 WEIGHTED MRI HAS HIGHER DIAGNOSTIC PRECISION AND ACCURACY THAN DARK BLOOD STIR MRI FOR ASSESSMENT OF THE ISCHAEMIC AREA-AT-RISK AND MYOCARDIAL SALVAGE IN ACUTE MYOCARDIAL INFARCTION
doi:10.1136/heartjnl-2011-300198.128

A R Payne, 1M Casey, 1J McClure, 2R McGeoch, 2A Murphy, 2R Woodward, 2A Saul, J Gilchrist, 2C Clark, 2K G Oldroyd, 1N Tzemos, 1C Berry. 1University of Glasgow, Glasgow, UK; 2Golden Jubilee National Hospital, Glasgow, UK
2

1

Abstract 126 Table 1 Preliminary cardiac investigations undertaken (pre-NICE) compared with those recommended by NICE (N¼595)
Pre-NICE No investigation Cardiac CT Functional cardiac assessment Invasive angiography 33 7 91 12 NICE 443 10 69 73 % change +1242% (p<0.001) +43% (p 0.436) À24% (p 0.06) +508 (p<0.001)

127

TIMING OF CARDIOVASCULAR MRI AFTER ACUTE MYOCARDIAL INFARCTION: EFFECT ON ESTIMATES OF INFARCT CHARACTERISTICS AND PREDICTION OF LATE VENTRICULAR REMODELLING
doi:10.1136/heartjnl-2011-300198.127

A N Mather, T A Fairbairn, N J Artis, J P Greenwood, S Plein. University of Leeds, Leeds, UK

Background The pathophysiological remodelling processes associated with acute myocardial infarction (AMI) evolve over time and the optimal acute imaging time point to predict medium-term surrogates for outcome has not been established. This study aimed to define the evolution of infarct characteristics by cardiovascular magnetic resonance (CMR), and to assess whether CMR data acquired at “day 2” or at “1 week” post-AMI are stronger predictors of infarct size and left ventricular (LV) function measured at 3 months. Methods Fifty-seven patients were recruited with first presentation ST elevation AMI treated successfully with primary percutaneous coronary intervention. Cine, T2- weighted and late gadolinium enhancement CMR imaging were performed at days 2, 7, 30 and 90 after index presentation. Results Infarct size and extent of myocardial oedema decreased significantly between “day 2” and “1 week” (mean %LV-scar (SD) 27.2 (13.9) vs 21.6 (14.1), p<0.001 and %LV-AAR (Area At Risk) (SD), 37.9 (15.2) vs 32.3 (14.3), p¼0.003). These changes were accompanied by a significant improvement in LV ejection fraction (%LVEF (SD), 41.7 (9.6) vs 44.6 (10.1), p<0.001). CMR data
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Background T2-weighted MRI reveals myocardial oedema and enables estimation of the ischaemic area-at-risk and myocardial salvage in patients with acute myocardial infarction (MI). We compared the diagnostic accuracy of a new bright blood T2-weighted with a standard black blood T2-weighted MRI in patients with acute MI. Methods A breath hold bright blood T2-weighted ACUTE pulse sequence with normalisation for coil sensitivity and a breath hold T2 dark blood short s inversion recovery (STIR) sequence were used to depict the area-at-risk in 54 consecutive acute MI patients. Infarct size was measured on gadolinium late contrast enhancement images. Results Compared with dark blood T2-weighted MRI, consensus agreements between independent observers for identification of myocardial oedema were higher with bright blood T2 -weighted MRI when evaluated per patient (p<0.001) and per segment of left ventricle (p<0.001). Compared to bright blood T2-weighted MRI, dark blood T2-weighted MRI under-estimated the area-at-risk compared to infarct size (p<0.001). The 95% limits of agreement for inter-observer agreements for the ischaemic area-at-risk and myocardial salvage were wider with dark blood T2-weighted MRI than with bright blood T2-weighted MRI. Bright blood enabled more accurate identification of the culprit coronary artery with correct identification in 94% of cases compared to 61% for dark blood (p<0.001). Conclusion Bright blood T2-weighted MRI has higher diagnostic accuracy than dark blood T2-weighted MRI. Additionally, dark blood T2-weighted MRI may underestimate area-at-risk and myocardial salvage.

129

MYOCARDIAL SALVAGE DURING PRIMARY PCI CAN BE PREDICTED IN THE CATH LAB
doi:10.1136/heartjnl-2011-300198.129

A R Payne, 1C Berry, 1O Doolin, 2M B McEntegart, 2R Woodward, 2A Saul, 2S D Robb, M C Petrie, 1I Ford, 2K G Oldroyd. 1University of Glasgow, Glasgow, UK; 2Golden Jubilee National Hospital, Glasgow, UK
2

1

Objectives This study investigated the relationship between the index of microcirculatory resistance (IMR) and myocardial salvage as determined by T2-weighted and contrast-enhanced cardiac magnetic resonance (CMR) imaging in patients undergoing primary percutaneous coronary intervention (pPCI) for ST elevation myocardial infarction (STEMI).
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BCS Abstracts 2011
Background IMR is a simple invasive measure of microvascular function available at the time of pPCI. T2-weighted non-contrast CMR can reveal myocardial oedema, and in the post-infarct population this represents the ischaemic area at risk (AAR). Contrastenhanced CMR delineates the area of myocardial infarction. The volume of myocardium within the AAR, but not contained within the infarct area is salvaged myocardium. Methods 108 patients with STEMI underwent invasive coronary physiology measurements during pPCI and had a subsequent CMR scan at a median of 19 h post pPCI. Short axis non-contrast T2weighted images were acquired and delayed enhancement imaging was performed following administration of intravenous gadolinium (0.1 mmol/kg). AAR was determined and myocardial salvage was calculated as AARdinfarct area. Results IMR was 29 (21), AAR 32% (13%) and myocardial salvage 6% (9%)dall mean (SD). Spearman rank correlation between IMR and AAR was 0.27 (p 0.02) and between IMR and salvage was À0.31 (p 0.01). IMR was also a multivariate predictor of AAR (p 0.01) and a negative multivariate predictor of myocardial salvage (p 0.02). Conclusions IMR measured acutely correlates with AAR and correlates negatively with myocardial salvage as determined by MRI. repeatability co-efficient (RC) 2.14; intra-observer R¼0.99, RC 1.49). Reproducibility of global ecc measurements by HARP was somewhat lower, but still high (inter-observer R¼0.89, RC 4.80; intraobserver R¼0.98, RC 2.73). There was much greater variability in segmental ecc measurements using both methods, particularly with HARP (Abstract 130 figure 2).

130

COMPARISON OF HARMONIC PHASE IMAGING WITH LOCAL SINE WAVE MODELLING FOR THE ASSESSMENT OF CIRCUMFERENTIAL MYOCARDIAL STRAIN USING TAGGED CARDIOVASCULAR MAGNETIC RESONANCE IMAGES
doi:10.1136/heartjnl-2011-300198.130

Abstract 130 Figure 1 Abstract 130 Table 1
Analysed segment for circumferential strain Anterior Anterolateral Inferolateral Inferior Inferoseptal Anteroseptal All 6 segments pooled HARP vs SinMod Mean Difference ± SD (%) À1.6866.38 À3.1868.07 1.4868.24 1.3366.17 À1.6665.63 À2.4766.77 À0.9967.11 HARP vs SinMod 95% Limits of agreement (%) À14.18 to 10.82 À18.99 to 12.64 À14.67 to 17.62 À10.76 to 13.42 À12.68 to 9.37 À15.73 to 10.79 À14.92 to 12.95 HARP vs SinMod Correlation Coefficient 0.59 0.22 0.24 0.48 0.59 0.52 0.43

A N Borg, 1C A Miller, 2C D Steadman, 2G P McCann, 1M Schmitt. 1University Hospital of South Manchester, Manchester; 2NIHR Leicester Cardiovascular Biomedical Research Unit, Leicester, UK

1

p-value for correlation 0.001 0.25 0.21 0.008 0.001 0.007 <0.001

Introduction Assessment of myocardial strain promises to become an important quantitative tool in early diagnosis of cardiac disease and treatment monitoring. Advances in image processing software have facilitated rapid and clinically feasible analysis of strain from tagged cardiac magnetic resonance (CMR) images. Harmonic Phase Analysis (HARP) or Local Sine Wave Modelling (SinMod) can be used for automated derivation of strain. We obtained tagged CMR images to compare measurements of left ventricular (LV) circumferential strain obtained using a HARP with a SinMod method. Methods Ten normal controls, 10 hypertrophic and 10 dilated cardiomyopathy patients (mean age 46.6614.8 years) were included. Spatial modulation of magnetisation using short-axis LV slices at mid-ventricular level, with a temporal resolution of 30e50 mS, were obtained using a 1.5 Tesla scanner (Siemens Avanto) with a 32-channel coil. Global and segmental transmural peak circumferential strains (ecc) were measured using HARP (Diagnosoft, USA, version 2.7) and SinMod (InTag, University of Lyons, France, version 3.6.1). Prior to running the algorithm, both methods involve manual tracing of the endocardial and epicardial borders, and localisation of right ventricle-to-septum insertion points, in one frame. Agreement between HARP and SinMod was assessed by Spearman’s correlation co-efficient R and Bland Altman methods. Repeated measurements were carried out on 10 randomly selected scans to assess reproducibility. Results There was a high level of agreement between HARP and SinMod for global ecc (HARPdSinMod mean difference: À0.12%, 95% limits of agreement: À5.69% to 5.45%, R¼0.83, p<0.001) (Abstract 130 figure 1). Agreement was much lower for segmental ecc, ranging from very poor in lateral segments to modest in inferoseptal segments (Abstract 130 table 1). Analysis time using SinMod was significantly shorter than for HARP (84642 vs 2016120 S, p¼0.02). Inter- and intra-observer reproducibility were extremely high for SinMod measurements of global ecc (inter-observer R¼0.99,
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Abstract 130 Figure 2 Inter- and intra observer variability for HARP local sine wave modelling: repeatability co-efficients.
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2 Freeman Hospital. 1H M Arthur. UK. the combined analyses included 3069 CHD cases and 7271 controls. 2L Sneddon. 3School of Mathematics & Statistics. The P415L mutant appeared to be hypomorphic whereas C484F appeared to be a null allele in the luciferase assay. Newcastle University. 1M McMahon. 1. This was confirmed in functional assays as both SMAD6 variants failed to inhibit BMP signalling compared with wild-type SMAD6. Newcastle University. P Avery. J J O’Sullivan. Heart June 2011 Vol 97 Suppl 1 Introduction Congenital cardiovascular malformation (CVM) exhibits familial predisposition but the specific genetic factors involved are unknown. Randomised trials of this question are not possible. Conclusions This is the first time that functional mutations in SMAD6 have been described in patients with CVM. 1B D Keavney. T Pierscionek. J Palomino-Doza. J Goodship.05) lower capacity to inhibit alkaline phosphatase generation in response to BMP signalling. Combination of our primary data with previous studies. D Hall. Functional effects of the wild-type and variant SMAD6 proteins were expressed in C2C12 cells and their capacity to inhibit ALK3 activated expression of a BMP-responsive reporter. however. Five genes of the BMP signalling were surveyed for novel variants predisposing to CVM risk. 5Department of Molecular Cell Biology and Center for Biomedical Genetics. Newcastle upon Tyne. Thus. A Topf. These ORs were significantly different from each other (p¼0. 2C Wren. P415L was identified in a patient with congenital aortic stenosis and C484F was identified in a patient with coarctation and calcification of the aorta. Conclusions We demonstrate genetic evidence in favour of a causal relationship between plasma folate and CHD. p¼0. Institute of Human Genetics. Studies conducted in countries with mandatory folate fortification showed no effect of C677T genotype on CHD risk (OR 0. The effect of TT genotype on plasma folate levels is greater in conditions of folate deficiency. A L Topf. 133 ACTIVITY AND PSYCHOSOCIAL HEALTH IN ADOLESCENTS WITH CONGENITAL HEART DISEASE (CHD) doi:10. which together included 1883 cases and 3069 controls in 25 studies. The MH2 domain of SMAD6 were further sequenced in additional 346 CVM patients. Leiden.44)). Results The primary genotyping data in 1186 cases and 4168 controls revealed a trend towards increased risk with the TT genotype. The population attributable fraction for the TT genotype was 3% of CHD. Leiden University.40)).96 (95% CI 0. but this did not reach statistical significance (OR 1. Patients aged 12e20 years were identified using the Northern Ireland regional database (HeartSuite). whereas studies conducted in countries without mandatory fortification showed a significant effect of genotype (OR 1. 2The Queen’s University of Belfast. UK. a higher frequency of TT genotype among CHD cases than among healthy controls would be anticipated. if lower plasma folate had a causal effect on CHD risk. including cardiac development. 2P P McKeown. poor reproducibility for segmental measurements using both techniques probably reflect user variability in identification of right ventricular septal insertion points and contour tracing.032). and higher levels of plasma homocysteine. 1Royal Belfast Hospital for Sick Children. functions as an inhibitory SMAD which preferentially inhibits BMP signalling. P415L and C484F. 4Institute for Cell and Molecular Biosciences. UK Background The existence of a causal relationship between lower levels of plasma folate and congenital heart disease (CHD) remains contentious. UK. A J Sands. but it is not known whether there is any effect on CHD. or to inhibit osteogenic differentiation (using an alkaline phosphatase assay) was assessed. Belfast.2F A Casey. Thus. There was no evidence of publication bias among the contributing studies. One of the genes. B Keavney. UK 3 1 1 1 1 2 V Mamasoula. C G McCusker. 132 NON-SYNONYMOUS SMAD6 MUTATIONS IMPAIRED INHIBITION OF BMP SIGNALLING IN PATIENTS WITH CONGENITAL CARDIOVASCULAR MALFORMATION doi:10. T Rahman. Like other patients with chronic illnesses they may be at higher risk of psychological/ emotional problems. Agreement is much lower for segmental measurements. Results We identified two novel non-synonymous variants. Newcastle University.45 (95% CI 1. The absence of a genetic association in countries practicing folate fortification suggests that fortification largely abrogates the risk of CHD attributable to folate deficiency. D H Hall. 4R J Lewis.12 to 1. J Gordon. We used randomeffects models to combine the data. We aimed to ascertain if activity and psychosocial health were reduced in adolescents with major CHD compared to those with a minor diagnosis.89). in view of the known protective effect of folate against neural tube defects (NTDs). We conducted sensitivity analyses to examine folate fortification of flour as a potential source of heterogeneity.131 H L Tan. Folate fortification of flour is known to reduce the incidence of NTDs. with good reproducibility for both individual methods. The TT genotype at MTHFR C677T is known to be associated with lower activity of MTHFR and plasma folate. Ability to exercise is an important quality of life measure and indicator of physical health. We present a genetic approach using “Mendelian randomisation” to determining the causality of folate in CHD risk. Methods We compared genotype frequencies at the methylene tetrahydrofolate reductase (MTHFR) C677T single nucleotide polymorphism (SNP) in 1186 CHD cases and 4168 controls. We placed our results in the context of a meta-analysis of all previously published studies of this question (to September 2010). 1 Institute of Human Genetics. BMPR1A. 5P ten Dijke. BMPR2 and SMAD6 were sequenced in 90 unrelated Caucasian cases of CVM. BMP4. Newcastle upon Tyne. that were not present in 1000 ethnically-matched controls. SMAD6.64 to 1.1136/heartjnl-2011-300198. 1J A Goodship. UK. UK. We hypothesised that rare functional variation in SMAD6 could predispose to congenital cardiovascular malformation (CVM). Newcastle upon Tyne. Clarity regarding the relationship between folate and CHD could potentially inform the practice of folate fortification. specifically those with calcific aortic malformations.63 (95% CI 1. Both mutations are in evolutionarily conserved amino acid residues and are predicted to be damaging by in silico analysis.1136/heartjnl-2011-300198. including aortic ossification. The SMAD6 knockout mouse is characterised by cardiac valve and outflow tract defects.94 to 1. Newcastle upon Tyne. Belfast.BCS Abstracts 2011 Conclusions HARP and SinMod methods show a high level of agreement for assessment of global mid-ventricular transmural circumferential strain. Methods The coding regions of BMP2.132 131 AETIOLOGICAL ROLE OF FOLATE DEFICIENCY IN CONGENITAL HEART DISEASE: EVIDENCE FROM MENDELIAN RANDOMISATION AND META-ANALYSIS doi:10. UK 1 1 1 1. 1B G Craig. revealed association in the larger dataset (OR 1.2 Many patients with CHD are now adolescents.133 M L Morrison.25)). The C484F mutant had a significantly (p<0.19 to 2. Our data suggest that inadequate inhibition of BMP signalling pathway due to genetic variation in SMAD6 may be an important factor in CVM.005). Bone morphogenetic proteins (BMPs) regulate many processes during development.15 (95% CI 0. E A Glen.1136/heartjnl-2011-300198. Participants were categorised as having major or minor CHD and divided into four diagnostic A75 . and this would be expected to be more marked in conditions of folate deficiency. We discovered folate fortification status to be a significant source of heterogeneity. Newcastle upon Tyne.

of which 23 were exclusive to the patient population. Family studies revealed additional members with LVNC for three of the probands. 30 cyanotic corrected (21.134 T Rahman. FOXC2. Nine of these variants cause change in the aminoacid sequence. Conclusions Mutations in MYH7 occur relatively frequently in Ebstein’s anomaly accompanied by LVNC. patients with major CHD had significantly higher activity counts. was found in HAND2.32. The Change Study ¨ Collaborators. Newcastle upon Tyne.1136/heartjnl-2011-300198. ie.01 (À8.73 mins (sd 3. Most patients presented just one variant. This study is another A76 Background Tetralogy of Fallot (TOF) is the most common cyanotic heart defect. S Hosmane. usually known to be deleterious. FOXA2. in this group. Berlin. Two patients had the same mutation. The secondary heart field gives origin to the right ventricle and the outflow tract. Methods We examined by standard Sanger method the full exonic and intron boundary regions of 14 secondary heart field genes. 64 probands had no associated cardiac anomalies. UK 1 1 Background Ebstein’s anomaly is a rare congenital heart malformation characterised by adherence of the septal and posterior leaflets of the tricuspid valve to the underlying myocardium. and had inherited them from one of their phenotypically normal parents (when parental information was available).6 years) consented to participate. 2B Mulder. Institute of Human Genetics.136 R Panayotova. and one patient presented up to 3 variants.08) in cyanotic palliated group. Participants also underwent an evaluation of exercise. a narrowed pulmonary valve and right ventricular hypertrophy. On formal exercise testing. age-appropriate questionnaires examining standard psychological parameters. The experience of growing up with a chronic condition may therefore have a positive effect on psychological health and interventions targeted around this area may influence activity. In addition. 75% of the variants were inherited from the mother.1136/heartjnl-2011-300198. The Netherlands. A Macnab.13)). Where mutations were discovered. HAND2. Germany. E Glen. we hypothesised genes involved in the regulatory network of the secondary heart field were particularly good candidates for TOF susceptibility. TBX1. 2Academic Medical Centre. 135 GENE SCREENING OF THE SECONDARY HEART FIELD NETWORK IN TETRALOGY OF FALLOT PATIENTS doi:10. it would seem more likely that susceptibility to TOF be determined by a larger number of small genetic contributions which are also modified by environmental factors.3%).74) compared to 8.42. affecting 3e6 infants for every 10 000 births. were absent from 1000 normal chromosomes. J A Goodship. The majority of young people with CHD.0%) and 13 (9%) cyanotic palliated patients. complex patients rate themselves to be as active as those with minor CHD. Institute of Human Genetics. the presence of multiple variants in the same proband may result in the disruption of gene-gene interactions in the secondary heart field pathway. p value 0. H R Griffin. UK Background Bicuspid aortic valve (BAV) disease is one of the most common congenital cardiac abnormalities with prevalence in the Heart June 2011 Vol 97 Suppl 1 . In these three pedigrees the mutation segregated with disease.1136/heartjnl-2011-300198. including formal exercise stress testing and measurement of free-living activity using an ActiGraph accelerometer. however 3 patients presented two. take part in regular exercise. parents of cases were screened to assess inheritance of the rare variant. ISL1 and FOXH1. of the seven distinct mutations. As there have been reports of abnormal left ventricular morphology and function in patients with Ebstein’s anomaly we hypothesised that mutations in the b-myosin heavy chain (MYH7) may be associated with Ebstein’s anomaly. Self-esteem and mood seem well preserved in adolescents with CHD as a whole. 4Institute of Human Genetics. UK. There was no significant difference in activity score between study groups. B D Keavney. 143 patients (mean age 15. 2K Engelen. P Waterworth. thus far we have not found any strong indication of unique causal effect. which in turn may lead to outflow tract defects. particularly cyanotic palliated patients. The most common associated cardiac malformation were atrial septal defect (48 probands) and left ventricular non-compaction (LVNC) (7 probands). as all variation found in probands was also present in their unaffected parents. However. UK 134 MUTATIONS IN THE SARCOMERE PROTEIN GENE MYH7 IN EBSTEIN’S ANOMALY doi:10. in a panel of 93 TOF patients. FGF8. Based on our results. Diagnostic subgroups included 39 acyanotic (27.135 A Topf. Each of these fields can be identified by the expression of specific markers. had higher anxiety scores (p value 0.7%). FGF10. Surprisingly. Among the 14 genes studied we found a total of 50 new variants. five were novel (four missense changes and an in-frame deletion) and two have been previously reported in patients with hypertrophic cardiomyopathy. 1J Goodship. they are limited in terms of peak exercise duration. one of whom also had a relative with Ebstein’s anomaly. In FOXC1 we found a contraction of both alanine and glycine tracts. Exercise time for acyanotic group 11. However. MEF2C. Methods MYH7 mutation analysis was undertaken in 141 unrelated affected individuals with Ebstein’s anomaly using next-generation sequencing on the 454 platform. We found a functional 19aa deletion of a highly conserved region of TBX1.7%) took part in regular exercise each week. 3S Klaassen. While accelerometer data indicate that the group may be more active day to day. 2A Postma. 61 acyanotic corrected (42. There were no significant differences across study groups for selfesteem or other psychological parameters.002 (1. Newcastle upon Tyne. Results Heterozygous mutations were identified in eight of the probands including six of the seven with LVNC. family studies were undertaken and the segregation of the mutation with disease was investigated. Results We re-sequenced a total of 80 exons and w30 Kb.26 mins (sd 4. 86 were male (60%) and 105 had major CHD (73%). An alanine expansion. University Hospital of South Manchester. FOXC1. namely NKX2-5. When available. Beck Youth Inventory demonstrated that individuals with major CHD. All patients were heterozygotes for the variants. BOP. À1. 4B Keavney. it consists of four heart abnormalities: a VSD. Correlation analysis showed that selfesteem and health locus of control were important predictor variables for activity. Conclusions Although genes of the secondary heart field seemed good candidates for TOF susceptibility. All newly discovered rare variants were checked in a panel of 1000 control chromosomes by multiplex Sequenom assays. 134 participants (93. During heart development two heart fields can be distinguished.61)). The first one gives origin to the left ventricle and contributes to the right and left atria. 5. 136 SHOULD FAMILIAL SCREENING BE ROUTINELY OFFERED TO PATIENTS WITH BICUSPID AORTIC VALVE DISEASE? doi:10. more complex patients performed worse at peak exercise. It is evident that larger scale analysis of significant numbers of whole genomes/exomes will be necessary to better understand the molecular aetiology of TOF. Manchester. example of mutations in a sarcomere protein causing congenital heart malformation. 3Max-Delbrueck-Center for Molecular Medicine. TOF is phenotypically well defined. Results were analysed using parametric methods. GATA4. Amsterdam.BCS Abstracts 2011 subgroups. TBX20. D H Hall. Newcastle upon Tyne. As TOF is a malformation of the outflow tract. Four non-synonymous changes were found in FOXA2. an over-riding aorta. Participants completed validated.

A M Shah. we used transgenic mice with endothelial-specific overexpression of Nox2 (TG) utilising the tie2 promoter construct. Conclusions The myocardial and capillary defects observed in myocardial loss of Cited2 are not associated with Pitx2c deficiency and suggests that Cited2 can cause myocardial and vascular defects via a mechanism that is distinct from its effect on the left-right patterning pathway. we generated chimeric mice by irradiation (10Gy. 1Kings College London BHF Centre of Excellence.360. lung.1%) compared to the WT:WT group (2. Texas. To overcome this problem we therefore investigated the role of Cited2 in the myocardium by conditional deletion in cardiomyocyte precursors. occurring at a younger age than in patients with idiopathic aortic aneurysms. UK.760. the extent of cardiac fibrosis was significantly greater in TG than WT by w2-fold (p<0. 138 CELL-SPECIFIC ROLE OF NOX2 NADPH OXIDASE IN DEVELOPMENT OF ANGIOTENSIN II-INDUCED CARDIAC FIBROSIS IN VIVO doi:10. UK. 1J Braganca.7%) or in WT receiving KO BM (2. We hypothesised that Nox2.1136/heartjnl-2011-300198. 1University of Oxford. A Ivetic. Thus. Patients with bicuspid aortic valve disease should be made aware of its familial pattern of inheritance and screening of their first degree relatives should be actively pursued in order to reduce the potential morbidity and mortality associated with this condition and its related aortopathy. Embryos were collected and processed for analysis by histology. BAV disease carries a 6% lifetime risk of aortic dissection.560. 1C Broadbent. Cited2 is a transcriptional cofactor that can inhibit hypoxia-activated transcription and also acts as a co-activator for transcription factors such as TFAP2. Zygotic and epiblastic deletion of Cited2 results in atrioventricular septation. and a reduction in Vegfa expression. liver.6%).137 1 1 S D Bamforth. However. However. 2S Heymans. which required prompt surgery. at least in part. D Vanhoutte. and indicate that coupling of myocardial and coronary vascular growth in the developing mouse heart occurs. X-Gal staining. Methods To investigate the role of Nox2 in inflammatory cells. There has been growing evidence supporting its familial predisposition with an autosomal dominant pattern of inheritance. Implementing such a programme is limited by adequate motivation to attend for a screening test if well. may be important for cardiac fibrosis in these cell types.1 mg/kg/day. The coupling of myocardial and coronary vascular development is mediated in part by VEGFA signalling. The selective effect of Nox2 on fibrosis may reflect its activation in a non-cardiomyocyte cell type. cardiac fibrosis assessed by Sirius red staining was significantly lower in KO mice receiving WT BM (0. Methods Cited2 was selectively deleted from cardiomyocytes by intercrossing mice transgenic for Cited2 and Nkx2-5Cre. Genetic evidence indicates that Cited2 is essential for cardiac left-right patterning via regulation of the Nodal-Pitx2c left-right patterning pathway. USA Introduction Myocardial development is dependent on the concomitant growth of cardiomyocytes and a supporting vascular network. to our knowledge. is not routinely done within the UK. and KO recipients with WT BM. Current ACC/AHA guidelines state that echocardiographic screening of first degree relatives of patients with BAV is recommended. Among the relatives of the 24 index patients. using the following permutations: wild-type (WT) recipient with either KO or WT BM. This. We identified a total of 47 patients who had undergone aortic valve surgery performed by the same Consultant Cardiothoracic Surgeon in the context of BAV disease in the period May 2007eSeptember 2009. as well as left-right patterning defects such as right-isomerism. This pathway may be targeted for the treatment of heart failure resulting from ischaemic heart disease.BCS Abstracts 2011 general population of up to 2%. We also show that CITED2 is present at the Vegfa promoter in mouse embryonic hearts. Houston. lens and placental development. 52 relatives (70%) actually attended for an appointment. 1A Brewer. Result AngII (1. Out of these. The Netherlands 1 1 1 1 1 2 137 A CITED2->VEGFA PATHWAY COUPLES MYOCARDIAL AND CORONARY VASCULAR GROWTH IN THE DEVELOPING MOUSE HEART doi:10.1136/heartjnl-2011-300198. 2University Hospital Maastricht. However. there were a total of 8 cases (3: 1 ratio) of bicuspid aortic valve diseasedeither known or newly diagnosed via screening. 1C-M Chen. Oxford. however. London. To assess the role of endothelial Nox2.138 S Chaubey. Methodology and Results We set out to explore the practicalities of running a routine echocardiographic screening programme for first degree relatives of patients with BAV disease.05). One of these asymptomatic individuals had a significant ascending aortic aneurysm. 1S Bhattacharya. TG mice developed the same level of systolic hypertension and hypertrophy as WT littermates after AngII infusion. These data suggested that resident Nox2-expressing cells are responsible for the protective effect observed in global Nox2 KO mice. It is often associated with ascending aortic dilatation and dissection. 14-day) infusion caused similar increase in systolic hypertension and cardiac hypertrophy in all 3 chimeric groups. The remainder did not undergo testing with us as they either lived in a different geographic region or expressed a personal preference not to be scanned at this time. the early requirement of Cited2 in Heart June 2011 Vol 97 Suppl 1 Introduction Mice globally deficient in Nox2 are protected against cardiac fibrosis in response to chronic AngII infusion even though the degree of hypertrophy was unaltered. outflow tract and aortic arch abnormalities. 15 min) to deplete resident bone marrow cells. However. Cited2 is also essential for adrenal. 2 Texas A&M Health Science Centre. Screening of first degree relatives was offered to these patients. 24 patients (51%) gave us information regarding family members who would like to attend for an echocardiogram. This is associated with a decreased ratio in the number of small vessels to large vessels. J E Schneider. 2R Schwartz. and that it stimulates human VEGFA promoter activity in cooperation with TFAP2 transcription factors in transient transfection assays. a known target of Cited2. the presence of BAV and dilatation of the ascending aorta requires regular monitoring with a view to timely pre-emptive surgery. chromatin immunoprecipitation and transient transfection assays. neural crest. quantitative reverse transcriptase PCR (Q-RTPCR). followed by bone marrow (BM) transplantation. Our results delineate a novel mechanism of Vegfa regulation by CITED2 and TFAP2 transcription factors. 9 times higher than that of the general population. B Yu. which is expressed in endothelial cells and inflammatory cells. A total of 75 first degree relatives were referredean approximate average of 3 per patient. through a Cited2->Vegfa pathway. Maastricht. 1S T MacDonald. Routine echocardiographic screening should be offered to these families. and by varying clinical practice in different geographic regions. C E Murdoch. left-right patterning and placental development makes it difficult to identify a later specific role for Cited2 in myocardial development. Results The cardiomyocyte specific knockout of Cited2 results in abnormal myocardial compact zone growth and ventricular septal defects. This was associated with a greater degree of infiltration by CD45+ A77 . The incidence of newly diagnosed bicuspid aortic valve disease in our cohort of first degree relatives was 8% (4 out of 52 relatives). Conclusions There is a relatively high prevalence and incidence of bicuspid aortic valve disease among first degree relatives of patients with this common congenital cardiac abnormality. MRI. we observed no change in the myocardial expression of the left-right patterning gene Pitx2c.

1136/heartjnl-2011-300198. UK. Although inflammatory cells may be important for the development of fibrosis.9616 154 mm2 vs 149 424. resulting in reduced expression of MMP1 and increased expression of collagen I. These effects are inhibited by an endoglin specific antibody. UK. is sufficient to promote atherosclerosis. 1S Wheatcroft. Mice then underwent surgical coronary artery ligation or sham operation. UK 1 2 2 3 140 IN VIVO DEPLETION OF ENDOGLIN RESULTS IN SIGNIFICANT LEFT VENTRICULAR REMODELLING doi:10. 1M Kearney. Conclusion These results indicate there is a cell-specific role of endothelial Nox2 in the development of fibrosis.8-fold. endoglin expression is up regulated following stimulation with angiotensin II and TGFb. This led us to investigate the effect of endoglin knockdown on normal heart structure and function in adult mice. and the transparent nature of the embryos.BCS Abstracts 2011 inflammatory cells (w1. p¼0. Endoglin heterozygous mice have been shown to have reduced fibrosis in response to renal injury. Furthermore.001) and ejection fraction significantly reduced (p¼0. 1S Galloway. M Kahn. systolic blood pressure. 1 Leeds University. Multiple features make this vertebrate model unique. to study in real time. insulin sensitivity and fasting glucose levels were similar in ApoE-/-ESMIRO and ApoEÀ/À mice.39).03). 1R Cubbon. Cine cardiac MRI was performed 28 days after injury. a TGFb co-receptor. The fact that cardiac function was preserved indicates that this is not a cardiomyopathic process and we hypothesise that the increased left ventricular volume in the endoglin-deficient mice may be the result of alterations in the extracellular matrix. We found that in the endoglin deficient mice. V M Bedell. was similar in ApoEÀ/ÀESMIRO and ApoEÀ/À mice (6.6%62. 1A Aziz.8%60. Tissue factor pathway inhibitor (TFPI) is a potent anticoagulant molecule. Cine cardiac MRI was therefore performed on mice without any surgical procedure after endoglin knockdown. 1H Viswambharan. including haemostasis.4% vs 16. localising to Heart June 2011 Vol 97 Suppl 1 . We then utilise transgenic fish with labelled endothelium (Fli1GFP) and erythrocytes (GATA1dsRed).141 E W Holroyd. TFPI mRNA became more abundant. Despite the divergence of jawed fish (teleosts) over 430 million years ago. 1P Sukumar. 1J Smith. R Redgrave.05) and 30% (p<0. Rochester. 141 TISSUE FACTOR PATHWAY INHIBITOR REGULATES VASCULAR DEVELOPMENT IN ZEBRAFISH doi:10. Subsequently. p<0.5% vs 5.8%62. Leeds. However. Absolute plaque size was also significantly increased in ApoEÀ/ÀESMIRO mice compared to ApoE controls (226 448. there is notable conservation of the constituent molecules of the clotting cascade.4%60. UK Background Global insulin resistance and endothelial dysfunction have been identified as predisposing factors for atherosclerosis.4%. Here we addressed this question by crossing Endothelial Specific Mutant Insulin Receptor Over-expressing (ESMIRO) mice with ApoE null mice.02).05) more leukocytes than WT upon AngII treatment. UK 1 1 1 2 Endoglin. C K Pierret. Using our conditional endoglin knockout mice we sought to investigate the role of endoglin in cardiac healing following myocardial infarction.41624 221 mm2. Newcastle Upon Tyne. B Keavney. p¼0. 1H Arthur. it is unclear whether selective insulin resistance in endothelial cells alone. However. in living zebrafish embryos. Newcastle University. inhibiting tissue factor-led coagulation. and parameters of cardiac function were calculated. is essential for cardiovascular development.5%. concomitant fluorescent imaging of both structural development and dynamic blood flow observation. This suggests that enhancing endothelial insulin sensitivity may be an appropriate target to prevent atherosclerosis in insulin-resistant conditions.01). UK. including its genetic accessibility. assessed by en-face oil red O staining. 1H Imrie. 1N Yuldasheva. 2Institute of Cellular Medicine. We are currently investigating this potential molecular mechanism for left ventricular remodelling in the absence of endoglin.05) more VCAM-1 positive blood vessels in AngII treated TG hearts. 2Mayo Clinic. They also have signifiA78 Introduction Angiogenesis requires the coordinate regulation of multiple biological pathways. 139 ENDOTHELIAL SPECIFIC INSULIN RESISTANCE PROMOTES THE DEVELOPMENT OF ATHEROSCLEROSIS doi:10. we also noticed LV volume and mass were increased in sham operated endoglin deficient mice. Heart rate. Measurement of left ventricular (LV) volumes and myocardial mass were made using ImageJ.139 1 1 M C Gage. 1Queen Elizabeth Hospital. cantly reduced cardiac function following myocardial infarction. Results TFPI expression was identified at 24 h post fertilisation (hpf) in the pronephros (Abstract 141 figure 1ddark blue staining denotes TFPI expression. 2C Jackson. 2R D Simari. none seen in control embryos). the role of TFPI in vascular development is unknown. J Townend. 2University of Bristol. Results ApoEÀ/ÀESMIRO mice were morphologically indistinguishable from ApoEÀ/À control littermates. p¼0. 2S C Ekker. 3Queen Elizabeth Hospital. Methods Male ApoEÀ/ÀESMIRO mice were compared with sexmatched littermate ApoEÀ/À mice (both on a C57Bl6 background) after feeding a Western-style diet for 12 weeks. atherosclerotic lesion area in cross sections of aortic sinus was significantly increased in ApoEÀ/À ESMIRO mice compared to ApoEÀ/À controls (24. Conclusions Endothelial specific insulin resistance is sufficient to promote atherosclerosis and increase lesion area in ApoE null mice. LV volume and mass were again significantly increased (p<0. Adult Eng fl/fl Rosa26-CreERT2 or control (Eng fl/fl) mice were treated with intraperitoneal injection of tamoxifen for 5 days to activate CreERT2 and deplete endoglin by Cre-lox recombination. ESMIRO mice over-express a human insulin receptor with Ala-Thr1134 mutation in the tyrosine kinase domain (which disrupts insulin signalling) selectively in endothelial cells under the control of the tie-2 promoter/enhancer. we demonstrate TFPI expression during early vertebrate development. 1Institute of Human Genetics. external embryonic development.1136/heartjnl-2011-300198. However. A Blamire. However. However. glucose tolerance. UK. However. Aortic lipid deposition. These results demonstrate that depletion of endoglin results in significant left ventricular remodelling and suggest that endoglin plays an essential role in the maintenance of normal cardiac structure. In rat cardiac fibroblasts. Zebrafish (Danio rerio) provide a unique model system to study vascular development in vertebrates. Newcastle University. Methods Using in-situ hybridisation techniques. with normal development and no difference between groups in body mass. Rochester. Bristol. ejection fraction did not differ significantly from controls. Newcastle Upon Tyne. We found that LV volumes and mass were significantly increased (p<0. our results indicate that Nox2 in these cells is not essential for any pro-fibrotic effect. endoglin also has an important role in fibrosis in adult life.140 B J Davison. possibly by enhancing inflammatory cell recruitment and influx via VCAM-1 expression.005) in endoglin deficient mice compared to controls.1136/heartjnl-2011-300198. isolated TG endothelial cells recruited w2-fold (p<0. the ability to titrate the degree of genetic knock-down. Endothelial Nox2 enhances AngII-induced cardiac fibrosis. Birmingham.

U Schotten. n¼19) with or without atrial structural remodelling secondary to surgical AV block (AVB.363. Statins improve NO-redox imbalance and decrease the occurrence of postoperative AF but are less effective in the secondary prevention of AF. NOX2 & p22phox protein level were increased after 2W-AF and in patients who developed AF post-operatively (n¼32). Athens.BCS Abstracts 2011 2EFHIK&L) were seen by 48hpf.1136/heartjnl-2011-300198. and in vitro in mature human endothelial cells. Control embryos did not demonstrate significant signs of coagulopathy (3.01) at 9 ng. Atrial NADPH oxidase activity (chemiluminescence and 2-OH ethidium. The molecular mechanisms and implications of this phenomenon in the management of patients with AF are poorly understood. 32 who developed AF post-operatively and 72 who were in normal sinus rhythm before and after surgery). UK. and was maintained by mitochondrial oxidases and uncoupled NOS (secondary to BH4 deplition). 3S Verheule. 2 First Department of Cardiology. 3Department of Physiology. The Netherlands 3 1 Abstract 141 Figure 1 developing kidney.3% (p<0. vessels sprouting from normal site but growing in abnormal direction. n¼10) or after 2 weeks (2W. Abnormally targetted (ie. 142 ATRIAL SOURCES OF REACTIVE OXYGEN SPECIES VARY WITH THE SUBSTRATE AND DURATION OF ATRIAL FIBRILLATION: IMPLICATIONS FOR THE ANTIARRHYTHMIC EFFECT OF STATINS doi:10. 1R Jayaram. Oxford. In line with this.8% (p<0. NOS activity remained coupled despite the increase in superoxide production. To further define the role of TFPI in vascular function.462. in patients with permanent AF. Ex-vivo inhibition of HMG-CoA reductase with atorvastatin (20 mMol/l) inhibited NADPH oxidase activity (via reducing activity of Rac1 and membrane translocation of cytosolic subunit p47phox and p67phox of NADPH oxidase) and caused a mevalonate-reversible reduction in A79 . 2C Anroniades. and from goats in sinus rhythm (SR. They support a model in which TFPI acts a molecular break to angiogenesis both in vivo.3%). University of Maastricht. CD: MO controls. and vasculature.01 cf.001 by ANOVA cf. white arrows in Abstract 141 figure Abstract 141 Figure 2 Heart June 2011 Vol 97 Suppl 1 Background Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with altered nitric oxide (NO)redox balance. John Radcliffe Hospital. EeP: TFPI knockdown). Knockdown of TFPI resulted in enhanced EC tube formation on Matrigel and EC migration in injury model associated with increased phosphorylation of Vascular Endothelial Growth Factor Receptor-2. 1B Casadei. the increased superoxide production in atrial tissue from goats with AVB or 6M-AF was exclusively driven by mitochondrial oxidases and uncoupled NOS (secondary to a reduction in atrial BH4 level and an increase in arginase activity). uninjected controls) at 3 ng and 23. In contrast.262. Increase in basal superoxide production in postoperative AF was associated with an apocynin-reversible increase in NADPH oxidase activity and protein level of the NOX2 and p22phox subunits. gut. white arrows Abstract 141 figure 2GJMP) in 25. increased superoxide production was not reversed by apocynin.865. left column: green endothelial Fli1GFP.142 S Reilly.6% (p<0. These findings were recapitulated in the right atrial appendage of patients. 1K M Channon. Greece. right column: red erythrocytes. during early vertebrate embryogenesis. AB: uninjected controls. secondary to constitutive regulation of VEGF signalling. Conclusion These data represent the first demonstration of TFPI expression in zebrafish and the first description of a unique phenotype following TFPI knockdown. Abstract 142 figures 1 and 2). 1University of Oxford. n¼15) or 6 months (6M. In contrast. Maastricht. University of Athens. atrial BH4 content was unaltered. Extra arteries occurred in 26. TFPI MO induced coagulopathy (a spontaneous clot or bleed. Methods and Results We investigated atrial tissue from 130 patients undergoing cardiac surgery (26 with permanent AF. n¼10) of pacing-induced AF. grey arrows) and extra vessels (ie. uninjected controls) of embryos injected with 3 ng of TFPI MO. RNAi-mediated knockdown of TFPI was performed in human endothelial cells (EC). suggesting that the sources of reactive oxygen species might vary with the substrate and duration of AF. 1N J Alp. Morpholino (MO)-based knockdown of TFPI resulted in coagulopathy and disordered vascular development (Abstract 141 figure 2. superfluous vessels not seen in controls.

Utilising the chimeric receptor. Survival (until 1-cm tumour dimension) of SM22áTFPI mice vs wild-type control (median survival 14 cf. 5. atorvastatin did not induce a mevalonate-reversible changes in the atrial BH4 concentration and NOS uncoupling in neither group. It currently affects almost one million people in the UK. B16 melanoma injection (n¼7 per group.1136/heartjnl-2011-300198.05. overexpression of TFPI inhibited endothelial cell tube formation on Matrigel and migration using an injury migration model. both in vivo and in vitro. which persisted throughout the experiment. This led us to suspect that the anti-angiogenic action of TFPI may be independent of TF. which lacks the heparin-binding domain of VEGF165.143 1 E W Holroyd. AP2 treated TAC Heart June 2011 Vol 97 Suppl 1 . p<0. Abstract 143 Figure 1 143 TISSUE FACTOR PATHWAY INHIBITOR REGULATES ANGIOGENESIS INDEPENDENTLY OF TISSUE FACTOR VIA INHIBITION OF VASCULAR ENDOTHELIAL GROWTH FACTOR SIGNALLING doi:10. We then defined the mechanism of these effects in vitro using Human Umbilical Vein Endothelial Cells (HUVECs) overexpressing TFPI or via exogenous addition of TFPI-derived peptides in assays of angiogenesis. SM22áTFPI showed significantly impaired recovery from ischaemia in the hindlimb ischaemia model after 3 days (p<0. EGDR. PMCA2 and PMCA3) or related ATPases which are expressed in the heart including the sarcoplasmic reticulum calcium ATPase and Na/K ATPase. Birmingham. n¼10 in each group.2. as the primary physiological inhibitor of tissue factor (TF)mediated coagulation.5. These data demonstrate. 2Mayo Clinic. hTFPIct did not inhibit VEGF121-induced migration. is ideally situated to modulate the proangiogenic effects of TF.560.1136/heartjnl-2011-300198. *p<0. 8. M Zi. thereby limiting angiogenesis. an inhibitory role for TFPI in angiogenesis that is TF-independent. 10 days) following s. However. Conclusions Together. A80 Abstract 143 Figure 2 Conclusion Angiogeneis is a key biological system in health and disease. n¼5 per group). S Prehar. Manchester University.BCS Abstracts 2011 superoxide release in atrial samples of patients with post-operative AF but had no effect in patients with permanent AF. Variation in atrial sources of reactive oxygen species with the duration and substrate of AF may explain the reported variability in the effectiveness of statins in the prevention and management of AF. which inhibited PMCA4 activity with high affinity (IC50¼300 nM) but not other PMCAs (PMCA1. AP2 showed dose dependent inhibition of phenylephrine-induced hypertrophy. Human TFPIct (hTFPIct) inhibited tube formation and migration through inhibition of Vascular Endothelial Growth Factor Receptor-2 (VEGFR2) tyrosine-951 phosphorylation. Endothelial-specific deletion of the TF-binding domain of TFPI failed to reveal a proangiogenic phenotype. a key event in migration. E J Cartwright.c.7 60. In vitro. 2D Mukhopadhyay. our group showed that plasma membrane calcium ATPase isoform 4 (PMCA4) knockout mice showed a reduced response to hypertrophic stress prompting us to hypothesise that a novel PMCA4 specific inhibitor would modify the development of cardiac hypertrophy. vehicle treated TAC mice. Similarly. Manchester. TFPI may also have effects on angiogenesis independent of its anti-TF ability. L Neyses. AP2 treated TAC mice. enabling cells in a hypoxic environment to stimulate new blood vessel growth. The compound AP2 was identified.325. Methods We determined the effects of altered TFPI expression on the regulation of angiogenesis in vivo using genetically-modified murine models of vascular overexpression (SM22áTFPI strain) and endothelial-specific deletion of the TF-binding domain of TPFI (Tie2TFPI). Systemic delivery of the murine TFPI carboxyl-terminus (mTFPIct) replicated the effects of endogenous overexpression. UK. which contains the extracellular domain of epidermal growth factor (EGF) and the intracellular domain of VEGFR2/KDR. D Oceandy. as mitochondrial oxidases and uncoupled NOS account for the statin-resistant increase in atrial superoxide production in permanent AF. 2K Larsen. In vivo studies showed that AP2 (5 mg/kg body weight/day IP) significantly reduced pressure-overload induced hypertrophy following 2 weeks transverse aortic constriction (TAC) (heart weight/tibia length (mg/ mm): sham. Minnesota. interferes with the interaction of VEGF165 with the extracellular domain of VEGFR2. 2R G Vile. 144 A DRUGGABLE INHIBITOR OF CARDIAC HYPERTROPHY IDENTIFIED THROUGH AN INNOVATIVE CHEMICAL LIBRARY SCREEN doi:10.144 R Abou Leisa. 7. indicated by an 85% reduction in cell surface area as well as in BNP activity. In addition to it classical role as a TF-antagonist.05). Recently. Proteases and inhibitors within the tissue factor (TF) pathway of coagulation have emerged as potential regulators of angiogenesis.3. F Baudoin. Tissue factor pathway inhibitor (TFPI). USA Introduction The biological systems of coagulation and angiogenesis show considerable interdependence. In isolated neonatal rat cardiomyocytes (NRCM). Few effective anti-hypertrophic agents with druggable properties have been identified. Results Vascular-directed over-expression of TFPI (SM22áTFPI strain) inhibited angiogenesis in vivo (Abstract 143 figure 1). a direct effect of TFPIct on the intracellular domain of VEGFR2 was excluded (Abstract 143 figure 2) TFPIct did not block phosphorylation of EGDR when stimulated with EGF. TFPI. Rochester. 2R D Simari.01). these findings indicate that upregulation of NOX2-NADPH oxidases is an early but transient event in the natural history of AF. 1Queen Elizabeth Hospital.0 60. c2¼4. UK Cardiac hypertrophy is a prerequisite for the development of heart failure. T M A Mohamed. A library of 1280 medically optimised compounds was screened using a novel in vitro assay which measures the Ca2+ dependent ATPase activity of PMCA4. via TFPIct.

gov number.146 C W Khoo. S Krishnamoorthy. TF. AFB and percentage of cumulative pacing were derived from pacemaker diagnostics.012 0. Patients on warfarin were excluded. AP2 treatment led to a significant reduction in the expression of the bona fide calcineurin target RCAN1. TF (r¼0. but showed no effect of electrogram amplitude. Barts and The London NHS Trust.096 0. from grade 1 to 5 (group 1) or grade 5 to 1 (group 2).2 0.8% of grade 3. and a resultant increase in mean AFCL $5 ms was regarded as significant.4 and a reduction in the NFAT phosphorylation level in vivo and the NFAT transcriptional activity in vitro.012).1136/heartjnl-2011-300198. location in the left or right atrium. G Y H Lip. p¼0.2% of grade 5 CFAE (p<0.0001 for grades 1. only 5 were ablated. Ablating certain grades of CFAE caused AFCL prolongation. 145 CHARACTERISATION OF FRACTIONATED ATRIAL ELECTROGRAMS CRITICAL FOR MAINTENANCE OF AF: A RANDOMISED CONTROLLED TRIAL OF ABLATION STRATEGIES (THE CFAE AF TRIAL) doi:10.1e0. we have identified AP2 as a novel PMCA4 specific inhibitor and shown its potential to modify the development of cardiac hypertrophy likely through inhibition of calcineurin/NFAT signalling. There were no significant differences in levels of vWf. M J Earley.0e99.2616. p<0. Lesions were regarded as individual observations. (76) 34. (%) Antiplatelet. suggesting they are more important in maintaining AF.8e81.0) 98.414 0. 33.91).1136/heartjnl-2011-300198.1 (6. Targeting these CFAE may reduce unnecessary left atrial destruction. AP2 treated TAC mice.9 mm2). Because grade 5 electrograms were considered normal.6 (41. G Dwivedi.6615.0) 94. The randomised strategy first controlled for any cumulative effect of ablation on AFCL. p¼0.3) 47. de-bulking normal tissue) on the cycle length of persistent AF (AFCL).8 12. ng/ml DDM.086). On linear regression analysis. 3 vs 5 not significant). both P-sel and DDM were independently associated with AFB (p<0. and second allowed assessment of the order of ablation on the number of CFAE lesions required.2) 63.7 152. Abstract 146 Table 1 No AHRE (n[70) Age. R J Schilling. AHREs were defined as atrialrate $220 beats/min and $5 minutes. until termination of AF or abolition of CFAE prior to DC cardioversion.643.739 0. There was no difference between groups in the number of grade 1 or 2 CFAE encountered.8e99.6% of grade 2.8 mm2.8 180.001) and DDM (r¼0. and 8.0e390. 2. Birmingham. with Grade 1 being most fractionated and grade 5 normal. I Diab. This compound has drug-like properties and thus lays the basis for a novel approach for treating cardiac hypertrophy and failure through PMCA4 inhibition. (71) 14. P-sel (r¼0.0e0. IS THERE AN ASSOCIATION BETWEEN THROMBOGENESIS MARKERS AND ATRIAL FIBRILLATION BURDEN IN PACEMAKER POPULATION? doi:10. S Sporton.5% of grade 1 CFAE. vehicle treated TAC mice.BCS Abstracts 2011 mice showed a significant reduction in the cardiomyocyte cross sectional area (sham.116 0.7% (l¼0.468. Methods We studied 87 patients with dual-chamber pacemaker.0611. although whether this is by eliminating focal drivers or simply de-bulking atrial tissue is unclear.5 (82.5) 21. The CFAE grade determined by rapid visual inspection for the 968 electrograms targeted agreed with that at off-line manual measurement in 92.045) correlated with AFB. 31963.795. Patients with AHREs had significantly higher cumulative percentage ventricular pacing (p¼0. tissue factor (TF). In this study. or the order in which CFAE were targeted. (54) 53.1 (0. (%) Percentage atrial pacing Percentage ventricular pacing vWf. NCT00894400).5) p value 0.0% of grade 4.105 0. translating to fewer CFAE targeted per patient in group 1 compared to group 2 (37614 and 58618 respectively. M Tayebjee.01). soluble P-selectin (P-sel) and D-dimer (DDM) were analysed using ELISA. but there were fewer grade 3 and 4 CFAE in group 2 than group 1 (both p<0. Conclusion Targeting CFAE is not simply atrial de-bulking.6 38.7 0. Plasma levels of von Willebrand factor (vWf). HS Lim. 26763. 48065. The AFB ranged from 0 to 99% in AHRE group.553 Heart June 2011 Vol 97 Suppl 1 A81 . L Richmond. 33. IU/dl TF. R J Hunter. 12. ng/ml P-sel. Patients were randomised to have CFAE grades eliminated sequentially. In conclusion. and 4 vs 5. Mean AFCL was determined manually over 30 cycles from bipolar electrograms recorded at the left and right atrial appendages before and after each CFAE was targeted.4 mm2. AFCL increased after targeting 49.9633. London 146 Introduction Targeting complex fractionated atrial electrograms (CFAE) in the ablation of atrial fibrillation (AF) may improve outcomes. p¼0.0) AHRE (n[17) 75. P-sel and DDM between patients with and without AHREs. It is also uncertain what electrogram morphology should be ablated. Binary logistic regression confirmed the effect of CFAE grade. ng/ml 71. UK Background and Objectives Contemporary pacemaker devices are able to quantify atrial high-rate episodes (AHREs) and atrial fibrillation burden (AFB) accurately. University Department of Medicine Centre for Cardiovascular Sciences.05).516. A significant reduction in the expression of the hypertrophic marker ANP and BNP and in the percentage of fibrosis was also observed in these mice compared with vehicle treated TAC mice. City Hospital.5e307. This randomised study aimed to determine the impact of ablating different CFAE morphologies compared to normal electrograms (ie. (82) 22.145 Abstract 145 Figure 1 Impact of CFAE grade on the proportion of lesions causing AF cycle length prolongation.6 (6. 10 s electrograms were classified by visual inspection according to a validated scale.9e65.015). Methods After pulmonary vein isolation CFAE were targeted systematically throughout the left then right atrium. Results Baseline characteristics and co-morbidities were comparable between groups (Abstract 146 table 1). Results 20 patients were randomised.9) 93. years Hypertension.2 (0.9 (1. B Balakrishnan.977 0.0 (82. we aim to assess the relationship of thrombogenesis markers in association with AHREs and AFB. (ClinicalTrials.055 0.4629.

diabetes. p<0.0 0. 148 THE ASSESSMENT OF TRANSIENT LOSS OF CONSCIOUSNESS: WE’RE STILL NOT ASKING THE RIGHT QUESTIONS doi:10. PAF episodes 3e4 times per year lasting <1 hour (NICE risk: high. “aspirin or warfarin” or “warfarin” therapy respectively.0 Aspirin or Warfarin (%) 2.0% GPs. ANTITHROMBOTIC AND ANTICOAGULATION USE FOR PATIENTS WITH ATRIAL FIBRILLATION.148 A E Bewick. 61 year old.3% or responders (24. L Ala. Inclusion required the TLOC to be complete. 7. UK Introduction Atrial fibrillation (AF) is the most prevalent arrhythmia in primary and secondary healthcare settings. hypertension. For example. PAF episodes weekly lasting 10e12 h (NICE risk: mod. PAF episodes occurring weekly and lasting several hours (NICE risk: high. NICE guidance stratifies patients with AF in to low. 43 year old. is recommended in both national and international guidelines.9 4.BCS Abstracts 2011 Conclusion AFB is independently associated with increased indices of P-sel and D-dimer which indicate platelet activation and thrombosis respectively.0 4. Only 4% of the initial assessments were undertaken by consultants. A Gasson. CHADS2 score 1/6). persistent (PersAF) or chronic (CAF)) does not influence TE risk assessment. (2) choice of AT/AC for increasing levels of risk. p¼0. Overall. Abstract 147 Figure 1 Conclusions TE risk stratification tools are reportedly widely used in UK clinical practice.7 95. 32.1 28. A further 123 patients were therefore excluded.2% cardiologists.0 0. 115 GPs). Methods We designed an audit questionnaire assessing: (1) use of risk stratification tools.001). R Kulanthaivelu.0 60. by AF episode frequency and subtype.14). D W Harrington.1% cardiologists.7 0.1136/heartjnl-2011-300198.0 87. In addition.7 0. 77 year old. Abstract 147 Table 2 CHADS2 Score Zero One Two Three Four Five Six None (%) 27. CHADS2 score 3/6). hypertension.3% (90. 4. previous TIA. CHADS2 score 3/6). The frequency of reported use of AT/AC for each risk level of the NICE assessment and CHADS2 score are shown in Abstract 147 tables 1 and 2 respectively. 78 year old.5 5.3 43. 80 year old. 5.6 0. 6. This left 165 data sets (58% male).001). 3.1 147 THROMBOEMBOLIC RISK STRATIFICATION. AT/AC use for NICE and CHADS2 risk levels are mostly appropriate.6 Accurately diagnosing patients with TLOC can be achieved in most cases with a detailed clinical history.9 Warfarin (%) 1. 76.3 3. We set out to assess how patients were assessed in the setting of a district general hospital (DGH) with 570 beds. 12% by a Specialist Registrar (SpR).0 0.3 45.3 2. Key diagnostic elements of the history are still being neglected. NICE risk assessment is used by 26.1 7.3% GPs. Thromboembolic (TE) risk assessment and initiation of anti-thrombotic or anticoagulation (AT/AC) therapy. 91. p¼0.9 2.0 Aspirin or Warfarin (%) 1.0 0. Using the ESC guidelines of 2009 we generated a 22-question study proforma for a retrospective review of the medical records. PAF episodes twice a year lasting 1e2 h (NICE risk: mod. CHADS2 by 79. Abstract 147 figure 1 demonstrates AT/AC usage for each of the following hypothetical patients: 1. UK Abstract 147 Table 1 NICE Risk Low Moderate High None (%) 16.4 Warfarin (%) 2. CAF (NICE risk: high. hypertension. 21% by a year 1 foundation program (FP1) doctor and the majority was assessed by FP 2 or core medical trainees (CMT).8 0. although warfarin is under recommended for patients with a CHADS2 score of 2/6.3 7. “aspirin or warfarin” or “warfarin” therapy respectively.0 Aspirin (%) 78. Royal Glamorgan Hospital. and (3) choice of therapy for a number of hypothetical patients with variable TE risk and variable AF subtype. CHADS2 score 3/6). or $2 recommends “aspirin”. Kent and Sussex Hospital. We audited UK cardiologists and general practitioners (GPs) to assess adherence to these guidelines. The age distribution was a typical bimodal distribution with 16% between 10 and 29 years of age and 48% over the age of 70 years. the symptoms at the onset of the TLOC were documented in only 58% of cases.0 0.0 Aspirin (%) 70. 73% were assessed in A&E.001).2% cardiologists. 18% were assessed in the Acute Medical Unit (AMU) and 7% were assessed in rapid access ambulatory clinics. moderate or high risk categories and recommends “aspirin”. Tunbridge Wells.9 66.6% of responders (24. 50. CAF (NICE risk: mod. 2. R A Bleasdale.1 97. 421 responses were received (306 cardiologists. CAF (NICE risk: mod. 46.8 0. p<0.4% of responders reported use of TE risk stratification tools (97. hypertension. 8 had insufficient details to identify the relevant patient.2 32. The questionnaire was distributed by electronic or postal mail to 1176 cardiologists and 621 randomly selected GPs. according to level of risk.1136/heartjnl-2011-300198. Therefore in total 288 notes were reviewed.5 0. A CLINICAL AUDIT doi:10. 26 of the case notes were not available to analyse. CHADS2 score 1/6). In addition. Cardiff. CHADS2 score 1/6).7 97. of rapid onset and short duration with spontaneous complete recovery.5% cardiologists. inappropriately. diabetes. the use of AT/ AC is influenced. Type of AF (PAF/PersAF/ CAF) reportedly influences the use of AT/AC for 34.7 94.2% GPs. 53 year old. receiving an unselected intake via general practice and an A&E. CHADS2 score 1/6).147 R A Veasey. P Patel. the recovery symptom A82 Heart June 2011 Vol 97 Suppl 1 . it is recommended that AF episode frequency or subtype (paroxysmal (PAF). diabetes.0 0.5% GPs.2 11. 76 year old. ACC/ESC guidance endorses use of the CHADS2 scoring system and for scores of 0. no other risk factors. 1. Results In total. We identified 322 cases for possible inclusion over a 4 month period.

No ablation was performed in any region other than the PV ostia. 2S Jones. 2 Imperial College Healthcare.149 1 1 L Malcolme-Lawes. We compared our data with several ICD studies of patients with specific ICCs (Abstract 150 table 1).BCS Abstracts 2011 profile was reported in only 37%. In this majority elderly study population. London. Abstract 149 Figure 1 Comparison of pre-ablation and post-ablation % scar using fixed threshold.360. In order to develop and objective method for delineating ablation-scar we compared pre and post DE-MRI after Cryo-balloon lesion on the basis that a more predictable lesion set would be created for validation. UK 1. (See Abstract 149 figure 1). An automatic segmentation of the LA was produced with custom software from the MRA sequence.75% in pre and post ablation scans respectively. P B Lim. The presence or absence of a family history of sudden cardiac death was only reported in 2% cases. Only 47% (n¼78) of records described a witness account.961. The scar proportion within these regions was calculated using commercially available software ITK-SNAP. 2P Kanagaratnam.150 R Bastiaenen.28% in the rest of the LA (p¼0. Methods and Results 12 patients undergoing cryoablation for PAF were enrolled in the study. R Karim.38% compared with 2.001). and selected manually for left and right sided veins prior to scar projection. 150 IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR LEAD COMPLICATIONS AND CLINICAL EFFECTIVENESS IN PATIENTS WITH INHERITED CARDIAC CONDITIONS doi:10. 2D W Davies. complications and ICD therapies were obtained from pacing and hospital records. Additional ablation by RF or Freezer Max was required to achieve PVI in 59%. Post-ablation DE-MRI was performed at 3 months. UK.661. key elements remained un-reported for example skin complexion was only reported in 35% of the 78. Pulmonary vein isolation (PVI) was confirmed in all patients at the end of the cryoablation procedure using a circular mapping catheter. 1N S Peters. Total LA scar proportion was 0. 1S Ben-Nathan. The increase in scar seen in the PV ostia was 24. Tongue biting in 27% and the presence or absence of abnormal movements was recorded in only 12% of this 78 patients.1136/heartjnl-2011-300198. The family history of a cardiomyopathy was only recorded in 1% and a family history of TLOC was recorded in 1%. We aimed to determine the ICD complication rate in our inherited cardiac condition (ICC) population compared with international reports. 1Imperial College London.02% vs 6. The preablation and postablation free breathing late gadolinium enhanced sequence was registered to the MRA and the maximum intensity within the LA wall was projected onto the post ablation LA surface.2 vs 8. 2M Gallagher.2S Sharma.1 SDs above the BPM in pre-and post-ablation MRIs respectively (p¼0. The brightest regions were 1. regions of brightest myocardium were initially selected in pre and post ablation MRIs. London. 2T V Salukhe. The blood pool was identified automatically using custom software as the region 1 cm inside the wall of the LA. and its mean (BPM) and SD used as a baseline. D Rueckert. The duration of the TLOC was recorded in only 44%. 1St George’s University of London. Particular importance was given to inappropriate shock therapy due to lead failure as there are new ICD technologies available. C Juli. 1.763. UK 1 2 2 Introduction Visualisation of the ablation-related atrial scar using delayed-enhanced MRI (DE-MRI) may reveal important underlying causes for atrial fibrillation (AF) recurrence following ablation. A threshold of 5 SDs above the BPM was therefore programmed into our custom software to identify regions of scar for all patients. 2D Ward. The ostial regions were defined as extending 1 cm both proximal and distal to the PVeLA junction. Heart June 2011 Vol 97 Suppl 1 Abstract 149 Figure 2 Conclusion We have demonstrated the feasibility an objective.2 1. To identify a universal threshold for scar.661. Methods Patients with ICCs who had ICD implantation or box change between January 2006 and September 2009 were included. A83 . particularly in young patients who live for many years with a device in situ. UK.1136/heartjnl-2011-300198. E R Behr. London. A patient past history of cardiac disease was asked about in 40% of cases while a past history of TLOC was only asked about in 35%. a recent change in drug therapy was only asked about in 2% of cases. This technique will now need to be validated against clinical outcomes. Within the witness accounts that were recorded. and underwent pre-ablation DE-MRI scans. automated method of DE-MRI analysis of left atrial ablation-scar.2 Background Implantable cardioverter-defibrillator (ICD) therapy can reduce sudden death due to ventricular arrhythmia (VT/VF) but is not without complication. the initial assessment of patients with TLOC is undertaken by junior medical staff who often do not document key diagnostically differentiating elements of the history and examination indicating an ongoing lack of adequate training regarding the most appropriate and accurate techniques for differentiating the causes of TLOC. 149 AUTOMATED ANALYSIS OF ATRIAL ABLATION-SCAR USING DELAYED-ENHANCED CARDIAC MRI doi:10. 2St George’s Hospital. Data on clinical characteristics.01) (See Abstract 149 figure 2).260. This study highlights that in a DGH environment. London.

0% biventricular. 1.3% of patients.151 A Shetty. particularly in pacing dependant patients who would otherwise require a TPW with its associated risks. 5 sensing errors (1 T-wave oversensing.7% of secondary and 6.2C A Rinaldi. S Duckett.2 1. HCM 21%. The high rate of appropriate therapy highlights the clinical effectiveness of ICD intervention in secondary prevention. 1.2 1. D Twomey.BCS Abstracts 2011 Abstract 150 Table 1 Long QT SGH ICC Syndrome HCM ARVC patients patients patients patients (n[101) (n[51) (n[506) (n[106) Follow-up (months.2R Razavi. Brugada syndrome 6%. extraction. mean6SD) 74653 Appropriate therapy (%) 26 Inappropriate therapy (%) Lead failure (%) Complication rate excluding lead failure (%) 18 21 26 87 24 29 25 31 44633 20 27 7 n/a 58635 24 19 2 34 Brugada Syndrome patients (n[220) 38627 8 20 9 20 Results 101 patients (mean age 44.6% dual chamber. Newcastle upon Tyne. 4 AF). 1 was managed with a TPW for 7 days prior to reimplantation and 1 underwent reimplantation at 14 days without TPW. London. Abstract 151 Table 1 Indication for device extraction Erosion Pocket infection Lead infection Threatened erosion Number of patients. UK Background The recommended management of cardiac implantable electronic device (CIED) infection is complete system A84 Introduction Optimal left ventricular (LV) lead placement via the coronary sinus (CS) is a critical factor in defining response to cardiac resynchronisation therapy (CRT). Indications were secondary prevention in 71.8 years. n[80 (%) 31 (39) 25 (31) 7 (9) 4 (5) 1 (1) Abstract 150 Table 2 Complication Lead failure Inappropriate shock Lead displacement Infection Pneumothorax/Haemothorax Box/Wound/Other revision procedure Thrombosis (venous/lead) Haematoma Chronic abdominal cavity postexplant Number of patients 21 18 5 5 5 7 2 5 1 % of patients 20. a small fragment of lead remained. UK 1. 1. This approach may be appropriate. Our results compare favourably to other similar studies.9 0. Inappropriate therapy occurred in 18 (17. This provides some supportive evidence that in patients with high surgical risk and pocket abnormalities. 1 with locking stylet and mechanical sheath and 2 with femoral snare.1136/heartjnl-2011-300198. ARVC 22%. 2King’s College London. M Ginks.7 days. 28/68 patients received a new device between 1 and 227 days later and 22/68 have not undergone reimplantation. similar to the LQT Study which reports 25% lead failure over 87 months (Abstract 150 table 1).2K Rhode. the patient requiring pocket washout had a fragment of lead remaining following their initial extraction. 9 with locking stylet.152 151 RISK OF RECURRENCE FOLLOWING EXTRACTION OF CARDIAC IMPLANTABLE ELECTRONIC DEVICES FOR INFECTION: WHEN SHOULD A NEW DEVICE BE RE-IMPLANTED? doi:10. A small series reported good results with simultaneous contralateral implantation. We evaluated this approach in our institution for patients without signs of systemic sepsis.2 months 2 patients died (1 inappropriate shocks. In 34 cases. DCM 17%. 1Guys and St Thomas’ Hospital NHS Foundation Trust.8 17.9 4. London. UK.1136/heartjnl-2011-300198. if fragments of lead may remain.9 6. Inappropriate and appropriate therapy rates are similar among all studies. Using novel semi-automated image acquisition.2 1. One patient with lead related endocarditis required a subsequent surgical procedure to remove a lead fragment and in 4 other patients who had erosion. An active fixation bipolar TPW (temporary pacing wire) was used in 6 patients for a mean 7. In addition. 59 male) were included (idiopathic VF 15%. Lead complications may be lower with the use of new ICD technology in selected patients. overlay and registration software Heart June 2011 Vol 97 Suppl 1 . 39. Methods The clinical records of all patients undergoing lead extraction in our institution since January 2008 were reviewed. Only one of the 4 patients with a residual lead fragment required reintervention for recurrent infection. 22 with locking stylet and laser sheath. There was complete hardware removal in 64 cases (94%). 1 generator fault. 1.2G Carr-White.2 1.862. With lead failure excluded the complication rate is comparable to shorter follow-up studies. Comparison with other studies indicates a high lead failure rate due to the long follow-up period. the device was removed with simple traction.9% of primary prevention patients received appropriate therapy. 12 out of 18 inappropriate shocks were due to lead failure. 1 pocket washout and 1 extraction. which may be expected given the high frequency of Sprint Fidelis leads implanted during this period and the long followup. 10/22 leads that failed were Medtronic Sprint Fidelis and these were responsible for 8/12 patients receiving inappropriate shocks including one death due to lead fracture. pocket infection or threatened erosion. We present clinical outcomes and completeness of extraction. In those individuals who required a TPW.8%) patients (Abstract 150 table 2). 18/68 patients were re-implanted with a new device on the contralateral side on the same day as the extraction.9 4. 4. 1. None of the 18 individuals simultaneously reimplanted with a new device on the contralateral side needed any further procedures during the follow-up period. 3 patients had a further device related procedure during a mean follow-up of 4456304 days: 1 lead reposition.9 Pain Conclusions There is a significant rate of ICD lead failure in patients with ICCs. There are limited clinical data on the optimal time for device re-implantation. long QT syndrome 17%. Y Ma. Results 68 patients underwent CIED extraction for infection during this time period (see Abstract 151 table 1).2 H E Thomas. ICD types were 56.2S Hamid. J Bostock. the patient may be treated conservatively and monitored for signs of recurrent CIED infection.9 1.2M Sohal. Appropriate therapy successfully terminated VT/VF in 27 (26. C J Plummer. the risk of recurrent infection in our series was 17% despite our use of an active fixation pacing lead and externalised pulse generator which has a lower reported complication rate.2P Mehta. E J Shepherd.8 4. segmentation.7%) patients 34.1614.8%) patients and lead failure (noise/wear/fracture) in 22 (20.4% single chamber. Freeman Hospital. M Das. 1. During a mean follow-up of 74. 152 REAL-TIME CARDIAC MR ANATOMY AND DYSSYNCHRONY OVERLAY TO GUIDE LEFT VENTRICULAR LEAD PLACEMENT IN CRT doi:10. Conclusion We report low rates of recurrent infections following CIED extraction. 1 stroke). 1.0653. others 2%).9 4. Of the 2 procedures carried out for recurrent infection.

Conclusion We have shown it is feasible to acquire.2Y Ma. The 3 latest mechanically activated segments with <50% scar were identified and this information was overlaid at CRT implant on to live fluoroscopic images using a prototype version of the Philips EP Navigator software. M Sohal.153 A K Shetty. It is not known. All dP/dt measurements were compared to baseline AAI or VVI (for those patients in AF) pacing at 5e10 beats/min above intrinsic rate. overlay and accurately register cardiac MR data on to fluoroscopic images at the time of CRT implant. Much larger differences in change in +dP/dt were seen. California. In 2 patients we were unable to place a LV lead successfully in any branch of the CS.3% when the CMR dyssynchrony-map defined target region was paced DDDLV.2 Abstract 152 Figure 1 Heart June 2011 Vol 97 Suppl 1 Introduction Cardiac resynchronisation therapy (CRT) usually involves placing the left ventricular (LV) pacing lead in the posterolateral or lateral region of the LV epicardial surface as this is thought likely to re-coordinate myocardial contraction most effectively. Sylmar. The mean overall percentage difference in AHR (measured by change in +dP/dt compared to baseline AAI pacing or VVI pacing in AF patients) between an individual CS branch bipole with the lowest +dP/dt and that with the highest was 6.361. whether there is a significant difference in haemodynamic response to LV pacing in different regions of the same coronary sinus (CS) vein. Subsequently.2C A Rinaldi. Results 15 of the 17 patients underwent successful placement of a LV pacing lead via the CS with satisfactory pacing parameters and no phrenic nerve stimulation at implant.2S Duckett. The initial results of this pilot study suggest that a MR dyssynchrony guided approach to LV lead placement may allow ideal LV lead positioning (Abstract 152 figures 1 and 2). The 3 ring electrodes are spaced 20 mm. UK 1. 1. 4 chamber and short axis cine images were processed using Tomtec software to give a 16 segment time volume-dyssynchrony map. London.1136/heartjnl-2011-300198.766. 1.9611.2S Hamid. 2. however. The mean time from insertion of the CS guide catheter into the venous sheath to successful cannulation of the CS was 1. 3.2R Razavi. We used a high fidelity pressure wire to assess the acute haemodynamic response (AHR) to pacing in different branches of the coronary sinus. lateral or posterior in all cases. The LV lead is standardly placed in a position with the best pacing parameters and satisfactory stability. The mean change in +dP/dt for the best lead position vs baseline+dP/dt was 15. 1. between different branches of the CS in the same patient with a mean difference in change in +dP/dt in the best CS vein compared to the worst CS vein of 16. 3D whole heart images were segmented to produce high fidelity anatomical models of the cardiac chambers and coronary veins. 1.9612. We paced in at least one of our 3 target segments in 11 patients. We used a high fidelity pressure wire to assess the acute haemodynamic response to pacing in different regions of the overlaid 16 segment model.2K Rhode. 1. In this study we aimed to evaluate the difference in acute haemodynamic response to pacing along individual branches of the CS. 1. 1.3%. Abstract 152 Figure 2 153 VENTRICULAR PACING ALONG INDIVIDUAL BRANCHES OF THE CORONARY SINUS USING A QUADRIPOLAR LV PACING LEAD doi:10. we did find that in some cases no pacing capture was found with one A85 . 67% of patients were responders as defined by a 10% increase in +dP/dt over baseline.2M Ginks.665. Methods 16 patients underwent an acute haemodynamic study during their CRT-defibrillator implant. 1. This appears to give close to the best acute haemodynamic response that can be achieved in any branch of the CS. USA) that has four poles on the LV lead―distal tip and 3 ring electrodes. Methods 17 patients underwent cardiac magnetic resonance (CMR) scans. the x-ray C-arm and table could be moved freely while automatically maintaining a registered roadmap.6%. St Jude Medical. In patients with myocardial scar the late gadolinium enhancement images were manually segmented and registered to the anatomical model along with the dyssynchrony map. Results DDDLV pacing was attempted in as many different CS branches as possible in each patient (total 56 different positions used). Although the difference in AHR seen between different bipoles within the same vein were not large. 2King’s College London. Our data suggest that it is also possible to identify and place the LV lead in at least one target region in most patients. This compares to a mean change in+dP/dt of 14. 30 mm and 47 mm from the distal tip electrode and the four poles allow bipolar pacing between them. The region of best+dP/dt response was postero-lateral.BCS Abstracts 2011 we set out to guide lead placement by avoiding scar and targeting the region of the LV with the latest mechanical activation.0 min. 1Guys and St Thomas’ Hospital NHS Foundation Trust. 1.2 1. however. It was thus possible for us to test pacing parameters and AHR along a significant proportion of a CS branch without having to reposition the LV lead.3% for DDDLV pacing. We used a novel quadripolar lead (Quartet. 1.2A Arujuna.2J Bostock.2P Mehta.

had a higher %VP (p<0. Conclusion Our data suggest that only a small difference in AHR is seen when pacing along the same branch of the CS compared to pacing within different branches of the CS within the same patient. National Institute of Clinical Excellence guidance TAO95 (NICE 2006) makes recommendations for primary prevention ICD implantation.03). however. Results Of 399 PGR procedures 342 subjects (86%).154 E L Berry.21. pacing variables and duration of pacing. UK. The presence of a single chamber device was associated with a poorer outcome (p<0. that problems with capture thresholds or PNS can be overcome without the need to reposition the LV lead.42. These differences were not seen in RR programmed dual chamber devices.002) despite patients with a single chamber device being of similar age as those with a dual chamber device. Leeds. mortality rate. long-term RV pacing is increasingly recognised to be detrimental to left ventricular (LV) systolic function. Mean left ventricular ejection fraction (LVEF) was 49 (1)%. Medical therapy included b-blockers in 60% and ACE inhibitors in 70%. a proximal or distal position within a CS branch is much less important than choosing the right branch in terms of acute haemodynamic response. 1J Gierula. comorbidities. 1Leeds General Infirmary. RR pacing was associated with higher %VP (p¼0. UK Background Right ventricular (RV) pacing is an accepted treatment for symptomatic bradycardia. 2K K Witte. attended. current medication and renal function.1136/heartjnl-2011-300198.001). However. and years since first implanted (p¼0. We performed echocardiography. There was a negative relationship between pVo2 and %VP (r¼0. exercise testing and recorded indications for pacing. All patients with a diagnosis of an acute STEMI had an echocardiogram at 6 weeks to assess left ventricular ejection fraction (LVEF).005). There was an inverse relationship between LVEF and %VP (0. Nottingham University Hospitals NHS Trust.09) but there was no effect on LVEF of age. Dual chamber devices were implanted in 77% (45% of all patients had rate responsive (RR) pacing programmed). the presence of AF and the pacing mode. associated features and predictors of LV systolic dysfunction (LVSD) and outcome in a contemporary group of patients with longeterm RV pacemakers.03) and worse renal function (p<0.01). This means that although the site of LV lead placement is important. RELATED TO THE PERCENTAGE OF RIGHT VENTRICULAR PACING doi:10.0001). Patients dead at the censor date were older at the time of the assessment (p<0.BCS Abstracts 2011 bipole but was found with another. 23 (7%) patients are dead. In an unselected population of patients with pacemakers. (44% had an LVEF <50%). Even with a short follow-up period of 16 (0. Our study investigated the feasibility of systematically screening patients following an acute ST elevation myocardial infarction (STEMI) to improve local ICD implant rates. We wanted to establish the prevalence. In single chamber devices. Furthermore. Leeds. left ventricular dysfunction and impaired pVo2 and suffer a high A86 Introduction The ICD implant rate for the United Kingdom is low compared with the European Union and United States of America. Patients with impaired LVEF then underwent screening for primary prevention ICD as per TA095 recommendations (Abstract 155 figure 1). p<0. differences in whether phrenic nerve stimulation (PNS) occurred were seen when using different LV lead bipoles within the same branch of the CS. Method A prospective single centre study was performed over 14months. Mean age (SE) was 76 (1). Mean percentage of ventricular pacing (%VP) was 61 (2)%. 1Z L Waldron. Nottingham. H C Padgett.3) years. A choice of bipoles on the LV lead may mean.1136/heartjnl-2011-300198. Conclusions Patients receiving standard pacemaker generator replacements frequently have cardiovascular comorbidities. Non-attendees had similar pacing variables and were of similar age as attendees. and mean duration of pacing was 10 (0. previous myocardial infarction in 15%. Abstract 155 Figure 1 Heart June 2011 Vol 97 Suppl 1 . Methods We prospectively recruited consecutive patients listed for PGR between 2008 and 2010 at Leeds General Infirmary. Whether an aggressive policy of limiting RV pacing in patients at risk reduces mortality is unknown. p<0. previous cardiac surgery in 26% and atrial fibrillation (AF) in 26%. but did not have significantly worse LVEF or pVo2. Mean peak oxygen uptake (pVo2) (in 107 subjects) was 17 (1) ml/kg/min and mean creatinine was 108 (3) mmol/l.5) months. A D Staniforth. University of Leeds. and a trend to worse LVEF (p¼0. we have established that the amount of RV pacing is related not only to important surrogate measures of outcome such as exercise tolerance and LVEF but also mortality. UK 1 2 G A Begg.155 154 PATIENTS RECEIVING STANDARD PACEMAKER GENERATOR REPLACEMENTS FREQUENTLY HAVE IMPAIRED LEFT VENTRICULAR FUNCTION AND EXERCISE INTOLERANCE. A J Ahsan. in tertiary centre setting.09). 184 men. 155 INCIDENCE SCREENING OF PATIENTS FOLLOWING ST ELEVATION MYOCARDIAL INFARCTION FOR PRIMARY PREVENTION IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICD) IMPLANTATION HAS A LOW THERAPEUTIC YIELD doi:10. Comorbidites were common: diabetes mellitus in 11%.

Clonidine was more effective than Ivabradine both in terms of reducing heart rate and treating symptoms for patients with inappropriate sinus tachycardia. 3(0. Introduction Inappropriate sinus tachycardia (IST) is a relatively rare disease that manifests with resting tachycardia. 2(0. 156 A SINGLE CENTRE EXPERIENCE OF IVABRADINE AND CLONIDINE FOR INAPPROPRIATE SINUS TACHYCARDIA doi:10. 2 Heart June 2011 Vol 97 Suppl 1 157 AN INSIGHT INTO IMPLANTERS’ PRACTICES OF ICD IMPLANTATION: A PHYSICIAN SURVEY doi:10. In total. Resting pre-treatment mean 24 h HR was 94610 (range 75e100) and mean HR on minimal exertion was 157620 (range 130e176). K C K Wong. Tilt table testing was considered in 3 patients due to their symptoms and it excluded postural orthostatic tachycardia syndrome. Ivabradine was exclusively used in 3 patients and clonidine in 2. All patients had a structurally normal heart on echocardiogram.8%) died during the investigation period (22 died during their initial acute event. 24(7. Treatment options include b-blockade or sinus node modification which are not 100% successful. patients had associated symptoms of hyperadrenergic surges. An alternative approach of opportunistic screening in patient groups with a high prevalence of impaired LV function might give a higher yield than our approach looking at disease incidence. Mean resting HR after 3 months of Ivabradine therapy was 9569 (range 88e105) and mean HR on exertion was 159623 (range 128e180).6%) were identified as having episodes of NSVT. 2(0.156 P P Sadarmin. Pretreatment with b-blockers had been unsuccessful in 5/6 patients. Oxford.157 P P Sadarmin. Results 5 out of 6 patients were women with a mean age of 27. UK Introduction The Implantable cardioverter defibrillator (ICD) is the mainstay of treatment for the prevention of sudden cardiac death (SCD) and the management of tachyarrhythmias.3%) self presented with a cardiac arrest before completion of their screening tests and received a secondary prevention ICD. Oxford. Medical case records were reviewed for each patient. 1(0. Methods We identified 6 patients from 2005 to 2009 with a diagnosis of IST (according to accepted international guidelines) who had been treated with either Ivabradine or Clonidine or both. both proceeded to have a primary prevention ICD implanted. 10(3. T R Betts. a normal ECG and absence of structural heart disease. A trial of Clonidine can be recommended before considering sinus node ablation.5 years (range 16e40 years). All 4 patients taking Ivabradine failed to gain symptom relief with no significant reduction in mean 24-h HR parameters. All patients had been symptomatic for alteast 6 months before presentation to our tertiary centre. Abstract 155 Figure 2 Conclusion The yield from this study was low. Both patients had EPS.4%) patients had Holter monitors.6%) patients were assessed as not clinically suitable for further investigation.9%) primary prevention ICDs were implanted (Abstract 155 figure 2).BCS Abstracts 2011 Results 326 STEMI patients were identified.7%) declined investigation. In contrast. Informed patient A87 . John Radcliffe Hospital.3%) had inducible VT and proceeded to have a primary prevention ICD implanted. 1 patient was started with Ivabradine but later switched over to clonidine as it was ineffective. John Radcliffe Hospital. Resting mean HR was 8163 (range 78e83) and mean HR with exertion was 144618 (range 132e164). 2(0.1%) requested follow-up in another geographical area.6%) had LVEF<30% and QRS>120 ms. Of these 12(3. Formal randomised controlled trials are needed to confirm our findings. Holter monitoring prior to treatment demonstrated sinus tachycardia. 3 patients (0. We present our experience of managing 6 patients with a diagnosis of IST with either Ivabradine or Clonidine or both. 1 patient (0. K Rajappan. The HR variability pre and post treatment is shown in Abstract 156 figure 1. 2/4 patients subsequently had complete sinus node ablation and AAIR pacemaker.1136/heartjnl-2011-300198. T R Betts. 3 died of non cardiac causes following discharge). 26(8%) patients were identified as LVEF<35%. 25(7.9%) proceeded to primary prevention ICD. It should also be noted that the methodology resultant from TA095 guidelines was labour and resource intensive. a rapid increase in heart rate (HR) with minimal exertion. UK Abstract 156 Figure 1 Discussion In our case series of 6 patients.1136/heartjnl-2011-300198. Patients with coexisting hyperadrenergic symptoms may benefit the most. The remaining patient had symptomatic asthma and was therefore unable to tolerate b-blockers. Newer agents like sinus node inhibitor (Ivabradine) or a centrally acting a-2 sympathomimetic (Clonidine) can be used but there is no success outcome data for either and there is also no evidence that one is better than the other. the 3 patients on clonidine had greater symptom resolution and fall in resting and exercise heart rates at 3 months follow-up. Y Bashir.

and then upgrading to CRT if required. and to the cost of implanting full CRT-D systems up front. All had LV EF<30%. Use of absolute risk reduction in percentages and number needed to treat while explaining the risks and benefits gained from ICDs were used by 22% and 26% respectively. yet are often felt likely to benefit from CRT in the future. 35% of the responders were between the age of 30e39 years and 39% were between 40 and 49 years.68 Abstract 158 Figure 1 A88 Per cent freedom from upgrade to LV lead. 83% of the responders were Consultants and 96% were working in an implantating centre.28:926e932) 5. 26 had ischaemic heart disease and 9 non-ischaemic dilated cardiomyopathy.08% (Br Heart J. K C K Wong. such that if an upgrade were to become necessary.1998. 0.98:663e670).64% (Circulation. with the LV port “plugged”.2005. inappropriate shocks and driving restrictions were performed by 96% of responders and device infections and lead failures discussed by 91%. Increasing awareness of ICD complication rates can help patients and physicians balance risk against benefit which could lead to improved patient satisfaction with their therapy.77% (Circulation. and to compare this cost to that of merely implanting a DDD device. All responders said they would personally discuss the therapy with the patient prior to the implantation regardless of the referral source. Information of the style and language of consent was requested. lets you live longer by an average of 3 months) (30%). Patient characteristics.6626.98:663e670).28 2. T R Betts. the estimated cost would have been £ 598 000.17 14. Results 35 patients (27 male) were identified. implanting CRT-D devices but without an LV lead. implanting CRT-D devices with LV leads in all patients in the first instance.1136/heartjnl-2011-300198. 0. Evidence based use of risk and benefit terminologies like ARR and NNT are needed to better inform the patient rather than abstract phrases. There was widespread use of phrases like “small risk” or “moderate risk” (61%) and life prolongation (eg.1998.98:663e670) 4.22:481e9) Background Many patients receiving ICD implants do not meet criteria for CRT therapy. There was widespread use of information leaflets (87%) and specialist ICD nurses (83%) to disseminate information to patients. 10% (Circulation. or implanting a full CRT-D system initially. K Rajappan. attitudes and factors influencing ICD prescription in the UK. If all patients had received full CRT-D the cost would have been £ 665 000.2762. to examine the cost implications of this approach.761.08 5. Mean (SD) age was 6768 years. UK Abstract 157 Table 1 Estimate of ICD complications Death as a complication of device implant Lead dislodgement requiring lead repositioning Lead failure requiring extraction or additional lead insertion Major haematoma requiring reoperation Device infection requiring removal/extraction Cardiac tamponade Pneumothorax Inappropriate shocks Mean % 0. indication for a plugged LV port.BCS Abstracts 2011 consent is an essential part of the implant process. lead dislodgement requiring re-positioning and major haematoma requiring reoperation.2005.98:663e670) 12% (PACE. Purpose This study analyses a retrospective cohort of patients who received CRT-D devices but without LV leads. as has been suggested by the recent Madit-CRT and RAFT studies. subsequent addition of a LV lead and reasons for doing so were taken from patient records.1998. 0. Y Bashir.1995:73:20e24) 5% (PACE. 0.89% (Circulation. it is predicted that an upgrade rate of 26%e31% would be required before using a plugged LV port becomes cost-effective.4 Published/Trial data % 0. The reasons for this include less severe NYHA class of HF symptoms at the time of implant. Replies also indicated that Imp under-estimate overall mortality in medicallytreated and ICD-treated patients.07 1.7263. Method A retrospective analysis of all patients receiving CRT-ICDs with plugged LV ports between September 2004 and June 2009 at our institution. only a new LV lead (and implant kit) would be required. 158 IS IT COST EFFECTIVE TO USE A PLUGGED LV PORT? doi:10.158 M A Jones. 83% of Imp were fully aware of Primary Prevention (PP) NICE guidelines while 78% were fully aware of Secondary Prevention (SP) NICE guidelines.1996.1% (PACE. 18% (Z Kardiol.2006:295:1901e1911) 0. 2. Guidelines and awareness about end-of-life care in ICD patients is needed and should be part of the initial consent process. narrow QRS.1998.28:926e932).2005. Total cost at end of FU period was £ 654 000. 17. at 10.1998. John Radcliffe Hospital. 17 and 21 months respectively. If all patients had initially been implanted with VVI or DDD ICDs and 6 new CRT systems implanted. Management options include only implanting DDD / VVI devices. 6 (17%) patients had an LV lead added.2005:28:926e932).8% (JAMA.6861. A discussion regarding the prevention of SCD. all for the development of NYHA III symptoms. Conclusion The majority of implanters are aware of UK ICD guidelines.77% (Circulation. only a small proportion subsequently required biventricular pacing.3760.0. Using a CRT-ICD with a plugged LV port is not a cost effective strategy (Abstract 158 figure 1). Results Replies were received from 23 implanters. 15. During a mean (SD) FU of 40 616 months. The total cost (surgery and hardware) was compared with the estimated cost of initially implanting single or dual chamber ICDs and upgrading the entire system. Taking into account the time to develop symptoms.07 2.92 Psychological problems associated with the device 22. Indications for a plugged LV port were LBBB and NYHA class I or II symptoms in 29 and NYHA class I or II with a narrow QRS but a high chance of becoming pacemaker dependent in 6.98:663e670) 1.98:663e670). The patient consent process is not universal. 11. full CRT-D system implantation is even less cost effective.5% (PACE.91% (Circulation. Conclusion In this series of ICD patients with potential CRT indications but minimal heart failure symptoms. Methods A questionnaire survey was sent to UK ICD Imp to test their knowledge of the risk and benefits of an ICD in patients who satisfy trial and national guideline criteria and the incidence of implant complications.7% (MADIT2 trial) 0.85:809e819) 13e38% (Clin Cardiol 1999. 14.1998. 28:926e932).8610. Imp overestimate infections leading to device removal and the incidence of pneumothorax when compared to published trial or study data.48 3. This questionnaire was specifically aimed at Imp and was part of the larger questionnaire looking at knowledge. Furthermore.467.2005. 28:926e932).562. Oxford. and finally. Our aim was to get an insight into implanters’ (Imp) practices prior to an ICD implantation.2% (PACE. and (progressive) atrio-ventricular conduction delay. 28:926e932). Heart June 2011 Vol 97 Suppl 1 .3% (PACE. N Qureshi. It is not clear which of these strategies is superior in terms of the cost-benefit ratio.2005.

The short-acting preparation was weaned following the second monthly injection.9 (16. propranolol. 160 HIGH DOSE OCTREOTIDE.5 5/7 6/7 1. 2P J Stafford.4) 9. Results Seven patients reached the endpoint of VA/death (median follow-up 24 months).14 24 (18) 7.4360.8) p 0.5) VA/death (n[7) 7268 100 106615 2767. Leicester. J Pitts-Crick.1136/heartjnl-2011-300198. 2University Hospitals of Leicester NHS Trust. 1C D Steadman. Octreotide was commenced using a short-acting preparation given 3 times daily (dosage 50e250 mg according to body mass) in conjunction with a longacting (monthly). 2M Jeilan. selective serotonin reuptake inhibitors. Both short-acting. secondary to cerebral hypoperfusion. intramuscular injection (dosage 10e30 mg).4260.031 0. a powerful splanchnic vasoconstrictor. subcutaneous (0.84 0.068 0.16 Introduction There is a need for better sudden cardiac death (SCD) risk markers. Methods Blinded retrospective study of 30 patients with ischaemic cardiomyopathy assessed for an implantable cardioverter defibrillator. C Parker. Heart June 2011 Vol 97 Suppl 1 Introduction Postural orthostatic tachycardia syndrome (POTS) is defined as symptomatic orthostatic intolerance with an increase in heart rate of 30 beats per minute within 10 min of head up tilt (HUT). 2S Yusuf. 2S Kundu. This dysautonomia causes wide-ranging symptoms including palpitations.4560.5 (8.8 (10.45 0. When POTS occurs in patients with preexisting Joint Hypermobility Syndrome (JHS). The R2I2 was derived from high resolution 12 lead ECG recorded during programmed electrical stimulation (PES). left ventricular ejection fraction and QRS duration (6/14 vs 1/15 p¼0. All patients had remained symptomatic despite pre-treatment with a mean of 5 POTS medications (range 5e7) including fludrocortisone. We report the first UK series of JHS patients with drug refractory POTS treated with high-dose octreotide.95 0. C Shepherd. J Tagney.7) 10. 1F S Schlindwein.41 0. 2G P McCann. A J Sandilands. Results During follow-up of 3 months (range 1e8). ECG surrogates were used to plot APD as a function of diastolic interval. intramuscular (10e20 mg) preparations have A89 .34 0. UK. symptoms begin approximately a decade earlier than non-JHS patients with a preponderance of neurological features.3960. No patients developed supine hypertension. Symptomatic improvements have been previously reported in POTS patients with the somatostatin analogue Octreotide. midodrine.4615 7/23 8/22 1.47 0.088 0. inferior and lateral leads normalised to the mean value for the total population. aged 21e52) were referred to our institution.055 0. neurological symptoms (headache and cognitive impairment) and diagnostic tilt-table testing with a mean increase in heart rate of 64 beats/min (range 47e73) with head-up tilt (HUT).057) (Abstract 159 figure 1). Bristol Heart Institute.41 p¼0. Mounting evidence suggests that the mechanism underlying risk of ventricular arrhythmia (VA) is increased heterogeneity of electrical restitution. 1University of Leicester.9 (17.1136/heartjnl-2011-300198. the extent of PIZ.4960. UK Abstract 159 Figure 1 Conclusions In this pilot study of ischaemic cardiomyopathy patients. gabapentin and erythropoietin. R2I2 > median was found to be predictive of VA/death independent of PES result.BCS Abstracts 2011 159 PILOT STUDY EXPLORING THE REGIONAL REPOLARISATION INSTABILITY INDEX IN RELATION TO MYOCARDIAL HETEROGENEITY AND PREDICTION OF VENTRICULAR ARRHYTHMIA AND DEATH doi:10.41 0.159 W B Nicolson. 3 (50%) patients reported a complete resolution of all postural and neurological symptoms which corresponded with a normalised response to HUT. Conclusion Octreotide is increasingly recognised as an effective therapy in POTS patients. G Thomas. A NOVEL THERAPY FOR THE TREATMENT OF DRUG REFRACTORY POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME IN PATIENTS WITH JOINT HYPERMOBILITY SYNDROME doi:10.5) No VA/death (n[23) 6569 96 107621 32. UK 2 1 Abstract 159 Table 1 Variable Age (years) Sex (% male) QRSD(ms) EF(%) PES result (positive/total) R2I2>median EDV index (ml/cm) SV index (ml/cm) Follow-up (months) PIZ % Scar % Whole Group (n[30) 6769 97 107620 31614 12/30 14/29 1. Methods Six patients (female. A Horne. chronic fatigue. the R2I2 was the maximal value of the mean squared residuals of the mean points for anterior. the R2I2 was shown to be an electrical measure of VA/ death risk with a moderately strong correlation with an anatomic measure of arrhythmic substrate. headache and cognitive difficulties. PIZ was measured from late gadolinium enhanced CMR images using the full width half maximum technique.093 0.67 (13. We investigated a novel measure of action potential duration (APD) restitution heterogeneity: the Regional Repolarisation Instability Index (R2I2) and correlated it with peri-infarct zone (PIZ) a cardiac magnetic resonance (CMR) anatomic marker of VA risk. Bristol.6 (8. Vascular laxity with splanchnic venous pooling has been implicated as a causative factor thus measures to expand plasma volume (thereby increasing mean arterial pressure and restoring cerebral perfusion) form the mainstay of therapy. The R2I2 may add value to existing markers of VA/death and merits further investigation. T Johnson.9 mg/ Kg) and long-acting. Modest correlation was seen between the R2I2 and PIZ (r¼0. Side effects including mild abdominal discomfort and transient diarrhoea were reported in 3 (50%) patients.5) 21. presyncope.031). The remaining patients reported a dramatic improvement but ongoing postural symptoms.14 24 (16) 7.160 A E French. 1P Brown.4860. Leicester. ivabradine. 1G A Ng.15 16 (16) 13. All had known JHS (4 requiring a wheelchair).

AVNRT. Introduction Following National Service Framework guidance on the management of sudden cardiac death (SCD). UK. examination. 162 THE CLINICAL MANAGEMENT OF RELATIVES OF YOUNG SUDDEN ARRHYTHMIC DEATH VICTIMS. fluoroscopy time. Standard technique employed was large area circumferential ablation using conventional RF energy or pulmonary vein isolation using duty cycled RF energy. N Khan. 2Department of Clinical Genetics. DCM (9). The number of ICDs inserted was very small (2%) and there have been no appropriate therapies in this A90 Heart June 2011 Vol 97 Suppl 1 . ECG and echo. major bleeding (requiring transfusion). There were no major bleeding complications. ARVC (12). during and after the procedure. Central Manchester University NHS Foundation Trust. age range between 21 and 73 years (mean 57 years). In sub therapeutic INR patients weight adjusted LMWH was used post procedure with warfarin until INR was >2. 1C J Garratt. Further imaging by CMR or contrast echo was performed in those with structurally abnormal hearts or with T wave inversion in V2/V3. Studies have examined the yield of different diagnostic strategies but the outcome of management in these patients has not been reported. Results Of the 193 patients. To date no deaths have occurred in those diagnosed with inherited causes of SCD (follow-up mean 20. 1 ARVC). Mean procedural INR was 2. this includes those with family histories of HCM (7). Central Manchester University NHS Foundation Trust. Conclusion These data demonstrate that CA for AF by both single and double transseptal technique using both standard RF and duty cycled RF while maintaining a therapeutic INR is a safe procedure.7e3. procedural INR. Results There were 128/173 male patients. UK 2 1 1 2 2 161 CATHETER ABLATION OF ATRIAL FIBRILLATION ON UNINTERRUPTED WARFARIN USING STANDARD AND DUTY CYCLED RADIOFREQUENCY ENERGY: SAFE AND EFFECTIVE doi:10.4 mins (range 8. Mean unfractionated heparin dose was 6000 units (range 1000e14 500). 13 failed to return to clinic and 47 are regular reviewed as the risk of developing an inheritable condition cannot be excluded.162 J C Caldwell. Of the 145 patients thought to be clinically normal. 2L Kerzin-Storrar. D J Fox. Data was gathered for demographics. Manchester. 21 had medication commenced by the clinic (b-blockers (21). St Mary9 s Hospital.BCS Abstracts 2011 previously been reported. University Hospital of South Manchester. ICDS ARE RARELY INDICATED doi:10. We wished to determine the safety of CA for AF with a therapeutic INR using both the single transseptal approach and duty cycled radiofrequency energy (RF) with non irrigated PVAC catheters and the double transseptal puncture technique using irrigated RF catheters and either CARTO or NAVX electroanatomical mapping. This technique is convenient for patients and avoids switching between LMWH and warfarin and ensures patient safety by maintaining therapeutic anticoagulation before. 43 individuals (22%) from 36 families (33%) were diagnosed with an inheritable cause of SCD and 145 patients were clinically normal (see Abstract 162 table 1).1136/heartjnl-2011-300198. Mean fluoroscopy time for the PVAC group was 23. pericardial tamponade and stroke/ TIA within 28 days of the procedure. Ajmaline provocative testing was performed in those with a history and/or ECG suggestive of Brugada syndrome. Five patients were found to have other conditions (LV non-compaction. To date no appropriate therapies have been administered (follow-up 8e29 months) but there was 1 inappropriate shock from a fractured lead. Manchester. 2K Metcalfe. 122 underwent ablation for PAF and 51 for persistent AF. Brugada (4) and LQT(1). Spironolactone[1]). covering the procedure with unfractionated heparin and “bridging” postoperative patients with low molecular weight heparins (LMWH) back onto warfarin. Mean fluoroscopy time for CARTO/NAVX group was 31mins (range 14.2%) both managed with percutaneous pericardial drainage. 85 were reassured and discharged.3e50. skeletal myopathy. 1 LQT). 1e52 range) or those clinically normal with ongoing review (follow-up mean 22 months. W Newman. All individuals underwent clinical assessment by history. N C Davidson. ACEi/ARB(2).1136/heartjnl-2011-300198. ICDs were implanted as per HRUK guidelines. 1Manchester Heart Centre. There were no stroke/TIAs. Many centres adopt a policy of discontinuing warfarin in the immediate run-up to the procedure. Inadequate anticoagulation leads to thrombotic complications and excessive anticoagulation can lead to bleeding risks. Endpoints were minor bleeding.44 mins). Methods We present data on 193 consecutive patients (108 families) referred to a regional inherited cardiac conditions clinic because of SCD/aborted cardiac arrest of a relative. regional inherited cardiac conditions clinics were established to identify and treat those at increased risk of dying from an arrhythmic condition. and type of radiofrequency energy used.4 (range 1. Of the 43 patients diagnosed with an inheritable condition.10e58.161 J R J Foley. The mean age on referral was 38617 yrs and mean duration of follow-up was 15 months (range 1 day to 56 months). resulting in 4 patients having an ICD inserted on clinic recommendation (2 HCM. Although ablation for paroxysmal AF (PAF) is associated with shorter procedure times and less extensive left atrial ablation vs persistent AF thromboembolic complications can occur in both sub-groups. mild AS and congenital sub-aortic membrane). 1e56 range).1 mins). Z Borbas. Maintaining a therapeutic INR reduces the risk of embolic events associated with “bridging” heparin without an increase in bleeding complications. Abstract 162 Table 1 Diagnosis of patient Clinically normal LQTS Brugada CPVT ARVC DCM HCM Numbers 145 12 2 5 7 7 10 Conclusion A diagnosis of an inheritable cause of SCD was obtained in 22% of individuals and 33% families with a history of SCD/ aborted cardiac arrest in a relative. There was 1 minor bleeding complication with a groin pseudoaneurysm.9). total dose of unfractionated heparin. If treadmill exercise test had not previously been performed this was undertaken. Methods A retrospective analysis of 173 patients who underwent CA for AF while taking uninterrupted warfarin. B D Brown. 1 DCM. N Moreton. Procedural target International Normalised Ratio (INR) was 2e3 with a peri-procedural target ACT of 300e350 s. We conclude that higher dosages of both preparations when administered together are effective and well tolerated in JHS patients with drug refractory POTS. There were 2 cases of pericardial tamponade (2/173%e1. UK Introduction Catheter ablation (CA) for atrial fibrillation (AF) is growing exponentially. CPVT (5). Three individuals had b-blockade withdrawn after negative genetic testing for an established familial mutations (2 CPVT. one ICD was removed and one deactivated (both negative for CPVT). Manchester. vascular complications.

1136/heartjnl-2011-300198. Conclusions The UK TAVI Registry has successfully captured the entire TAVI activity of England and Wales incorporating the learning curves of every centre. A Bhan. Median (IQR) age was 82 (78e87) yrs. There was also no difference in survival between patients treated with CoreValve or Edwards technologies. without the need for thoracotomy or cardiopulmonary bypass. 68% were transfemoral. Two ICDs have been removed/deactivated after exclusion of a known familial mutation. and not different between those with a LES<21 compared with LES 21e40. B Brickham. London. Abstract 163 Figure 1 Heart June 2011 Vol 97 Suppl 1 Abstract 164 Figure 1 A91 . Patients needing a transapical route had more comorbid conditions than those treated by a transfemoral route (LES 25.1136/heartjnl-2011-300198. More details of the 2010 cohort will be available at the time of presentation (Abstract 163 figure 1).2%. A unique patient identifier (the NHS number) is used to link with the NHS Central Register to track mortality.9% at 1 year (443 at risk) and 72. or the presence of concomitant coronary artery disease. Outcomes following TAVI are excellent in a high risk patient population. the remainder being mainly transapical.164 R Dworakowski. P MacCarthy. The registry has captured all cases in England and Wales. Outcomes are better in the population who are suitable for a transfemoral approach (with less comorbidity) than those treated with the transapical approach. all centres complete an agreed dataset.9%). M Monaghan.4% in 2007 to 29. NYHA class. UK Purpose Transfemoral (TF) TAVI is a novel procedure for the treatment of severe aortic stenosis. On Behalf of the UK TAVI Steering Group. UK Introduction The United Kingdom Transcatheter Aortic Valve (TAVI) Registry was established to define the clinical and procedural details of all patients being treated by TAVI. and a change in demographics with the proportion of patients with prior CABG rising from 16.5% vs 81. and we have demonstrated no systematic difference in outcome between the two commercially available technologies. 90% of CoreValve implants and 46% of Edwards used a transfemoral approach. 164 EARLY HAEMODYNAMIC CHANGES AND MYOCARDIAL INJURY AFTER TRANSFEMORAL TRANSCATHETER AORTIC VALVE IMPLANTATION (TAVI) doi:10. This analysis is based on all procedures performed up to 31st December 2009. or between proctored and non proctored cases. There was a significant improvement in survival over the 3 years of the registry. 66 in 2007. but little is yet known about the periprocedural haemodynamic effects. Kings College Hospital. 52% were male.9% in 2009.2% vs 20. Kings Health Partners.1%. 163 THE UNITED KINGDOM TRANSCATHETER AORTIC VALVE REGISTRY . and mean logistic Euroscore (LES) was 22. Survival was also poorer in those with poorer LV ejection fraction. and to assess their outcomes. Methods In 16 patients undergoing TF TAVI haemodynamics were characterised with a number of tD and 3D TTE measurements.OUTCOMES TO DECEMBER 2009 AND UPDATE doi:10. with moderate or severe post procedural aortic regurgitation and with a LES>40. These data suggest that careful proctoring allows the introduction of a new treatment method without an adverse effect on patient outcome. 273 in 2008 and 538 in 2009. Results 25 centres in England and Wales performed a total of 877 procedures in 870 patients. Birmingham. The total number of cases in the UK TAVI registry has risen to 1490 as of 29 Nov 2010. We aimed to describe these effects using 3D and tissue Doppler (tD) transthoracic echocardiography (TTE) and Cardiac Output monitoring. regardless of access route or technology used.4%). Survival at 30 days was 93. The data are encrypted and sent electronically to servers at the Central Cardiac Audit Database (CCAD) for analysis.BCS Abstracts 2011 group. Survival was significantly poorer in those needing non-transfemoral approaches (1 year survival 73.163 P F Ludman. 78. Survival was not associated with age. Methods For every TAVI performed. The procedure results in almost instantaneous normalisation of transvalvular gradients. O Wendler. Mortality tracking was successful in 100% of patients.3% at 2 years (114 at risk). A M Shah. Median number of cases per centre was 24.

differs between patients with bicuspid and tricuspid valvular disease with comparable transvalvular gradients. Results Uptake was 46% (age range 65e96 years.BCS Abstracts 2011 These were taken at multiple time points (baseline. Participants underwent a standard transthoracic echocardiogram (TTE) according to A92 S Bull. UK Background Bicuspid aortic valves (BAV) are a common inherited abnormality with a very high rate of adverse cardiac events at an earlier age than tricuspid aortic valves (TAV). However. VHD was detected in 33% of participants and prevalence increased with increasing age (see Abstract 165 figure 1). Mitral regurgitation and aortic regurgitation were the most common lesions detected (present in 17% and 14% respectively).3. were invited to attend their GP surgery where routine demographic and cardiac data were collected and a focused examination undertaken. and the majority of detected VHD is mild. Oxford. It is unknown whether pathological left ventricular (LV) remodelling. 4D Mant. Methods 42 subjects were recruited in total: 24 patients with moderate to severe BAV (age 55 615 yrs.05).8 ml. 1B D Prendergast. Conclusion Successful TF TAVI results in an immediate improvement in cardiac output. within the first 24 h both systolic and diastolic dysfunction occurs.9 to 33. none expressed significant levels of worry or tension. Results TAVI resulted in an immediate increase in cardiac output (3. Methods Patients >65 years.5 l/min (24 h). 98% would be prepared to undergo repeat echocardiography as screening for VHD. The threshold for inclusion in the screen positive group was deliberately low to capture all manifestations of VHD. 6 h post-TAVI there was a significant decrease in systolic function as measured by dP/dt max/EDV (see Abstract 164 figure 1A) and co-existent impairment of diastolic function as indicated by medial E:E9 values (see Abstract 164 figure 1B). using a low threshold for detection. p<0. The majority of participants (99%) described themselves as calm or relaxed at the time of screening. However. Abstract 165 Figure 1 Prevalence of VHD in $65s by age group. 1John Radcliffe Hospital.05).05. Echocardiographic screening for VHD is feasible in the primary care setting and acceptable in this group of patients. 165 THE OXVALVE STUDY: ECHOCARDIOGRAPHIC SCREENING FOR VALVULAR HEART DISEASE IN THE COMMUNITY SETTING: METHODOLOGY. to assess the acceptability of echocardiographic screening for VHD. p<0. 6 and 24 hours post procedure). UK. Studies addressing the contemporary epidemiology and natural history of VHD are scarce but demonstrate an increasing prevalence in the elderly. J M Francis. A J Farmer. In addition. registered with participating general practices (GP) and with no known VHD. overlying this. Cardiovascular magnetic resonance (CMR) tagging provides detailed characterisation of global and regional contractility. 1292 and 1367 dyn*s/cm5). we present preliminary data for the first 1050 patients. N Blundell.2 cm/s. prospective community echocardiographic screening study within the adult Oxfordshire population.05 baseline vs 24 h and 6 h vs 24 h). to determine the epidemiological characteristics of VHD in the UK for the first time. B Prendergast.7 (baseline). peak transHeart June 2011 Vol 97 Suppl 1 .1). stroke volume (SV) and systemic vascular resistance in real-time. UK. associated with significant morbidity and mortality. uses a clinically validated algorithm to provide continuous cardiac output (CO). we observed a significant decrease in EDV and ESV at 24 h post-TAVI (EDV: 94. 6. FEASIBILITY AND PRELIMINARY RESULTS doi:10. Oxford. British Society of Echocardiography guidelines. remains a significant clinical challenge.4. p<0. A Pitcher. which was associated with an appropriate increase in LA volume (70.05 baseline vs 6 h). J Suttie. there was a recovery of both systolic and diastolic indices.5 baseline vs 6 h and 24 h) with no significant change in systemic vascular resistance (1162.6 and 72. Diastolic function was monitored using the indices mean E:E9 and systolic function/ contractility was measured with dP/dt max and early peak systolic velocity (S9 ). Following this. The rise in the markers of myocardial injury suggest this may be due to myocardial stunning and/or some periprocedural myocardial damage. only 1% of VHD detected was severe. The majority of VHD was graded as mild (84%). with enrolment ongoing. S Neubauer. 82. T D Karamitsos. valve morphology and LV hypertrophy in patients with bicuspid and tricuspid aortic valve disease matched for transvalvular gradient. is approximately 33% and increases with age. Cohort studies in the USA are ongoing but there are no European or UK studies to date. female 21%. UK. The FloTrac system (consisting of the Vigileo monitor and sensor). Principle limitations are the diverse nature of patients with VHD. Calculated volumetric parameters included 3D enddiastolic volume (EDV) and end-systolic volume (ESV).06 vs 1.4 ml (p<0.166 Introduction Valvular heart disease (VHD) is poorly researched in comparison with other areas of cardiovascular disease. male to female ratio 1:1.6. ESV 41. Mitral regurgitation is the most common lesion. Concurrent with this recovery.1136/heartjnl-2011-300198. J D’Arcy. p<0. 4Department of Public Health and Primary Care. University of Oxford.6 vs 6. We therefore assessed left ventricular strain (using CMR tagging). stroke volume (SV) and 3D LA volume (LAV). These changes in haemodynamics were associated with significant increase of troponin I levels at 24 h and increase in CK-MB at 6 h after the procedure (troponin: 0. 8. p<0. a strong predictor of adverse cardiac events. Oxford. UK 1 2 3 4 166 CARDIOVASCULAR MAGNETIC RESONANCE (CMR) TAGGING IDENTIFIES DIFFERENTIAL VENTRICULAR REMODELLING IN PATIENTS WITH BICUSPID VS TRICUSPID AORTIC VALVE DISEASE doi:10. Herein. and is a powerful investigative tool in the assessment of myocardial disease. P Grimwade. 2Didcot Health Centre.165 Conclusions The prevalence of VHD in adults aged over 65 in the Oxfordshire population. We have developed a large scale. in both bicuspid and tricuspid disease.19 mg/l. Oxford.05)). 3Bampton Medical Practice. J L d’Arcy. another marker of systolic function. before completing a shortened Spielberger STAI questionnaire. Participants were given preliminary results. John Radcliffe Hospital.1136/heartjnl-2011-300198. S9 increased after 24 h (6. CK-MB 1.9 to 83. D Ebbs. S G Myerson. 4. and establish cohorts with well-characterised genetic and echocardiographic phenotypes for future study.6 mg/l.6 (6 h) 4. Risk stratification for moderate to severe aortic stenosis.5 ml (p<0. inability to identify individuals at the earliest stages of disease and lack of an appropriate investigational infrastructure. Oxford. Recovery of contractility is observed after 24 hours.

despite being younger and having lower systolic blood pressure.15 0. 1John Radcliffe Hospital & University of Oxford. SBP 127 614 mm Hg DBP 76 610 mm Hg) and 18 patients with velocity-matched TAV (age 74 66 years. 1A P Banning. The best predictors of progression to symptoms and other conventional indications for surgery were determined. but prognosis is already reduced by this time.6/ ms.93 (p<0.50 0. female 28%. tagging and cine imaging. Background The timing of valve surgery in asymptomatic patients with significant aortic regurgitation can be challenging. despite the younger age and lower blood pressure. Heart June 2011 Vol 97 Suppl 1 Abstract 167 Figure 1 Kaplan-Meier survival curve showing survival without surgery for conventional indications. compared to 6% for those with a regurgitant fraction $37% (see Abstract 167 figure 1).91 and 0. J M Francis.04).BCS Abstracts 2011 aortic velocity 3.6 172648 127614 76610 2063 1962 1764 Tricuspid aortic valve (TAV) 7466 28 3. Royal Brompton Hospital and the National Heart and Lung Institute.09 for regurgitant volume).04) despite similar degrees of valve stenosis. Patients were scanned using a 1. J P Greenwood. and we examined whether either could predict symptom development and the need for aortic valve surgery. Regurgitant fraction and volume were the only independent outcome predictors on multiple logistic regression analysis. 1T D Karamitsos. Supporting data also comes from a comparison Abstract 166 Figure 1 Velocity matched tricuspid and bicuspid aortic valves showing valve morphology. LV volumetric indices also predicted outcome. UK.0001). have more severe hypertrophy and lower myocardial contractility. J D’Arcy. p<0. Auckland. velocity 3. but less strongly than measures of regurgitation: LV end-diastolic volume >267 mls (AUC 0. Conclusion Ventricular remodelling differs between BAV and TAV patients with equivalent transvalvular gradients.01 0. Quantification of the regurgitation has not previously been used to guide management. 3University of Leeds. 2CMR Unit. New Zealand).160. Regurgitant volume >38 mls and regurgitant volume index >25 ml/m2 were also good predictors (AUC 0. LV mass 172648 g. p¼0. 4J P Christiansen. Survival without surgery was 88% for patients with a regurgitant fraction <37%.26 compared to 1. New Zealand 1 1 1 2 3 Abstract 166 Table 1 Bicuspid vs tricuspid aortic valve disease Bicuspid aortic valve (BAV) 55615 21 3. Peak systolic global circumferential strain was calculated at each ventricular level using CimTag2D software v.160.7 (Auckland MRI Research Group.1136/heartjnl-2011-300198. 4North Shore Hospital. and subsequent clinical followup occurred for up to 7 years (mean 2. mid-ventricular and apical short axis tagging images were acquired. Leeds. 167 AORTIC REGURGITATION QUANTIFICATION WITH CARDIOVASCULAR MAGNETIC RESONANCE PREDICTS CLINICAL OUTCOME doi:10.160.6/ms. The predictive ability of CMR applied to patients with both moderate and severe aortic regurgitation on echocardiography. Methods 94 asymptomatic patients with moderate or severe aortic regurgitation on echocardiography were identified from four high volume CMR centres. 1S Neubauer.04 0. Current indications focus on symptoms and left ventricular (LV) dilation/ dysfunction. likely due to the difficulty of achieving this with echocardiography. R Mohiaddin.07. LV end-systolic volume >88 mls (AUC 0.78). Germany) and basal.85). SBP 136617 mm Hg.04 0.31 0. LV mass 147627 g.07 0. apical BAV 1764% vs TAV 1963%. Results Aortic regurgitant fraction was the best predictor of clinical outcome. Cardiovascular magnetic resonance (CMR) can accurately quantify aortic regurgitation and LV volumes.90 respectively).5 T Avanto scanner (Siemens Healthcare.04. A93 . though regurgitant fraction had significantly greater predictive power (OR 1. UK.04 Results Patients with BAV had significantly greater left ventricular hypertrophy (BAV 172 648 g vs TAV 147627 g. CMR scans were performed to quantify aortic regurgitation and LV volume indices.04 0.6 147627 136617 7967 2263 2162 1963 Morphology Age (yrs) Female (%) Transvalvular velocity (msÀ1) Left ventricular mass (g) Systolic blood pressure (SBP) Diastolic blood pressure (DBP) Basal circumferential systolic strain (%) Mid ventricular circumferential strain (%) Apical ventricular circumferential strain (%) p Value <0. UK. DBP 7967 mm Hg. Oxford.662. Abstract 166 table 1). Mid BAV 19 6 2% vs TAV 21 6 2% p¼0.167 S G Myerson. reduced contractility) in patients with BAV than TAV (Basal BAV 2063% vs TAV 2263% P¼0. Peak systolic circumferential strain was lower (ie. London. Erlangen. area under the curve (AUC) on receiver operating characteristics analysis 0. This finding may have implications for monitoring disease progression or more timely medical or surgical intervention in patients with BAV.160. with a specificity of 93% and sensitivity of 78% for predicting the progression to symptoms and surgery.1 years). BAV patients.

mid-wall or infarct patterns of late gadolinium enhancement by blinded independent observers.4%).96 (95% CI. p¼0.32. B¼ Infarct LGE. consecutive patients with moderate or severe aortic stenosis (aortic valve area <1.7 * Geometric mean (95%) Mid-wall LGE 54 70611 42 58621 1.37 92. 5. S Joshi.6* (86.0. Scotland was linked through a unique patient identifier to the Tayside echocardiography database (>110 000 scans). we sought to assess the prognostic significance of mid-wall and infarct patterns of myocardial fibrosis in aortic stenosis.169 1. Abstract 169 Table 1 No LGE Number of patients Mean age yrs Documented CAD % Ejection fraction % Aortic valve area Indexed LV mass g/m2 Mortality rate (deaths / 1000 pt years) 49 64616 37 69613 1. 97 male) were followed up for 2.6) 15. UK.4 years. Subjects who remained asymptomatic had a significantly lower regurgitant fraction: 25. T Murigu. Its use in patients with aortic regurgitation should be encouraged. Edinburgh.56 to 0. Using late gadolinium enhancement.7* (104. 1. A Gulati. 168 b-BLOCKER THERAPY IMPROVES CLINICAL OUTCOMES IN PATIENTS WITH MODERATE TO SEVERE MITRAL REGURGITATION doi:10. Results A total of 4437 patients with moderate to severe MR (mean age 74 Â611 years. Cox regression model (adjusted for age. Hence.31 113. morbidity and mortality database for the population of Tayside. Abstract 169 Figure 1 Kaplan-Meier curves of cardiac mortality (left) and all cause mortality (right) according to pattern of LGE (A¼ No LGE. London. University of Dundee. Conclusions This large observational study suggests that BB therapy is associated with an improved survival and a lower risk of CV events in patients with moderate to severe MR. D H Elder.8* (90. Compared to those with no late gadolinium enhancement (n¼49). 72 underwent aortic valve replacement and 27 died. It has incremental prognostic value to ejection fraction and may provide a useful method of risk stratification in patients with advanced disease (Abstract 169 figure 1).368. p<0.9 years there were 2287 (51%) all-cause deaths and 2333 (52%) CV events.061. MR was categorised as functional in 2523 (57%) and organic in 1894 (43%) while 1324 (30%) were on BBs.031 <0. Those treated with BBs had a significantly lower all-cause mortality with an adjusted HR of 0. Results 143 patients (aged 68614 years.0001).0560. 2 Centre for Cardiovascular Sciences.005 169 MID-WALL FIBROSIS IS AN INDEPENDENT PREDICTOR OF MORTALITY IN PATIENTS WITH AORTIC STENOSIS doi:10.8%610.94 to 0. left ventricular dimensions and function. C¼ Mid-wall LGE).111 0. Patient follow-up was completed using the National Strategic Tracing Scheme. gender.2) 173.168 A Nadir. 1Royal Brompton Hospital. Methods The Health Informatics dispensed prescribing.5 cm2) underwent cardiovascular magnetic resonance with assessment of myocardial fibrosis by late gadolinium enhancement. UK 1 1 1 1 1 Introduction Predicting adverse clinical outcomes in aortic stenosis is challenging. S D Pringle.0001) and fewer CV events with an adjusted HR of 0. Late gadolinium enhancement (LGE) has been asso- A94 Heart June 2011 Vol 97 Suppl 1 . 105.0001 vs both the planned surgical group and the symptom progression group). F Alpendurado. 1S Prasad.5. cardiovascular (CV) history and concurrent CV medications) was used to assess the impact of BB therapy on all-cause mortality and cardiovascular events (CV death or hospitalisations).1136/heartjnl-2011-300198. Patients were categorised into absent. Experimental data have reported protective effects of beta-blockers (BBs) on myocardial function in MR suggesting that BB therapy may be beneficial in MR.8) 142.90. 0. University of Edinburgh. Dundee.35 (95% CI. the effect of BB therapy on clinical outcomes in MR has not been defined. Conclusion: Mid-wall fibrosis is an independent predictor of mortality in patients with moderate and severe aortic stenosis.99). 46% males) were identified.4%612. These observations needs to be confirmed in prospective studies and support the rationale for undertaking a future randomised clinical trial.7 Infarct LGE 40 70613 98 44618 0.BCS Abstracts 2011 with patients already planning to undergo surgery at the time of CMR scanning.03) and ejection fraction (HR 0.26 97. However.7 p Value e 0. C C Lang. Patients with an infarct pattern (n¼40) had a six-fold increase. p¼0. Mid-wall fibrosis (HR. Over a mean follow-up of 3.0060. 2D Newby.65 (95% CI 0.001 0.1136/heartjnl-2011-300198. left atrial diameter. p<0.9160.001 <0.1%) compared to the initially asymptomatic patients who developed symptoms or other indications for surgery (42. UK Background Volume overload seen in mitral regurgitation (MR) leads to neuro-endocrine activation including heightened sympathetic activity. 123. M G MacArtney. R Mohiaddin.9. J Pepper. 99. ciated with an adverse prognosis in a range of other cardiac conditions. 1D Pennell. Patients with a diagnosis of moderate or severe MR from 1993 to 2008 were identified. in this large observational study we investigated the impact of BB therapy on clinical outcome in patients with moderate to severe MR.16 to 24. 81 patients had coronary artery disease.69 to 0.6% (p<0.2 1 M R Dweck. Methods Between January 2003 and October 2008. A M Choy. which showed similar regurgitant fractions in the surgical group (mean 6SD: 45. univariate analysis revealed that patients with mid-wall fibrosis (n¼54) had an eightfold increase in all-cause mortality despite similar aortic stenosis severity and coronary artery disease burden.75.79 (95% CI 0. Conclusions CMR quantification of aortic regurgitation and LV volumes accurately predicts the progression to symptoms/surgery. p¼0. A D Struthers.01) were independent predictors of all cause mortality by multivariate analysis.56).

Echocardiography provided measurements of RVI. N Chandra.039 0. 103 WP) were assessed in 3 specialist cardiomyopathy clinics in South London.9% 7.2% 9.035 0.6% 11. A Zaidi. UK.967.7% 3. p¼0.7 40.8 39.5616. Current studies are based on predominantly Caucasian cohorts (white patients.534 0.1 17.552 0.5% 3.026 0. 3G Whyte. p¼0.1% 11.967.0% 0.270 0.6760.5% 23. Data in athletes and hypertensive patients indicate that black ethnicity is associated with a greater prevalence of repolarisation abnormalities on the ECG as well as a greater magnitude of left ventricular hypertrophy (LVH).20 0.9% vs 60.8% 33. which may represent the initial expression of HCM.0%) (p¼0.3 0.466. The greater prevalence of deep T wave inversions and T wave inversions in the lateral leads underscores the importance of further evaluation of black individuals with such ECG repolarisation abnormalities. A significant proportion of black patients exhibit concentric LVH. St. Black patients also tended to display more ST segment depression (50.281 0. BP) are not fully realised.038) and deep ($À0.0% vs 35. UK Purpose Hypertrophic Cardiomyopathy is a heterogeneous condition with variable phenotypic expression.170 N Sheikh.8% 1.445 0.0% 0.163 171 THE RIGHT VENTRICLE OF THE ENDURANCE ATHLETE: THE RELATIONSHIP BETWEEN MORPHOLOGY AND DEFORMATION doi:10.9% 9.864. has received less attention.071 0.364.8% 26.985 0.58 37. London. Methods Between 2001 and 2010. 5S Sharma.2 mV) T-wave inversions (69.1 0. A recent guideline paper from the American Society of Echocardiography (ASE) has provided a range for normal RV dimensions and functional deformation.9 vs 18.1136/heartjnl-2011-300198. Patients subject to therapeutic interventions potentially affecting repolarisation patterns were excluded. UK.8% 44.7 39.3% 30. Leeds.593 0. although this was not statistically significant.422 0.9% 3. M Papadakis.989 0.7% 5.44 23.2% 51.747 0.5 40.038 0. 4Leeds Teaching Hospitals NHS Trust. Relating to ECG repolarisation abnormalities.2260. and a similar diagnostic challenge with arrhythmogenic right ventricular cardiomyopathy (ARVC). 5St Georges University Hospital.469.364.1 61. RV length.3 44.1%) and apical (28. A recent paper also suggested that an RVOT dimension >36 mm or 21 mm/m2 is a major criterion for the diagnosis of ARVC and furthermore longitudinal RV deformation has been shown to be impaired in these patients.2% 69.27 1. 1K Birch.7% 55. 155 consecutive patients with HCM (52 BP.004).3% 17.3 44.363.066.265. p¼0. These guidelines suggest the RV inflow (RVI) should be <42 mm while the proximal outflow tract (RVOT) <35 mm. Liverpool.1160.2% vs 30.2% vs 51. 2R Shave.6% 39.2% 9.641 0.171 D Oxborough. S Sharma.3% vs 25.5% 34.851 0.787 0.8% 60.9% 53. London.5%.123 0.197 0. To provide normal athlete data for indices of RV strain (3) and strain rate (SR).18 0.8% 1. H Raju. highlighting the importance of defining the HCM phenotype in this ethnic group.1 mm.9% 76. 4N Artis. WP).2%.033 0.0% 7.480 0.269 0.8% 28.1 18.767 0.7% 9.0% 35. BP exhibited more T wave inversions in the lateral leads (76. University of Leeds. p¼0. 3K George.7%) hypertrophy compared to WP who exhibited more asymmetric septal hypertrophy (57.6% 1.1% 32. S Ghani. p¼0.1% 50.7% 13.5 62. WP had significantly more pathological Q waves (23. Leeds.1% 12.8% 5.6% 7. The impact of physiological conditioning on RV structure and function.7% 1. A 2D strain technique was utilised to provide indices of RV3 and systolic and diastolic SR.2% 28.9% 49.1 287.9% 5. RVOT and RV diastolic area (RVDarea).6% 50% 57.1617.991 0.868. UK 1 1 Introduction It is well established that endurance exercise results in cardiac adaptation including eccentric hypertrophy of the left ventricle which can complicate the differential diagnosis of the athletic heart from some cardiac pathologies that may pre-dispose to sudden cardiac death.004 white HCM (n[103) p Value cardiac evaluation including 12-lead ECG and echocardiography.864. In view of this. Black patients exhibited a similar magnitude of LVH compared to WP (17.035).8% vs 11. All subjects were either endurance runners or cyclists and were scanned at peak condition. George’s University of London.069).071). 2. The values for RVI A95 Heart June 2011 Vol 97 Suppl 1 . highlighting the diagnostic challenges in distinguishing HCM from hypertensive heart disease and physiological adaptation to exercise in black individuals. M Muggenthaler. 2UWIC.942 0.039). Methods and Results One hundred and two (102) endurance athletes (86 males and 16 females) with a broad age range (mean 6 SD age (range)¼36 6 11 (21e71) years) volunteered and were consecutively enrolled in the study.987 0.18 1.8% 46.9% 69. In contrast.BCS Abstracts 2011 170 ETHNIC DIFFERENCES IN PHENOTYPIC EXPRESSION OF HYPERTROPHIC CARDIOMYOPATHY doi:10. Conclusions Ethnicity appears to exert a significant effect on ECG and echocardiographic patterns in patients with HCM. 48.6%.1% 23.086 0. UK.5% 9. To provide a range of absolute values for RV dimensions in 102 endurance athletes as well as providing a range of data indexed for body surface area (BSA).66106. with more concentric (44.080 0. 3Liverpool John Moores University.66112.5% 82.069 0. Results Black patients revealed significantly different echocardiographic patterns of LVH. the aims of this study are twofold: 1. Cardiff. S Gati.6660.9 279.064 0.8% 31.9% 34. UK. therefore the phenotypic manifestations of HCM in individuals of African/Afro-Caribbean origin (black patients.0%.7% 35.7060.3% vs 9.443 0.1136/heartjnl-2011-300198.7460. All individuals underwent comprehensive Abstract 170 Table 1 Black HCM (n[52) Demographics Age of diagnosis (years) Gender (males) FH of HCM/SCD NYHA functional class III or IV Patients on treatment B-blockers Calcium antagonists Amiodarone Diuretics Disopyramide Intracardiac defibrillator in situ Echocanliographic characteristics Ao (mm) LA (mm) LVED (mm) mLVWTd (mm) LV mass (g) FS (%) E wave (m/s) A wave (m/s) E/A SAM LVOT gradient ¼ 30 mm Hg LVH pattern ASH Concentric Apical No hypertrophy Echocanliographic characteristics LVH (Sokolow & Lyon) Left atrial enlargement Pathological Q waves Left axis deviation Inverted T-waves T-wave inversions in V1eV4 T-wave inversions in inferior leads T-wave inversions in lateral leads Deep T-wave inversions ST-segment elevation ST-segment depression 25% 44.

862 (8. When indexed (ratio scaling) for BSA proximal RVOT ranged from 13 to 25 mm/m2 with 6% of the population meeting the major criteria for ARVC.65 l/s.76) 1. Results Iron II exposure significantly increases systolic Ca transient amplitude (mean increase 82. mean decrease 48. The same manoeuvre in in tempol delayed the onset of SACRE to 17.63) 2. which mediate oxidative damage.001). Conclusion RV dimensions in endurance athletes are higher than those proposed as “normal” and likewise may be consistent with the criteria for ARVC. Manchester.861. the effects of iron II were irreversible.065. Methods Single rat ventricular cardiomyocytes were loaded with fluo-3 to monitor intracellular Ca changes upon stimulation while bathed in control Tyrode solution and after adding ferrous iron (iron II). Proximal RVOT ranged from 26 to 49 mm with 40% of the population above the normal range. which empties SR Ca stores. 28% of the population had RVOT values greater than the proposed “major criteria” for ARVC. Sarcolemmal Ca extrusion rate was also significantly reduced upon iron II exposure (measured as the rate of fall of the caffeine response. We have previously found that iron exposure impairs cardiomyocyte Ca homeostasis. n¼9) and causes spontaneous arrhythmogenic Ca release events (SACRE). The onset of these Ca disruptions was significantly delayed in the presence of the ROS scavenger tempol (p<0.7%. Furthermore. UK. with the ROS scavenger Tempol.060. Peak RV3 ranged from À18 to À41% and peak RV SRS9 from À0. In contrast.87 to 3. Conclusions Our data show that iron II disrupts cardiomyocyte Ca handling.765.8 min (n¼7).03 (0. These changes corresponded with increased SR Ca content (mean increase 21. with increased susceptibility to arrhythmias and sudden death.6 min (n¼22) following iron II exposure. leading to SR Ca overload and SACRE.28 to 2. SACRE onset occurred after 6. Data are provided as mean6SEM. which is known to impact on systolic Ca release and spontaneous activity in cardiomyocytes.43 (À0. Iron is known to participate in the Fenton reaction to produce reactive oxygen species (ROS). 2University of Manchester. n¼8). Without tempol. Edinburgh.5360.05.8%.75 to À2. F R Millar.88) 1.61 (0.8621. Sarcoplamic reticulum (SR) Ca load and sarcolemmal Ca extrusion rates were estimated during exposure to caffeine. consistent with an overall gain of Ca by the cardiomyocyte. the cellular mechanisms responsible are unknown.54 N/A N/A N/A Indexed (ratio scaling) for BSA 1763 (13 to 25) mm/m2 2263 (15 to 30) mm/m2 4565 (32 to 61) mm/m2 12. These are the initiators of most fatal non-reentrant arrhythmias and cardiac sudden death in A96 Heart June 2011 Vol 97 Suppl 1 . Abstract 171 Table 1 Parameter RVOT (mm) RVDI (mm) RV Length (mm) RVDarea (cm2) RV 3 (%) RVSRS9 (l/s) RVSRE9 (l/s) RVSRA9 (l/s) RVSR E9 /A9 Mean ± SD (range) 3465 (26 to 49) 4465 (30 to 55) 9269 (70 to 110) 2665 (13 to 38) À2766 (À18 to À41) À1.49 to 7. Significance was tested using paired student t test and defined as p<0.1136/heartjnl-2011-300198. RV function in endurance athletes is preserved and therefore the role of RV strain imaging may provide additional diagnostic value in differentiating physiological from pathological adaptation.2560.7 to 17. could be cardioprotective in the presence of iron. as well as SACRE upon washout of iron II. n¼8). in cardiomyocytes not exposed to tempol.6) N/A N/A N/A N/A N/A 172 INCREASING ANTI-OXIDANT CAPACITY REVERSES IRON OVERLOAD MEDIATED DYSFUNCTION IN CARDIOMYOCYTES doi:10.BCS Abstracts 2011 ranged from 30 to 55 mm with 57% of the population having values greater than the normal range. increasing ROS scavenging reversed the increase in systolic Ca transient amplitude.060. consistent with normal ranges proposed by the ASE. respectively.75 to À2.25) ASE Normal Values <35 <42 <86 <25 À18 to À39 0.56 (0.5%.2560.8961.960.172 1 ´az.7 to 2. UK Abstract 171 Figure 1 Introduction Iron overload-cardiomyopathy (IOCM) is an increasing clinical problem worldwide.56 l/s). 1D T Baptista-Hon. We therefore tested the hypothesis that increasing the anti-oxidant capacity of cardiomyocytes. 70% of patients who receive compulsory blood transfusion die of IOCM. RV length ranged from 70 to 110 mm and RVDarea from 13 to 38 cm2 with values falling above ASE cut-offs in 69% and 59% of the population. 1M E Dı 1University of Edinburgh. The ROS scavenger tempol was used to dissect ROS-mediated pathways from the direct effects of iron II on Ca handling. This is mediated via inhibition of sarcolemmal Ca extrusion. RV diastolic deformation indices displayed marked individual variability with a dominant SRE9 (mean 6 SD¼2. Despite this enlargement.61 l/s) and smaller SRA9 (1. However. 2S C O9 Neill.

6 W (OR 8. Leeds. we have developed a new method of directly assessing the individual patient’s cardiac functional reserve through stress testing. and crucially rendering the effects reversible upon iron-washout.6 W and all non-pregnant women had PkCPO exceeding 2. 2N Lewis.766.005). Only a small proportion of the cardiac patients had PkCPO values lower than the 2. 2G Mason.1560.173 1 D Barker. 173 A GENERIC METHOD TO ASSESS THE ADEQUACY OF INDIVIDUAL MATERNAL CARDIAC RESERVE TO TOLERATE THE DEMANDS OF PREGNANCY AND LABOUR doi:10. The healthy controls had a mean peak CPO (PkCPO) of 3.1. Cardiac power output (CPO) was calculated as the product of CO and mean arterial pressure. This value was adopted for investigation as the minimum required for an average woman to cope with the circulatory demands of normal labour.1136/heartjnl-2011-300198. The majority of heart disease patients were able to achieve PkCPO values overlapping their healthy counterparts. Employing data from a previous study of haemodynamics during labour in healthy women. which can be safely undertaken during pregnancy. A composite endpoint including maternal death. p<0.0. A cutoff value of PkCPO 2.9860. NS). 1Liverpool Heart and Chest Hospital. emergency caesarean section for maternal distress and significant morbidities was determined. the mean CPO required during peak labour is 2. p¼0. 95% CI 1. Heart June 2011 Vol 97 Suppl 1 A97 . UK. Measurement of PkCPO allows pregnant patients to be further classified into those with adequate vs limited cardiac reserve.668.6 weeks) and 102 healthy pregnant women (mean age 31.6 W. Results All tests were performed without significant complications.6 W was identified as the lower limit for healthy women. and all asymptomatic (NYHA I) and low risk cardiac patients had PkCPO values similar to controls. To complement current evaluation.2 weeks) underwent maximal symptom-limited treadmill cardiopulmonary exercise testing. corresponding to that required for normal labour.6 W cutoff. fetal death.77 W.023). Women were significantly more likely to have uncomplicated pregnancy.169. Methods Fifty-one pregnant women with heart disease (mean age 30. Cardiac output (CO) was measured at peak exercise using the CO2 re-breathing method. The observed effects are partly due to iron IImediated oxidative damage. Pregnant mothers with and without heart disease were studied to test the hypothesis that pregnant cardiac patients who possess cardiac reserve equivalent to that of controls can tolerate the usual demands of pregnancy. whereas symptomatic pregnant women had significantly lower values (mean 3.71W. mean gestation 25. supplementary to existing risk stratification methods. These effects of tempol suggest a novel therapeutic target for the treatment of IOCM patients. mean gestation 25. Fifty-nine non-pregnant women (mean age 32.765.1 (range 20e41) years) were similarly tested and used as a control group. (range 19e41). 2Leeds General Infirmary. labour and puerperium.465. Liverpool. Most cardiac patients studied had PkCPO values comfortably above this cutoff. This was confirmed by the presence of a ROS scavenger delaying the onset of the effects of iron II. Conclusions Direct measurement of cardiac functional reserve capacity can be performed by maximal cardiopulmonary exercise testing with non-invasive assessment of PkCPO.8 to 37. Pregnant women in NYHA class I had PkCPO values indistinguishable from controls (mean 3.BCS Abstracts 2011 experimental models. UK Introduction Clinicians often feel apprehensive when managing pregnant patients with heart disease. labour and puerperium if able to achieve PkCPO>2.6 W.5 (range 21e42). 2L B Tan.0.7960.

A30 Bowater S. A5 Ayers L. A39 Aggarwal R. A59 Bapat V. A83 Baudoin F. A36 Clark C. A43 Ahsan AJ. A82 Alahmar A. A88 A98 Bastiaenen R. A5 Adams PC. A82 Bloomer LDS. A90 Borg A. A11 Cannon DT. A25 Behr E. A41. A3 Abidin N. A18 Baker S. A72 Crossman D. A61 Chico TJA. A84 Carre F. A58 Christiansen JP. A52 Birch K. A43 Cook SA. A93 d’Arcy JL. A56 Ball SG. A83 Bennett MR. A72. A3. A55 Beatt K. A60. A11 Blamire A. A70 Borg AN. A48. A45 Bellamy MF. A2. A77 Banerjee A. A64 Berry C. A72 Balmforth AJ. A34. A7 Banerjee R. A70 Bedell VM. A43 Chinchapatnam P. A52. A30 Danesh J. A50 Behan M. A78 Begg G. A92 Bonser RS. A35. A38. A86 Betts TR. A71 Chong E. A24. A57 Connelly K. A2 Braund PS. A24 Choudhury RP. A60. A62 Blake J. A49. A7 Barmby D. A96 Dall’Armellina E. A41 Bamforth SD. A42 Collerton J. A19 Cowie MR. A70 Abozguia K. A36. A79 Casey FA. A38 Behr ER. A7 Angelini G. A15 Anand A. A55 Bowen TS. A61 Ahmed R. A56 Begg GA. A80 Baumbach A. A10 Beadle RM. A94 Choy AMJ. A7 Cook DG. A72 Bell J. A28. A12. A78 Bland MB. A75 Artis N. A21 Barnes S. A38 Carrick D. A53 Cox RD. A68 Barsan A. A60. A92. A2. A1. A79 Chaubey S. A64 Camara O. A92 ´az Dı ME. A52 Chinnappa S. A80 Casadei B. A86 Begley D. A66. A1. A49 Barth J. A85 Boston-Griffiths E. A77 Biasiolli L. A61 Austin D. A73 Berry EL. A52. A9 Al Fakih K. A48 Borbas Z. A4 Corbett S. A16. A90 Calver A. A33. A62. A53 Alpendurado F. A97 Barker J. A40 Banerjee G. A16 Cotton J. A12 Damm E. A84. Abbas A. A90 Brown P. A89 Bryan L. A16 D’Arcy J. A75 Crean A. A91 Bhattacharya S. A19. A29 Brown BD. A74 Bostock J. A33. A15 Behar JM. A43 Das D. A41 Blundell N. A77 Cheng A. A63 Banerjee S. A27 Archbold A. A33 Bashir Y. A52 Curzen N. A46 Brickham B. A7 Banner NR. A68 Balakrishnan B. A70 Clarke B. A12 Channon KM. A7 Clack L. A85 Augustine D. A16 Behar J. A78 Arthur HM. A77 Braganza D. A75 Awan M. A41 Craig BG. A26 Clarke SC. A23 Alp NJ. A5 Appleby C. A33. A62 Chalmers RTA. A73 Clark D. A73 Arujuna A. A21 Blair E. A3 Chambers J. A70 Chowienczyk P. A95 Artis NJ. A78 Babar J. A52 Campbell M. A86 Aitma TJ. A93 Banypersad SM. A38. A22 Connolly S. A63 Aung N. A43 Chandra N. A41 Cook S. A58 Basavarajaiah S. A24 Bechar I. A41. A93 Christie J. A60 Caldwell JC. A56 Caplin JL. A64 Banning AP. A27 Chen C-M. A57 Chiribiri A. A41. A57. A81 Baliga V. A73 Cassar TE. A77 Brewster S. A21 Bleasdale RA. A24 Anroniades C. not the abstract number. A19 Clapp B. A16 Christofidou P. A51. A5 Cartwright EJ. A5 Arthur H. A60. A87. A36 Ala L. A91 Broadbent C. A43 Heart June 2011 Vol 97 Suppl 1 . A24 Cubbon R. A63 Baker CSR. A35. A62 Bijnens BH. A18 Ben-Nathan S. A68. A60 Barth JH. A23 Bull S. A55 Abu-Own H. A5 Avery P. A82 Bhabra M. A96 Barker D. A17 Baruah R. A60 Barrington S. A27 Alamgir MF. A42 Brewer A. A25 Adam Z. A2 Cleary N. A75 Casey M. A24 Bawamia BR. A79 Antoniou S. A46 Archbold RA. A46 Clesham G. A56 Braganca J. A32 Claridge S. A94 Amersey R. A32 Choy AM. A16 Carter J. A72 Buchanan L. A37 Blaxill JM. A60. A22. A19 Baptista-Hon DT. A41 Churchhouse AMD. A30 Codd V. A50 Aziz A. A13 Cruddas E. A8. A4 Akhtar M. A77 Chaudhry U. A92 Byrom R. A12. A88 Bewick AE. A23 Carr-White G. A30 Aggarwal S. A16 Calvert PA. A78 Cunliffe E. A40 Bhan A. A79 Alpendurada F.Author index The number next to the author indicates the page number. A87. A95 Channon K. A77 Brown AJ. A83 Bell D. A95 Blackman DJ.

A58. A9 Dixit A. A53 Hall A. A85 Glen E. A92. A5 Galloway S. A5. A36 Holbrook I. A20 Gosling OE. A34 Irwin RB. A75 Goodall AH. A49 Gordon J. A29 Eftychiou C. A65 Jackson C. A83 Joshi NV. A26 Debiec R. A41. A84. A68. A34 de Belder A. A95 George DA. A41 Deaton C. A17 Hawkins NM. A71 Ingram TE. A16 Ford I. A7 Frampton C. A13. A71 Deanfield JE. A34 Jamieson S. A62 Fox DJ. A49. A76 Grimwade P. A49 French AE. A52. A32 Hunter A. A12. A55 Gage M. A78 Gamble D. A10 Diab I. A90 Foo F. A63. A44 Heneghan C. A11 Francis DP. A13 Fox KAA. A88 Jones S. A76 Glen EA. A24. A31 Gallagher SM. A63 Francis JM. A16 Hodson J. A92 Guha K. A16 Eve S. A48 Engelen K. A94 Elder DHJ. A50. A36 Gray C. A30 Hawkins PN. A54 Davies JE. A41 Juli C. A63 Digby J. A53 Guilcher A. A51. A41 Gibbs SDJ. A52 Hancock J. A60. A95 Ghani S. A75 Hall DH. A90 Gasson A. A12 Finch S. A51. A81 Dworakowski R. A76 Hall JA. A1. A93 Frangi AF. A59 Hayward PA. A39 Haran H. A84. A13. A10. A12 Forfar JC. A38 Heart June 2011 Vol 97 Suppl 1 Flint J. A78 Jagger C. A81 Hussain S. A41 Densem CG. A11 Diesch J. A37 Donald A. A76 Englyst N. A7 Garden OJ. A32 Donald AE. A46 Flather M. A73 Forfar C. A43 Gray H. A31 Jain AK. A63 Davison BJ. A92 Fath-Ordoubadi F. A78. A23 Hughes A. A64 Gordon B. A61 Foley C. A7 Graham TR. A28. A50 Dweck M. A10 Joshi S. A86 Gilchrist J. A60. A13. A7 Fox KF. A9 Guttmann OP. A45. A47 Fairbairn TA. A76 Gopalan D. A10 Davies MJ. A68 Iles-Smith H. A60 Holroyd EW. A83 Gallagher S. A3. A71 Ivetic A. A25. A89 Jones D. A11 Imrie H. A40 George K. A37 Hall D. A75 Gosling O. A13 Guttmann O. A78 Gale CP. A42 Goodship J. A78 Dawson A. A90 Fox K. A45 Edwards R. A79 Jeilan M. A93 Griffin HR. A68. A3 Garratt CJ. A81 Ebbs D. A25. A62 Haq IU. A41 Hall ASH. A59 Durham N. A70 Ishida M. A90 Davies DW. A66 Francis J. A80 Horne A. A52 Fraser AG. A5 Jones DA. A10 Jamshidi Y. A76 Hoye A. A66 Hunt J. A35. A60. A73 Douglas-Hill C. A83 Kahn M. A15. A65 Graham A. A59 Gillivray TJMac. A37 Gallagher M. A82 Harwood SM. A24 Hamid S. A53 Dhillon OS. A75. A41 Donin A. A70 Greenwood JP. A3 Gage MC. A14 Davidson J. A92 Eccleston D. A94 Dwivedi G. A78 Indermeuhle A. A5 De Silva K. A60 Hunter RJ. A8. A13 Hall AS. A45 Gibbons SM. A19 Drury-Smith M. A13 Foley JRJ. A9. A3. A31. A13. A2 Dent H. A49 Harrington DW. A15. A41 Doolin O. A6 Davis E. A3 Dweck MR. A81 Dick AJ. A60 Gale CPG. A49 Hughes AD. A50. A89 Frenneaux MP. A72. A66. A9 Hedger M. A42 Dickens C. A58 Ellins E. A26 Dixon G. A19 Duckett S. A89 Hosmane S. A11 Ferguson E. A1. A7. A37. A75. A85 Duckett SG. A15 James PE. A61. A85 Hamid SG. A5 Ferreira V. A37. A18. A94 Joysurry D. A30. A77 Iyengar S. A24 Indermuhle A. A91 Earley MJ. A76 Goodship JA. A73 Farmer AJ.Author index Das M. A16 Denvir MA. A59 Ginks M. A75. A78 A99 . A37. A28 Gulati A. A41 Emin A. A17. A34 Fraser D. A34. A26 Elder DH. A13. A31 Haga KK. A5 Hall R. A21. A89 Johnson T. A59 Gierula J. A31. A21 Ekker SC. A40 Heymans S. A16 Greaves M. A78 El-Omar M. A30 Jones MA. A62. A6 Gibbins A. A94 Gunn J. A52 Dungu J. A82 Gati S. A15. A17. A45 Dobrzynski H. A8. A84. A24. A15 Graham C. A84 Davidson C. A4 Jayaram R. A73. A22 Dick KJ. A95 Gholap NN. A83 Davies J. A49 Hegab Z. A1. A19 Hards R. A70 Dinh DT. A52 Gill PS. A3 Gillmore JD. A35 Davidson NC. A26 Freemantle N. A57 Jain A. A19 Handa A. A60 Dutka DP. A22. A73 Gill JS. A31 Jones JD. A4 Doherty PD. A77 Hobson A. A9. A45 de Belder MA. A38 Edmunds L.

A13 Mole G. A74. A91 Lundmark P. A81 Lim PB. A6 Kilcullen N. A57 Kervio G. A7 Macnab A. A11 McKeown PP. A13. A3 MacGowan G. A89 Kylintireas I. A51. A70 Kyriacou A. A6 Menon A. A25. A95 Muir DF. A27 Mavroudis CA. A48. A52 Kapur A. A66 McCann GP. A80 Mohammed TMA. A5. A11 Mascaro J. A37 Lewinter CL. A23 Khan N. A68. A25 Kooner J. A37 Ludman A. A22. A92. A17. A50 Khan MF. A83 Malik N. A93 Nadir A. A70 Nevill AM. A91 MacDonald ST. A93. A7 Mitchell AG. A44 Mamas MA. A24. A78 Kearney MT. A78 Keavney BD. A26. A20 May S. A9. A51. A68. A58. A62. A53 McEntegart MB. A74 Mills NL. A91 Moraldo M. A44 Mohiaddin R. A81 Khunti K. A15. A43 Kotecha D. A90 Morgan-Hughes G. A58. A43 Mcclean DR. A50. A19 Khoo CW. A41. A40 Morrison ML. A64 Mittal TK. A62 Kenny A. A76 Kellman P. A48 Lim HS. A28 Margulescu A. A80 Mulder B. A60. A66. A62 Neubuer S. A80 Lazdam M. A73 McGill LA. A68 Majumder B. A20 Makri L. A34 Markl M. A55 Lewandowski AJ. A90 Newton T. A3 McLenachan JM. A13 Mayet J. A97 Mather AN. A73 Mathur A. A37. A5 Mukhopadhyay D. A21 Llewellyn-Griffiths H. A94 Nadra I. A24 Kettle AJ. A75 McKillop G. A12 Lindsay AC. A81 Little A. A25 Karamitsos TD. A5. A13 Morton G. A15. A28 Loh PH. A55 Kuijer JPA. A66. A75 Leyva F. A25. A46 Khogali S. A69. A3. A72. A94 Mohiddin S. A65 Morrell C. A84. A68. A68. A1. A37. A60. A12 Karim R. A42 Ma Y. A63. A68. A3. A23 Lovell MJ. A37 Kelly P. A36 Masi S. A36 Metcalfe K. A85 MacArtney MG. A66 Moreton N. A61. A82 Kumar D. A43 Muckett PJ. A35 Macgillivray K. A37. A10 Nayar V. A25 McGowan L. A49 McDonagh T. A29 Murdoch CE. A92. A12 Khattar R. A19 Khimdas K. A46 Liu A. A89 A100 Heart June 2011 Vol 97 Suppl 1 . A76 Mahadevan V. A77 MacDonald TM. A62 Marshall CJ. A58 Mant D. A2 Mehta P. A94 Newby DE. A96 Miller C. A66. A56 Murigu T. A38 Krishnamoorthy S. A75. A21 Malcolme-Lawes L. A63 Leadbeater P. A60 Kearney M. A50. A71 Muckett P. A5. A92 Marber M. A14 Monaghan M. A9. A5 Lowdell M. A75. A57. A26 Nallaratnam M. A40 New G. A7 Newman D. A12 Kelly B. A19 Macgilivray TJ. A97 Lewis RJ. A35 Myerson SG. A44. A41. A29 McCusker CG. A24 Morton GDJ. A39 Kanagaratnam P. A90 Khan S. A73 McCormick LM. A76 Knight C. A64 Moccata T. A93 Karia N. A94 MacCarthy P. A75 McDiarmid A. A59 McCarthy MI. A63 Leisa RA. A61 Lip GYH. A37. A59. A21 McMahon M. A53 Neubauer S. A12. A59 Lang CC. A57 Kirkwood T. A9. A26 Khawaja MZ. A83 Kapetanakis S. A3 Kaier T. A83 Kearney L. A83 Lindsay A.Author index Kahn MB. A51. A62 Ling HZ. A39 Kharbanda RJ. A69 Kuker W. A75 McNab D. A20 Lucas A. A66. A80 Leon FL. A53 Musameh MD. A85 Mehta RL. A77 Murgatroyd SR. A75 Manisty C. A8 Morrice D. A62. A26 Maher A. A57 Klaassen S. A26. A76 Mullen LJ. A30 Kemp I. A62 Kulanthaivelu R. A13 Leeson P. A70 Neyses L. A57. A75 Morton AC. A84. A90 Kesavan S. A37 Lewis N. A35. A60 Keavney B. A40 Newman W. A15. A89 McCarthy CA. A80 Ng GA. A42 Ness A. A8 Kingston A. A65 Lockie TPE. A41 Mamasoula V. A38 Newby D. A19 Mahmod M. A66 Lachmann HJ. A9 Ludman PF. A93 Neubauer SN. A27 Kemp S. A31 Knight CJ. A73 Murray SA. A11 Mckenzie JL. A38 Kerzin-Storrar L. A76. A12. A41 Mason G. A62. A94 Langrish JP. A50. A63 Lewin BL. A31 Kennedy J. A22 Mamas M. A11 Khan FZ. A19 Nagel E. A62. A41. A49 MacLeod M. A81 Krum H. A92. A94 Murphy A. A35. A46 Kundu S. A70 Lee KK. A7 Lees B. A50 Manisty CH. A11 Mohamed TMA. A31 Mavroudis C. A13. A31 Kapur AK. A54 Loader R. A70 Miller CA. A50 Nelson CP. A11 McClure J. A73 McGeoch R. A4 Muggenthaler M. A16 Lee JM. A11 Narayan HK. A38 Kuehl M. A90 Millar FR. A3 Larsen K. A71 Nair S. A33.

A2. A49 Palomino-Doza J. A86 Padley S. A79 Rekhraj S. A72 Paul GA. A95 Pabari P. A49 Postma A. A71 Schwartz R. A72 Nicolson WB. A95 Sheikh N. A78. A84 Poole R. A1. A87 Salaheen D. A51 Sayer J. A84. A49 Simpson I. A91 Shah NH. A33 A101 . A88 Rahman T. A81 Rider O. A88 Raju H. A84 Shetty A. A80 Simon A. A17 Rudd JHF. A71 Perry R. A70 Rogers C. A76 Heart June 2011 Vol 97 Suppl 1 Prasad S. A75 Panayotova R. A68 O’Donnell M. A60. A15 Rathod KS. A89 Shepherd EJ. A54 Simari RD. A10 Nicol E. A36 Palmieri V. A64 Oceandy D. A33. A38. A41. A30 Sicard P. A35 Rhode K. A70 Pennell D. A70 Shome J. A84. A9. A53 Sharma S. A92 Prescott M. A71 Rees I. A15. A92 Pitts-Crick J. A22. A59 Saul A. A53. A33. A48 Sandilands AJ. A49 Robson MD. A52 Patel P. A52. A25 Smith J. A52. A28 Sim V. A49. A2 Schotten U. A12. A75 O’Sullivan M. A77 Schofield PM. A60 Peebles C. A22 Payne AR. A62. A52 Shah A. A83 Petersen SE. A43 Salukhe TV. A38. A79 Schueler S. A63.Author index Ng LL. A4. A23 Ordoubadi F. A66 Padgett HC. A63 Popov AF. A50 Pye M. A95 Shelton RJ. A61 Oldroyd K. A52 Razvi NA. A31. A30 Perry RA. A95 Shave R. A54 Russell SJ. A46 Roughton M. A17 Qureshi N. A75 Snell KIE. A64 Panoulas V. A27 Peters NS. A43 Semple SI. A67 Russell S. A84. A85 Shi WY. A55 O’Doherty M. A81 Schlindwein FS. A56 Rothman A. A28. A89 Schmitt M. A69 Redgrave R. A23 Shantsila E. A85 Richards JMJ. A95 Rajwani A. A58. A65 Rooney SJ. A94 Perera D. A75 Pinney JH. A16 Sammut E. A75 Sattianayagam P. A35. A49 Norrie J. A72 Spath N. A62 Petrie MC. A78 Redwood S. A8. A19. A26 Oriolo V. A11 Rogers CA. A41. A33. A76 Panicker MG. A4 Prehar S. A19 Singhal A. A30 Schilling RJ. A59 Pitcher A. A24 Siebes M. A24. A74 Schneider JE. A12. A50. A41 Owen J. A24. A33. A15 Rawling A. A3 Rathod B. A31 Rathod K. A94 Penswick A. A70 Sadarmin PP. A7 Shah AJ. A28 Roobottom C. A73 Pearson IR. A94 Pravanec M. A85 Somauroo J. A95 Parameshwar J. A7. A45. A89 Parry G. A83 Rusk RA. A38. A47 Ormerod OO. A54 Rossiter HB. A2 Shardey GC. A41 Rueckert D. A92 Prendergast BD. A2 Raybould A. A48 Simon AR. A8. A17 Rana B. A3 Sermesant M. A62. A33. A22. A30 Nijjer SS. A5 Showkathali R. A83 Samani NJ. A48 Rogers T. A31 Rathod KR. A55 Sabharwal NS. A55 Reid CM. A48 Parker C. A51. A73 Plummer CJ. A60 Oxborough D. A75. A70. A68. A72 Pagano D. A10 Qureshi AC. A69 Sohal M. A96 Obaid DR. A49 Schuster A. A73 Robinson N. A20. A46 Pepper J. A31. A78 Smith JA. A53 O’Sullivan JJ. A45 Pringle SD. A70 Rinaldi CA. A31 Somers K. A64 Rudnicka AR. A2 O9 Neill SC. A49 Pashaei A. A85 Razavi RS. A73 Sayan S. A45. A27 Rampat R. A9 Sneddon L. A89 Plein S. A11 Richards T. A72. A38 Papadakis M. A36 Rose H. A15 Rathod VS. A17. A9 Reid J. A77. A67 Rapala A. A37. A94 Pugh PJ. A13 Sanderson JE. A9 Shirodaria C. A28. A38 Ray KK. A70 Owen CG. A83. A39 Smith EJ. A61 Richmond L. A46. A16 Nyawo B. A53 Reilly S. A84. A89 Nightingale CM. A3 Rakhit RD. A58 Pabari PA. A82 Paterson E. A36 Rolandi C. A38. A63. A9 Sharma R. A73 Oliver M. A78 Pierscionek T. A37 Sinha M. A16 Singh R. A13. A68. A50 Rawlins J. A87. A42 Sambu N. A30 Pierret CK. A41 Nijjar M. A76 Rajappan K. A85 Ring L. A54 Oliver RM. A15. A3 Richards M. A21 Shepherd C. A77 Sehmi J. A63 Shah AM. A25 Sammut EC. A29 O’Callaghan P. A80 Prendergast B. A7 Patterson C. A67 Robb SD. A41 Rashid S. A41 Pretsell G. A16 Oldroyd KG. A59 Shapiro LM. A21 Sorbron S. A73 Pettit S. A31. A80 Okonko DO. A25. A51. A54 Razavi R. A47 Sivananthan UM. A89 Sands AJ. A17 Skinner JS. A84 Shetty AK. A60 Quinn PA. A48. A13 Rothman M.

A22 Tagney J. A31 Wilkinson S. A35. A58 Topf A. A33. A26 Witte KK. A4 Williams C. A92 Suttie JJ. A49 A102 Heart June 2011 Vol 97 Suppl 1 . A77 Yuldasheva N. A29 Westwood M. A59 Whincup PH. A58. A89 Staniforth AD. A41 Whinnett Z. A89 Tai ES. A3. A1. A68 Sutton AGC. A79 Vile RG. A82 Venables P. A43 Tan HL. A86 Walker S. A75 Wright GA. A54. A8 Waldron ZL. A69 Vanhoutte D. A51 Wilson IC. A41 Tooze P. A5 Syvanen AC. A75 Tan LB. A58 White J. A6. A65 Strauss BH. A88 Woodcock T. A55 Yu B. A62 Wragg A. A60 Watson OJ. A10 Stables RH. A3 Williams P. A60 Wheatcroft S. A78 Wheatcroft SB. A23 Unsworth B. A51 Whinnett ZI. A73 Ungvari T. A45. A10 Struthers AD. A45 Yousaf F. A48 Thomas M. A29 Templeton C. A62. A14 Watson J. A50 Viswambharan H. A61 Wells TA. A9. A17 Yellowlees D. A74. A25. A60. A20 Surr J. A25. A61 Thompson CA. A4 Warner T. A66 Van den Bruel A. A89 Stegemann B. A70 Strain WD. A91 Wenzelburger FWG. A78 Suresh V. A56. A31. A21 Whelan CJ. A66 Suttie J.Author index Sporton S. A69. A60. A34. A42 ¨ Szwejkowski BR. A36 Wilson K. A20 Verheule S. A24. A87. A3 Sutaria N. A80 Virdee MS. A73 Wordsworth BP. A55 Williams M. A78 Tsui S. A3. A60 Wong KCK. A62 Wechalekar A. A13. A46 Weissert S. A83 Ware JS. A40 van Eeden FJ. A75 Topf AL. A25 Tilling LM. A23 Thomas G. A35. A86 Woldman S. A89 Thomas HE. A34. A59 Weerackody R. A76 ¨ Taggu W. A78 Yusuf S. A86 Steadman CD. A95 Zaman A. A97 Tan YT. A27 Stafford PJ. A43 Watt H. A75 Thackray S. A21 Topf A. A80 Zych B. A19 Wilson SJ. A5 Wheatcroft AC. A22 Wright RA. A77 Veasey RA. A1. A3. A76 Watson D. A7 Wallace W. A35 Ward D. A57. A1. A2. A58. A72 Zhang W. A43 van Rossum AC. A89 Zaidi A. A9 Yaqoob MM. A15. A81 Taylor R. A48 West NEJ. A3 Wang WYS. A53 Yeo Y. A34 Williams LK. A16 Wassef N. A47 Wendler O. A84 Thomas HL. A20 Wiper A. A60 Whyte G. A28. A57 Yousef ZR. A19. A48 Tayebjee M. A78 Viswanathan K. A59 Waterworth P. A75 Townend J. A39 Willson K. A19 Young S. A63. A49 Yap CH. A26 Williams R. A5 Wrightson N. A94 Sukumar P. A5 Swanson NM. A32 Tomaszewski M. A31 Wren C. A60. A46. A22 Struck J. A15. A34 ten Dijke P. A43 Young C. A48 Twomey D. A47. A49 Stoll VMS. A10. A84 Tzemos N. A72 Woodward R. A81 Squire IB. A95 Wicks E. A41. A43 Zi M.