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JC1009

JC1009

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JOURNAL WATCH (AND ITS DESIGN) IS A REGISTERED TRADEMARK OF THE MASSACHUSETTS MEDICAL SOCIETY.AN EDITORIALLY INDEPENDENT LITERATURE-SURVEILLANCE NEWSLETTER SUMMARIZING ARTICLES FROM MAJOR MEDICAL JOURNALS. ©2010 MASSACHUSETTS MEDICAL SOCIETY.ALL RIGHTS RESERVED. DISCLOSURE INFORMATION ABOUT OUR AUTHORS CAN BE FOUND AT
http://cardiology.jwatch.org/misc/board_disclosures.dtl
Bystander CPR: Chest Compression Aloneor with Rescue Breathing?
 A randomized trial shows no differencein adult patient outcomes with the twoapproaches.
A previous nonrandomized study showedimproved outcomes from adult cardiac ar-rest with compression-only cardiopulmo-nary resuscitation (CPR) compared withconventional CPR (
 JW Cardiol 
May 2007,p. 44, and
Lancet 
2007; 369:920). Now, re-searchers compared outcomes with the twomethods in a randomized study of consecu-tive 911 calls for cardiac arrest to threeemergency medical services systems (2 inWashington State and 1 in London). Afterdetermining patient eligibility (uncon-scious, not breathing normally, bystanderCPR not already under way), dispatchersrandomly assigned patients to chest com-pression only or conventional CPR andprovided instructions to bystanders abouthow to perform the assigned method. Pa-tients who were younger than 18 years orwho had arrest because of trauma, drown-ing, or asphyxiation were excluded. Duringthe study period, which ranged from 3 to 5years at the three sites, 1941 patients wereenrolled.No significant differences were notedbetween the chest-compression–only andconventional CPR groups in rates of sur- vival to hospital discharge — the primary outcome — (12.5% and 11.0%) or favor-able neurological status at discharge (14.4%and 11.5%). Prespecified subgroup analysisof patients with cardiac causes of arrestshowed no significant difference inoverall survival rate between the chest-compression–only and conventionalCPR groups (15.5% and 12.3%) but asignificant improvement in the rate of neurologically favorable survival in thechest-compression–only CPR group(18.9% vs. 13.5%).
COMMENT
The finding that chest compression alone isnot inferior to chest compression plus res-cue breathing is important, because doingaway with breathing might increase theprevalence of bystander CPR. This simplertechnique should be adopted for bothbystanders and basic-level prehospital pro- viders. The authors note that the findingfrom the subgroupanalysis should prompt research in“targeted application of type-specificCPR.”
 — J. Stephen Bohan, MD, MS,FACP, FACEP,
 Journal Watch EmergencyMedicine
Rea TD et al. CPR with chest compression alone or with rescue breathing.
N Engl J Med
2010 Jul 29;363:423.
CPR: Conventionalor Compressions Only?
Survival rates at 30 days are similar in patients with out-of-hospital cardiac arrest who receive either type.
A growing body of evidence indicates thatchest compressions alone are as effective asconventional cardiopulmonary resuscitation(CPR) for out-of-hospital cardia arrest inadults (see previous article,
N Engl J Med 
 2010; 363:423;
 JW Cardiol 
May 2007, p. 44;and
Lancet 
2007; 369:920).In a prospective national study, re-searchers in Sweden compared outcomesin patients older than 8 years who experi-enced witnessed out-of-hospital primary cardiac arrest (not from trauma, airway obstruction, drowning, or intoxication)and underwent chest compression–only CPR or traditional CPR by bystanders.Dispatchers randomly assigned patientsto one of the two methods and instructedbystanders about how to perform theassigned method.Of 3809 calls to dispatchers from 2005to 2009 for patients with suspected cardiacarrest, 1828 met inclusion criteria and 1276with complete data were included in theprimary analysis. The standard-CPR andchest compression–only groups did not dif-fer significantly in the rate of survival at 30days (the primary endpoint; 7.0% and 8.7%)or rate of survival at 24 hours. Subgroupanalysis by age, sex, location of arrest, time
SUMMARY & COMMENT
Bystander CPR: Chest CompressionAlone or with Rescue Breathing? .........................69CPR: Conventional or Compressions Only? ............69Improving Outcomes of Cardiac Arrest:Don’t Forget About CPR! .........................................70Microvascular Outcomes in the ACCORD Trial .....70Retinopathy in the ACCORD Trial ..............................71Blood Pressure Control in Patientswith Diabetes and CAD ...........................................71Self-Management of HypertensionOutperforms Usual Care .........................................72A New, but Not Yet Approved,Weight Loss Drug .....................................................72HDL and Cardiovascular Risk in thePresence of Very Low LDL......................................72Adherence to CardiovascularPerformance Measures in Outpatients ...............74Allopurinol for Chronic Stable Angina? ...................74Antibiotic-Induced Hyperkalemia andRenin-Angiotensin–System Inhibitors.................74Treating Heart Failure in Hospitalized Patients:How Are We Doing? ................................................75Is Exercise Testing Necessary to AssessDegenerative MR? ........................................75Multivessel Interventions for Stable STEMI:Still a No-Go! .............................................................75Why Don’t ICDs Prevent SCDAfter Recent MI? ......................................................76
FEATURE
Diagnosing Acute Coronary Syndromes:The Troponin Conundrum........................................73
CONTENTS
CARDIOLOGY
September 2010 Vol. 16 No. 9
From the publishers of 
The New England Journal of Medicine
 
to EMS response, and initial rhythm simi-larly revealed no differences in outcome.
COMMENT
Rescue breathing in out-of-hospital by-stander CPR does not seem to improvesurvival compared to chest compressionsalone, and, given its drawbacks — difficultto perform and potential transmission of infection — it should be abandoned.
 — J. Stephen Bohan, MD, MS, FACP,FACEP,
 Journal Watch EmergencyMedicine
Svensson L et al. Compression-only CPR or standard CPR in out-of-hospital cardiac arrest.
N Engl J Med
2010 Jul 29; 363:434.
Improving Outcomes of CardiacArrest: Don’t Forget About CPR!
The 2005 AHA resuscitation guidelines,which emphasize high-quality CPR, havehad a positive effect.
In the late 1990s and early 2000s, many predicted that automated external defi-brillators would markedly improve car-diac arrest outcomes; unfortunately, thesehopes were not realized. In 2005, theAmerican Heart Association publishedresuscitation guidelines reemphasizingthe importance of circulatory supportwith properly performed chest compres-sions in addition to defibrillation. Changesfrom previous recommendations includeda compression-to-ventilation ratio of 30:2, ventilation at
10 breaths per minute, anda more-vigorous compression technique.To evaluate the effects of the new guide-lines, investigators compared outcomes in1605 cardiac arrest patients treated ac-cording to the 2005 guidelines and 1641controls treated before guideline imple-mentation in five U.S. emergency medicalservices (EMS) systems.Age, sex, rates of bystander cardio-pulmonary resuscitation (CPR), and timefrom 911 call to arrival of EMS personneldid not differ significantly between the twogroups. The rate of survival to hospital dis-charge was significantly higher in patientstreated after guideline implementationthan in controls (13.1% vs. 10.1%). In pa-tients with ventricular tachycardia or fib-rillation, the rate of survival to dischargewas 32.3% and 20.0%, respectively. Neuro-logical function was also significantly im-proved in survivors treated according to2005 protocols, compared with controls.
COMMENT
Increased emphasis on cardiopulmonary circulation has improved outcomes of car-diac arrest. Yet further improvement islikely to be possible, not only in survivalbut in survival with good neurologicalfunction. The path to improvement will bemultifactorial, including higher rates andquality of bystander CPR and improvedpostarrest treatment.
 — Mark S. Link, MD
 Aufderheide TP et al. Implementing the 2005 American Heart Association Guidelines improvesoutcomes after out-of-hospital cardiac arrest.
Heart Rhythm
2010 Apr 24; [e-pub ahead of print]. (http://dx.doi.org/10.1016/j.hrthm.2010.04.022)
Microvascular Outcomesin the ACCORD Trial
Intensive glycemic control did not lower theincidence of microvascular adverse outcomes.
In the ACCORD trial, 10,000 patients withtype 2 diabetes (mean age, 62; average du-ration of diabetes, 10 years) were random-ized to receive intensive or standard glyce-mic control; choice of antidiabetic agentswas individualized. The main purpose of ACCORD was to determine whether inten-sive treatment (target glycosylated hemo-globin [HbA
1c
] level,
6%) improved car-diovascular outcomes. The trial was haltedafter an average follow-up of 3.5 years,when overall and cardiovascular mortalitwere significantly higher with intensivethan with standard treatment (
 JW Cardiol 
 Jul 2008, p. 53, and
N Engl J Med 
2008;358:2545). Now, the researchers presentmicrovascular outcomes.The principal composite microvascularoutcome was end-stage renal disease, riseof serum creatinine to >3.3 mg/dL, or needfor photocoagulation or vitrectomy to treatretinopathy. This outcome occurred in simi-lar proportions of patients in the intensiveand standard treatment groups, both duringthe study itself (9%) and after 1.5 additionalyears of follow-up (11%). Although inten-sive treatment appeared to slow the progres-sion of neuropathy, the incidence of a com-posite endpoint that included neuropathy (along with nephropathy and retinopathy)remained similar between groups. Somesecondary endpoints (e.g., incident albu-
EDITOR-IN-CHIEF
Harlan M. Krumholz, MD, SM,
Harold H. Hines, Jr.,Professor of Medicine, Section of CardiovascularMedicine, Yale University School of Medicine,New Haven
EXECUTIVE EDITOR 
Kristin L. Odmark
Massachusetts Medical Society
DEPUTY EDITOR 
Howard C. Herrmann, MD,
Professor of Medicine,Director, Interventional Cardiology and CardiacCatheterization Laboratories, University ofPennsylvania Medical Center, Philadelphia
ASSOCIATE EDITORS
JoAnne M. Foody, MD,
Director, CardiovascularWellness Center, Brigham and Women’s Hospital,Boston
Joel M. Gore, MD,
Edward Budnitz Professorof Cardiovascular Medicine, University ofMassachusetts, Worcester
Mark S. Link, MD,
Associate Professor of Medicine,New England Medical Center and Tufts UniversitySchool of Medicine, Boston
Frederick A. Masoudi, MD, MSPH,
Division ofCardiology, Denver Health Medical Center andAssociate Professor of Medicine, University ofColorado at Denver
Beat J. Meyer, MD,
Associate Professor ofCardiology, University of Bern; Chief, Division ofCardiology, Lindenhofspital, Bern, Switzerland
CONTRIBUTING EDITORS
 William T. Abraham, MD,
Professor of Medicine,Chief, Division of Cardiovascular Medicine,The Ohio State University Heart Center, Columbus
Hugh Calkins, MD,
Professor of Medicine andDirector of Electrophysiology, The Johns HopkinsHospital, Baltimore
FOUNDING EDITOR 
Kim A. Eagle, MD,
Albion Walter Hewlett Professorof Internal Medicine and Chief of ClinicalCardiology, Division of Cardiology, University ofMichigan Medical Center, Ann Arbor
MASSACHUSETTS MEDICAL SOCIETY
Christopher R. Lynch,
Vice President forPublishing;
Alberta L. Fitzpatrick,
Publisher
Betty Barrer, Christine Sadlowski, Sharon S.Salinger,
Staff Editors;
Kara O’Halloran,
CopyEditor;
Misty Horten,
Layout;
Matthew O’Rourke,
 Director, Editorial and Product Development;
Robert Dall,
Editorial Director;
Art Wilschek,Christine Miller, Lew Wetzel,
Advertising Sales;
 William Paige,
Publishing Services;
Bette Clancy,
 Customer ServicePublished 12 times a year. Subscription rates peryear: $119 (U.S.), C$166.67 (Canada), US$165 (Intl);Residents/Students/Nurses/PAs: $69 (U.S.), C$96.19(Canada), US$80 (Intl); Institutions: $219 (U.S.),C$256.19 (Canada), US$230 (Intl); individual printonly: $89 (U.S.). Prices do not include GST, HST,or VAT. In Canada remit to: Massachusetts MedicalSociety C/O #B9162, P.O. Box 9100, Postal Station F,Toronto, Ontario, M4Y 3A5. All others remit to:
Journal Watch Cardiology,
P.O. Box 9085, Waltham,MA 02454-9085 or call
1-800-843-6356
. E-mailinquiries or comments via the
 
Contact Us page at
JWatch.org
. Information on our conflict-of-interestpolicy can be found at
JWatch.org/misc/conflict.dtl
70
CARDIOLOGY
Vol. 16 No. 9
 
minuria) occurred less often with intensivethan with standard therapy.
COMMENT
In ACCORD, intensive glycemic controldid not lower the incidence of a compositeendpoint of advanced microvascular ad- verse outcomes. When this finding is con-sidered against the background of excessmortality noted in the intensively treatedgroup, a target HbA
1c
level of 6% clearly isnot appropriate for patients like those en-rolled in ACCORD.
 — Allan S. Brett, MD,
 Journal Watch General Medicine
Ismail-Beigi F et al. Effect of intensive treatmenof hyperglycaemia on microvascular outcomesin type 2 diabetes: An analysis of the ACCORDrandomised trial.
Lancet
2010 Aug 7; 376:419.
Retinopathy in theACCORD Trial
Findings from the ACCORD Eye Study arenot straightforward.
In the ACCORD study of patients withtype 2 diabetes (mean age, 62; averageduration of diabetes, 10 years), intensiveglycemic control led to excess mortality and did not lower the incidence of adversecardiovascular events (
 JW Cardio
Jul 2008,p. 53, and
N Engl J Med 
2008; 358:2545).Moreover, in the ACCORD Lipid andBlood Pressure substudies, neither fenofi-brate nor intensive antihypertensive thera-py resulted in fewer adverse cardiovascularoutcomes (
 JW Cardiol 
Apr 2010, p. 29, and
N Engl J Med 
2010; 362:1563 and 1575).Now, ACCORD researchers presentretinopathy outcomes in 2856 patients. Theprimary endpoint was a 3-step change on a17-step retinopathy scale (determinedfrom serial retinal photographs) or devel-opment of proliferative retinopathy requir-ing photocoagulation or vitrectomy. A sec-ondary outcome was moderate vision losson a visual acuity chart. Findings at 4 yearswere as follows:Intensive glycemic therapy (vs. stand-ard therapy) significantly lowered theincidence of progressive retinopath(7.3% vs. 10.4%) but not vision loss(16.3% vs. 16.7%).Fenofibrate plus simvastatin (vs. sim- vastatin alone) significantly loweredthe incidence of progressive retinopa-thy (6.5% vs. 10.2%) but not visionloss (16.0% vs. 15.2%).Intensive antihypertensive therapy (vs.standard therapy) did not lower the in-cidence of either progressive retinopa-thy or vision loss.
COMMENT
Intensive glycemic control and fenofibratelowered the incidence of progressive reti-nopathy but not moderate vision lossduring 4 years of follow-up. However,ACCORD’s intensive glycemic target(glycosylated hemoglobin [HbA
1c
], 6%)cannot be recommended to prevent pro-gressive retinopathy, because it also resultedin excess mortality. The effect of inten-sive glycemic control on all microvascularoutcomes in ACCORD — retinopathy,nephropathy, and neuropathy — also waspublished recently (see previous article and
Lancet 
2010; 376:419). As for fenofibrate,it did not prevent adverse cardiovascularevents in ACCORD; using it solely to limitretinopathy is premature until we knowthat it will prevent vision loss, with anacceptable number needed to treat andwithout adverse effects during long-termadministration.
 — Allan S. Brett, MD,
 Journal Watch General Medicine
The ACCORD Study Group and ACCORD EyeStudy Group. Effects of medical therapies on reti-nopathy progression in type 2 diabetes.
N Engl JMed
2010 Jul 15; 363:233.
Blood Pressure Control inPatients with Diabetes and CAD
 No benefit for lowering BP to <130/80 mm H
Several organizations recommend a bloodpressure (BP) goal of <130/80 mm Hg forpatients with diabetes. To determinewhether this goal is appropriate for pa-tients with diabetes and known coronary artery disease (CAD), researchers con-ducted a secondary analysis of data fromthe INVEST study, a randomized trial inwhich hypertensive patients with CADreceived
β
-blocker–based or calcium-channel blocker–based regimens (
 JAMA
 2003; 290:2805). Researchers reportedpreviously that overly aggressive BP low-ering in these patients was associated withexcess risk for adverse cardiovascularevents (
 JW Cardiol 
Aug 2006, p. 67, and
 Ann Intern Med 
2006; 144:884); now, they focus on subset of 6400 INVEST patientswith diabetes.Patients were divided into three groupsaccording to their average systolic BP dur-ing the trial: tight control (<130 mm Hg),usual control (130–139 mm Hg), or un-controlled (>139 mm Hg). During medianfollow-up of 3 years, the primary outcome(all-cause mortality or nonfatal myocardi-al infarction or stroke) occurred in 12.7%of the tight-control group, in 12.6% of theusual-control group, and in 19.8% of theuncontrolled group. In adjusted analysesthat included secondary outcomes, re-searchers found no difference betweentight and usual control. After an additional5-year follow-up, all-cause mortality washigher in the tight-control group than inthe usual-control group (22.8% vs. 21.8%;
=0.04).
COMMENT
Because this was a post hoc analysis of observational data from patients whoweren’t randomized to different BP tar-gets, confounding factors could have in-fluenced the findings. However, in therecently published ACCORD BP trial,high-risk patients with diabetes
were
ran-domized to one of two systolic BP targets(120 mm Hg or 140 mm Hg), and re-searchers found no difference in adversecardiovascular events between the groups(
 JW Cardiol 
Apr 2010, p. 29, and
N Engl  J Med 
2010; 362:1575). Taken together,INVEST and ACCORD suggest that a sys-tolic BP goal in the 130s is reasonable forhypertensive diabetic patients with CADor multiple cardiovascular risk factors.
 — Thomas L. Schwenk, MD,
 Journal Watch General Medicine
Cooper-DeHoff RM et al. Tight blood pressurecontrol and cardiovascular outcomes among hyper-tensive patients with diabetes and coronary arterydisease.
JAMA
2010 Jul 7; 304:61.
Is internship depressing?Read about a study that showsincreased depressivesymptoms in interns.Listen to our latest podcasts,including “Survivors of childhood cancer facemanageable reproductiverisks.”
 JWatch.org/online
 JOURNAL WATCH ONLINE
September 2010
JWatch.org
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