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R MAHARAJ EMERGENCY MEDICINE
INTRODUCTION ± EPIDEMIOLOGY/PREVALENCE/DEFINITION PATHOPHYSIOLOGY OF ACUTE CORONARY SYNDROMES APPROACH TO SUSPECTED ACUTE CORONARY SYNDROME ± GUIDELINE UPDATE TREATMENT/MANAGEMENT UPDATE
Coronary Artery Disease ± leading cause of morbidity & mortality in industrialised nations. Although decrease in cardiovascular mortality still major cause of morbidity & burden of disease. South African perspective of cardiovascular disease: ³A World in One Country´ - Yusuf et al Epidemiological transitions of cardiovascular disease.
896 000 for MI Higher prevelance for NSTEMI. unit for chest pain/acs related (stats 1Jan 2009 ± 28 Feb 2009) 150/628 entries. . HIGH RISK POPULATION FOR CAD/ACS: INDIAN/WHITE/COLOURED INCREASING rate in Black population ± lifestyle/socioeconomic changes. In US ± 2004 ± 1.8% of admissions to resus.56 million admissions for ACS ± 669 000 for unstable angina. urbanisation GF Jooste stats: 23.
DEFINITIONS CAD is a continuum of disease«. Angina -> unstable angina -> AMI -> sudden cardiac death Acute coronary syndrome encompasses unstable angina.usually relieved with rest/NTG. frequency constant over time. reproducible. . Classification of angina ± Canadian Cardiovascular Society classification. NSTEMI. STEMI Stable angina ± transient episodic chest pain d/t myocardial ischaemia.
Canadian Cardiovascular Association Classification of Angina CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY ± PAIN OCCURS WITH WALKING. PAIN AT REST . CLIMBING STAIRS.STRESS SEVERE LIMITATION OF DAILY ACTIVITY ± PAIN OCCURS ON MINIMAL EXERTION CLASS 3 CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN.
T wave changes . duration Angina becoming resistance to drugs that previously gave good control. NB! ECG ± normal.5mm). ST depression(>0. increases in frequency. UNSTABLE ANGINA ± Pain occurring at rest ± duration > 20min. within one week of first visit New onset angina ± ~ Class 2 severity. onset with last 2 months Worsening of chest pain ± increase by at least 1 class.
ACUTE MYOCARDIAL INFARCTION ± ECC/ACC DEFN ±rise and fall in cardiac enzymes with one or more of the following: Ischaemic type chest pain/symptoms ECG changes ± ST changes, pathological Q waves Coronary artery intervention data Pathological findings of an acute MI NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS + POSITIVE CARDIAC ENZYMES STEMI = ST ELEVATION ON ECG + SYMPTOMS
WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH UNSTABLE ANGINA?? 5 -17% suffer an MI within a week after admission. 3 -15% die within a year.
Distruption of coronary artery plaque -> platelet activation/aggregation /activation of coagulation cascade -> endothelial vasoconstriction ->intraluminal thrombus/embolisation -> obstruction -> ACS Severity of coronary vessel obstruction & extent of myocardium involved determines characteristics of clinical presentation
Thorough history required: Character of pain Onset and duration Location and radiation Aggravating and relieving factors Autonomic symptoms TYPICAL VS ATYPICAL HISTORY Failure to recognise symptoms other than chest pain -> approx 2 hr delay in seeking medical attention .APPROACH Identifying those with chest pain suggestive of IHD/ACS.
NOT TENDER TO PALP.CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSEN¶S. WITH BREATHING/MOVING ABSENT . <20 MIN GRADUAL SUBSTERNAL. WITH EXERTION/ACTIVITY PRESENT USUALLY LESS SUGGESTIVE OF ANGINA SHARP/STABBING DURATION ONSET LOCATION/CHEST WALL TENDERNESS REPRODUCIBALITY AUTONOMIC SYMPTOMS SECONDSTO HOURS/CONTINUOUS RAPID LATERAL CHEST WALL/TENDER TO PALP. EMERGENCY MEDICINE) CHARACTERISTIC TYPE OF PAIN SUGGESTIVE OF ANGINA DULL PRESSURE/CRUSHING PAIN 2-5 MIN.
delayed intervention . no prior history of MI ATYPICAL SYMPTOMS: GIT symptoms Syncope SOB Pleuritic/positional pain Chest wall tenderness No chest pain/symptoms NRMI 2 STUDY ± MI without chest pain -> increased risk of death (23% vs 9%) More complications ± hypotension. elderly. dementia. stroke Delayed ED presentation.heart failure. females. non white patients.ATYPICAL PAIN RISK FACTORS FOR DEVELOPING ATYPICAL PAIN: Diabetes.
high risk -> admission to high care Helps decongest the ED and make available medical resources to more needy patients Risk stratification should be ongoing ± at admission. 24hrs.RISK STRATIFICATION IN ACS Reasons : Provides prognostic information Determines treatment and level of intervention -> low risk patients ± early discharge. 6-8 hrs. discharge .
TOOLS USED IN RISK STRATIFICATION HISTORY ECG BIOCHEMICAL MARKERS .
4% unstable angina .ECG First point of entry into ACS algorithm Abnormal or normal Neither 100% sensitive or 100% specific for AMI Single ECG for AMI ± sensitivity of 60%. specificity 90% Represents single point in time ±needs to be read in context Normal ECG does not exclude ACS ± 1-6% proven to have AMI.
RV 4 (Class 2a B) Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs (Class 2a B) . GUIDELINES: Initial 12 lead ECG ± goal door to ECG time 10min. read by experienced doctor (Class 1 B) If ECG not diagnostic/high suspicion of ACS ± serial ECGs initially 15 -30 min intervals (Class 1 B) ECG adjuncts ± leads V7 ±V9.
BIOCHEMICAL MARKERS IDEAL MARKER: High concentration in myocardium Myocardium specific Released early in injury Proportionate to injury Non expensive testing Troponins CKMB Myoglobin Other markers .
TROPONINS T/I Troponin T vs I ± both equivalent in diagnostic and prognostic abilities ( except in renal failure ± Trop T less sensitive) Elevation ~ 2hrs to 12hrs ~30 ± 40% of ACS patients without ST elevation ± had normal CKMB but elevated troponins on presentation Meta-analysis (Heindereich et al) ± odds of death increased 3 to 8 fold with positive troponin .
Mortality at 42 days in troponin positive patients .
MYOGLOBIN Rapid release within 2 hours Not cardiac specific Rule out for NSTEMI rather than rule in. CKMB Used in conjunction with troponins Useful in diagnosing re-infarction .
.MARKER CHANGE SCORES 2 hour delta CKMB mass Aim ± to exclude MI within 6hrs of symptom onset Determine changes in serum marker levels over certain time intervals ±delta values Increasing values while still within normal range suggestive of ischaemia ± more rapid anti.ischaemic mxn.
hsCRP. IL6. d dimer.OTHER MARKERS INDICATORS OF INFLAMMATION OR ACTIVATION OF COAGULATION CASCADE: Myeloperoxidase. soluble CD40 ligand. prothrombin fragment 1 & 2 Elevated before onset of irreversible injury Lack specificity Complex lab assays .
ISCHAEMIA MODIFIED ALBUMIN Measured with albumin cobalt binding assay In ischaemia -> decreased binding of albumin to cobalt Increased with minutes of ischaemia ± elevated for 6-12hrs ± gone by 24hrs ~90% negative predictive value Combined with myoglobin/CKMB/troponin ± increases diagnostic sensitivity of ischaemia by 40% Possible role for rule criteria in low risk patients Positive IMA ± high risk patients ± more aggressive mxn Positive in hypoxic disorders ± poor specificity in this setting .
no ECG changes. atrial arrythmias. Studies ± BNP not a specific marker but a strong predictor of ACS especially in patients with chest pain. PE. Also positive in heart failure. non diagnostic troponins. renal failure Pregnancy Associated Plasma Protein A (PAPP-A): Released when plaque ruptures Predictor of ischaemia . B ±type Natriuretic Peptide: released from heart muscle in response to increased ventricular wall stress.
but also expressed outside heart Therefore may be sensitive but not specific for injury Possible role in multi-marker strategy IMAGING MODALITIES Cardiac MRI Multidetector CT for coronary calcification Coronary CT angiography Undergoing clinical evaluation . HEART FATTY ACID BINDING PROTEIN (HF ABP) Identifies AMI <4hrs after onset Protein involved in myocardial lipid synthesis.
repeat 8-12hours later(Class 1 B) Remeasuring of positive biomarkers to determine infarct size/necrosis (Class 2a B) Patients presenting within 6 hours of symptom onset ± myoglobin in conjunction with troponin measured (Class 2b B) 2hr delta CKMB/Delta troponin considered in <6hr presentation (Class 2b B) BNP level ± for global risk assessment(Class 2b B) Class 3 ± AST/LDH/CK without CKMB . 2007 ACC/AHA guidelines: Cardiac biomarkers measured in all patients with suspicion of ACS (Class 1 B) Troponin preferred marker( Class 1 B) If troponin negative within 6 hours of onset.
RISK STRATIFICATION MODELS .
TIMI RISK SCORE ±increase in mortality with increasing score ~40% all cause mortality at 14 days for patients requiring urgent revascularisation .
WHICH MODEL IS MOST APPROPRIATE?? 2007 ACS/AHA GUIDELINES: Risk stratification models useful in decision making with regard to treatment options ( Class 2a B) TIMI vs GRACE vs PURSUIT PURSUIT & GRACE risk scores allow better discrimination of in hospital and 1 year mortality in patients compared to TIMI. (Andrew et al. Risk scores for risk stratification in ACS «) What¶s appropriate in our setting??? .
MANAGEMENT ALGORITHM .
non diagnostic ECG/biomarkers ± observed in facility with cardiac monitoring (Class 1 C) Alternative to in patient treatment: for those with 12hr ECG/markers negative ± stress ECG in 72hrs (Class 1 C) Giving precautionary treatment for those for OPD stress (Class 1 B) .MANAGEMENT UPDATE 2007ACS/AHA GUIDELINES: Rapid catergorisation of patient (Class 1 C) Possible ACS.
ischaemia at rest or minimal activity Elevated troponins New ST depression Signs of heart failure/worsening mitral regurg. High risk factors include: Recurrent angina. hemodynamic instability (LOE B) Early invasive strategy for stabilised patients with elevated risk for clinical events. Ventricular tachycardia Prior CABG PCI in last 6 months High TIMI/GRACE scores LVEF < 40% .INITIAL INVASIVE VS INITIAL CONSERVATIVE STRATEGY CLASS 1 RECOMMENDATIONS: Early invasive strategy for refractory angina.
CLASS 2b May opt for initial conservative strategy in stabilised high risk patients ± dependent on patient/physician preference (LOE B) CLASS 3 Invasive strategy -not recommended in patients with multiple co morbidities.(LOE C) . low risk patients. patients not consenting.
UA/NSTEMI ±PHARMACOTHERAPY UPDATE GENERAL: IV B Blockers downgraded from Class 1 to 2a recommendation. cardiogenic shock and reactive airway disease. (COMMIT Trial) Oral B Blockers in first 24hrs still Class 1 ± but not used in signs of heart failure.(LOE B) MORPHINE downgraded from Class 1 to 2a ± findings from CRUSADE Registry .
PHARMACOTHERAPY UPDATE ANTIPLATELET THERAPY: CLASS 1 RECOMMENDATION Aspirin to all patients as soon as possible and continued (if no C/I) (LOE A) Initial dose 162 -325mg Maintenance 75 -162mg No added benefit from higher doses except post stenting Clopidogrel for those allergic to aspirin or major GI bleeding (LOE A) For initial invasive strategy ± aspirin + clopidogrel or IV glycoprotein 2b/3a therapy (LOE A) Abciximab if no delay in angiography/PCI. eptifibatide/tirofiban if delayed angiography(LOE B) .NSTEMI.
(LOE C) Invasive strategy ± can use clopidogrel + glycoprotein inhibitors(LOE C) CLASS 2b In patients managed conservatively ± can add glycoprotein inhibitor therapy. CLASS 2a In patients managed conservatively who develop recurrent ischaemia ± on clopidogrel/ASA/Anticoagulant ± can add glycoprotein inhibitor. in addition to aspirin & anticoagulant (LOE B) .
CLASS 3 ABCIXIMAB should not be given if PCI not planned (LOE A) .
Clopidogrel or Glycoprotein 2b/3a inhibitors should be added before angiography. . continued ideally up to 1 year(LOE B) If initial conservative strategy selected but patient has recurrent ischaemic symptoms/heart failure/arrythmias ± diagnostic angiography recommended. For initial conservative strategy: Aspirin + Clopidogrel + anticoagulant ± administered for 1 month(LOE A).
ANTICOAGULANT THERAPY CLASS 1 Anticoagulant therapy should be added as soon as possible For patients undergoing angiography/PCI ± enoxaparin/UFH (LOE A) of Bivalirudin/ fondaparinux (LOE B) For conservative strategy: enaxaparin. fondaparinux For patients with increased risk of bleeding with conservative strategy ± fondaparinux . UFH (LOE A).
CLASS 2a Enoxaparin /fondaparinux vs UFH Enoxaparin/fondaparinux preferred except in those undergoing CABG within 24hrs (LOE B) .
ADDITIONAL MANAGEMENT STRESS TEST should be performed for those managed conservatively. ideally up to 1 year(LOE B) . If stress test positive/ high risk ± needs diagnostic angiography(Class 1 LOE A) If classed as low risk ± need to continue aspirin indefinitely ( LOE A) Clopidogrel for at least 1 month(LOE A).
UA/NSTEMI ALGORITHM.INVASIVE STRATEGY .
UA/NSTEMI ALGORITHM ±CONSERVATIVE STRATEGY .
STEMI PHARMACOLOGICAL UPDATE: ANALGESIA ± changes from 2004 guidelines MORPHINE: still remains Class 1 C for STEMI. heart failure. re infarction. myocardial rupture) Class 1 C NSAIDS should not be administered in hospital for MI (Class 3) . titrated doses NSAIDS/COX 2 INHIBITORS: those on it should have it discontinued ( increased risk of mortality.
BETA BLOCKERS Modified recommendation Oral Beta Blockers should be initiated in first24rs. risk of cardiogenic shock . risk of cardiogenic shock) Class 1 B Patients with early contraindications -> re. if no contraindications (heart failure.evaluated later for possible use Role of IV B blockers ± used in hypertensive patients with STEMI Class 2a B Class 3 LOE A ± IV B blockers should not be administrated to patients with heart failure.
Emphasis on decreasing ischaemic time. Increase use of prehospital 12 lead ECG emphasised. No major changes to reperfusion strategies. (Class 1 B) . In PCI capable hospital ± door to PCI time 90 min (Class 1 A) In non PCI capable hospital ± door to needle time 30 min or timeous transfer to PCI capable hospital.
REPERFUSION STRATEGY .
0. ffd.5hrs . tPA/heparin cf comb.3% vs 1%) GUSTO 1 trial ± early vessel patency post infract assoc.FIBRINOLYTICS AVAILABLE FIBRINOLYTICS: STREPTOKINASE ± 1. with better survival.15mg IV bolus. tPA -> lower mortality rates . Accl. marginally higher stroke rate with tPA (1. 10U IV after 30 min WHICH FIBRINOLYTIC TO USE??? GISSI 2 trial ± tPA vs Streptokinase . 0.5mu infusion over 30min (1hour ±ACLS) rtPA ± accelerated infusion over 1. Streptokinase/tPA/heprain cf strep with IV vs S/C heparin Outcome ± better flow rates with accl.75mg/kg over 30 min. no difference in mortality.5mg/kg over 1hr ANISTREPLASE ± 30 U IV over 5 min TENECTEPLASE ± 30 TO 50 MG RETEPLASE ± 10 U IV bolus.
tenecteplase was equally or minimally more effective. especially in those presenting > 4hrs after symptom onset. Fibrinolysis combined with glycoprotein 2b/3a inhibitors ± no overall advantage (ASSENT 3. ASSENT 2 TRIAL ± tenecteplase vs aTPA . GUSTO 5 trials) .
or large area of myocardium injured) LOE B Class 3 ± angiography performed if invasive strategy contraindicated. ventricular dysrythmias Class 2a ± persistent ischaemic symptoms post fibrinolysis. electrical instability (LOE C) New recommendation ± PCI for failed fibrinolytic therapy (less than 50% decrease in ST elevation in worst lead.PCI in patients (<75 yrs)with cardiogenic shock. RESCUE PCI: CLASS 1 LOE B ± angiography with +/. 90min post fibrinolytic therapy. severe heart failure. haemodynamic instability. or patient refusal (LOE C) .
LOE A Anti coagulants with proven efficacy: Unfractionated Heparin . caution in renal impairment (LOE A) Fondaparinux ± 2.keeping aPTT 1.5 ± 2 sec above control (LOE C) Enoxaparin (Clexane) ± initial dosage of 30mg IV bolus ± ffd by 1mg/kg 12hrly. ffd by 2.5mg dly S/C maintenance for duration of hospitalisation (LOE B) .ANTICOAGULANT ADJUNCTS NEW RECOMMENDATIONS: CLASS 1 Patients undergoing fibrinolysis should be kept on anticoagulants for atleast 48 hrs and preferably the duration of hospital stay.5mg IV.
ANTICOAGULANTS CLASS 2a recommendation to use anticoagulants in STEMI without reperfusion. UFH (LOE B) LMWH (LOE C) Fondaparinux (LOE B) .
THIENOPYRIDINES CLASS I CLOPIDOGREL ± now recommended in all STEMI patients in addition to aspirin. whether undergoing reperfusion or not. Dosage 75mg daily(LOE A) Duration -14 days (LOE B) CLASS 2 A In patients < 75yrs ± Clopidogrel 300mg loading dose recommended(LOE C) Long term maintenance therapy should be considered. 75mg dly for 1 year (LOE C) .
SECONDARY PREVENTION INCREASED FOCUS ON SECONDARY PREVENTION: SMOKING CESSATION DIET MODIFICATION/WT CONTROL BP CONTROL LIPID MANAGEMENT EXERCISE DIABETES MANAGEMENT .
older age SYMPTOMS OF INFARCT BUT NO ESTABILISHED ECG CHANGES . Despite good reperfusion strategies approx. complicated disease presentation.keep in mind aortic dissection. Attributed to ± delayed presentation. atypical presentation. 1/3 of patients worldwide miss out. other chest pathology . GIT disease.
Emphasis should also be placed on primary &secondary prevention of ACS. decreases morbidity & mortality The way forward ± fully equipped CHEST PAIN OBSERVATION UNIT . Early intervention helps prevent complications.CONCLUSION With increase burden of CVD. and lack of health resources risk stratification becomes important.
CARDIOLOGY AT THE LIMITS IV.REFERENCES EDITORS MARX ET AL. KEY ARTICLES IN MANAGEMENT OF ACS & PCI -2007 UPDATE. YELLON DM FOX KA. ACC/AHA 2007 GUIDELINES FOR MXN OF U/A. NETH. HEART J.16(6):191 -196 . PHARMACOTHERAPY 2007:27(12). 2008 JUNE. ROSEN¶S EMERGENCY MEDICINE: CONCEPTS AND CLINICAL PRACTICE. MANAGEMENT OF ACS: AN UPDATE. THE GLOBAL EPIDEMIC OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE. DEFINING THE LIMITS OF ACS.2004 JUNE. CHEST PAIN IN THE ER: VALUE OF THE HEART SCORE.onlinejacc. CARDIOLOGY AT THE LIMITS IV. YELLON DM YUSUF S. EDITORS: OPIE LH. HEART.NSTEMI ± EXECUTIVE SUMMARY ± DOWNLOADED content. 1722 -1750 WHITE HD. 6TH EDITION PAUL PD ET AL. EDITORS: OPIE LH. 90(6):698 -706 ANDERSON ET AL.org SIX AJ ET AL.
EUROPEAN HEART JOURNAL 2008. ANTMAN EM ET AL.29(23): 2843 -2850 KING III SB ET AL. NOVEL BIOMARKERS IN EARLY DIAGNOSIS OF AMI COMPARED WITH CARDIAC TROPONIN T.ahajournals. VOL 51. NO 2.. JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY.FOR PCI. DOWNLOADED http://circ. 2007 FOCUSSED UPDATE OF ACC«. 2007 FOCUSSED UPDATE OF ACC/AHA 2004 GUIDELINES FOR MAXN OF PATIENTS WITH STEMI.org McCANN CJ ET AL. 2008 .
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