1	Importance of Risk Stratification of Non-ST Elevation ACS Heart Center , Beijing Chaoyang Hospital & Cardiovascular Institute,Affiliate of Capital University of Medical Sciencies Lefeng Wang M.D.
2	New terminology in ACS
3	Overview of 2002 Update to the ACC/AHA Guidelines for UA/NSTEMI Assess likelihood of CAD Risk stratification Target therapy: more aggressive treatment in higher-risk patients Anti-ischemic, antithrombotic therapy Invasive vs. conservative strategy Discharge planning (risk-factor modification and long-term medical therapy)
4	ED ® CCU ® Cath Lab Risk Stratification for Chest Pain Three levels of risk stratification are pertinent to the ED: Low, intermediate, or high risk that ischemic symptoms are a result of CAD Low, intermediate, or high risk of short-term death or nonfatal MI from ACS Dynamic, ongoing risk-oriented evaluation of low- or intermediate-risk patients for “conversion” to high-risk status that is linked to intensity of treatment
5	Risk Stratification Tools in the ED History and Physical Standard ECG and Non-standard ECG leads Cardiac Biomarkers Troponin I or T, CK-MB, myoglobin Predictive Indices / Schemes Better as research tools than for real-time clinical decision-making Non-Invasive Imaging Studies Echocardiogram Exercise testing Technetium-99m-sestamibi: stress and rest
6	Clinical Assessment (1) Rapid, focused evaluation Decisions based on this evaluation have substantial clinical and economic consequences Are the symptoms a manifestation of ACS? If so, what is the prognosis? Identify signs of life-threatening instability Triage to most appropriate area Typically an ED or chest pain unit
7	Clinical Assessment (2) Risk status determined in the ED by: Assessment of anginal symptoms Careful physical examination Electrocardiogram Cardiac biomarkers CAD risk factors Illicit drug use Initial risk stratification assignment drives pace of subsequent evaluation and treatment
8	Clinical Assessment (3) High-risk features apparent in the ED: Accelerated pattern of angina Ongoing rest pain > 10 min Signs of CHF Hemodynamic instability Arrhythmias – atrial or ventricular Advanced age (> 75 years) Ischemic ECG changes Elevated cardiac markers
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12	Electrocardiogram (1) Carries diagnostic and prognostic value Especially valuable if captured during pain ST-segment depression or transient ST-segment elevation are primary ECG markers of UA/NSTEMI 75% of patients with + CK-MB do not develop Q waves Differentiation between UA and NSTEMI relies upon positive biomarkers Inverted T-waves suggestive of ischemia, particularly with good chest pain story
13	ST Depression is The Most Common ECG Abnormality Noted in Patients Presenting with Non-ST Elevation ACS
14	GUSTO IIb: Correlation of 6-month mortality with baseline ECG findings in patients with ACS
15	ST Depression is a Major Predictor of Mortality in Patients Presenting with NSTE ACS
16	Patients with ST¯: Likely to Have Higher-Risk Medical Histories than Patients with ST
17	ST Depression Signifies Likelihood to Require High-risk Revascularization
18	Anemia in NSTE ACS: ST deviation
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20	Electrocardiogram (2) Guidelines suggest that serial ECGs increase both sensitivity and specificity Guidelines withhold recommendation regarding utility of continuous ST-segment monitoring Guidelines recommend mathematical models based on ECG findings only for identification of low-risk patients and for prognosis in those with ischemia
21	Biomarkers
22	Relationship Between Extent of Myocardial Necrosis and Long-Term Morbidity and Mortality
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24	Long Term Survival and Troponin-T Status
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27	Baseline troponin and outcomes in ACS. Influence of LMWH
28	Baseline troponin, GP IIb/IIIa antagonists, and outcomes in ACS patients
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30	Biomarkers: Troponins Very useful in diagnosis and prognosis of ACS Normally not detectable in blood of healthy persons; cTnI or cTnT can be positive with negative CK-MB = “minor myocardial damage” Predictive of death when elevated, independent of CK-MB levels Elevated troponin validated as a predictor of enhanced treatment benefit from aggressive therapies
31	Biomarkers: Myoglobin Utility limited by release kinetics (early) and by lack of cardiac specificity Isolated elevation of myoglobin 4-8 hours after pain onset with a a non-diagnostic ECG must be supplemented by a more cardiac-specific marker Sufficiently sensitive that a negative myoglobin 4-8 hours after pain onset is useful in excluding myocardial necrosis
32	Serial Cardiac Markers
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34	B-type natriuretic peptide (BNP) and mortality in ACS patients
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40	Biomarkers: Bedside Testing Consideration of bedside marker assay recommended when hospital lab turn around time > 30-60 minutes Ready-for-use availability must be balanced against need for stringent QC and training of ED personnel, CLIA concerns, etc
41	Predictive Indices / Schemes
42	TIMI risk score for UA/NSTEMI
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44	In-hospital Mortality Rate for Patients Treated versus Not with an Early GP IIb/IIIa Inhibitor Stratified by NSTEMI Risk Score
45	CRUSADE: A National Quality Improvement Initiative Can Rapid Risk Stratification of Unstable Angina Patients Suppress ADverse Outcomes with Early Implementation of the ACC/AHA Guidelines
46	Inclusion Criteria: High-Risk NSTE ACS Ischemic symptoms lasting ³ 10 minutes within previous 24 hours and at least one of the following: Positive cardiac markers CK-MB or TnI / TnT above ULN Positive bedside troponin assay ST-segment ECG changes: ST-segment depression ³ 0.5 mm Transient ST-segment elevation 0.6 - 1 mm (lasting < 10 mins) Transfer patients (with any of the above) must arrive at CRUSADE hospital within 24 hrs of symptoms
47	Tools for Risk Stratification in ACS Demographics Age Phisical Exam Killip class,BP,HR ECG ST-segment deviation Biomarkers Troponins,hsCRP,BNP/NT-proBNP,CD40L,CrCI,WBC,etc Risk Scores TIMI,NRMI,GRACE,PURSUIT,etc
48	Goal of ACS Risk Stratification Identify those who are at ‘high risk’ for death or MI. Identify those who can benefit from acute medical and procedural intervention Identify those with long-term disease risk
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