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ED Risk Stratification for Chest Pain

Non-ST-Segment Elevation Acute Coronary Syndromes: Risk Stratification Based on the ACC/AHA UA / NSTEMI Guidelines. ED Risk Stratification for Chest Pain. For the past 20 years. In 2002: Does this patient need fibrinolytic therapy?

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ED Risk Stratification for Chest Pain

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  1. Non-ST-Segment ElevationAcute Coronary Syndromes:Risk Stratification Based on the ACC/AHA UA / NSTEMI Guidelines

  2. ED Risk Stratification for Chest Pain For the past 20 years . . . In 2002: • Does this patient need fibrinolytic therapy? • Should this patient get anti-thrombin and anti-platelet agents? • Can I safely send this patient home? R/O MI

  3. ED  CCU  Cath Lab Risk Stratification for Chest Pain Three levels of risk stratification are pertinent to the ED: • Low, intermediate, orhigh risk that ischemic symptoms are a result of CAD • Low, intermediate, or highrisk 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

  4. Chest Pain History, Physical EKG Definite Non-Cardiac STEMI UA/NSTEMI/ High Risk Mod Risk Low Risk Initial Risk Stratification Scheme

  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 • Non-Invasive Imaging Studies • Echocardiogram • Exercise testing • Technetium-99m-sestamibi: stress and rest

  6. I IIa IIb III Initial EvaluationRisk Stratification (1) Early risk stratification by symptoms, physical findings, ECG, cardiac markers 12-lead ECG within 10 min for ongoing pain, or ASAP if pain has resolved at presentation Cardiac markers, Troponins and CK-MB, for initial assessment Monitoring, repeat ECG and cardiac markers in 6-12 hours, if initial results normal

  7. I IIa IIb III Initial EvaluationRisk Stratification (2) If <6 hours after symptom onset, add early myoglobin or CK-MB to troponin C-reactive protein, other markers of inflammation Total CK, SGOT, HBDH, LDH

  8. 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

  9. 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

  10. Clinical Assessment (3) • High-risk features apparent in the ED: • Accelerated pattern of angina • Ongoing rest pain > 20 min • Signs of CHF • Hemodynamic instability • Arrhythmias - Atrial or ventricular • Advanced age (> 75 years) • Ischemic ECG changes • Elevated cardiac markers

  11. Electrocardiogram • 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

  12. Six-Month Mortality by Baseline ECG Findings -GUSTO-IIb Results 10% ST  8% ST  6% % Mortality 4% NS ST-Ts 2% 0% 0 30 60 90 120 150 180 Days from Randomization Savonitto, JAMA 1999

  13. Biomarkers: CK/CKMB • Until recently the principal serum marker used in evaluation of ACS despite known limitations: • Low levels in healthy persons limits specificity • MB band may be elevated in skeletal muscle damage • Different MB isoforms exist in myocardium (MB2) and in plasma (MB1), and differentiating assay is not widely available

  14. 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 MI and death when elevated, independent of CK-MB levels • Elevated troponins validated as a predictor of enhanced treatment benefit from aggressive therapies (LMW heparins, GP IIb/IIIa inhibitors, early invasive strategy)

  15. Troponin as a Marker of Increased Risk in ACS

  16. Long Term Survival and Troponin-T Status GUSTO-IIa Results 1-Year Mortality Rates: Troponin-T Positive: 14% Troponin-T Negative: 5% TnT - p < 0.001 TnT +

  17. 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

  18. Integration of Biomarkers with Clinical History • Time since symptom onset should be a factor in marker selection and in repeat assay strategy • Elevated serum levels of troponins persist for 7-14 days after initial release • Delta values, as close as 2 hours apart, may be sufficiently sensitive to assist with serial evaluations • Serial cardiac marker strategy not specified

  19. Myoglobin CK-MB (mass) Troponin T Myoglobin CK-MB (mass) Troponin T 100% 100% 75% 75% 50% 50% 25% 25% 0% 0% 3 4 5 6 8 12 3 4 5 6 8 12 Serial Cardiac Markers Serial Testing in 309 Patients with Suspected MI Sensitivity Hours After Symptom Onset Hours After Symptom Onset Hours After Symptom Onset Winter, Circulation, 1995

  20. Biomarkers: Bedside Testing • Consideration of bedside marker assay recommended when hospital lab turnaround time > 30-60 minutes • Ready-for-use availability must be balanced against need for stringent QC and training of ED personnel, CLIA concerns, political hazards, etc • Prognostic value limited because many assays are qualitative, not quantitative

  21. “Vein-to-Brain” Reporting Times for Cardiac Markers - St. Agnes Hospital Bedside Test (mean=15 mins) Laboratory Test (mean=128 mins) 180 160 140 120 100 Reporting Times (mins) "Vein-to Brain" 80 60 40 20 n = 939 SD = 46.74 0 Test Type Christenson R: Md Med 2001 Spring:Suppl:98-103

  22. Distribution of Reporting Times for Cardiac Markers - St. Agnes Hospital 284 mins = Latest Reporting Time (201.3 mins) 95th percentile (147 mins) 75th percentile (Median , 117 mins) 50th percentile Range of Lab Reporting Times (85 mins) 25th percentile (62.6 mins) 5th percentile 40 mins = Earliest Reporting Time Christenson R: Md Med 2001 Spring:Suppl:98-103

  23. Noninvasive Studies • Guidelines do not consider use of these tests in the ED setting, although: • Many EDs now use rest sestamibi scanning in the risk stratification process • Stress testing used after patients have “ruled out” • Reality dictates that appropriate provocative testing often not likely after patient leaves ED • ED is the “first, last, and best shot” at intervening in patients with risk concerns

  24. Predictive Indices - Risk Scores in the ED • Combine clinical history, physical exam findings, ECG signs of ischemia, and cardiac marker results • PURSUIT and TIMI Risk Scores • Therapies such as LMW heparin and GP IIb/IIIa inhibitors have greater benefit in patients with higher risk scores • Have not been tested prospectively in the ED • Risk scores not specifically recommended by the ACC/AHA Guidelines

  25. I IIa IIb III Immediate Management Classify as non-cardiac, chronic stable angina, possible ACS, or definite ACS Evaluate for immediate reperfusion therapy if definite ACS and ST-segment  present Pharmacological or exercise stress test, if possible ACS and serial biomarkers and ECGs are normal Admit pts with definite ACS, ongoing pain,  biomarkers, new ST  or deep T-wave inversion, abnormal hemodynamics, or (+) stress test

  26. The “Key” to Risk Stratification • Link ongoing evaluation of risk to changes in intensity of therapy • Develop risk stratification schemes that reflect capabilities of ED and needs/preferences of cardiologists • Develop treatment pathways that provide for independent response of emergency physicians to recognition of higher risk levels

  27. The “Rallying Cry” for CRUSADE . . . . . . starts with a successful risk stratification strategy A seamless transition of optimal care—diagnostic and therapeutic—from the ED to the Cardiology Service . . .

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