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Acute Coronary Syndrome

Acute Coronary Syndrome. Steven R. Bruhl MD, MS 3 rd Year Cardiology Fellow Internal Medicine Didactics July 14, 2010. Goals and Objectives. Discuss the definition & pathophysiology of ACS Recognize the clinical features of low, intermediate and high risk ACS

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Acute Coronary Syndrome

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  1. Acute Coronary Syndrome Steven R. Bruhl MD, MS 3rd Year Cardiology Fellow Internal Medicine Didactics July 14, 2010

  2. Goals and Objectives • Discuss the definition & pathophysiology of ACS • Recognize the clinical features of low, intermediate and high risk ACS • Be able to identify and treat patients appropriate for a conservative or invasive strategy • Discuss new and controversial pharmacological treatments

  3. Gold Standard for Treatment of ACS ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction http://circ.ahajournals.org/cgi/content/full/102/10/1193

  4. Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.

  5. ACS Overview • Overview of ACS • Assessment of “Likelihood of ACS” • Early Risk Stratification • Invasive vs Conservative Strategy • Pharmacotherapy • Long-term Therapy/Secondary Prevention

  6. Scope of the Problem • 5 million ER visits nationwide for CP • 800,000 experience an MI each year • 213,000 die from their event • ½ of those die before reaching the ER • Pre-CCU, mortality for MI was >30% • Fell to 15% with CCU • With current interventions, in hospital mortality of STEMI is 6-7%

  7. Overview of ACS Acute Coronary Syndromes* 1.57 Million Hospital Admissions - ACS UA/NSTEMI† STEMI 1.24 millionAdmissions per year 0.33 millionAdmissions per year *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA. Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.

  8. Acute Coronary Syndrome (ACS) • Definition: The spectrum of acute ischemia related syndromes ranging from UA to MI with or without ST elevation that are secondary to acute plaque rupture or plaque erosion. [----UA---------NSTEMI----------STEMI----]

  9. Pathophysiology of Stable Angina and ACS Pathophysiology ACS • Decreased O2 Supply • Flow- limiting stenosis • Anemia • Plaque rupture/clot • Increased O2 Demand Asymptomatic Angina Myocardial Infarction O2 supply/demand mismatch→Ischemia Myocardial ischemia→necrosis

  10. Pathophysiology of ACSEvolution of Coronary Thrombosis

  11. Unstable Angina STEMI NSTEMI • Non-occlusive thrombus • sufficient to cause • tissue damage & mild • myocardial necrosis • ST depression +/- • T wave inversion on • ECG • Elevated cardiac • enzymes • Non occlusive • thrombus • Non specific • ECG • Normal cardiac • enzymes • Complete thrombus • occlusion • ST elevations on • ECG or new LBBB • Elevated cardiac • enzymes • More severe • symptoms

  12. STEMI • Name 3 situations in which you cannot diagnose STEMI

  13. STEMI • Name 3 situations in which you cannot diagnose STEMI • Left Ventricular Hypertrophy • Chronic or Rate Dependent LBBB • Paced Rhythm

  14. Cardiac Catheterization • Name the only 3 situations that demand emergent cardiac catheterization.

  15. Cardiac Catheterization • Name the only 3 situations that demand emergent cardiac catheterization. • STEMI or new LBBB • ACS with hemodynamic or electrical instability despite optimal medical management • Uncontrolled CP despite optimal medical management

  16. At least 2 of the following History ( angina or angina equivalent) Acute ischemic ECG changes Typical rise and fall of cardiac markers Absence of another identifiable etiology Diagnosis of ACS

  17. Initial Evaluation and management of Non ST-elevation ACS

  18. History/Examination Pain in Chest or Left Arm CP Radiation Right Shoulder Left Arm Both Left & Right Arm Diaphoresis 3rd Heart Sound SBP < 80 mm Hg Pulmonary Crackles Panju AA. JAMA. 1998;280:1256. Suggesting AMI LR 2.7 LR 2.9 (1.4-6.0) LR 2.3 (1.7-3.1) LR 7.1 (3.6-14.2) LR 2.0 (1.9-2.2) LR 3.2 (1.6-6.5) LR 3.1 (1.8-5.2) LR 2.1 (1.4-3.1) Likelihood of ACS by Hx/PE

  19. Likelihood of ACS by Hx/PE • Clinical Examination – • Pleuritic Chest Pain • Sharp or Stabbing Pain • Positional Chest Pain • Reproducible Chest Pain Panju AA. JAMA. 1998;280:1256. Against AMI LR 0.2 (0.2-0.3) LR 0.3 (0.2-0.5) LR 0.3 (0.2-0.4) LR 0.2-0.4

  20. Risk Stratification by ECG • Simple, quick, noninvasive tool • Universally available, cheap • Correlates with risk and prognosis • Guides treatment decisions • Can identify alternative causes

  21. Risk Stratification by ECG • ECG Findings and Associated LR for AMI • New ST-E > 1mm LR 5.7-53.9 • New Q waves LR 5.3-24.8 • Any ST-E LR 11.2 (7.1-17.8) • New Conduction Defect LR 6.3 ( 2.5-15.7) • New ST-D LR 3.0-5.2 • NORMAL ECG LR 0.1-0.4 Panju AA. JAMA. 1998;280:1256.

  22. Risk Stratification by ECG CAVEATS • 1-8% AMI have a normal ECG • Only Approx 50% of AMI patients have diagnostic changes on their initial ECG Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40.

  23. Risk Stratification by ECG CAVEATS cont. • 1 ECG cannot exclude AMI • Brief sample of a dynamic process • Small regions of ischemia or infarction may be missed Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40.

  24. How Sensitive is the ECG Alone?

  25. How Predictive is NTG response?

  26. Timing of Release of Various Biomarkers After Acute Myocardial Infarction Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.

  27. % % % % Mortality at 42 Days % % 831 174 148 134 50 67  Risk Stratification by Troponin

  28. Non ACS causes of Troponin Elevation • Trauma (including contusion; ablation; pacing; ICD firings,, endomyocardial biopsy, cardiac surgery, after-interventionalclosure of ASDs) • Congestive heart failure (acute and chronic) • Aortic valve disease and HOCM with significant LVH • Hypertension • Hypotension, often with arrhythmias • Noncardiac surgery • Renal failure • Critically ill patients, especially with diabetes, respiratory failure • Drug toxicity (eg, adriamycin, 5 FU, herceptin, snake venoms) • Hypothyroidism • Coronary vasospasm, including apical ballooning syndrome • Inflammatory diseases (eg, myocarditis, Kawasaki disease, smallpox vaccination, • Post-PCI • Pulmonary embolism, severe pulmonary hypertension • Sepsis • Burns, especially if TBSA greater than 30% • Infiltrative diseases: amyloidosis, hemachromatosis, sarcoidosis, and scleroderma • Acute neurologic disease, including CVA, subarchnoid bleeds • Rhabdomyolysis with cardiac injury • Transplant vasculopathy • Vital exhaustion Modified from Apple FS, et al Heart J. 2002;144:981-986.

  29. Combined Sensitivities for ACS

  30. Early Invasive Conservative

  31. Unstable angina/NSTEMI cardiac care • Evaluate for conservative vs. invasive strategy based upon: • Likelihood of actual ACS • Risk stratification by TIMI risk score • ACS risk categories per AHA guidelines Low High Intermediate

  32. TIMI Risk Score Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

  33. TIMI Risk Score T:Troponin elevation (or CK-MB elevation) H:History or CAD (>50% Stenosis) R:Risk Factors: > 3 (HTN, Hyperlipidemia, Family Hx, DM II, Active Smoker) E:EKG changes: ST elevation or depression 0.5 mm concordant leads A2:Aspirin use within the past 7 days; Age over 65 T:Two or more episodes of CP within 2 hours

  34. Deciding between Early Invasive vs a Conservative Strategies • Hemodynamic instability • Elecrical instability • Refractory angina • PCI in past 6 months • CABG • EF <40%

  35. Specifics of Early Hospital Care Anti-Ischemic Therapy Anti-Platelet Therapy Anticoagulant Therapy

  36. Early Hospital CareAnti-Ischemic Therapy • Class I • Bed/Chair rest and Telemetry • Oxygen (maintain saturation >90%) • Nitrates (SLx3 Oral/topical. IV for ongoing iscemia, heart failure, hypertension) • Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa indication) • Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-blockers • ACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other pts) (ARBs for those intolerant) • Statins

  37. Early Hospital CareAnti-Ischemic Therapy • Class III • Nitrates if BP<90 mmHg or RV infarction • Nitrates within 24-hrs of Sildenafil or 48 hrs of Tadalafil • Immediate release dihydropyradine Ca-blockers in the absence of B-Blocker therapy • IV ACE-inhibitors • IV B-blockers in patients with acute HF, Low output state or cardiogenic shock, PR interval >0.24 sec, 2nd or 3rd degree heart block, active asthma, or reactive airway disease • NSAIDS and Cox-2 inhibitors

  38. Early Hospital CareAnti-Platelet Therapy • Class I • Aspirin (162-325 mg), non enteric coated • Clopidogrel for those with Aspirin allergy/intolerance (300-600 mg load and 75 mg/d) • GI prophylaxis if a Hx of GI bleed • GP IIb/IIIa inhibitors should be evaluated based on whether an invasive or conservative strategy is used • GP IIb/IIIa inhibitors recommended for all diabetics and all patient in early invasive arm

  39. Early Hospital CareAnticoagulant Therapy • Class I • Unfractionated Heparin • Enoxaparin • Bivalarudin • Fondaparinux • Relative choice depends on invasive vs conservative strategy and bleeding risk

  40. Early Hospital CareStatin Therapy • MIRACL TrialInclusion Criteria • 3086 patients with Non ST ACS • Total cholesterol <270 mg/dl • No planned PCI • Randomized to Atorvastatin vs Placebo • Drug started at 24-96 hours

  41. Statin Evidence: MIRACL Study Primary Efficacy Measure Placebo 17.4% 15 14.8% Atorvastatin 10 • Time to first occurrence of: • Death (any cause) • Nonfatal MI • Resuscitated cardiac arrest • Worsening angina with new objective evidence and urgent rehospitalization Cumulative Incidence (%) 5 Relative risk = 0.84P = .048 95% CI 0.701-0.999 0 0 4 8 12 16 Time Since Randomization (weeks) Schwartz GG, et al. JAMA. 2001;285:1711-1718.

  42. 2 Placebo 1.5 Cumulative Incidence (%) 1 Atorvastatin 0.5 Relative risk = 0.49 P = .04 95% CI 0.24-0.98 0 0 4 8 12 16 Time Since Randomization (weeks) Statin Evidence: MIRACL Study Fatal and Nonfatal Stroke Waters DD, et al. Circulation. 2002;106:1690-1695. S24

  43. 0 30 3 6 9 12 15 18 21 24 27 PROVE-IT Trial All-Cause Death or Major CV Events in All Randomized Subjects 30 Pravastatin 40mg (26.3%) 25 20 % with Event Atorvastatin 80mg (22.4%) 15 10 16% RR (P = 0.005) 5 0 Months of Follow-up

  44. Summary of PROVE-IT Results • In patients recently hospitalized within 10 days for an acute coronary syndrome: • “Intensive” high-dose LDL-C lowering (median LDL-C 62 mg/dL) compared to “moderate” standard-dose lipid-lowering therapy (median LDL-C 95 mg/dL) reduced the risk of all cause mortality or major cardiac events by 16% (p=0.005) • Benefits emerged within 30 days post ACS with continued benefit observed throughout the 2.5 years of follow-up • Benefits were consistent across all cardiovascular endpoints, except stroke, and most clinical subgroups

  45. Invasive vs Conservative Strategies

  46. Invasive vs Conservative Strategy Clinical Trials ISAR-COOL ICTUS (05) RITA-3 (02) VANQWISH (98) VINO MATE TRUCS TIMI IIIB (94) TACTICS-TIMI 18 (01) FRISC II (99) Weight of the evidence ConservativeStrategy Favored N=920 InvasiveStrategy Favored N=7,018 No difference N=2,874

  47. How Early is Early?

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