Assessment and Management of Non-Q-Wave Myocardial Infarctions

1. Assessment and Management ofNon-Q-Wave Myocardial Infarctions by Michael R. Tamberella, MD Resident Grand Grounds November 17, 1998

2. Case Presentation • Ms. A.L. is an 84 y/o WF with CHF who presented to the OPD clinic with cough productive of yellow sputum and fever. • She denied any CP, SOB, N/V, diaphoresis or abdominal pain

3. Case Presentation • PMHx: hyperlipidemia, remote pneumonia • PSHx: hysterectomy 1975, bladder tack 1997 • Medications: Zocor 40mg/day • Allergies: NKDA • Social Hx: lives with daughter, works in the catering business, Øtobacco, ØEtOH • FmHx: Father died of CVA, Mother died of MI

4. Case Presentation • Physical Exam: • VS: BP-110/70, P-105, R-24, T-101.0 • Gen: Thin WF A+Ox4 in moderate respiratory distress • HEENT: WNL • CV: RRR with 2/6 holosystolic murmur at LLSB • Lungs: Bilateral coarse crackles, rhonchii but no wheezes • Abd: WNL • Ext: No C/C/E. 2+ peripheral pulses • Skin: W/D/I

5. Labs: 12.5 19.8 185 135 101 30 39.5 3.9 24 1.0 CXR: RML infiltrate Case Presentation

6. Case Presentation Discussion: Patient was admitted and treated for community acquired pneumonia however, she deteriorated rapidly with acute respiratory distress was intubated and found to have EKG changes consistent with lateral ischemia. She was transferred to the CCU and ruled in for acute NQWMI with peak CK of 647 and MB% of 22. She was treated with heparin, IV NTG, and ECASA. An echo revealed no resting segmental wall motion abnormalities and an ejection fraction of 20%. Over 48 hours her condition improved, she was extubated and transferred back to the floor where she continued to do well and completed a 14 day course of antibiotics in the TCU then discharged to home and returned to her baseline level of activity.

7. Introduction • Differences between Q and NQWMI • Incidence • Pathogenesis • Clinical Presentation • ECG • Prognosis • Evidence behind post MI testing

8. Introduction • Distinction between QWMI and NQWMI was first proposed in the early 1980’s based on evidence that the terms transmural and non-transmural did not correlate with anatomic findings at autopsy. • NQWMI’s represent less extensive area of infarction with lower peak CK’s but with larger degree of jeopardized myocardium.

9. Incidence • Up to 71% of all MI’s • Increasing over the last 10 years • newer treatments • increased public awareness of warning signs • increased public awareness of risk factors • HTN, Hyperlipidemia, tobacco

10. Pathogenesis • Unstable eccentrically located plaques rupture causing lipid extravasation and a local pro-thrombotic state which leads to clot formation and obstruction of the lumen of an epicardial artery.

11. Pathogenesis • QWMI’s are characterized by occlusion of a proximal section of a coronary artery with an extensive area of cardiac necrosis • NQWMI’s are associated with transient reductions in blood flow without complete occlusion

12. Pathogenesis • NQWMI’s vs QWMI’s • smaller infarcted areas • lower peak CK’s • higher percentage of patent infarct related arteries • larger area of viable but jeopardized myocardium in the infarct zone

13. Pathogenesis • NQWMI vs Unstable Angina • greater degree of incomplete occlusion • lower flow rate through the culprit artery • myocardial necrosis

14. Pathogenesis • Reflow in NQWMI occurs rapidly due to • early thrombolysis • decreased vasospasm • rapid healing of underlying plaque rupture • collateral blood flow • anterograde flow through a subtotal thrombotic burden

15. Pathogenesis • Patients with collaterals have • better cardiac function • more effective remodeling • and are more likely to have NQWMI

16. Pathogenesis • Keen et al • Coronary angiography within 6 hours of AMI • 58 Q and 28 NQWMI • 91% of QWMI’s had total occlusion of IRA vs 39% of NQWMI’s (p=0.0001) • 84% of QWMI’s had thrombus vs 43% in NQWMI (p=0.0002) • 19% QWMI’s had collaterals vs 45% in NQWMI (p=0.06)

17. Pathogenesis • Keen et al • Findings suggest that the key angiographic difference between QWMI and NQWMI is the presence of some form of residual perfusion through the infarct related artery • This perfusion pattern contributes to the high incidence of post-MI angina, infarct extension and recurrent MI

18. Clinical Presentation • Diagnosis made by combination of history, ECG findings and laboratory evaluation

19. Clinical Presentation • Symptoms range from no pain to mild epigastric discomfort to severe crushing substernal chest pain. • i.e. similar to any acute chest pain syndrome

20. Clinical Presentation • Typical picture is that of substernal chest pain with autonomic symptoms, and ST segment depression which persists following the resolution of the pain

21. Clinical Presentation • Unstable presentations such as hypotension, CHF, and cardiogenic shock are rare with NQWMI since there tends to be a smaller area of damaged myocardium

22. ECG Findings • Unlike QWMI which often present with ST segment elevation, NQWMI’s often present with a variety of ECG changes including ST segment depression, ST segment elevation, T wave inversion and no ST segment changes at all.

23. ECG Findings • Kleiger et al • Found that up to 14% of patients with suspected NQWMI developed late Q-waves (after 3 days) with no evidence of infarct extension. • Thus ECG’s should be repeated for up to 3 days following enzyme peak before categorizing patients as having a Q or Non-Q MI

24. Prognosis • Depends on: • Size of myocardial infarction • left ventricular function • presence of arrhythmias

25. Prognosis • Nicod et al • 1869 patients with acute MI, 1425 Q and 444 NQ • One year follow-up • Primary end point - in-hospital and one year mortality

26. Prognosis In hospital mortality 1-year mortality Q-wave 11.5% 9.2% Non-Q-wave 8.1% 13.7% p-value P<0.06 P<0.05

27. Prognosis • Zareba et al • 549 patients with acute MI, 363 Q and 186 NQ • Primary end point - any subsequent cardiac event • Follow-up 40 months

28. Prognosis - Zareba et al 0.30 0.20 0.10 0 Cardiac Event Rate 0 200 400 600 800 1000 Days

29. Prognosis Zareba et al Cardiac event Q-wave 15.7% Non-Q-wave 16.7% p value NS

30. Prognosis - Zareba et alPost infarct angina 0.40 0.30 0.20 0.10 0.0 Q-wave p=0.0452 Non-Q p=0.0002 Chest pain Chest pain Cardiac Event Rate No chest pain No chest pain 0 400 600 1000 0 400 600 1000 Days

31. Prognosis - TIMI II • Secondary analysis of 2634 patients • All patients received thrombolytics • Primary end point - Death or MI • 1867 Q-wave and 767 Non-Q-wave MI’s

32. Prognosis - TIMI II • Analysis of differences between Q and NQWMI • At baseline • ECG • Angiography • Discharge testing • Follow-up period

33. Prognosis - TIMI II • Findings at Baseline • Patients with Q-wave MI’s were more likely to be male, have anterior MI’s and were less likely to have used nitrates in the week prior to their MI compared to the NQWMI counterparts.

34. Prognosis - TIMI II • ECG Findings • QWMI’s - More leads with ST segment elevation • Greater deflection of the ST segments • Higher percentage of patients with more than 0.3mV ST segment deflection.

35. Prognosis - TIMI II • ECG Findings • Patients with NQWMI were more likely to have normalization of ST segments following thrombolytics than their counterparts with QWMI.

36. Prognosis - TIMI II • Angiographic findings • TIMI 3 flow more likely in NQWMI • No difference in degree of stenosis • Similar collateral flow

37. Prognosis - TIMI II • Pre-discharge testing • NQWMI patients had better ejection fractions • QWMI patients were more likely to have CHF • NQWMI patients had more reinfarction • One year mortality rate was similar

38. Prognosis - TIMI II NQ p=0.24 Cumulative Death rate 0 10 20 Q 0 13 26 39 52 Weeks

39. Prognosis - Chung et al • Predictors of Mortality (age >70) • Advanced age • Advanced NYHA classification • Advanced Killip classification • Higher peak CK’s • Depressed LVEF

40. Post MI Testing Low Level Exercise Stress Symptom Limited Exercise Stress Nuclear Imaging Dobutamine Echocardiography Coronary Angiography

41. Post MI Testing • Why test • Who has inducible ischemia after MI? • Evaluate the presence of viable myocardium behind stenotic lesions • Who will benefit from early revascularization

42. Post MI Testing • Issues to consider • Hemodynamic Stability of Patient • Cost • Risk Stratification - who has jeopardized myocardium

43. Post MI Testing - Bissett et al 100 Jeopardized Myocardium 75 50 % with jeopardized myocardium 25 Ant. NQ Inf NQ Ant Q Inf Q

44. Which testing modality best predicts recurrent cardiac event? Post-MI Testing Rest ECG Ambulatory ECG Recurrent Event Exercise ECG Thallium Scintigraphy ?

45. Post-MI Testing - Moss et al • 936 patients with MI within last 6 months • All patients underwent rest ECG, ambulatory ECG, exercise ECG and stress thallium • Primary end-point first recurrent cardiac event (death, MI or unstable angina) • Follow-up every 4 months for an average of 23 months

46. Post-MI Testing - Moss et al Rest Ambulatory 0.0 0.1 0.2 0.3 0.4 0.0 0.1 0.2 0.3 0.4 Cardiac Event Rate Cardiac Event Rate 0 200 400 600 800 1000 0 200 400 600 800 1000 Days Days Exercise Thallium 0.0 0.1 0.2 0.3 0.4 Cardiac Event Rate 0.0 0.1 0.2 0.3 0.4 Cardiac Event Rate 0 200 400 600 800 1000 0 200 400 600 800 1000 Days Days

47. Post MI testing - Moss et al • ST segment depression on exercise testing or ambulatory ECG did not predict subsequent cardiac events • Reversible defects by thallium correlated with late cardiac events but results were not statistically significant

48. Post MI testing - Moss et al • Only resting ECG ST segment depression accurately predicted risk of recurrent cardiac event • Study included Q and Non-Q-wave MI but subgroup analysis did not differ

49. Low-level Exercise Stress • Can patients with recent MI exercise? • What is a low-level exercise test? • What is the implication of a positive low-level exercise stress test

50. Low-level Exercise Stress • Krone et al • 141 patients with NQWMI within 2 months of MI • Exercise Stress to 5 mets • Follow-up q 3 months x4 then yearly up to 4 • Endpoint - cardiac death and non-fatal MI