Atherosclerotic Heart Disease Part II: Myocardial Infarction

1. Atherosclerotic Heart DiseasePart II: Myocardial Infarction Humayun J. Chaudhry, D.O., M.S., S.M., FACP, FACOI Chairman, Department of Medicine and Assistant Dean for Health Policy New York College of Osteopathic Medicine of NYIT September 21, 2005

2. Acute Myocardial Infarction • When it happens… • Usually caused by sudden thrombotic occlusion of a coronary artery at the site of an atherosclerotic plaque that has become unstable due to a combination of ulceration, fissuring and rupture • CHF ensues if 25% or more of the left ventricle is infarcted • Cardiogenic shock ensues if 40% or more of the left ventricle is infarcted • Right ventricular ischemia or infarction occurs in up to ½ of inferior wall infarctions

3. EKG Findings • EKG Patterns for Localization of Infarct • Inferior wall MI: see changes in leads II, III and aVF • Anterior septal MI: see changes in leads V1, V2 and V3 • Anterior wall MI: see changes in leads V2, V3 and V4 • Lateral wall MI: see changes in leads V5, V6, I and aVL • ST segment elevation and T wave changes occur first, then Q waves form

4. Coronary syndromes have exploded since the early 1920’s

5. Trends in the Leading Causes of Death in the U.S., 1970-2002 • Absolute # of deaths and age at death continue to increase • There have been decreases in death rates from stroke (63%), ASHD (52%) and accidents (41%) • There have been increases in death rates from COPD (200%) and DM (45%) since 1987 • Source: Ahmedin Jemal et al, JAMA, 294(10): 1255-1259, September 14, 2005

9. Pathophysiology • Atherosclerotic plaques rich in foam cells that are susceptible to sudden plaque will rupture and hemorrhage into the vessel wall. This may result in the sudden partial or total occlusion of the coronary artery • After total occlusion, myocardial necrosis is complete in 4-6 hours. Flow to ischemic area must remain above 40% of pre-occlusion levels for that area to survive

10. Myocardial infarctions can be divided into Q-wave and non Q-wave, with the former being transmural and associated with totally obstructed infarct-related artery and the latter being non-transmural (subendocardial) and associated with patent vessels • Total occlusion of the left main coronary artery, which usually supplies 70% of the LV mass, is catastrophic and results in death in minutes.

11. Common Signs/Symptoms Pain - Arm, back, jaw, epigastrium, neck, chest Anxiety Lightheadedness, pallor, weakness, syncope Nausea, vomiting, diaphoresis Chest heaviness, tightness Cough, diaphoresis, dyspnea, crackles, and wheezing

12. Hypercholesterolemia (increased LDL; decreased HDL) Premature (<55) familial onset of coronary disease Smoking Diabetes mellitus Hypertension Sedentary life style Aging Hostile, frustrated personality Hypertriglyceridemia Obesity Pertinent Risk Factors

13. Estimating future ASHD, developed by Framingham Heart Study Group, stratifies patients by their age, number and severity of their risk factors

15. S4/S3 heart sounds Arrhythmias Hypertension, hypotension Levine’s sign Jugular venous distention (JVD) Diaphoresis Pallor Bradycardia, tachycardia, or irregular pulses Physical Exam

16. Serum Cardiac Markers • Troponin I • Becomes positive in 3-12 hours • Peaks at 24 hours • Remains elevated for 4-10 days • Highly sensitive in early detection of cardiac injury • Can be used to help decide whether it is safe to discharge patients who present to the emergency department with acute chest pain • Patients without ST segment elevations during pain and 2 negative troponin I determinations (one at least 6 hours after the onset of symptoms) have a low risk of death or fatal acute MI (0.3%) during the next 30 days.

17. Serum Cardiac Markers • CK-MB Fraction • CK-MB1 (plasma) and CK-MB2 (tissue)-myocardial necrosis can be detected earlier with subform analysis then with traditional CK-MB measurement • Within 6 hours CK-MB2 greater than 1.0 U/L with a ratio of CK-MB2/CK-MB1 greater than 1.5 is more sensitive and specific than CK-MB alone for diagnosis of MI • If a patient presents more than 24 hours after a presumed MI, and the CK isoenzymes are inconclusive, troponin I is now preferred over LDH

20. Early Assessment of Infarct Size • Currently, 2-D echocardiography is the technique used most frequently in the hospital course to evaluate acute MI infarction size • 2-D Echo reveals • Extent and location of ventricular wall abnormalities • Provides an assessment of overall ventricular function • Demonstrates left ventricular thrombus • Color flow doppler provides information about the extent of valvular disease and mechanical complications of acute MI

21. Approach to the patient with Acute MI • A. History I. Aspirin • B. Physical J. Oxygen • C. EKG K. Thrombolytic Therapy • D. Enzymes L. Heparin • E. Chest X-Ray M. Angiography • F. Nitrates N. PTCA with stenting • G. Beta-blockers O. CABG • H. Morphine sulfate P. GPIIB/IIIA inhibitors

22. Acute Reperfusion Therapy • Rapid reperfusion of the infarct related artery with IV thrombolytic therapy or primary PTCA is the main treatment strategy for acute MI • The main goal is to improve survival and outcome (decrease incidence of CHF) • The benefits of reperfusion therapy are time dependent: the sooner the blood flow is restored to the ischemic zone the greater the advantage in terms of survival and functional recovery

23. 80 t-PA * * 70 60 SK 62 % ofPatients 40 43 *P<0.001 31 20 0 Reperfusion of Patency at 90 minutes occluded arteries TIMI 1 Primary Outcome Comparison of t-PA and Streptokinase TIMI Study Group, N Engl J Med, 1985 (312): 397-401

24. Acute Reperfusion Therapy • Risk of hemorrhage • Age greater than 65 • Weight less than 70 kg • Female • Hypertension • Although patients greater than 75 years have a greater risk of hemorrhage and stroke with thrombolytic therapy, they have a net benefit in overall outcome because of a significant mortality reduction with thrombolytic therapy

25. Thrombolytic therapy within the first six hours of a coronary event

26. After the first 10 hrs the mortality benefits decrease

29. Pt presents to ED s/p chest heaviness X3hrs

30. 30 min post-arrival, terminal inverted T waves are noted septally

31. 1 hr post-arrival the patient develops ST segment elevation in the anteroseptal walls

32. The lack of ST segment elevation decreases the mortality of a coronary event

33. Those with new LBBB (left bundle branch block) have worst prognosis

34. Management Protocol

35. No one thrombolytic has been shown to be superior, they differ really only by the Bolus and infusion rates…as well as price

36. Most important factor in treatment success with thrombolytics is time

38. TIMI 1 Monitoring Reperfusion TIMI Grade Flow Scoring System Mortality at 42 Days TIMI 0 Complete occlusion TIMI 1 Penetration of obstruction by contrast but no distal perfusion TIMI 2 Perfusion of entire artery but delayed flow TIMI 3 Full perfusion, normal flow P < 0.005 Flygenring BP et al. JACC 1991 (17): 275

39. GUSTO trial shows that the higher the TIMI grade for flow rate, the lower the mortality

40. 2004 ACC/AHA STEMI Guidelines • 3 Major Areas of Revision • Preference for PCI over fibrinolysis in patients who present less than or equal to 12 hrs after symptoms and… • If PCI can be performed within 90 minutes of presentation by experienced personnel • Aggressive treatment of cardiogenic shock • Greater clarity regarding adjuvant therapy

41. Those patients Tx with frontloaded t-Pa as compared to streptokinase had achieved TIMI grade 3 in 54% of the time as compared to 33%

43. Meta-analysis shows the benefits of ß-blockade

44. Pt’s treated with B-blockers post infarction are seen to have a significant reduction in re-infraction

45. Adding an ACE-I dramatically reduces mortality

49. What about Nitrates?

50. And if Mg++ was added…