1. Acute Myocardial Infarctions Howard L. Sacher, D.O. Chief, Division of Cardiology Adjunct Clinical Associate Professor of Medicine New York College of Osteopathic Medicine

2. Learning Objectives To understand current concepts of the pathophysiology of acute myocardial infarction (AMI). To understand and apply current strategies in the evaluation of patients with AMI. To understand and apply current strategies in the management of patients with uncomplicated AMI. To understand and apply current strategies in the evaluation and management of patients with complications of AMI.

3. Acute Myocardial Infarction Acute Myocardial infarction A. usually caused by sudden thrombotic occulusion of a coronary artery at the site of an atherosclerotic plaque that has become unstable due to a combination of ulceration, fissuring and rupture. B. CHF if 25% of the left ventricle is infarcted C. Cardiogenic shock if 40% of left ventricle is infarcted D. Right ventricular ischemia or infarction occurs in up to ½ of inferior wall infarctions.

4. E. EKG 1.inferior wall myocardial infarction changes leads II, III and aVF. 2. Anterior septal MI-V1, V2, V3 3. Anterior wall MI- V2, V3, V4 4. Lateral wall MI-V5,V6, I, aVL ST segment elevation and T wave changes occur first, then Q waves form

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

7. The Progress of Atherosclerosis Foam cells – beginning of fatty streak Endothelial cell Activated macrophage T-cell Adhesion molecules LDL particle IL-6 IL-1 TNF-  Smooth muscle cells ‘Oxidised’ LDL Monocyte IL-6 IL-1 TNF-  Liver Bone marrow Excess LDL-C leads to Accumulation in Intima Trapped LDL particles undergo oxidation Oxidized LDL are not recognized - Activate macrophage which produces, and stimulates endothelial cells to produce IL-6, IL-1, TNF-a, neopterin. This in turn causes endothelial cells to produce adhesion molecules. Monocytes attach and drop from circulation, mature to macrophages and engulf LDL = Foam Cell

13. There is a direct correlation between the amount of fatty streaks in the intralumenal surface and coronary events in young individuals

14. Pathophysiology Atherosclerotic plaques rich in foam cells that are susceptible to sudden plaque rupture and hemorrhage into the vessel wall, which 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.

15. The 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 and associated with patent Total occlusion of the left main coronary artery which usually supplies 70% of the LV mass is catastrophic and results in death in minutes.

16. Common Signs/Symptoms Pain - arm, back, jaw, epigastrium, neck, chest Anxiety Lightheadedness, pallor, weakness, syncope Nausea, vomiting, diaphoresis Chest heaviness, tightness Cough, diaphoresis, dyspnea, rales, wheezing

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

18. Estimating future CHD,developed by Framingham Heart Study Group, stratifies Pt’s by their age number and severity of their risk factors. Separate one for men and women

20. Physical Exam S4/S3 heart sound Arrhythmias Hypertension, hypotension Levine’s sign Jugular venous distention Diaphoresis Pallor Bradycardia, tachycardia, or irregular pulses Fourth heart sound

21. Serum Cardiac Markers A. cTnI/Troponin I 1.Becomes positive in 3-12 hours 2. Peaks at 24 hours 3. Remains elevated for 4-10 days 4. Highly sensitive for early detection of myocardial injury 5. Can be used to help decide whether it is safe to discharge patients who present to the emergency room with acute chest pain

22. Cont’d 6. 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 (.3%) during the next 30 days.

23. Cont’d B.CKMB subforms, 1. CKMB1 (plasma) and CKMB2 (tissue)- myocardial necrosis can be detected earlier with subform analysis then with traditional CKMB measurement. 2.Within 6 hours CKMB2 greater than 1.0 U/L with a ratio of CKMB2/CKMB1 greater than 1.5 is more sensitive and specific than CKMB for diagnosis of MI

24. Cont’d 3. 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.

27. Early Assessment of Infarct Size A. Currently two dimensional echocardiography is the technique used most frequently in the hospital course to evaluate acute MI infarction size. B. Echo reveals 1. Extent and location of ventricular wall abnormalities 2. Provides an assessment of overall ventricular function 3. Demonstrates left ventricular thrombus 4. Color flow doppler provides information about the extent of valvular disease and mechanical complications of acute MI.

28. Approach to the patient with Acute MI A. HistoryI. Aspirin B. PhysicalJ. O2 C. EKGK. Thrombolytic Therapy D. EnzymesL. Heparin E. Chest X-RayM. Angiography F. NitratesN. PTCA with stenting G. Beta-BlockersO. CABG H. MorphineP. GPIIB/IIIA antagonists

29. Acute Reperfusion Therapy A. 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 benefit 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.

30. Cont’d B. Risk of hemorrhage 1. Age greater than 65 2. Weight less than 70 kg. 3. Female 4. 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.

31. Thrombolytic therapy with in the 1 st 6hr of a coronary event

32. After the 1 st 10hrs the benefits mortality benefits decrease

35. Pt presents to ED s/p chest heaviness X-3hrs

36. 30min post arrival terminal inverted T waves are noted septally

37. 1hr post arrival the patient develops ST segment elevation in the anteroseptal walls

38. The lack of ST segment elevation decrease the mortality of a coronary event

39. Those with a new onset LBBB has the worst Px

40. Management Protocol

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

42. The most important factor in tx with thrombolytics is time

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

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

46. Heparin – yes or no?

48. Gusto I

49. Pharmacokinetics ASA GP IIb IIIa Ticlopidine Anti-Thrombins Dipyridomol Epoprostenol

51. Meta-analysis shows the benefits of B-blockade

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

53. Adding an ACE-I dramatically reduces mortality

57. What about Nitrates?

58. And if Mg was added:

59. Rx d/c after MI A. Beta-blocker B. ACE-Inhibitor or if not tolerated, ARB C. Aspirin D. Lipid lowering drug- Statin E. Folic Acid, Vit B6, Vit B12 ? F. Clopidogrel

63. Hemodynamic Compromise A. Patients who develop hemodynamic compromise (CHF, Hypotension, Cardiogenic shock) following AMI have a worse prognosis than those with little or no hemodynamic impairment. B. Management of hemodynamic compromise is aided by balloon flotation Swan-Ganz catheter. This catheter makes it possible to measure cardiac output and PCWP that reflect LVEDP and helps the physician adjust therapy according to the patients hemodynamic subset

69. Right Ventricular Infarction A. Nearly 50% of patients with inferior wall MI have some evidence of right ventricular ischemia or infarction (It is hemodynamically significant in only about 10% of these patients). B. Should be suspected with inferior MI when patient presents with a triad of hypotension, clear lung fields, and jugular venous distention (right atrial pressure greater than 10 mmHg).

70. Cont’d C. Right sided EKG should be done in patients with inferior wall myocardial infarction. D. Treatment 1. Reperfusion therapy 2. Increasing preload by volume expansion(1 or more Liters of normal saline) 3. Cautious administration of Dobutamine 4. Diuretics and Vasodilators should be avoided

73. Papillary Muscle Rupture A. Has mortality of 80-90% with medical therapy B. Prompt surgical therapy indicated C. Intra-aortic balloon pump prior to surgery

75. Ventricular Septal Defect A. Has mortality of 50% with surgical treatment and at least 90% with medical treatment. B. Surgical repair and CABG C. Intra-aortic balloon pump prior to surgery

76. Rupture of LV free wall A. Occurs 10% of patients who die of an AMI B. Sudden hemodynamic collapse often accompanied by severe chest pain suggests possibility of rupture of free wall C. Echocardiogram diagnostic D. Emergency pericardiocentesis and use of intra aortic balloon pump to stabilize E. Emergency surgery is definitive therapeutic approach F. Event is almost always fatal even when emergency surgery attempted

77. LV Aneurysm and Mural Thrombus A. Occurs 10% of AMI patients B. 80% located in anterior apical segment and result from occlusion of LAD coronary artery C. Mural thrombus develops in about 50% of patients with anterior apical Q wave MI usually during the first week after infarction D. Thrombi are uncommon in inferior wall AMI and rare in non-Q wave infarctions

78. Cont’d E. Echocardiography useful for identifying LV aneurysm and mural thrombi F. 4% of AMI patients have embolic events during the first week after infarction G. There is a 5-fold increase in embolic events in patients with anterior apical MI’s found to have a mural thrombus by echo

79. Cont’d Other complications of LV aneurysms are CHF and ventricular aneurysms H. Treatment- anticoagulation with Heparin followed by Warfarin for 3-6 months significantly decreases frequency of embolic events

92. Using Dipi Tc99m MIBI imaging to stratify patients at risk for an event within the year

93. Assessment of Resting LV function A. Prognosis following AMI is related to degree of LV disfunction. B. Evaluation is done by echocardiogram, radionuclide imaging (MUGA study), positron emission tomography. C. Identify stunned and hybernating myocardium

94. Non-Invasive Strategies for Identifying Risk of Sudden Death A. Holter moniter- PVC’s, nonsustained ventricular tachycardia B. Signal averaged EKG C. Heart rate variability D. Patients at high risk of non-sustained V- tach, low EF(less than 40%) consider electrophysiologic testing and implantable cardioverter defibrillator (AICD)

95. Cont’d E. Multi-center automatic defibrillator implantation trial revealed (MADIT trial) 1. LV dysfunction less than 35% 2. Asymptomatic non-sustained V-tach (3 beats-30 beats) 3. Inducible, sustained, non-supressible V- tach Patients with these criteria had improved survival with AICD.

98. CHD really is worth preventing

104. At the end….. The acute coronary event (AMI) can be devastating…as clinicians, let’s do our part to try and prevent these events from occurring. Remember the old saying… “An once of prevention is worth a pound of cure”