1. Acute Myocardial Infarction Willis E. Godin D.O., FACC

2. Acute Myocardial Infarction  Definition:  Decreased delivery of oxygen and nutrients to the myocardium  Myocardial tissue necrosis causing irreparable tissue/cell death

3. Pathophysiology  The most frequent cause of an acute MI is a disruption in the vascular endothelium that is associated with myocardial plaque  Plaque occurs over a period of years to decades  This combination causes the development of an intra-coronary thrombus, which causes the coronary artery to occlude  Within 20-40 minutes of an occlusion, irreversible myocardial cell damage/death occurs

4. Pathophysiology  2 primary characteristics of plaque development are 1) a fibromuscular cap and 2) an underlying lipid rich core.  The overall loss of structural stability of the plaque usually occurs at the junction between the fibromuscular cap and the vessel wall (shoulder region)  Thrombus develops (due to the platelet- mediated activation of the coagulation cascade) and partial or complete occlusion occurs causing an acute myocardial infarction.

7. Pathophysiology  The severity of an MI depends on three factors  1) The level of the occlusion in the coronary artery  Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium that will be at risk of necrosis  2) The length of time of the occlusion  The longer the period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion  3) The presence or absence of collateral circulation

8. Pathophysiology  STEMI  “complete” blockage of a coronary artery  NSTEMI  “near-complete” blockage of a coronary artery

9. Pathophysiology  Left Coronary Artery  Left Anterior Descending Artery (LAD)  “widow maker”  Anterior MI  Lateral MI  Left Circumflex Artery (LCx)  Lateral MI  Posterior MI  Right Coronary Artery  Inferior MI  RV MI

11. Prevalence  Myocardial Infarction is the leading cause of death in the United States  Approximately 450,000 people in the US die from coronary disease per year  50% of all acute MI’s in the US occur in people under the age of 65  No longer considered a “disease of the elderly”

12. Risk Factors  Dyslipidemia  Diabetes Mellitus  Hypertension  Tobacco use  Family History  Male gender

13. Diagnosis  Symptoms (gained by an accurate history)  Electrocardiogram (ECG)  Laboratory Tests  CK  CK-MB  Troponin  Echocardiogram

14. Symptoms  Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax  Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back  Associated dyspnea or shortness of breath  Associated epigastric discomfort with or without nausea and vomiting  Associated diaphoresis or sweating  Syncope or near syncope without other cause  Impairment of cognitive function without other cause

16. Electrocardiogram  ST elevation myocardial infarction (STEMI)  > 1mm ST elevations in contiguous leads  Non-ST elevation myocardial infarction (NSTEMI)  ST depression  T wave inversions  No obvious ECG changes

17. ECG - STEMI

19. ECG -NSTEMI

22. Cardiac Enzymes  Serial blood draws  Every 4 hours x 4 sets  Myoglobin peaks first (detectable in 1-4 hrs)  Troponin  peaks last (detectable in 3-12 hrs)  most specific  remains detectable in serum the longest

23. Cardiac Enzymes

25. Imaging (Echocardiography)  An echocardiogram can be performed to assess areas of the left ventricle that are not contracting normally as compared to areas that are contracting normally  After normal blood flow is interrupted, the area of the myocardium affected by the occluded artery will not function normally.  This abnormal wall motion can be detected by echocardiography

26. Treatment  Antiplatelets  Supplemental oxygen  Nitrates  Pain control  Beta Blockers  Statin Therapy  Heparin (unfractionated / low-molecular-weight heparin)  Fibrinolytics  Angiotensin-Converting Enyme Inhibitors / Angiotensin Receptor Blockers  Glycoprotein Iib/IIIa Antagonists  Aldosterone Antagonists

27. Other Treatment Options  Percutaneous Coronary Intervention  PCI / coronary stenting  Surgical Revascularization  CABG  Implantable Cardiac Defibrillators  AICD

33. Treatment Outcomes  Long-term medications  Smoking cessation  Cardiac Rehabilitation

34. Long-Term Medications  Most oral medications instituted in the hospital at the time of acute MI will be continued long term  Aspirin, beta blockade, and statin therapy is continued indefinitely in all patients  ACE inhibitors are continued indefinitely in patients with CHF, left ventricular dysfunction, hypertension, or diabetes  Diet modification, regular exercise

35. Smoking Cessation  Smoking is a major risk factor for coronary artery disease and MI  For patients who have undergone an MI, smoking cessation is essential to recovery, long- term health, and prevention of re-infarction  In one study, the risk of recurrent MI decreased by 50% after 1 year of smoking cessation

36. Smoking Cessation  All STEMI and NSTEMI patients with a history of smoking should be advised to quit and offered smoking cessation resources  Nicotine replacement therapy  Pharmacologic therapy  Referral to behavioral counseling or support groups  Smoking cessation counseling should begin in the hospital, at discharge, and during follow up

38. Cardiac Rehabilitation  Provides a venue for continued education, reinforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI including exercise training  Participation in cardiac rehabilitation programs after MI is associated with decreases in subsequent cardiac morbidity and mortality  Other benefits include improvements in quality of life, functional capacity, and social support

39. Summary  MI results from myocardial ischemia and cell death, most often because of an intra-arterial thrombus superimposed on an ulcerated or unstable atherosclerotic plaque  Despite advances in therapy, MI remains the leading cause of death in the United States.  MI risk factors include hyperlipidemia, diabetes, hypertension, male gender, and tobacco use.  Diagnosis is based on the clinical history, ECG, and blood test results, especially creatine phosphokinase (CK), CK-MB fraction, and troponin I and T levels.

40. Summary  Outcome following an MI is determined by the infarct size and location, and by timely medical intervention.  Aspirin, nitrates, and beta blockers are critically important early in the course of MI for all patients.  Post-discharge management requires ongoing pharmacotherapy and lifestyle modification.