Acute Myocardial Infarction Willis E. Godin D.O., FACC
Acute Myocardial Infarction Definition: Decreased delivery of oxygen and nutrients to the myocardium Myocardial tissue necrosis causing irreparable tissue/cell death
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
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 plateletmediated activation of the coagulation cascade) and partial or complete occlusion occurs causing an acute myocardial infarction.
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
Pathophysiology STEMI complete blockage of a coronary artery NSTEMI near-complete blockage of a coronary artery
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
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
Risk Factors Dyslipidemia Diabetes Mellitus Hypertension Tobacco use Family History Male gender
Diagnosis Symptoms (gained by an accurate history) Electrocardiogram (ECG) Laboratory Tests CK CK-MB Troponin Echocardiogram
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
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
ECG - STEMI
ECG - STEMI
ECG -NSTEMI
ECG - NSTEMI
ECG - NSTEMI
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
Cardiac Enzymes
Cardiac Enzymes
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
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
Other Treatment Options Percutaneous Coronary Intervention PCI / coronary stenting Surgical Revascularization CABG Implantable Cardiac Defibrillators AICD
Treatment Outcomes Long-term medications Smoking cessation Cardiac Rehabilitation
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
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, longterm health, and prevention of re-infarction In one study, the risk of recurrent MI decreased by 50% after 1 year of smoking cessation
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
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
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.
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.