Causes and Incidence
More than 90% of all myocardial infarctions (MIs) are caused by obstruction of a plaque-lined coronary artery by an acute thrombus. MI also may be caused by arterial embolization from valvular stenosis or endocarditis and by arterial spasm after cocaine ingestion. Each year more than 1 million people in the United States suffer an MI; one in four dies, and more than half of the deaths occur within 1 hour of onset.
Occlusion of a coronary artery causes a persistent cellular ischemia that interferes with myocardial tissue metabolism, causing rapid, permanent cell damage and necrosis. The extent of necrosis is dictated by the size of the infarct, the vessel occluded, and the length of time it remains occluded. Damage initially occurs to the left ventricle but often extends to other cardiac chambers. Infarcts may be classified by the thickness of the myocardial tissue involved. Transmural infarcts (Q wave) involve the full thickness of the myocardium from the epicardium to endocardium and cause abnormal Q waves on the ECG. Nontransmural infarcts (non–Q wave) do not extend through the ventricular wall and cause ST segment or T wave ECG abnormalities.
Most individuals have prodromal symptoms such as fatigue, shortness of breath, and crescendo angina days or weeks before the acute attack. The first symptom of the attack is usually a deep, substernal, visceral pain that may be described as aching, squeezing, or crushing, or as a heavy weight on the chest. The pain may radiate to the back, neck, jaw, teeth, or left arm, and it is not relieved by rest, nitroglycerin, or antacids. Other signs and symptoms include anxiety; restlessness; sweating; nausea; vomiting; cold, clammy skin; low-grade fever; and dyspnea.
Complications include arrhythmia, cardiogenic shock, heart failure, pulmonary edema, cerebral or pulmonary emboli, myocardial rupture, pericarditis, postmyocardial infarction syndrome, and sudden death.
The diagnosis is made using a clinical history; electrocardiography, which illustrates an elevation in the ST segment, T wave inversion, and deep Q waves; laboratory tests of cardiac enzymes (aspartate aminotransferase, creatine phosphokinase, lactate dehydrogenase), which are elevated for days after the event; a complete blood count, which reveals an elevated white count and erythrocyte sedimentation rate; a thallium perfusion scan, to determine the size and location of the infarct and resulting ischemia; and an echocardiogram, to detect contraction abnormalities of ventricles.
Angioplasty post thrombolysis is contraindicated; recent clinical trials have shown no benefit and possible harm from angioplasty performed within the first few days after an attack; angioplasty may have a rescue role in cardiogenic shock that is unresponsive to other treatment.
Thrombolytic drugs are given within 6 hours of onset to interrupt MI evolution; aspirin and anticoagulants for antiplatelet, anticoagulant effects; beta-adrenergic blockers to reduce reinfarction and infarct size; vasodilators and narcotic analgesics for pain; stool softeners to avoid straining at stool; sedatives and tranquilizers to increase rest.
Cardiovascular monitoring; oxygen therapy; bed rest; decreased environmental stimuli; monitoring for and treatment of depression, particularly about the third day; quitting smoking; restriction of caffeine and cholesterol; antiembolism hose; rehabilitation with stepped exercise program; sexual counseling; regular medical follow-up.