The pathophysiology of acute myocardial infarction is currently based on observations made in 1912 by Herrick and reconfirmed in 1980 by Dewood. They described occlusion of stenotic coronary arteries by thrombus in the setting of acute myocardial infarction. Thrombus formation most often results in the setting of a ruptured atherosclerotic plaque. The degree of obstruction and thrombus is variable and due of multiple factors including dysfunctional coronary endothelium, extent of obstruction, platelet aggregation, and altered vasomotor tone. These mechanisms are believed to be responsible for at least 85% of all myocardial infarctions.
Other mechanisms of myocardial infarction include coronary artery vasculitis, embolic phenomena, coronary artery spasm, congenital abnormalities, and increased blood viscosity. Cocaine-induced myocardial infarction is thought to be multifactorial since severe vasospasm and acute thrombus have been described in both stenotic and normal coronary arteries.
In most patients, no precipitating cause for ruptured plaques resulting in myocardial infarction can be found. A modest relationship to heavy exercise, emotional stress, trauma, and neurologic disturbances has been described. Early-morning predilection for acute myocardial infarction has also been demonstrated and may be related to circadian rises in catecholamines and platelet aggregation.
Describe the typical signs and symptoms of acute myocardial infarction.
The classic symptoms of myocardial infarction include dull substernal chest pain, dyspnea, nausea, diaphoresis, palpitations, or sense of impending doom. The chest pain typically lasts at least 15-30 minutes and may radiate into the arms, jaw, or back. The elderly often have atypical presentations, such as dyspnea, confusion, vertigo, syncope, and abdominal pain. Approximately 25% of myocardial infarctions are either asymptomatic or unrecognized and are termed silent.
General examination findings include pallor, diaphoresis, and anxiety. Abnormalities in blood pressure, heart rate, and respiratory rate are variable, depending on the type and extent of infarction. A low-grade fever may be present. A fourth heart sound is almost always present. Jugular venous distention and a third sound may occur, depending on the site and extent of infarction. Precordial friction rubs and peripheral edema may be present later but are not usually present in the first few hours after infarction. In the setting of papillary muscle dysfunction or rupture, the murmur of mitral regurgitation may be present, although it is often much shorter and softer than expected.