ACUTE MYOCARDIAL INFARCTION



Myocardial infarction refers to irreversible ne­crosis of myocardium. It usually results from atherosclerotic narrowing of a major coronary artery that creates an unfavorable balance of myocardial oxygen supply versus demand. Initially ischemia occurs and if severe and prolonged, myocardial infarction follows, the extent of which depends on the severity of the ischemia, the area of muscle supplied by the obstructed coronary artery, the extent of collateral blood flow, and” the oxygen demands of the tissue supplied by the artery. My­ocardial infarction may be transmural, that is, in­volving the full thickness of the left ventricular wall, or nontransmural, involving only the sub-endocardium and adjacent myocardium. The electrocardiographic findings of “transmural” versus “subendocardial” infarction do not cor­relate well with the pathological extent of infarc­tion. No gross pathological changes occur in the myocardium until approximately six hours after myocardial infarction, and even light microscopic findings until that time are subtle. The myocar­dium initially appears pale and slightly edema­tous and over the next few days changes color as exudate and neutrophil infiltration occur. Eight to ten days after infarction the myocardium in the region of the infarction thins as debris is removed by mononuclear cells, and granulation tissue forms that by three to four weeks extends through the necrotic tissue. Subsequently, a thin scar de­velops that becomes firm over a six-week interval. Ninety per cent of transmural myocardial in­farctions are associated with complete obstruc­tion of a coronary artery, consisting of fresh thrombus superimposed on a critically stenotic lesion. Nontransmural myocardial infarctions fre­quently occur distal to severely stenotic but still patent arteries. Mechanisms by which thrombosis occurs in the region of atherosclerotic plaques may include changes in the atherosclerotic intima promoting thrombosis, hemorrhage into the ath­erosclerotic plaque, ulceration of the plaque with activation of clotting factors, platelet thrombi, or coronary spasm at the site of a plaque causing sludging of blood flow and deposition of platelets and fibrin. Reperfusion can be achieved in many cases using intracoronary or intravenous fibri­nolytic agents; however, residual high-grade ath­erosclerotic lesions are usually present at the site of occlusion after thrombi dissolution.