MI, also known as heart attack, is overwhelmingly the most important form of IHD and alone is the leading cause of death in the United States and industrialized nations. About 1.5 million individuals in the United States suffer an acute MI annually and approximately one third of them die. At least 250,000 people a year die of heart attack before they reach the hospital.

Transmural Versus subendocardial Infarction

Most myocardial infarcts are transmural in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. This pattern of infarction is usually associated with chronic coronary atherosclerosis, acute plaque change, and superimposed completely obstructive thrombosis . In contrast a subendocardial infarct constitutes an area of ischemic necrosis limited to the inner one third or at most one half of the ventricular wall; it may extend laterally beyond the perfusion territory of a single coronary artery. As previously pointed out the subendocardial zone is normally the least well perfused region of myocardium and therefore most vulnerable to any reduction in coronary flow. In the majority of subendocardial infarcts, there is diffuse stenosing coronary atherrosclerosis and reduction of coronary flow but neither plaque disruption nor superimposed thrombosis. The two types of infarcts however are closely interrelated because, in experimental models, the transmural infarct begins with a zone of subendocardial necrosis that progressively encompasses the full thickness of the ventricular wall. Therefore a subendocardial infarct can occur as a result of aplaque disruption of followed by a coronary thrombus that becomes lysed before myocardial necrosis extends across the major thickness of the wall. Subendocardial infarcts, however can also result from sufficiently prolonged and severe reduction in systemic blood pressure, as in shock in cases of global hypotension resulting subendocardial infarcts are usually circumferential rather than limited to the distribution of a single major coronary artery.

Incidence and Risk factors

The risk factors for atherosclerosis the major underlying cause of IHD in general. MI may occur at virtually any age but the frequency rises progressively with increasing age and when predispositions to atherosclerosis are present, such as hypertension, cigarette smoking, diabetes mellitus, genetic hypercholesterolemia, and other causes of hyperlipoproteinemia. Nearly 10% of myocardial infarcts occur in people under age 40 yars 45% occur in people under age 65. Blacks and whites are affected equally often. Through out life, men are at significantly greater risk of MI than women the differential progressively declining with advancing age. Except for those having some predisposing atherogenic condition, women are remarkably protected against MI during the reproductive years. The decrease of estrogen after menopause can permit rapid development coronary heart disease. Epidemiologic evidence strongly suggests that postmenopausal hormone replacement therapy protects women against MI through favorable adjustment of risk factors, albeit with slightly increased risk of breast and endometrial cancer.

Coronary Arterial Occlusion

In nearly all transmural acute myocardial infarcts a dynamic interaction has occurred among several or all of the following severe coronary atheroscelerosis, acute atheromatous plaque change superimpsed platelet activation thrombosis and vasospasm- eventuating in an occlusive intra coronary thrombus overlying a disrupted plaque. In addition either increased myocardial demand or hemodynamic compromise can worsen the situation. Collateral circulation may provide perfusion to ischemis zones from a relatively unobstructed branch of the coronary tree, bypassing the point of obstruction and protecting against the effects of an acute coronary occlusion.

In the typical case of MI the following sequence of events can be proposed:

The initial event is a sudden change in the morphology of an atheromatous plaque- manifest as intraplaque hemorrhage, errosion or ulceration or rupture or fissuring.

Exposed to subendothelial collagen and necrotic plaque contents platelets undergo adhesion , aggregation activation and release of potent aggregators, including thromboxane A2 serotonin and platelet factors 3 and 4 vasospasm is stimulated.

Other mediators activate the extrinsic pathway of coagulation and add to the bulk of thrombus.

Frequently within minutes, the thrombus evolves to occlude completely the lumen of the culprit coronary vessel.