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 coronary atherosclerosis, acute plaque change, and superimposed thrombosis (as discussed previously). In contrast, a subendocardial

(nontransmural) infarct constitutes an area of ischemic necrosis limited to the inner one third or at most one half of the ventricular wall; under some circumstances, 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 is

most vulnerable to any reduction in coronary flow. A subendocardial infarct can occur as a result of a plaque disruption followed by coronary thrombus that becomes lysed before

myocardial necrosis extends across the major thickness of the wall; in this case the infarct will be limited to the distribution of one coronary artery with plaque change. However,

subendocardial infarcts can also result from sufficiently prolonged and severe reduction in systemic blood pressure, as in shock, often superimposed on chronic, otherwise noncritical,

coronary stenoses. In cases of global hypotension, resulting subendocardial infarcts are usually circumferential or nearly so, 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, are discussed in Chapter 11 and are not reiterated here. Suffice it to say that 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, and 45% occur in people under age 65. Blacks and whites are equally affected. Throughout life, men are at significantly greater risk of MI

than women; the differential progressively declines with advancing age. Except for those having some predisposing atherogenic condition, women are remarkably protected against MI

during the reproductive years. Nevertheless, the decrease of estrogen following menopause can permit rapid development of coronary artery disease (CAD), and IHD is the overwhelming

cause of death in elderly women. Moreover, recent epidemiologic evidence suggests that postmenopausal hormone replacement therapy does not protect women against MI.[53]

Pathogenesis.

We now consider the basis for and subsequent consequences of myocardial ischemia, particularly as they relate to the typical transmural myocardial infarct.

Date: 2016-04-22; view: 1100