Pathophysiology of Acute Myocardial Infarction

Acute coronary occlusion results in immediate systolic bulging (dyskinesia) of the ischemic muscle segment.15,17,10 Passive bulging occurs because the noncontracting ischemic region is stretched during systole by remote contracting muscle. In order to maintain a sufficient cardiac output to sustain life, remote myocardium not subject to infarction must hypercontract to compensate for dissipation of energy during passive stretching of the ischemic segment.15 Loss of more than 40% of contracting left ventricular muscle results in cardiogenic shock84,8 which can occur, e.g., with very proximal coronary occlusions. Survival after an acute coronary occlusion that renders less than 40% of the left ventricle nonfunctional depends upon the compensatory capacity of the remote "nonischemic" myocardium.15,17,27,77 Left ventricular power failure will develop even if the acute coronary occlusion leads to an ischemic region of the left ventricle less than 40%, if the mass of unaffected myocardium has been reduced by a previous myocardial infarction: reduced contractility (hypokinesis) or even "normal" contractility (normokinesis) in viable remote muscle has grave prognostic implications.15,50

Studies of the natural history of acute regional ischemia after coronary occlusion22 have shown that acute occlusion of a coronary artery not only affects the ischemic myocardium, but causes structural, functional, and metabolic alterations in the remote and adjacent myocar-dium.15-17 These changes in the remote myocardium are even more severe if the remote myocardium is supplied by a stenotic artery.15

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