ABSTRACT
Myocardial infarction results from the interaction of multiple cardiac risk factors and a genetic predisposition for atherosclerosis that triggers intramural plaque instability, rupture of the fibrous cap and acute thrombotic occlusion. The resulting interuption in coronary flow causes loss of contracting myocytes. This chapter describes the effects of reperfusion on postinfarction remodeling of (LV) myocardium and potential mechanisms by which the beneficial impact on clinical outcome may be mediated. LV remodeling is a well-characterized process through which the heart responds to cellular injury and to changes in loading conditions. Remodeling may be physiologic and reversible, or pathologic and irreversible—or only partially reversible. Immediately after acute myocardial infarction, the ischemic region stops contracting and within one hour, the infarct zone expands and the LV begins to diiate. Stroke volume and ejection fraction acutely decrease as both ischemic and nonischemic myocardium adapt to the mechanical overload from early LV dilatation and myocardial stretching.
