Patterns of left ventricular dilatation with an opened artery after acute myocardial infarction: missing links to long-term prognosis.

Ventricular remodeling, the geometric adaptation to injury after acute myocardial infarction, affects the function of both non-infarcted and infarcted muscle, as well as prognosis. Ventricular dilatation bodes especially poorly for late survival.1 It has long been recognized that early infarct expansion is the result of lengthening of the noncontractile region undergoing a stress response with secondary volume overload hypertrophy, a process which maybe progressive over time.2–4 The extent of the initial myocardial damage is linked both to the magnitude and, to a lesser degree, the timing of left ventricular (LV) dilatation and ultimately survival.5 Moreover, ventricular remodeling (enlargement) is influenced not only by infarct size but also the type of infarct healing and coexistent LV wall stresses.5