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

Abstract

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 See p 2351 The most effective interventions to limit or prevent ventricular dilatation after infarction are those addressing the initial myocardial insult through the earliest and most sustained reperfusion therapies.6 The re-establishment of coronary blood flow to the infarcted region, even if delayed in some circumstances, is thought to attenuate ventricular remodeling. Modification of those biochemical and physiological factors that deform the compromised ventricle also influences late ventricular adaptive responses and prognosis. It is now common knowledge that instituting afterload reduction improves ventricular remodeling, attenuates infarct expansion, and provides long-term clinical improvement.1 However, of the three major factors involved in the acute infarct remodeling sequence, cardiologists can exert the most influence only at the onset through the timeliness and …