Left ventricular remodelling after acute myocardial infarction--solved and unsolved issues

Abstract

Left ventricular remodelling after acute myocardial infarction, through long-term left ventricular chamber dilatation and increased wall stress can result in alteration of the contractile properties of the non-infarct zone, impairment of the systolic and diastolic performances of the left ventricle, and eventually congestive heart failure. Left ventricular remodelling is influenced by several factors, among which the role of systemic and tissue renin angiotensin systems is determinant. Pharmacological interventions on the renin angiotensin systems were shown to limit left ventricular remodelling and reduce mortality from acute myocardial infarction in rats and humans, although the results of some trials remain controversial. To date, the beneficial effects of ACE inhibitors have only been demonstrated in patients with a low residual ejection fraction. Recent observations of changes in left ventricular chamber dilatation and left ventricular wall hypertrophy occurring over the course of time after acute myocardial infarction allow better definition of the subset of patients who are at risk of progressive left ventricular dysfunction and congestive heart failure. An akinetic surface >20%, a left ventricular ejection fraction <0 x 40, an anterior location of the infarction, a stroke volume <31 ml.m(-2) during the acute phase, and persistent occlusion of the infarct-related artery are the most powerful predictors of late left ventricular function impairment. Some issues remain controversial, such as the optimal time for introducing ACE inhibitors after the onset of symptoms, the potential additive effects of ACE inhibitors given in conjunction with thrombolytic therapy, and the role of systemic angioplasty of the infarct-related artery.