Left ventricular dilatation after acute
myocardial infarction (MI) is a powerful predictor of progressive functional deterioration, culminating in
heart failure and death. The most important determinants of post-MI
left ventricular remodeling are the size of the
infarct, the degree of residual
stenosis in the
infarct-related artery, and the viability of the
infarct zone. In addition to reperfusion
therapy and
angiotensin-converting enzyme inhibition, metabolic intervention with
L-carnitine may represent a therapeutic approach for preventing left ventricular dilatation and preserving cardiac function. Ongoing studies with early metabolic intervention with
carnitine in the acute phase of
infarction may prove successful in protecting the microcirculation against ischemic damage and enhancing its ability to respond to blood flow resumption. The results of the multicenter, randomized, double-blind
Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) trial suggest that the early and long-term administration of
L-carnitine attenuates progressive left ventricular dilatation after acute anterior MI. Results show significant, consistent reductions in end-diastolic volume and end-systolic volume in patients who received
L-carnitine compared with placebo. The ongoing CEDIM-2 trial (projected 4000 patients with acute MI) will assess the efficacy of
L-carnitine in reducing the combined incidence of death and
heart failure at 6 months. In addition to standard reperfusion
therapy and
angiotensin-converting enzyme inhibition, metabolic intervention with
L-carnitine may be a therapeutic approach for preventing left ventricular dilatation and preserving cardiac function by limiting
infarct size, decreasing residual
stenosis in the
infarct-related artery, and increasing viability of the
infarct zone.