Left ventricular dilatation after acute myocardial infarction (MI) is a pow
erful predictor of progressive functional deterioration, culminating in hea
rt failure and death. The most important determinants of post-Mi left ventr
icular remodeling are the size of the infarct, the degree of residual steno
sis in the infarct-related artery, and the viability of the infarct zone. I
n addition to reperfusion therapy and angiotensin-converting enzyme inhibit
ion, metabolic intervention with L-carnitine may represent a therapeutic ap
proach for preventing left ventricular dilatation and preserving cardiac fu
nction. Ongoing studies with early metabolic intervention with carnitine in
the acute phase of infarction may prove successful in protecting the micro
circulation 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) tr
ial suggest that the early and long-term administration of L-carnitine atte
nuates progressive left ventricular dilatation after acute anterior MI. Res
ults show significant, consistent reductions in end-diastolic volume and en
d-systolic volume in patients who received L-carnitine compared with placeb
o. The ongoing CEDIM-2 trial (projected 4000 patients with acute MI) will a
ssess the efficacy of I-carnitine in reducing the combined incidence of dea
th and heart failure at 6 months. in addition to standard reperfusion thera
py and angiotensin-converting enzyme inhibition, metabolic intervention wit
h L-carnitine may be ct therapeutic approach for pro venting left ventricul
ar dilatation and preserving cardiac function by limiting infarct size, dec
reasing residual stenosis in the infarct-related artery, and increasing via
bility of the infarct zone.