[The role of metabolic therapy in myocardial infarct]

During acute myocardial ischemia the metabolism of free fatty acids is impaired. Since the rate of beta-oxidation is reduced, the levels of acil-CoA and long-chain acyl-carnitine increase. The activity of carnitine, which permits the transport of fatty acids into the mitochondria, is reduced both by its transformation in acyl-carnitine and by its release from the cells induced by acute ischemia. The accumulation of fatty acids induces a deterioration of hemodynamic parameters and some impulse formation and conduction disturbances. Since in experimental studies L-carnitine prevents the occurrence of hemodynamic and arrhythmic complications, clinical studies with this compound have been performed during acute ischemia in man. In patients with acute myocardial infarction high doses of L-carnitine induce: a statistically significant increase in urinary concentrations of long- and short-chain carnitine esters; a statistically significant reduction of ventricular arrhythmias during the second day after the onset of symptoms; a reduction of the necrotic area as assessed by electrocardiographic and enzymatic methods.