The protective effect of carnitine in human diphtheric myocarditis.
Carnitine, an important cofactor in the transport of fatty acids to the interior of cell mitochondria, is depleted in myocardial tissue of guinea pigs submitted to diphtheric toxin administration. Mortality rates were reduced in these animals by supplying exogenous amounts of carnitine. The accumulation of fatty acids in the cytoplasm of human heart cells reported in cases of diphtheria suggests that carnitine might possibly be depleted in human myocardium as well. For the purpose of studying the effect of carnitine administration, 132 diphtheric patients were randomly divided into two groups, one of them (carnitine-treated group, n = 73) receiving DL-carnitine, 100 mg/kg/day during 4 days after admission, in addition to routine treatment, which was prescribed for this and the control group (n = 59). The presence of myocardial damage was evaluated by clinical, electrocardiographic, radiological, and enzymatic criteria. Carnitine administration resulted in decreased incidence of heart failure (P = 0.0475), of pacemaker implants (P = 0.0256), and of lethality indexes due to myocarditis (P = 0.013). We suggest that carnitine can play an important role in the treatment of diphtheric patients.
D000293:Adolescent; D002331:Carnitine / Q000378:metabolism / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D003402:Creatine Kinase / Q000378:metabolism; D004165:Diphtheria / Q000188:drug therapy* / Q000378:metabolism; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000517:prevention & control; D006801:Humans; D007223:Infant; D007527:Isoenzymes; D008297:Male; D009205:Myocarditis / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology
D007527:Isoenzymes; D003402:Creatine Kinase; D002331:Carnitine