High doses of L-carnitine in acute myocardial infarction: metabolic and antiarrhythmic effects

Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs...

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Veröffentlicht in:European heart journal 1989-06, Vol.10 (6), p.502-508
Hauptverfasser: RIZZON, P., BIASCO, G., DI BIASE, M., BOSCIA, F., RIZZO, U., MINAFRA, F., BORTONE, A., SILIPRANDI, N., PROCOPIO, A., BAGIELLA, E., CORSI, M.
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Sprache:eng
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Zusammenfassung:Fatty acids accumulate in the muscle cells in some carnitine deficiency syndromes due to a variety of genetic defects in intermediary metabolism. L-Carnitine administration may relieve this excess by transporting acyl compounds out of the cell as acylcarnitine. Similar fatty acid accumulation occurs during myocardial ischae-mia because of the decreased rate of fi-oxidation, and this has been put forward as a cause of ventricular arrhythmias. This study was carried out to investigate whether administration of high doses of i.v. L-carnitine in patients with acute myocardial infarction could increase urinary excretion of acylcarnitine and reduce early ventricular arrhythmias. Fifty-six patients suffering from acute myocardial infarction, admitted to the Coronary Unit between 3 and 12 h after the onset of symptoms, were included in the study. The design of the study was double blind, parallel and placebo controlled. Allocation of treatment to patients was done randomly after stratification (time from onset of pain and site of infarction). The first group (28 patients) received intravenous L-carnitine at a dose of 100 mg kg−1 b.w. every 12 h for 36 h while the second group (28 patients) received placebo intravenously. Immediately before starting treatment two blood samples were taken (at 5-min intervals) and a further 16 samples were taken at regular intervals over the following 48 h. Patients' urine was collected over the same period of time. Concentrations of free carnitine, short chain acylcarnitine esters and long chain acylcarnitine esters in serum and urine were measured. On days 1 and 2, 24-h ECG monitoring (Holler) was carried out. Analysis of results showed that: (1) in patients receiving placebo, free carnitine serum levels increased significantly during the first 48 h after infarction; (2) in the same group of patients, free and total urinary carnitine excretion was significantly higher than in normal subjects; (3) administration of high doses of L-carnitine considerably increased urinary excretion of long and short chain carnitine esters; (4) this metabolic effect might explain the reduction in premature ventricular beats on the second day of treatment.
ISSN:0195-668X
1522-9645
DOI:10.1093/oxfordjournals.eurheartj.a059519