Cardiovascular Disease

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l-Carnitine supplementation in doses ranging from 2 g to 4 g/day has been investigated in a number of controlled studies involving subjects with angina, heart failure, cardiogenic shock, cardiomyopathy and post myocardial infarction. Overall, positive results have been obtained and reduced mortality reported for some populations.

Chronic stable angina Controlled studies indicate that l-carnitine supplements increase exercise tolerance and reduce frequency of angina attacks, enabling some patients to reduce nitrate requirements.

One RCT of 47 patients with chronic stable angina found that 2 g l-carnitine taken daily for 3 months moderately improved the duration of exercise and the time taken for ST changes to recover to baseline (Iyer et al 2000). This study confirmed the results of an earlier multicentre, double-blind, randomised, placebo-controlled crossover trial that examined the effects of l-carnitine 1 g twice daily for 4 weeks in 44 men with stable chronic angina (Cherchi et al 1985). This study showed that active treatment resulted in increased exercise tolerance and reduced ECG indices of ischaemia in stable effort-induced angina. A meta-analysis also highlighted a significant reduction in the number of angina attacks and nitrate requirements with doses of 2 g/day (Fernandez & Proto 1992).

Post myocardial infarction A dose of 4 g/day l-carnitine over 12 months improved quality of life and increased life expectancy in patients who had suffered a Ml, according to a controlled study (Davini et al 1992). This included an improvement in heart rate, systolic arterial pressure, a decrease in anginal attacks, and improve

ment in the lipid profile. Changes were also accompanied by lower mortality in the treated group (1.2% vs 12.5% in the control group).

In a randomised, double-blind placebo-controlled trial, the effects of oral l-carnitine (2 g/day) for 28 days were assessed in patients with suspected acute Ml. Total cardiac events, including cardiac deaths and non-fatal infarction, were 1 5.6% in the carnitine group and 26.0% in the placebo group. Angina pectoris (17.6 vs 36.0%), New York Heart Association class III or IV heart failure plus left ventricular enlargement (23.4 vs 36.0%) and total arrhythmias (13.7% vs 28.0%) were significantly less in the carnitine group compared with placebo (Singh et al 1996). Cardiomyopathy Cardiomyopathy appears to cause leakage of carnitine from heart stores, which may make cardiac tissue vulnerable to damage; however, it is unclear whether carnitine leakage is a cause or effect of cardiomyopathy (Baker et al 2005). Long-term placebo-controlled studies (10-54 months) using an oral dose of 2 g/day l-carnitine for treatment of heart failure caused by cardiomyopathy found a statistically significant advantage in survival rates with carnitine treatment (Rizos 2000). In patients with idiopathic dilated cardiomyopathy associated with coeliac disease, a gluten-free diet has been shown to increase serum carnitine levels (Curione et al 2005).

Cardiogenic shock Several studies confirm the role of l-carnitine in the reversible phase of cardiogenic shock in terms of enzymic protection in the course of cellular oxidative damage. This has been reflected in improved survival rates (Corbucci & Lettieri 1991, Corbucci & Loche 1993).

Congestive heart failure In congestive heart failure a specific myopathy secondary to myocyte apoptosis triggered by high levels of circulating TNF-alpha has been described. The role of carnitine in preventing apoptosis in skeletal muscle and reducing TNF-alpha provides a theoretical basis for its use in the treatment of myopathy associated with congestive heart failure (Vescovo et al 2002). Myocarditis resulting from diphtheria Two studies using d,l-carnitine (100 mg/kg/day in two divided doses orally for 4 days) found a reduction in the incidence of, and mortality from, myocarditis in diphtheria (Ramos et al 1984, 1992).

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