Statin Drug

The mechanism of action of the statin group of drugs is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)-reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. Inhibition of this enzyme also adversely effects the intrinsic biosynthesis of CoQ10, as demonstrated in laboratory animals and humans and reduces plasma and myocardial levels of CoQ10 (Bargossi et al 1994b, Folkers et al 1990, Rosenfeldt et al 2005). Studies have indicated that reductions of 20-30% in circulating coenzyme Q10 concentrations may be expected in response to treatment with statins (Nawarskas 2005); however, it is uncertain whether reduced serum levels are of clinical consequence. It is more likely that reduced muscle CoQ10 concentrations are of greater concern because they may be associated with impaired cardiac function. The results obtained by Folkers et al (1990) and Silver et al (2004) provide some support for this rationale; however, a study by Colquhoun et al (2005) casts doubt on this relationship. Folkers et al showed that oral administration of CoQ10 to five hospitalised patients with cardiac disease made worse with lovastatin, produced an improvement in cardiac function (1990). Silver et al found that left ventricular diastolic function worsened in 10 of 14 patients after atorvastatin therapy, as observed with Doppler echocardiography (2004). When CoQ10 (300 mg/day) was administered to 9 of these patients, 8 experienced a reversal of diastolic abnormality. In contrast, Colquhoun et al (2005) studied left ventricular EF in 21 hypercholesterolaemic subjects with normal function receiving simvastatin over 6 months. After 1 month, EF significantly decreased; however, no significant changes were observed after 3 or 6 months and washout of simvastatin. No association was found between the size of the reduction in EF and the reduction in plasma CoQ10 level after 1 month.

There has been some suggestion that the side-effects of myalgia, fatigue and rhabdomyolisis associated with statin treatment may be dependent on CoQ10 depletion. A recent study identified that statin-induced myopathy can be associated with a mild decrease in muscle CoQ10 concentration, providing some support for this theory (Lamperti et al 2005). Numerous anecdotal reports suggest that some patients using statin therapy long-term and experiencing fatigue find benefit with CoQ10 © 2007 Elsevier Australia

supplementation; however, controlled trials are unavailable to determine the significance of these observations. A case study by Walravens et al (1989) illustrates the point.

A 48-year-old physician was taking lovastatin 20 mg/day for moderate hypercholesterolemia and he also jogged three times a week, with occasional high-altitude cycling. After 2-3 weeks of lovastatin treatment, exercise became difficult because of muscle soreness and fatigue and at 7 weeks he had severe cramps while cycling. Soreness and weakness continued for 6 months, after which he began taking CoQ10 (30 mg daily). After a few days' treatment, muscle fatigue after exercise ceased and the severe cramps did not recur. Restarting lovastatin 10 mg 5-6 times weekly did not result in muscle cramping while CoQ10 was taken.

Currently it is still not clear whether CoQ10 supplementation should be considered a necessary adjunct to all patients taking statin drugs; however, those patients considered at risk of deficiency may benefit, in particular, patients with a family history of heart failure, elevated cholesterol levels and who are over 65 years of age and taking statin drugs long-term (Levy & Kohlhaas 2006).

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