Coenzyme Q.sub.10 (2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone) is a redox component in the respiratory chain and is found in all cells having mitochondria. It is thus an essential co-factor in the generation of metabolic energy and is particularly important in muscle function. For example, Folkers et al., Proc. Natl. Acad. Sci., 82: 901 (1985) have measured the levels of Coenzyme Q.sub.10 (CoQ.sub.10) in endomyocardial biopsy samples taken from patients with varying stages of cardiomyopathy. Folkers et al. states that these data show decreasing tissue levels of CoQ.sub.10 with increasing severity of the symptoms of cardiac disease. Folkers et al., Proc. Natl. Acad. Sci., 82: 4513 (1985) in a double-blind study have reported improved cardiac output for some patients upon receiving an oral administration of CoQ.sub.10.
HMG-CoA reductase inhibitors represent a new class of cholesterol-lowering drugs. Relatively low doses of these drugs effectively reduce plasma cholesterol levels. These drugs are believed to function by inhibiting the chemical transformation HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. A branch of the mevalonate cholesterol biosynthetic pathway in mammalian cells leads to the formation of CoQ.sub.10. [reviewed by Brown and Goldstein J. Lipid Res., 21, 505 (1980)]. Furthermore high levels of lovastatin can reduce CoQ.sub.10 in the liver (MK-803 NDA report) and compactin reduces LDL-bound CoQ.sub.10 at doses employed in humans [H. Mabuchi et al, N. E. J. Med., 478 (August 1981].
The Physician's Desk Reference, 42d Ed., 1366 (1988) states that myalgia has been associated with lovastatin therapy. Tobert, N. E. J. Med., 48 (Jan. 7, 1988) states that in a very small number of patients (0.5 percent) myopathy appeared to be associated with lovastatin therapy. Concomitant therapy with immunosuppressant drugs, including cyclosporine, with gemfibrozil or niacin or a combination, appears to increase the risk of myopathy. (J. A. Tobert, Am. J. Cardiol. 1988, 62: 28J-34J). The myopathy is reversible upon discontinuance of lovastatin therapy.
Although cholesterol-lowering therapy through the use of HMG-CoA reductase inhibitors is generally free of side reactions, it would be of considerable benefit to counteract the myopathy observed in a small percent of patients. Since CoQ.sub.10 is of benefit in congestive heart failure patients the combination with HMG-CoA reductase inhibitors should be of value in such patients who also have the added risk of high cholesterol levels.