Abstract

I concur with Stricker and Goldberg, who reemphasize the need for caution when it comes to prescribing statin therapy. Because 10- to 20-year follow-up data are lacking for 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, the possibility of carcinogenicity-related risk must be a concern when prescribing these agents for extended periods of time. Careful consideration of treatment indications includes stratification of cardiac risk to determine when intervention with this powerful class of pharmacotherapeutic agents is indicated. Although it is imperative to avoid overusing statin therapy for cholesterol lowering, the risk-to-benefit ratio is tipped in favor of this drug intervention for patients at high cardiac risk. This population includes patients with a documented history of coronary artery disease, unstable angina, and acute coronary syndrome, as well as patients in whom high calcium burdens are identified (>1,000 score on the basis of electron beam computed tomography). In these special populations, measures to improve plaque stabilization and promote plaque reversal must be initiated. Research has consistently suggested that statin drugs do modify inflammatory mediators for high-risk populations for whom double-blind, placebo-controlled trials correlate statin therapy with major reductions in death, myocardial infarction, and stroke. 1 In patients with cardiac vulnerability, statin use can certainly be justified, and underuse in such high-risk cardiovascular patients should be avoided. Statin drugs inhibit the synthesis of 3-hydroxy-3-methylglutaryl-coenzyme A reductase liver enzyme and in turn block manyother biochemical pathways, one of which is the endogenous formation of coenzyme Q10 (CoQ10). Diminished CoQ10 levels have been associated with both cancer and impaired cardiac function in an animal model and in humans. 2–4 At the third conference of the International Coenzyme Q10 Association, held in November 2002 in London, England, the results of a pilot study were presented. The study involved six patients who were undergoing statin therapy for hyperlipidemia. Abnormalities of diastolic dysfunction occurred with a frequency of 67% after 6 months of statin therapy. 5 AltShough it may take 10 to 20 years for diastolic dysfunction to manifest as impaired systolic function, long-term statin use could be undesirable in some patients, particularly those whose baseline CoQ10 levels are suboptimal. Carcinogenicity and cardiomyopathy could prove to be serious long-term effects of statin therapy. Although high-risk cardiovascular patients stand to benefit the most from statin therapy, overuse of this treatment modality to lower cholesterol in otherwise healthy individuals is not smart medical practice.Stephen T. Sinatra, MD, FACC