Heart failure—Low endogenous coenzyme Q10 levels have been associated with worse heart failure outcomes, but this association is likely because low levels are a marker for more advanced heart failure, rather than a predictor of disease. Despite these findings, coenzyme Q10 is often advocated to improve heart muscle function in patients with heart failure. According to the most recent meta-analysis, coenzyme Q10 was shown to improve ejection fraction by 3.7% when used short term (2–28 weeks). It is unclear whether improvements in ejection fraction are applicable to all patients with heart failure, including those receiving the current standard of care for heart failure management. More research is required to assess the role of coenzyme Q10 in heart failure and its impact on disease severity, particularly with concomitant prescription medications.
3.
Ischemic heart disease—The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium by reducing proinflammatory markers (including interleukin-6 and C-reactive protein) that contribute to oxidative stress. Double-blind, placebo-controlled trials have suggested that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein (a), high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%).
4.
Prevention of statin-induced myopathy—Statins reduce cholesterol by inhibiting the HMG-CoA reductase enzyme (see Chapter 35). This enzyme is also required for synthesis of coenzyme Q10. Initiating statin therapy has been shown to reduce endogenous coenzyme Q10 levels, which may block steps in muscle cell energy generation, possibly leading to statin-related myopathy. It is unknown whether a reduction in intramuscular coenzyme Q10 levels leads to statin myopathy or if the myopathy causes cellular damage that reduces intramuscular coenzyme Q10 levels. A meta-analysis evaluating the effect of coenzyme Q10 on statin-induced myopathy as measured by muscle pain and plasma creatine kinase activity found that coenzyme Q10 supplementation (30 days to 3 months) did not demonstrate any benefit in reducing myopathy. More information is needed to determine which patients, if any, with statin-related myopathy might benefit from coenzyme Q10 supplementation, especially as it relates to the specific statin, the dose, and the duration of therapy.
Coenzyme Q10 is well tolerated, rarely leading to any adverse effects at doses as high as 3000 mg/d. In clinical trials, gastrointestinal upset, including diarrhea, nausea, heartburn, and anorexia, has been reported with an incidence of less than 1%. Cases of maculopapular rash and thrombocytopenia have very rarely been observed. Other rare adverse effects include irritability, dizziness, and headache.
Coenzyme Q10 shares a structural similarity with vitamin K, and an interaction has been observed between coenzyme Q10 and warfarin. Coenzyme Q10 supplements may decrease the effects of warfarin therapy. This combination should be avoided or very carefully monitored.
As a dietary supplement, 30 mg/d of coenzyme Q10 is adequate to replace low endogenous levels. For cardiac effects, typical dosages are 100–600 mg/d given in two or three divided doses. These doses increase endogenous levels to 2–3 mcg/mL (normal for healthy adults, 0.7–1 mcg/mL).