In reply—Coenzyme Q10 and Statin-Induced Myopathy


Maciej Banach, MD | Dimitri P. Mikhailidis, MD | On behalf of theLipid and Blood Pressure Meta-analysis Collaboration (LBPMC) Group
First published: March 2015 |


We thank Drs Keller and Braillon for their interest in our article. Dr Keller suggests that there is a need to evaluate higher dosages of coenzyme Q10 (CoQ10) (at least 600 mg/d) in patients with statin-induced myopathy (SIM), an issue we mentioned in our meta-analysis. However, actually conducting such a study is problematic. Specifically, a considerable amount of research now depends on the financial interests of the pharmaceutical industry. The limited amount of research on CoQ10 to date probably reflects their current interest and offers a preview of future interest.
Additionally, all cases of SIM are not due to a single cause. It follows that CoQ10 supplements, even if effective, may not benefit all cases of SIM. Studies evaluating the role of CoQ10 supplements in patients with SIM would have to involve very large numbers of patients and/or exclude SIM not potentially related to CoQ10 deficiency. These requirements have considerable methodological and cost implications. First, SIM/statin intolerance should be classified using a uniform method.

 Another question is whether higher dosages of CoQ10 have adverse effects. Contemporary data concerning the administration of CoQ10 at dosages higher than 1200 mg/d are limited. It is usually recommended to administer up to 400 mg/d of CoQ10 for patients older than 18 years. Despite the fact that CoQ10 appears to be generally very safe with no major adverse effects, it is known that it may, among other effects, slightly lower blood glucose concentrations, interfere with chemotherapy medications, interfere with antihypertensive and anticoagulant therapies, affect thyroid hormone concentrations, and interact with thyroid hormone replacement therapy. Thus, studies with high dosages of CoQ10 are needed.

We agree with Dr Braillon that there is no definitive link between SIM and CoQ10. Nevertheless, as outlined previously, there is enough evidence to consider this topic further. In our study, the small increase of plasma creatine kinase activity (mean, 11.69 U/L) was not statistically significant, and there was also a wide confidence interval of −14.25 to 37.63 U/L. This means that this topic still needs to be investigated in larger trials with longer follow-up (and at higher dosages of CoQ10).

We also agree that there are several options for the management of statin intolerance, but they may not always be effective. For example, we can use ezetimibe after the recently encouraging results of the IMProved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT). Another choice may be to correct vitamin D deficiency. New lipid-lowering drugs may also prove useful in reducing the risk of SIM altogether.

Statin discontinuation (or reducing statin dosage) is a very relevant clinical issue because it may increase the risk of cardiovascular events.Therefore, we need to continue our efforts to provide optimal treatment of hyperlipidemia while avoiding (or appropriately treating) SIM.

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