CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Leo Marcoff, MD and
Paul D. Thompson, MD, FACC*
* Hartford Hospital, Cardiology, 80 Seymour Street, P.O. Box 5037, Hartford, Connecticut 06102-8000 (Email: pthomps{at}harthosp.org).
Dr. Wolinsky raises an interesting issue. Statins block the rate-limiting enzyme in the mevalonate pathway reducing cholesterol production, but also reduce production of farnesyl and geranylgeranyl pyrophosphate. These molecules participate in post-translational modification or prenylation of the Ras superfamily guanosine triphosphatases or small G proteins. Small G proteins are involved in cell signaling and proliferation. Statin inhibition of these G proteins decreases vascular smooth muscle hypertrophy and proliferation, improves endothelial function, and reduces angiotensin I receptor expression (1). It may also explain the statin antiarrhythmic effect in atrial fibrillation (2).
Coenzyme Q10 (Q10) supplementation should not affect small G protein production since Q10 is not involved in the G protein prenylation process. Furthermore, we recommended that Q10 supplementation be "tested" or "trialed" (3) only in statin myalgic patients to allow ongoing statin treatment.
 |
References
|
|---|
1. Liao JK. Effects of statins on 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibition beyond low-density lipoprotein cholesterol Am J Cardiol 2005;96:24F-33F.[Web of Science][Medline]2. Adam O, Frost G, Custodis F, et al. Role of Rac1 GTPase activation in atrial fibrillation J Am Coll Cardiol 2007;50:359-367.[Abstract/Free Full Text] 3. Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy: a systematic review J Am Coll Cardiol 2007;49:2231-2237.[Abstract/Free Full Text]
|
Top
References