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.
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References
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- 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.[ISI][Medline]
- 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]
- 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]
Related articles in JACC:
- Coenzyme Q10 in Statin-Associated Myopathy
- Harvey Wolinsky
JACC 2007 50: 1911.
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