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补充辅酶Q(10)对辛伐他汀所致肌痛的影响。

Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.

作者信息

Young Joanna M, Florkowski Christopher M, Molyneux Sarah L, McEwan Roberta G, Frampton Christopher M, George Peter M, Scott Russell S

机构信息

Lipid and Diabetes Research Group, Christchurch Hospital, Christchurch, New Zealand.

出版信息

Am J Cardiol. 2007 Nov 1;100(9):1400-3. doi: 10.1016/j.amjcard.2007.06.030. Epub 2007 Aug 16.

DOI:10.1016/j.amjcard.2007.06.030
PMID:17950797
Abstract

Myalgia is the most frequently reported adverse side effect associated with statin therapy and often necessitates reduction in dose, or the cessation of therapy, compromising cardiovascular risk management. One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain. This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia. Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day. Patients experiencing significant myalgia reduced their statin dose or discontinued treatment. Myalgia was assessed using a visual analogue scale. There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47). In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.

摘要

肌痛是与他汀类药物治疗相关的最常报告的不良副作用,常需要减少剂量或停止治疗,从而影响心血管风险管理。一种关于他汀类药物相关肌痛的假设机制是通过辅酶Q10(线粒体电子传递链的关键组成部分)耗竭导致线粒体功能障碍。这项初步研究评估了补充辅酶Q10对既往有他汀类药物相关肌痛患者的他汀类药物耐受性和肌痛的影响。44例患者被随机分为辅酶Q10组(200毫克/天)或安慰剂组,为期12周,同时辛伐他汀从10毫克/天开始向上滴定剂量,如果耐受,每4周加倍,最大剂量为40毫克/天。出现明显肌痛的患者减少他汀类药物剂量或停止治疗。使用视觉模拟量表评估肌痛。联合治疗与单纯使用他汀类药物在肌痛评分变化方面(中位数6.0[四分位间距2.1至8.8]对2.3[0至12.8],p = 0.63)、耐受40毫克/天辛伐他汀的患者数量方面(辅酶Q10组22例中的16例[73%]对安慰剂组22例中的13例[59%],p = 0.34)或继续治疗的患者数量方面(辅酶Q10组22例中的16例[73%]对安慰剂组22例中的18例[82%],p = 0.47)均无差异。总之,补充辅酶Q10并未改善他汀类药物耐受性或肌痛,尽管有必要进行进一步研究。

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