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他汀类药物使用对运动诱导的心肌肌钙蛋白升高的影响。

Impact of statin use on exercise-induced cardiac troponin elevations.

机构信息

Henry Low Heart Center, Department of Cardiology, Hartford Hospital, Hartford, Connecticut; Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands.

Cardiovascular Performance Program, Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts.

出版信息

Am J Cardiol. 2014 Aug 15;114(4):624-8. doi: 10.1016/j.amjcard.2014.05.047. Epub 2014 Jun 6.

DOI:10.1016/j.amjcard.2014.05.047
PMID:25015693
Abstract

Marathon running commonly causes a transient elevation of creatine kinase and cardiac troponin I (cTnI). The use of statins before marathon running exacerbates the release of creatine kinase from skeletal muscle, but the effect of statin use on exercise-induced cTnI release is unknown. We therefore measured cTnI concentrations in statin-using (n = 30) and nonstatin-using (n = 41) runners who participated in the 2011 Boston Marathon. All runners provided venous blood samples the day before, within an hour of finishing, and 24 hours after the marathon. cTnI was assessed at each time point via both a contemporary cTnI and high-sensitivity cTnI (hsTnI) assay. Before the marathon, cTnI was detectable in 99% of runners with the use of the hsTnI assay. All participants completed the marathon (finish time: 4:04:09 ± 0:41:10), and none had symptoms of an acute coronary syndrome. cTnI increased in all runners (p <0.001) immediately after the marathon, and half (hsTnI = 54% vs contemporary cTnI = 47%) exceeded the diagnostic cut-point for an acute myocardial infarction. Statin use did not affect the magnitude of cTnI release (group*time p = 0.47) or the incidence of runners with cTnI elevation greater than the diagnostic cut-point for myocardial infarction (57% vs 51%, p = 0.65). In addition, there was no significant association between statin potency and cTnI release (r = 0.09, p = 0.65). In conclusion, marathon-induced cTnI increases are not altered by statin use.

摘要

马拉松跑通常会导致肌酸激酶和心肌肌钙蛋白 I(cTnI)短暂升高。在马拉松跑之前使用他汀类药物会加剧骨骼肌中肌酸激酶的释放,但他汀类药物使用对运动引起的 cTnI 释放的影响尚不清楚。因此,我们测量了参加 2011 年波士顿马拉松比赛的使用他汀类药物(n=30)和未使用他汀类药物(n=41)的跑步者的 cTnI 浓度。所有跑步者在马拉松跑前一天、完赛后 1 小时和 24 小时提供静脉血样。在每个时间点通过当代 cTnI 和高敏 cTnI(hsTnI)检测来评估 cTnI。在马拉松跑之前,使用 hsTnI 检测法,99%的跑步者都可以检测到 cTnI。所有参与者都完成了马拉松跑(完赛时间:4:04:09±0:41:10),并且没有人出现急性冠状动脉综合征的症状。所有跑步者的 cTnI 都在马拉松跑后立即升高(p<0.001),有一半(hsTnI=54%,而当代 cTnI=47%)超过急性心肌梗死的诊断切点。他汀类药物的使用并不影响 cTnI 释放的幅度(组*时间 p=0.47)或 cTnI 升高超过心肌梗死诊断切点的跑步者的发生率(57% vs 51%,p=0.65)。此外,他汀类药物的效力与 cTnI 释放之间没有显著关联(r=0.09,p=0.65)。总之,他汀类药物的使用不会改变马拉松跑引起的 cTnI 增加。

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