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Impact of Statin Use on Exercise-Induced Cardiac Troponin Elevations

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...

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Published in:The American journal of cardiology 2014-08, Vol.114 (4), p.624-628
Main Authors: Eijsvogels, Thijs M.H., PhD, Januzzi, James L., MD, Taylor, Beth A., PhD, Isaacs, Stephanie K., BS, D'Hemecourt, Pierre, MD, Zaleski, Amanda, MS, Dyer, Sophia, MD, Troyanos, Chris, ATC, Weiner, Rory B., MD, Thompson, Paul D., MD, Baggish, Aaron L., MD
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creator Eijsvogels, Thijs M.H., PhD
Januzzi, James L., MD
Taylor, Beth A., PhD
Isaacs, Stephanie K., BS
D'Hemecourt, Pierre, MD
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Dyer, Sophia, MD
Troyanos, Chris, ATC
Weiner, Rory B., MD
Thompson, Paul D., MD
Baggish, Aaron L., MD
description 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
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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 &lt;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). 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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). 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subjects Adult
Cardiovascular
Cholesterol
Female
Follow-Up Studies
Healthy Volunteers
Heart attacks
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Male
Marathons
Metabolic disorders
Middle Aged
Myocardial Ischemia - blood
Myocardial Ischemia - prevention & control
Prognosis
Retrospective Studies
Running - physiology
Statins
Troponin I - blood
Troponin T - blood
title Impact of Statin Use on Exercise-Induced Cardiac Troponin Elevations
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