Journal
AMERICAN JOURNAL OF CARDIOLOGY
Volume 103, Issue 10, Pages 1467-1472Publisher
EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
DOI: 10.1016/j.amjcard.2009.01.294
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- St. Boniface 'General Hospital and Research Foundation, Winnipeg, Manitoba, Canada.
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Although previous studies including endurance athletes after marathon running have demonstrated biochemical evidence of cardiac injury and have correlated these findings with echocardiographic evidence of cardiac dysfunction, particularly of the right ventricle, a study of marathon athletes incorporating biomarkers, echocardiography, and cardiac magnetic resonance (CMR) imaging has not been performed to date. The aim of this study was to demonstrate the cardiac changes associated with participation in a marathon using serial cardiac biomarkers, echocardiography, and CMR imaging. Fourteen participants (mean age 33 +/- 6 years, 8 men) completed the full marathon. Myoglobin, creatine kinase, and troponin T were elevated in all athletes after the race. There was a strong linear correlation between right ventricular (RV) fractional area change as asses sed, by echocardiography and the RV ejection fraction as assessed by CMR imaging (r = 0.96) after the marathon. RV function, using echocardiography, transiently decreased from before to after the race (RV fractional area change 43 +/- 4% vs 33 +/- 5%, p <0.05). There were also postrace changes in left ventricular and RV diastolic filling. Although RV systolic changes were transient, left ventricular and RV diastolic abnormalities persisted up to I week after the marathon. No evidence of delayed enhancement of the left ventricular myocardium was found on CMR imaging, suggesting that the increase in cardiac biomarkers after the marathon may not have be due to myocardial necrosis. In conclusion, RV systolic dysfunction transiently occurs after a marathon and has been validated for the first time by CMR imaging. The increase in cardiac troponin after marathon running is likely due to the cytosolic release of the biomarker, not to the true breakdown of the myocyte, as confirmed by delayed enhancement CMR imaging. (c) 2009 Elsevier Inc. (Am J Cardiol 2009;103:1467-1472)
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