Published online before print November 13, 2006, doi: 10.1161/CIRCULATIONAHA.106.647461
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(Circulation. 2006;114:2325-2333.)
© 2006 American Heart Association, Inc.
Exercise Physiology |
Myocardial Injury and Ventricular Dysfunction Related to Training Levels Among Nonelite Participants in the Boston Marathon
From the Cardiac Ultrasound Laboratory (T.G.N., J.L.J., T.-T.T.-N., D.M.Y., D.S.J., J.E.M., M.H.P., M.J.W.), Division of Cardiology, Pathology (E.L.-L., K.B.L.), and Pediatric Surgery (D.L.), Massachusetts General Hospital, and the Department of Medicine (A.J.S.), McLean Hospital, Harvard Medical School, Boston, Mass; and the Division of Cardiovascular Medicine (P.S.D.), Duke University Medical Center, Durham, NC.
Correspondence to Dr Malissa J. Wood, Cardiac Ultrasound Laboratory, Division of Cardiology, Massachusetts General Hospital, 55 Fruit St, VBK 508, Boston, MA 02115-2696. E-mail mjwood{at}partners.org
Received June 21, 2006; revision received August 23, 2006; accepted August 25, 2006.
Background— Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction.
Methods and Results— We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler–derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, >60% of participants had increased cTnT >99th percentile of normal (>0.01 ng/mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (
0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P<0.001). The increase in biomarkers correlated with post-race diastolic dysfunction, increased pulmonary pressures, and right ventricular dysfunction (right ventricular mid strain, r=–0.70, P<0.001) and inversely with training mileage (r=–0.71, P<0.001). Compared with athletes training >45 miles/wk, athletes who trained 
35 miles/wk demonstrated increased pulmonary pressures, right ventricular dysfunction (mid strain 16±5% versus 25±4%, P<0.001), myocyte injury (cTnT 0.09 versus <0.01 ng/mL, P<0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P<0.001).
Conclusions— Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.
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