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Right ventricular dysfunction and injury following marathon running: correlating biomarkers with cardiac MRI

  • Negareh Mousavi1,
  • Andrew Czarnecki1,
  • Kanwal Kumar1,
  • Nazanin Fallah-Rad1,
  • Matthew Lytwyn1,
  • Song-Yee Han1,
  • Andrew Francis1,
  • Iain D Kirkpatrick1,
  • Tomas G Neilan2,
  • Sat Sharma1 and
  • Davinder S Jassal1
Journal of Cardiovascular Magnetic Resonance200911(Suppl 1):O74

Published: 28 January 2009


Right VentricularRight Ventricular FunctionRight Ventricular Ejection FractionFractional Area ChangeSerum Myoglobin


Although previous studies including endurance athletes following marathon running have demonstrated biochemical evidence of cardiac injury and have correlated these findings with echocardiographic evidence of cardiac dysfunction, in particular the right ventricle, a study of marathon athletes incorporating biomarkers, echocardiography and cardiac MRI (CMR) has not been performed to date.


To demonstrate the cardiac changes associated with participation in a marathon using serial cardiac biomarkers, echocardiography and CMR.


Fourteen participants (mean age 33 ± 6 years; 8 males) completed the full marathon. Serum myoglobin, creatine kinase and troponin T were elevated in all athletes post-race. There was a strong linear correlation between right ventricular (RV) fractional area change (FAC) as assessed by echocardiography and RV ejection fraction as assessed by CMR (r = 0.96) post marathon (Figure 1). RV function, using echocardiography, transiently decreased from pre- to post-race (RV FAC 43 ± 5% vs. 34 ± 7%, p < 0.05). There were also post-race changes in LV and RV diastolic filling. While RV systolic changes were transient, both LV and RV diastolic abnormalities persisted up to one week post marathon. We did not find evidence of delayed enhancement of the LV myocardium on CMR suggesting that the increase in cardiac biomarkers post-marathon is not due to myocardial necrosis.
Figure 1

Figure 1


Right ventricular systolic dysfunction transiently occurs post marathon, and has been validated for the first time by CMR. The increase in cardiac troponin following marathon running is due to cytosolic release of the biomarker, and not due to true breakdown of the myocyte as confirmed by delayed enhancement CMR.

Authors’ Affiliations

St. Boniface General Hospital, University of Manitoba, Winnipeg, Canada
Massachusetts General Hospital, Harvard Medical School, Boston, USA


© Mousavi et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.