The Open Sports Medicine Journal


ISSN: 1874-3870 ― Volume 9, 2015

Assessment of Mechanical Cardiac Function in Elite Athletes

The Open Sports Medicine Journal, 2011, 5: 26-37

J. Patrick Neary, David S. MacQuarrie, Veronica Jamnik, Norman Gledhill, Scott Gledhill, Edward F.G. Busse

Faculty of Kinesiology & Health Studies, University of Regina, Regina, SK, S4S0A2, Canada.

Electronic publication date /12/2011
[DOI: 10.2174/1874387001105010026]


Hypertrophic cardiomyopathy (HCM) is the number one cause of sudden cardiac death in elite athletes. This project used resting 12-lead electrocardiography (ECG) and ballistocardiography (BCG) to assess cardiac cycle timing events as simple screening techniques to rule out cardiac abnormalities for the safety of a group of elite ice hockey players. Clinical cardiac (ECG) and physiological (maximal aerobic power [VO2max], anaerobic [Wingate peak power, Watts] and musculoskeletal strength) data is presented here on an elite group of ice hockey players (n=34; age=17-18 yrs) that participated in a professional medical and fitness evaluation. Subsequently one subject was diagnosed with #1 Apical HCM and his cardiac data is compared with the group. The HCM subject performed all fitness testing and was determined to be physically fit (%BF=7.2%; VO2max=59.4 mL•kg-1•min-1; Wingate peak power output=15.1 Watt•kg-1; Heart Rate max=200 beats•min-1). However, the ECG showed extreme voltage and deeply inverted T-waves, and the BCG showed abnormal waveform complexes and cardiac timing events in comparison to the group means. Mean BCG systolic timing events for isovolumic contraction time (54.7±7.1 vs 49.5±12.4 msec), acceleration time (49.1±1.8 vs 56.3±9.1 msec), diastole (470.8±25.3 vs 531.4±166.7 msec), and isovolumic relaxation time (88.5±7.4 vs 100.8± 16 msec) were significantly different (p<0.05). Atrial systole amplitude was statistically higher for this subject (9.2±3.7 vs 5.3±3 mG). Subsequent follow-up assessment showed abnormal echocardiogram (Echo) dimensions (ventricular septum [12mm]; posterior wall [16 mm]), velocities (mitral valve deceleration [233 msec], LV systolic strain [14%]), and volumes (LV stroke volume [38 mL•metre-1 body surface area]), with normal E:A ratio (1.75) and LV ejection fraction (62%). Cardiac magnetic resonance imaging (MRI) showed apical septal wall thickness (24-25 mm) in the HCM player. In conclusion, BCG was able to corroborate a cardiac abnormality that was later confirmed with echocardiography and MRI, suggesting that BCG is a potential technology to detect anomalies that alter cardiac timing and amplitude.

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