Why the study?
Does ballistocardiography (BCG) combined with ECG detect mechanical cardiac abnormalities in elite athletes during screening?
Does ballistocardiography (BCG) combined with ECG detect mechanical cardiac abnormalities in elite athletes during screening?
Ballistocardiography (BCG) is a potential non-invasive screening technology to detect mechanical cardiac anomalies, such as hypertrophic cardiomyopathy, in elite athletes.
BCG timing differences in one HCM athlete are hypothesis-generating; larger studies needed before screening consideration.
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 [VO 2 max], 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%; VO 2 max=59.4 mLkg -1 min -1 ; Wingate peak power output=15.1 Wattkg -1 ; Heart Rate max=200 beatsmin -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 (54.77.1 vs 49.512.4 msec), acceleration time (49.11.8 vs 56.39.1 msec), diastole (470.825.3 vs 531.4166.7 msec), and isovolumic relaxation time (88.57.4 vs 100.8 16 msec) were significantly different (p<0.05). Atrial systole amplitude was statistically higher for this subject (9.23.7 vs 5.33 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 mLmetre -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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J. Patrick Neary (2011) studied this question.
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