ATHLETIC HEART RESEARCH and lectures

 

Prof John Somauroo was awarded a Professorship to the University of Chester in Cardiovascular, Sports and Exercise Medicine in 2010 in recognition for his ongoing lecturing and research programmes at the University. He lectures on screening for sudden cardiac death and the effects of training on the heart nationally and internationally.


He has ongoing research programmes at the University of Chester and the Research Institute for Sport and Exercise Sciences (RISES) at Liverpool John Moores University. He continues to research physiological versus pathological changes in athletes’ hearts. Current research includes effects of exercise on ultra-endurance runners (pictured above at the Lakeland 100 mile trail race in 2009 with Prof Keith George and his team), footballers and rugby players (pictures at Wigan Warriors Rugby League Club in 2010 below).




Research Team 2010 (Left to right): Dr Marwan Al-Dawoud, Mrs Kath Giles, Miss Karen Williams, Prof John Somauroo, Dr Robert Cooper, Prof Keith George



Latest research presentation:  European Society of Cardiology, Stockholm  August 2010


     

Comparison of ECGs and Troponin I in ultra-endurance athletes before and after 50 and 100 mile trail race in UK

    1. JD Somauroo1, RE Shave2, KL Williams2, J Forster3, C George2, T Bett2, DC Gaze4, KP George2. 1Countess of Chester NHS Trust, 2Liverpool John Moores University, 3Leeds General Infirmary, 4St Georges Hospital London.


OBJECTIVES: Reports of elevated levels of blood borne biomarkers of cardiomyocyte insult and the observation of reduced systolic and/or diastolic function during recovery from ultra-endurance activity have generated significant clinical, scientific and media interest. Relatively little attention has been paid to changes in cardiac electrical activity in such athletes and whether elevations in cardiac Troponin I (cTnI) correlate with specific ECG changes.


METHOD: We recruited 25 Caucasian male competitors (aged 24-62) at the Lakeland 50 and 100 mile trail race in the UK (31.7.09 to 2.8.09). 9 athletes competed in 100 mile race and 16 in 50 mile race. Prior to race start a resting 12-lead ECG was recorded after 15 min supine rest and 24 hr after any previous intense exercise. All were normotensive, free of known cardiovascular disease and had been training for a minimum of 2 years for ultra-endurance sports events. Venous blood samples were taken before and after the race and serum was analysed for cTnI using a high-sensitive assay (Centaur, Siemens Healthcare Diagnostics) with a detection limit of 0.02 ng/ml.


RESULTS: cTnI prior to race was <0.02 in 23 (92%), =0.02 in 1 (4%) and 0.03 in 1 (4%). cTnI post race was <0.02 in 1 (4%) and 0.02 to 0.07 in 21 (84%). cTnI levels of 0.11, 0.15, and 0.51 were recorded post-race. ECGs at rest had typical features of athletic heart syndrome with sinus bradycardia, 1st degree AV block, left atrial (LA) enlargement, left ventricular hypertrophy (LVH) on voltage and additional criteria, partial RBBB, anterior ST elevation with predominantly 'peaked and tall' morphology and T flattening or <2mm inversion in 2 adjacent leads. Post-race further ST elevation and/or increase in T waves with ‘peaked and tall’ morphology occurred in anterior +/- lateral leads in 14 (56%), and inferior leads in 3 (12%). Maximum peaked T wave of 18mm and ST elevation 3mm. Most cTnI levels in this cohort were 0.07 or less, but also 0.11 and 0.15. Normalisation of baseline T inversion in inferior leads occurred in 4 (16%) with no cTnI greater than 0.07. New T inversion <1mm  in AVL with slight increase in T in V5 and V6 occurred in 1 (4%) with cTnI of 0.51. Less frequent changes seen were new T inversion in V1 or T inversion normalising, changes in cardiac axis, p wave morphology and prolongation of QTc (428 to 448 and 465 to 495).


DISCUSSION: cTnI pre-race was very low (<0.02) in 92% runners. It became detectable in 24 (96%) mostly 0.02-0.07 (84%). Increase in ‘peaked and tall’ morphology across anterior +/- lateral leads was seen in 56% runners and in inferior leads in 12%. cTnI was 0.07 or less in majority.  cTnI of 0.51 developed in 1 runner which correlated with new T inversion in AVL <1mm with slight increase in T amplitude in V5 and V6. Whether these changes reflect athletic status and effects of extreme exercise alone or in combination with undiagnosed cardiac disease was not determined.




Previous teenage professional football player paper, Somauroo et al. Heart 2001;85:649-654


             


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1. Sudden Cardiac Death in Athletes

2. Cardiac Screening to prevent Sudden Cardiac Death

3. Athletic Heart Research and Lectures



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