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S Fyyaz, A Merghani, S Al-Turaihi, N Chatrath, R Bhatia, H Maclachlan, G Finocchiaro, S Papatheodorou, G Parry-Williams, S David, J O’driscoll, M Papadakis, K Alfakih, S Sharma. European Journal of Preventive Cardiology. 13 June 2024.
Abstract:
Introduction
Cross-sectional studies of master athletes with a low risk atherosclerotic risk profile demonstrate a greater prevalence of high coronary artery calcium (CAC) scores, coronary plaque and luminal stenoses than matched controls. We sought to assess the progression of coronary disease amongst an ostensibly fit cohort of lifelong athletes compared with controls.
Methods
72 male master-athletes and 24 controls of similar age without cardiovascular risk factors at baseline underwent evaluation with health questionnaire, cardiopulmonary exercise testing (CPET) and computed tomography coronary angiography (CTCA) with CAC score at baseline and at 8 year follow-up. Athletes were required to continue running at least 10km/week.
CTCA was interpreted in accordance with established guidelines assessing luminal stenosis severity and plaque morphology (i.e. calcified, mixed or non-calcified). CAC was calculated using the Agatston method and adjusted for age and sex. A 3-vessel plaque score was calculated based on the coexisting presence of any plaque in the LAD, LCX or RCA irrespective of severity.
Results
Athletes remained well matched with respect to cardiovascular risk factors at follow-up, weighed significantly less, had higher HDL cholesterol, and achieved significantly greater CPET metrics with respect to maximum workload, peak VO2 and % predicted peak VO2 (p<0.001). Athletes were more likely to demonstrate a peak systolic blood pressure exceeding 220mmHg on exercise than controls.
There were no significant differences between athletes and controls with respect to CAC scores, proximal or 3-vessel plaque at baseline or follow-up. Albeit only athletes demonstrated CACS >300 and 400 AU and luminal stenoses >50% at baseline. Amongst athletes, 80% of plaques were of calcified at baseline versus 20% in controls (p<0.001). The dominant plaque morphology in controls was mixed plaque (67%).
At follow-up, athletes demonstrated a similar proportion of calcific and mixed plaque accounting for 48% and 43% of plaques respectively. However, controls continue to demonstrate significantly more mixed-morphology plaque (67%, p=0.027).
Discussion
Plaque composition amongst athletes changes with increasing age with an increasing prevalence of mixed plaque compared with calcific plaque at baseline, whereas the relative proportion of plaques amongst control subjects remained stable. This may suggest exercise induces plaque stabilising effects which is progressively offset with increasing age. Further longitudinal studies are required to understand cardiovascular event rates relative to plaque composition in athletes.
