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215 Longitudinal study of plaque morphology in masters athletes
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  1. Saad Fyyaz1,
  2. Ahmed Merghani1,
  3. Samar Al-Turaihi1,
  4. Nikhil Chatrath1,
  5. Hamish Maclachlan1,
  6. Raghav Bhatia1,
  7. Gherardo Finocchiaro1,
  8. Stathis Papatheodorou1,
  9. Gemma Parry-Williams1,
  10. Sarojini David1,
  11. Michael Papadakis1,
  12. Khaled Alfakih2,
  13. Sanjay Sharma1
  1. 1St George’s, University of London, Cardiology Clinical Academic Group, St George’s Uni, Cranmer Terrace London, London, LND SW17 0RE, UK
  2. 2Lewisham & Greenwich NHS Trust

Abstract

Introduction Cross-sectional studies of Master’s athletes with a low atherosclerotic risk profile have identified a greater prevalence of high coronary artery calcium (CAC) scores, coronary plaque and luminal stenoses than matched controls. Athletes exhibited predominantly calcified plaque which is purportedly more stable and less prone to rupture.

We sought to assess the progression of coronary disease amongst a cohort of male athletes and controls.

Methods 72 ostensibly fit male Master’s-athletes and 24 matched controls of similar age without cardiovascular risk factors at baseline underwent evaluation with health questionnaire, cardiopulmonary exercise testing (CPET) and CT coronary angiography (CTCA) with CAC score at baseline and 8-year follow-up. Athletes were required to continue running or cycling at least 10km or 30km/week respectively.

CTCA was interpreted in accordance with established guidelines assessing luminal stenosis severity and plaque morphology (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, demonstrated higher HDL cholesterol, and achieved significantly greater CPET metrics in regard to maximum workload, peak VO2 and % predicted peak VO2 (p<0.001). Only athletes demonstrated a peak systolic blood pressure exceeding 220 mmHg.

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.

At baseline amongst athletes, 79.5% of plaques were calcified versus 20% in controls (p<0.001). The dominant plaque morphology in controls was mixed plaque (66.7%).

At follow-up, athletes demonstrated a significant change in plaque composition with calcific and mixed plaque now accounting for 47.6% and 43.3% of plaques respectively (p<0.001). There were no significant differences in plaque composition amongst controls, who continued to demonstrate significantly more mixed-morphology plaque than athletes (63.2% vs 43.3%, p=0.027).

Discussion Plaque composition amongst athletes’ changes with increasing age from a predominantly calcified plaque morphology at baseline to a similar proportion of both calcified and mixed plaque at follow-up. By contrast, the relative proportions of plaques amongst control subjects remained stable, largely attributable to mixed plaque. Exercise may induce plaque stabilising effects which is progressively offset by age. Further longitudinal studies are required to understand cardiovascular event rates relative to plaque composition in athletes.

Abstract 215 Table 1
Abstract 215 Table 2

Conflict of Interest None

  • Master’s Athletes
  • CAC
  • Coronary Disease

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