<p>Participating in lifelong endurance sports is associated with an increased risk of atrial fibrillation (AF), potentially mediated through the process of left atrial (LA) remodeling which includes the progression of atrial fibrosis. This cross-sectional cohort study aimed to investigate LA remodeling including the presence and localization of LA fibrosis in lifelong endurance athletes. 42 master endurance athletes (76% male, age 54 ± 9 years), participating in Ironman races, (ultra) marathons and the Cape Epic Mountain Bike races, underwent clinical assessment with questionnaires, physical examination, and cardiac MRI (CMR). LA function, volumes, and left ventricular volumes were assessed. The extent of LA fibrosis, both global and regional, was derived from post-processed 3D late gadolinium-enhanced images using ADAS 3D. The median LA fibrotic burden as assessed by LGE-CMR was 2.5% (interquartile range, 1.1 to 7.6%). Fibrosis was heterogeneously distributed across the LA wall, with the highest burden observed along the left aspect of the posterior wall. There were no significant associations between LA fibrotic burden and atrial volume or functional parameters. Similarly, no associations were observed between fibrotic burden and sports level or training duration. LA fibrotic burden was significantly higher in participants who competed in long-distance mountain bike races versus participants who did not (7.3% [4.1–9.5] vs. 2.0% [0.5–5.6], <i>p</i> = 0.03). This study demonstrates the limited amount of LA fibrosis in lifelong master endurance athletes, with uneven distribution along the LA wall, most notably around the posterior side of the left inferior pulmonary vein. Participants engaged in long-distance mountain bike races exhibited significantly higher LA fibrotic burden, underscoring the potential impact of specific sports disciplines on LA remodeling, which may play a role in AF development.</p>

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Left atrial function and fibrosis in lifelong endurance athletes: a cardiac magnetic resonance imaging study

  • Luuk H.G.A. Hopman,
  • Jan-Peter Smedema,
  • Jeroen Swart,
  • Mayamiko J. Steenhoek,
  • Irene M. Frenaij,
  • Vijay Dahya,
  • Marco J.W. Götte

摘要

Participating in lifelong endurance sports is associated with an increased risk of atrial fibrillation (AF), potentially mediated through the process of left atrial (LA) remodeling which includes the progression of atrial fibrosis. This cross-sectional cohort study aimed to investigate LA remodeling including the presence and localization of LA fibrosis in lifelong endurance athletes. 42 master endurance athletes (76% male, age 54 ± 9 years), participating in Ironman races, (ultra) marathons and the Cape Epic Mountain Bike races, underwent clinical assessment with questionnaires, physical examination, and cardiac MRI (CMR). LA function, volumes, and left ventricular volumes were assessed. The extent of LA fibrosis, both global and regional, was derived from post-processed 3D late gadolinium-enhanced images using ADAS 3D. The median LA fibrotic burden as assessed by LGE-CMR was 2.5% (interquartile range, 1.1 to 7.6%). Fibrosis was heterogeneously distributed across the LA wall, with the highest burden observed along the left aspect of the posterior wall. There were no significant associations between LA fibrotic burden and atrial volume or functional parameters. Similarly, no associations were observed between fibrotic burden and sports level or training duration. LA fibrotic burden was significantly higher in participants who competed in long-distance mountain bike races versus participants who did not (7.3% [4.1–9.5] vs. 2.0% [0.5–5.6], p = 0.03). This study demonstrates the limited amount of LA fibrosis in lifelong master endurance athletes, with uneven distribution along the LA wall, most notably around the posterior side of the left inferior pulmonary vein. Participants engaged in long-distance mountain bike races exhibited significantly higher LA fibrotic burden, underscoring the potential impact of specific sports disciplines on LA remodeling, which may play a role in AF development.