Key result
Marathon running may induce systemic vascular maladaptations and arterial stiffness that promote lethal arrhythmias.
Why the study?
Does marathon running cause systemic vascular maladaptations that contribute to arrhythmogenic remodeling and sudden death?
Does marathon running cause systemic vascular maladaptations that contribute to arrhythmogenic remodeling and sudden death?
Prolonged strenuous exertion like marathon running may induce systemic vascular maladaptations that contribute to arrhythmogenic remodeling and sudden cardiac death.
May warrant vascular monitoring in endurance athletes; leaves open causal role in sudden cardiac death.
Subacute and chronic cardiac adaptations to marathon running may increase risk for sudden death. Herein, it is proposed that cardiac arrhythmogenic remodeling resulting from prolonged strenuous exertion may also have a systemic vascular component. Marathon running reduces coronary perfusion pressure and causes acute endothelial damage, possibly via altering concentrations of circulating angiogenic growth factors with novel vasoregulatory properties. Marathon runners have increased arterial stiffness and augmented pressure from wave reflections contributing to a widening of pulse pressure. Pulsatile hemodynamics may contribute to target organ damage. Moreover, each of these vascular maladaptations (increased arterial stiffness, augmented pressure from wave reflections, and widened pulse pressure) has been associated with atrial fibrillation and may provide a substrate for lethal arrhythmogenesis in the marathon runner. Clin. Cardiol. 2012 DOI: 10.1002/clc.21009 The author has no funding, financial relationships, or conflicts of interest to disclose. This article first published online 28 November 2011. It has since changed. The term “coronary pulse pressure” has been changed to “coronary perfusion pressure.”
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Kevin S. Heffernan (2011) conducted a review in Cardiovascular adaptations to marathon running. Marathon running was evaluated. Marathon running may induce systemic vascular maladaptations, including increased arterial stiffness and widened pulse pressure, potentially providing a substrate for lethal arrhythmogenesis.
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