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      Atrial fibrillation in athletes: implicit literature-based connections suggest that overtraining and subsequent inflammation may be a contributory mechanism.

      Medical Hypotheses
      Atrial Fibrillation, epidemiology, Causality, Comorbidity, Cumulative Trauma Disorders, Exercise, Exercise Movement Techniques, statistics & numerical data, Humans, Incidence, Inflammation, Periodicals as Topic, Sports

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          Abstract

          Research on atrial fibrillation (AF), a common heart arrhythmia in the elderly, over many decades has resulted in a literature of more than 16,000 articles indexed in Medline. An exploratory Medline search was conducted in which the subheadings for epidemiology and etiology of AF were combined to form a small subset of the initial records. Further computer-assisted selection led to a few articles that reported an unexpectedly high prevalence of AF in groups of otherwise healthy middle-aged endurance runners and other athletes. Why athletes should be unusually susceptible to AF is mysterious and puzzling. Because relatively few articles are about both AF and endurance exercise, a computer was used first to create a list of important terms that these two separate literatures had in common. Several inflammation-related terms, including C-reactive protein (CRP) and interleukin-6, were on that list. Further searching and literature analysis revealed that excessive endurance exercise or overtraining can lead to chronic systemic inflammation and, separately, that there is a solid association between CRP and AF and that anti-inflammatory agents have been reported to lower CRP and ameliorate AF. No articles were found that brought together all three concepts - AF, inflammation, and exercise. The following hypothesis is plausible, readily testable, and apparently novel: Older athletes diagnosed with AF but otherwise healthy who have engaged in rigorous aerobic endurance exercise for more than a decade will have CRP levels that are higher than those of a similar population of athletes without AF. Corroboration of this hypothesis would then justify a prospective clinical trial of anti-inflammation therapy. It is of particular interest to extend recent studies of inflammation in AF to athletes; athletic behavior that can induce inflammation may contribute to understanding the origins of AF.

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