Journal of cardiovascular electrophysiology · 1998
Atrial fibrillation in elite athletes.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Furlanello F, Bertoldi A, Dallago M, Galassi A, Fernando F, Biffi A, Mazzone P, Pappone C, Chierchia S
Аннотация
INTRODUCTION: Atrial fibrillation (AF) is a rare event in people younger than 25 years of age, but is probably more frequent in competitive athletes. We analyzed the presence of AF, paroxysmal or chronic, in a population of young elite athletes, including previous Olympic and World champions, who were studied for arrhythmias that endangered their athletic careers.
METHODS AND RESULTS: From 1974 to June 1977, 1,772 athletes identified with arrhythmias (1,464 males and 308 females; mean age 21 years) underwent individualized work-ups. Among these, 146 (122 males and 24 females; mean age 24 years) were young elite athletes. They were studied from 1985 to 1997, with a mean follow-up of 62 months. Of the 146 young elite athletes, 13 (9%) had AF (paroxysmal in 11 and chronic in 2); all were male. The paroxysmal AF occurred during effort (n = 7), after effort (n = 1), or at rest (n = 3) and was reinduced by transesophageal pacing or endocavitary electrophysiologic testing under the same clinical circumstances. AF was the cause of symptoms in 13 (40%) of 22 young elite athletes with long-lasting palpitations. Five young elite athletes had a substrate for AF: Wolff-Parkinson-White syndrome (WPW) in 3, arrhythmogenic right ventricular dysplasia (ARVD) in 1, healed myocarditis in 1, and was considered idiopathic in 8. All elite athletes are alive with a mean follow-up of 62 months and 7 continue in their sports: 3 after radiofrequency catheter ablation (of WPW in 2 and AF with maze-type nonfluoroscopic approach in 1) and 4 after a period of de-training.
CONCLUSIONS: AF, occurring in young elite athletes and affecting only males, is one of the most frequent causes of prolonged palpitations and is reproduced easily by transesophageal atrial pacing or electrophysiologic testing. AF may be a cause of disqualification from sports eligibility, but may disappear if the athletic activity is stopped for an adequate period of time, if trigger mechanisms are corrected (i.e., WPW), or if the substrate is modified.
METHODS AND RESULTS: From 1974 to June 1977, 1,772 athletes identified with arrhythmias (1,464 males and 308 females; mean age 21 years) underwent individualized work-ups. Among these, 146 (122 males and 24 females; mean age 24 years) were young elite athletes. They were studied from 1985 to 1997, with a mean follow-up of 62 months. Of the 146 young elite athletes, 13 (9%) had AF (paroxysmal in 11 and chronic in 2); all were male. The paroxysmal AF occurred during effort (n = 7), after effort (n = 1), or at rest (n = 3) and was reinduced by transesophageal pacing or endocavitary electrophysiologic testing under the same clinical circumstances. AF was the cause of symptoms in 13 (40%) of 22 young elite athletes with long-lasting palpitations. Five young elite athletes had a substrate for AF: Wolff-Parkinson-White syndrome (WPW) in 3, arrhythmogenic right ventricular dysplasia (ARVD) in 1, healed myocarditis in 1, and was considered idiopathic in 8. All elite athletes are alive with a mean follow-up of 62 months and 7 continue in their sports: 3 after radiofrequency catheter ablation (of WPW in 2 and AF with maze-type nonfluoroscopic approach in 1) and 4 after a period of de-training.
CONCLUSIONS: AF, occurring in young elite athletes and affecting only males, is one of the most frequent causes of prolonged palpitations and is reproduced easily by transesophageal atrial pacing or electrophysiologic testing. AF may be a cause of disqualification from sports eligibility, but may disappear if the athletic activity is stopped for an adequate period of time, if trigger mechanisms are corrected (i.e., WPW), or if the substrate is modified.