Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Szeged, Dóm tér 12, 6720, Szeged, Hungary.
Pflugers Arch. 2010 Jun;460(1):31-40. doi: 10.1007/s00424-010-0798-0. Epub 2010 Feb 26.
Sudden death among athletes is very rare (1:50,000-1:100,000 annually) but it is still 2-4 times more frequent than in the age-matched control population and attracts significant media attention. We propose a mechanism underlying sudden cardiac death in athletes that does not relate to myocardial ischemia but is based on repolarization abnormalities due to potassium channel downregulation and can also be best explained by the concurrent presence of several factors such as cardiac hypertrophy (athlete's heart), and/or hypertrophic cardiomyopathy, increased sympathetic tone, genetic defects, drugs, doping agents, food, or dietary ingredients. These factors together can increase the repolarization inhomogeneity of the heart ("substrate") and an otherwise harmless extrasystole ("trigger") occurring with a very unfortunate timing may sometimes induce life-threatening arrhythmias. The effective and possible prevention of sudden cardiac death requires the development of novel cost effective cardiac electrophysiological screening methods. Athletes identified by these tests as individuals at higher proarrhythmic risk should then be subjected to more costly genetic tests in order to uncover possible underlying genetic causes for alterations in ionic channel structure and/or function.
运动员猝死非常罕见（每年每 5 万人至 10 万人中有 1 例），但仍比同龄对照组高出 2-4 倍，因此引起了媒体的广泛关注。我们提出了一种与心肌缺血无关的运动员心源性猝死的发生机制，其基础是由于钾通道下调导致复极异常，同时还可以通过多种因素（如运动员心脏的心脏肥大和/或肥厚型心肌病、交感神经张力增加、遗传缺陷、药物、兴奋剂、食物或膳食成分）来最好地解释这种机制。这些因素共同增加了心脏复极的不均匀性（“基质”），而原本无害的偶发性早搏（“触发”）如果发生在非常不幸的时间，可能会引发危及生命的心律失常。有效的、可能的预防心源性猝死需要开发新的具有成本效益的心脏电生理筛查方法。通过这些测试确定的、处于更高致心律失常风险的运动员，应该进一步接受更昂贵的基因测试，以发现离子通道结构和/或功能改变的潜在遗传原因。
