Guasch E, Mont L, Sitges M
Institut Clinic Cardiovascular, Hospital Clínic de Barcelona; IDIBAPS; Universitat de Barcelona; CIBERCV., 08036, Barcelona, Catalonia, Spain.
Neth Heart J. 2018 Mar;26(3):133-145. doi: 10.1007/s12471-018-1080-x.
Exercise is an emerging cause of atrial fibrillation (AF) in young individuals without coexisting cardiovascular risk factors. The causes of exercise-induced atrial fibrillation remain largely unknown, and conclusions are jeopardised by apparently conflicting data. Some components of the athlete's heart are known to be arrhythmogenic in other settings. Bradycardia, atrial dilatation and, possibly, atrial premature beats are therefore biologically plausible contributors to exercise-induced AF. Challenging findings in an animal model suggest that exercise might also prompt the development of atrial fibrosis, possibly due to cumulative minor structural damage after each exercise bout. However, there is very limited, indirect data supporting this hypothesis in athletes. Age, sex, the presence of comorbidities and cardiovascular risk factors, and genetic individual variability might serve to flag those athletes who are at the higher risk of exercise-induced AF. In this review, we will critically address current knowledge on the mechanisms of exercise-induced AF.
运动是无并存心血管危险因素的年轻个体发生心房颤动(AF)的一个新出现的原因。运动诱发心房颤动的原因在很大程度上仍不清楚,且明显相互矛盾的数据危及了相关结论。已知运动员心脏的某些成分在其他情况下具有致心律失常性。因此,心动过缓、心房扩张以及可能的房性早搏在生物学上是运动诱发房颤的合理促成因素。动物模型中的挑战性发现表明,运动也可能促使心房纤维化的发展,这可能是由于每次运动后累积的轻微结构损伤所致。然而,在运动员中支持这一假设的直接数据非常有限。年龄、性别、合并症和心血管危险因素的存在以及基因个体差异可能有助于识别那些运动诱发房颤风险较高的运动员。在本综述中,我们将批判性地阐述关于运动诱发房颤机制的当前知识。