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Background: The incidence of atrial fibrillation (AF) is increased by an average of approximately 2.5-fold in recreational and elite athletes, depending on the intensity of exercise. It is, however, difficult to determine the exact duration or intensity of exercise that increases the risk of AF. The pathophysiological mechanisms of AF in athletes are a combination of pulmonary vein ectopy as a trigger, myocardial changes such as fibrosis and remodeling processes, and modulators such as changes in the autonomic nervous system. However, gastroesophageal reflux also seems to play an important role., Material and Methods: The classic AF diagnosis is performed by means of 12-lead or Holter ECG; arrhythmia recordings via chest belts and pulse watches are not sufficient for the differentiation of the arrhythmia. However, wearables with the capability of ECG recording can also be used for AF screening. The first AF documentation in an athlete should be followed by cessation of physical exercise and initiation of detailed cardiac diagnostics. Thereafter, evaluation of oral anticoagulation is important. Long-term antiarrhythmic therapies are usually not tolerated or desired by athletes. Thus, valuable therapeutic options are either a "pill in the pocket" therapy with antiarrhythmic drugs or catheter ablation., (© 2022. The Author(s).)

Rhythm disturbances are life-threatening cardiovascular diseases, accounting for many deaths annually worldwide. Abnormal electrical activity might arise in a structurally normal heart in response to specific triggers or as a consequence of cardiac tissue alterations, in both cases with catastrophic consequences on heart global functioning. Preclinical modeling by recapitulating human pathophysiology of rhythm disturbances is fundamental to increase the comprehension of these diseases and propose effective strategies for their prevention, diagnosis, and clinical management. In silico, in vivo, and in vitro models found variable application to dissect many congenital and acquired rhythm disturbances. In the copious list of rhythm disturbances, diseases of the conduction system, as sick sinus syndrome, Brugada syndrome, and atrial fibrillation, have found extensive preclinical modeling. In addition, the electrical remodeling as a result of other cardiovascular diseases has also been investigated in models of hypertrophic cardiomyopathy, cardiac fibrosis, as well as arrhythmias induced by other non-cardiac pathologies, stress, and drug cardiotoxicity. This review aims to offer a critical overview on the effective ability of in silico bioinformatic tools, in vivo animal studies, in vitro models to provide insights on human heart rhythm pathophysiology in case of sick sinus syndrome, Brugada syndrome, and atrial fibrillation and advance their safe and successful translation into the cardiology arena.