Cover Story

Management of Atrial Fibrillation in Athletes

Auras R. Atreya, MD, MPH and Eugene H. Chung, MD, MSc

Frankel Cardiovascular Center, University of Michigan

Ann Arbor, Michigan

Auras R. Atreya, MD, MPH and Eugene H. Chung, MD, MSc

Frankel Cardiovascular Center, University of Michigan

Ann Arbor, Michigan


Atrial fibrillation (AFib) is the most common arrhythmia in the general population as well as the elite athlete population.1,2 Middle-aged male athletes appear to be at higher risk of developing AFib than younger athletes. Possible explanations for higher risk of AFib include longer years of endurance training, higher vagal tone, and structural remodeling of the heart that occurs due to longstanding pressure and volume changes following endurance training.3-5 The prevalence rates vary widely for AFib in athletes, between 0.3% and 9% reported based on the population studied.6,7

While the precise pathophysiology of AFib in athletes is not fully understood, it is proposed that atrial stretch, progressive dilatation, and atrial fibrosis create an arrhythmogenic substrate for AFib, while atrial ectopy (predominantly pulmonary veins) and enhanced parasympathetic activity (which shortens atrial effective refractory periods) serve as triggers and modulators of AFib.8 Additionally, genetic predilection, nutritional supplements, electrolyte abnormalities, and gastrointestinal reflux may contribute to AFib in certain cases.2 Figure 1 summarizes the potential mechanisms of exercise-induced AFib.

The large majority of AFib in young athletes manifests as paroxysmal AFib in structurally normal hearts, or so-called lone AF, while middle-aged athletes may present with persistent AFib. The management of AFib in this population has several special considerations, as even routine therapeutic options such as anticoagulants and beta-blockers may have significant implications for the athlete.

In the following article, we present two brief cases and discuss approaches to evaluation and management.

Case Descriptions

Case #1

A professional baseball player in his late 30s was referred for the management of symptomatic paroxysmal AFib. The patient denied use of alcoholic beverages, nicotine, recreational drugs, or supplemental drug use. He had a structurally normal heart on echocardiogram, and due to marked symptoms interfering with game participation, a rhythm control strategy was chosen. An antiarrhythmic option consisting of a Class IC medication (propafenone) and a beta-blocker (low-dose metoprolol) versus catheter ablation was discussed. After consultation with his team physician, the patient opted for an ablation approach to avoid long-term medications. Cryoballoon ablation was performed in sinus rhythm to achieve pulmonary vein isolation of 5 veins (additional right middle pulmonary vein). Phrenic nerve pacing was performed during right-sided cryoballoon ablation. No arrhythmias were inducible post ablation. 

Three months following ablation, the patient was arrhythmia free. He was taken off of metoprolol and his oral anticoagulant (CHA2DS2-VASc score of 0). A 14-day wireless wearable event monitor documented no arrhythmias, including during professional games. He resumed his sporting activities after a brief recovery period.

Case #2

A professional basketball player in his early 30s was referred for the management of recurrent, symptomatic paroxysmal AFib. He had episodes brought on by physical exertion, during practice, or during basketball games, as well as several episodes at rest, around 7-8 AM. Echocardiography revealed a structurally normal heart with a mildly dilated left atrium (43 mm). Several antiarrhythmic drugs were either not tolerated well or were ineffective (Class IA: disopyramide; Class IC: flecainide; Class III: amiodarone, dofetilide). A radiofrequency ablation procedure was discussed, but the patient wished to hold off due to potential complications. Eventually, due to recurrent symptoms, he underwent pulmonary vein isolation and cavotricuspid isthmus linear ablation due to inducible typical atrial flutter during the procedure. He remained arrhythmia free for 3 months post ablation, and all medications (including anticoagulation) were discontinued to allow resumption of contact sports.

He participated in professional sports for 2 years and subsequently had recurrence of his arrhythmia, requiring redo pulmonary vein isolation and repeat ablation along the cavotricuspid isthmus due to recovery of conduction. He had no clinical arrhythmias for several years thereafter.


The American Heart Association and American College of Cardiology Task Force recommends that the routine evaluation of all athletes with atrial fibrillation should include drug use questions (performance-enhancing or illicit), thyroid function testing, electrocardiography, and echocardiography (Class I).9 If there is clinical suspicion for coronary artery disease or structural/infiltrative abnormalities, an exercise stress test and/or cardiac magnetic resonance imaging may also be appropriate. AFib in an adolescent athlete should also raise the suspicion for an accessory pathway, and event monitoring or serial electrocardiograms to look for intermittent pre-excitation would be reasonable. Testing for sleep apnea is important as well, as it is being increasing recognized that athletes are at risk for sleep apnea.10,11

Subsequent management options depend on the AFib burden and symptoms associated with it. It is reasonable to manage paroxysmal, low-burden, asymptomatic AF with rate control as needed or as a “pill-in-the-pocket” antiarrhythmic approach, with continued participation in sporting activities.8 In conjunction, stroke risk should be assessed using standard approaches, and anticoagulants are not indicated if the CHA2DS2-VaSc score is 0 or 1. As a result, athletes with low-burden, minimally symptomatic AFib may be able to avoid long-term medications that hinder athletic participation.

In patients with symptomatic or high-burden AFib, rhythm control is the preferred strategy for athletes. First, AFib is invariably poorly tolerated or associated with rapid rates that preclude or diminish athletic performance. Second, even if rate control were to be exercised, sporting performance is either impaired due to effect of atrioventricular nodal blockers or certain competitive participation may be prohibited due to beta-blocker use (World Anti-Doping Agency).12 Although antiarrhythmic drugs are an option for rhythm control, there are concerns regarding the proarrhythmic effects these drugs possess, which may be exacerbated in adrenergic states. Additionally, Class IC antiarrhythmics (flecainide, propafenone) — the first-line option in structurally normal hearts, require the concomitant use of a beta-blocker or calcium channel blocker, which most athletes prefer to avoid. Therefore, catheter ablation is often discussed as the first-line rhythm control therapy, and if successful, allows the athlete with a low risk of stroke to stop all medications (rate/rhythm/anticoagulant) in the long term. The caveat here is that the complications of catheter ablation or the need for anticoagulation immediately post ablation may preclude any contact sports for a period of time. These potential side effects should be discussed in detail with the patient to inform his/her decision.8

With regard to ablation strategy, there are no randomized studies comparing cryoballoon ablation with radiofrequency ablation in this specific population. Decision making is extrapolated from studies consisting of the general population.13 As such, either approach is reasonable to achieve pulmonary vein isolation based on operator and center experience. However, one consideration is the small risk of phrenic nerve injury with cryoballoon ablation. Shortness of breath experienced from this complication may potentially be very problematic for a professional athlete, and close monitoring with phrenic nerve pacing/compound motor action potential is critical.14,15

As an adjunct to rhythm control strategies with antiarrhythmic drugs or with catheter ablation, decreased training or detraining for a short period of time (2 months) may be considered. Indeed, this is recommended as an initial strategy by the European Society of Cardiology Study Group on Sports Cardiology.16 The rationale for this is the recognition of the association between intense endurance training and AFib risk.17,18 It is important to understand the “U-shaped” arrhythmia risk association with intensity of exercise, as low to moderate intensity exercise is recommended to aid rhythm control.19,20 Therefore, at the outset, it is worth discussing the athlete’s willingness to consider detraining for a short period of time, and further treatment plans can be formulated based on the AFib burden. Realistically, most athletes may not choose this option, and detraining can instead be incorporated into the post-ablation or post-cardioversion phase, when anticoagulation is mandated and contact sports are to be avoided.


Atrial fibrillation is the most common arrhythmia encountered in elite athletes, particularly middle-aged men. The pathophysiology is multifactorial — cardiac remodeling as a consequence of sustained endurance training and increased vagal tone are key elements. The approach to management is weighted in favor of rhythm control, given the relatively young age of patients, as well as the significant impact on quality of life and sports participation (Figure 2). Temporary detraining for 2 months is a consideration either as a first-line or adjunct therapy to facilitate rhythm control, if the athlete is amenable to it. 

Disclosures: The authors have no conflicts of interest to report regarding the content herein.   

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