Ablation of Atrial Fibrillation in Athletes: PRO

Editor's Note: This is the Pro article of a two-part Pro/Con Expert Analysis. Click here for the Con article.

Atrial fibrillation (AF) is widely recognized as the most common arrhythmia in clinic practice and its prevalence is expected to increase over the next decade.1 AF is responsible for considerable morbidity and may dramatically affect quality of life. AF is not limited to those with underlying heart disease and other conditions, but is also observed in quite healthy athletes. Regular exercise is recommended by the American College of Cardiology and the American Heart Association as it improves cardiovascular fitness and reduces mortality.2 In fact, vigorous exercise may increase the risk of cardiac arrhythmias. This potentially puts athletes at increased risk of developing atrial fibrillation. Recent meta-analysis suggested the rate of AF in athletes is higher than controls, though the data were of poor quality.3 Even the type of physical activity may also play a role. Studies suggest atrial fibrillation (AF) and atrial flutter may be more common in aerobically-trained athletes than non-aerobically trained athletes.4

Current theories suggest the etiology of AF in athletes is multifactorial and may include different mechanisms than in the general population. Physiologic adaptations to intense exercise serve to increase oxygenation of skeletal muscle during rigorous activity. It is theorized that some of these adaptive mechanisms to recurrent atrial pressure overload may lead to higher rates of AF. In fact, one of the greatest independent predictors of AF risk is left atrial size.5 Prior studies have demonstrated the left atrial dimensions are increased in athletes when compared to the general population. The increase in atrial wall stretch/strain may play a mechanistic role in the development of AF.6

The autonomic nervous system also plays an important role in both the initiation and maintenance of AF. Highly trained athletes develop increased parasympathetic tone, some have attributed to high vagal tone.7 With deconditioning, episodes of AF may be diminished. Vagal-mediated AF may be one of the mechanism by which athletes develop higher rates of AF.8

Regardless of the mechanism, non-valvular AF is associated with increased rates of morbidity and mortality in both athletes and the general population. In addition, the effects of AF on quality of life, in particular for the athlete, can be extreme. However, the optimal treatment algorithm for managing athletes with AF has not been well elucidated.

Treatment

AF is known to cause a variety of symptoms in the general population including palpitations, dyspnea, and generalized fatigue.9 When present in the highly trained athlete, these symptoms are of particular concern and may result in a decrease in performance or even render the athlete ineligible for further competition. In the athlete, aggressive rhythm control may allow the patient to continue to train and compete with minimal interruption.

Initial recommendations for athletes' participation in competitive sports were driven largely by the ventricular rate during exertion. Both United States and European guidelines suggests athletes with both symptomatic and asymptomatic AF without structural heart disease with appropriate rate responsiveness may continue to play sports.10,11 Traditional rate-controlling methods focus on beta-adrenergic and/or calcium-channel blocking agents. However, titrating AV nodal blockade to allow for high-performance activities at high heart rates, while preventing AF with a rapid ventricular response can prove difficult, if not impossible in many athletes. Both drug classes can have limiting side effect profiles in athletes and non-athletes alike. Additionally, beta-blockers are banned from some competitive sports.10 Antiarrhythmic agents for a rhythm control strategy may be an alternative. However, these agents are not without their risk, including proarrhythmia and sudden cardiac death. In addition both short term side effects and long term toxicities limit their use in a younger healthier population. As such, catheter ablation has emerged as an attractive therapeutic option in athletes with AF.

As is true for most treatments of the athlete, most of the data on catheter ablation is from a more general population of individuals, who are largely non-athletes. In this general population, the likelihood of procedural success is more directly related to patient characteristics than to the specific technique. Those most likely to derive benefit are those with paroxysmal AF, no underlying cardiac disease and a non-dilated left atrium. Paroxysmal AF is defined as AF less than 7 days in duration. Success rates with these patients approaches 80%.12-14 However, those with persistent (>7 days), and longstanding persistent (continuous AF >1 year) may benefit.15-17 It was once thought that patients need fail at least one antiarrhythmic agent prior to AF ablation. However, given the known toxicities of antiarrhythmic agents and the success of ablation, ablation is now acceptable as an initial rhythm control strategy, at least for paroxysmal AF.15,16

In the general population, randomized clinical trials comparing ablation to antiarrhythmic drug therapy have shown a higher likelihood of arrhythmia-free survival with ablation. In the RAAFT (First Line Radiofrequency Ablation Versus Antiarrhythmic Drugs for Atrial Fibrillation Treatment) Study, paroxysmal AF patients randomized to catheter ablation had a higher 2 year likelihood of sinus rhythm (45% vs 28%; p=0.02).18 In A4, ablation patients had a one year sinus rhythm incidence of 89% compared to 23% (p<0.001) in the antiarrhythmic arm.12 In MANTRA-PAF (Radiofrequency Ablation Versus Antiarrhythmic Drug Treatment in Paroxysmal Atrial Fibrillation), patients randomized to ablation were more likely to be free of AF at 2 year follow-up (85% vs 71%, p=0.004), and quality of life was higher.13 In the cryoablation STOP-AF (Atorvastatin Therapy for the Prevention of Atrial Fibrillation) trial, 70% of those randomized to ablation remained free of AF at 12 months as compared to 7.3% of those randomized to antiarrhythmic drugs.14 And there are several other RCTs which show a higher likelihood of sinus rhythm with ablation.14, 18-20

There are no randomized control trials of ablation limited to athletes. Initial ablation studies in athletes with AF were conducted in participants with disabling symptoms after failing drug therapy. Of the twenty participants recruited who underwent pulmonary vein isolation (PVI), 90% were free of AF during a 36-month follow-up period, and all participants demonstrated an improved post-ablation exercise capacity and improved quality of life.21 Importantly, all participants were deemed eligible to participate in their sport and were able to reinitiate their sport activity.

Follow-up studies of PVI using radiofrequency ablation (RFA) reinforced good initial success rates and evidence of durability in endurance athletes. Endurance athletes who underwent PVI showed similar long-term freedom from AF after a single ablation procedure as non-athletes after three years.22,23 When multiple PVI ablations were performed, athletes with lone AF actually demonstrated higher arrhythmia-free rates at one year when compared to their non-athlete controls.23

Currently the treatment of AF in athletes lacks high quality evidence and randomized, controlled clinical trials to help guide therapy. However, available case-control studies have demonstrated encouraging results for RFA as a therapy for athletes with symptomatic AF.

In the final analysis, treatment decisions should be shared between the athlete and the physician. Athletes with infrequent episodes and minimal symptoms may chose a simple strategy of rate control. Athletes with more troubling symptoms or with more frequent episodes will likely desire normal sinus rhythm. In these athletes, the risks and benefits of antiarrhythmic agents must be balanced against the risks and benefits of ablation.

References

  1. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: the anticoagulation and risk factors in atrial fibrillation (ATRIA) study. JAMA 2001;285:2370-5.
  2. Eckel RH, Jakicic JM, Ard JD, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:2960-84.
  3. Abdulla J, Nielsen JR. Is the risk of atrial fibrillation higher in athletes than in the general population? A systematic review and meta-analysis. Europace 2009;11:1156-9.
  4. Baldesberger S, Bauersfeld U, Candinas R, et al. Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur Heart J 2008;29:71-8.
  5. Henry WL, Morganroth J, Pearlman AS, et al. Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 1976;53:273-9.
  6. Pelliccia A, Maron BJ, Di Paolo FM, et al. Prevalence and clinical significance of left atrial remodeling in competitive athletes. J Am Coll Cardiol 2005;46:690-6.
  7. Coote JH, White MJ. Crosstalk proposal: bradycardia in the trained athlete is attributable to high vagal tone. J Physiol 2015;593:1745-7.
  8. Carpenter A, Frontera A, Bond R, Duncan E, Thomas G. Vagal atrial fibrillation: what is it and should we treat it? Int J Cardiol 2015;201:415-21.
  9. Dorian P, Paquette M, Newman D, et al. Quality of life improves with treatment in the canadian trial of atrial fibrillation. Am Heart J 2002;143:984-90.
  10. Maron BJ, Zipes DP. Introduction: eligibility recommendations for competitive athletes with cardiovascular abnormalities-general considerations. J Am Coll Cardiol 2005;45:1318-21.
  11. Pelliccia A, Fagard R, Bjornstad HH, et al. Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J 2005;26:1422-45.
  12. Jais P, Cauchemez B, Macle L, et al. Catheter ablation versus antiarrhythmic drugs for atrial fibrillation: the A4 study. Circulation 2008;118:2498-505.
  13. Cosedis Nielsen J, Johannessen A, Raatikainen P, et al. Radiofrequency ablation as initial therapy in paroxysmal atrial fibrillation. N Engl J Med 2012;367:1587-95.
  14. Packer DL, Kowal RC, Wheelan KR, et al. Cryoballoon ablation of pulmonary veins for paroxysmal atrial fibrillation: first results of the North American Arctic Front (STOP AF) pivotal trial. J Am Coll Cardiol 2013;61:1713-23.
  15. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 3014;64:e1-76.
  16. Camm AJ, Lip GY, De Caterina R, et al. 2012 focused update of the ESC guidelines for the management of atrial fibrillation: An update of the 2010 ESC guidelines for the management of atrial fibrillation: developed with the special contribution of the European Heart Rhythm Association. Eur Heart J 2012;33:2719-47.
  17. Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design: a report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Developed in partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Society (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bodies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Society, and the Heart Rhythm Society. Heart Rhythm 2012;9:632-96.
  18. Morillo CA, Verma A, Connolly SJ, et al. Radiofrequency ablation vs. antiarrhythmic drugs as first-line treatment of paroxysmal atrial fibrillation (RAAFT-2): a randomized trial. JAMA 2014;311:692-700.
  19. Pappone C, Santinelli V, Manguso F, et al. Pulmonary vein denervation enhances long-term benefit after circumferential ablation for paroxysmal atrial fibrillation. Circulation 2004;109:327-34.
  20. Wilber DJ, Pappone C, Neuzil P,et al. Comparison of antiarrhythmic drug therapy and radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation: a randomized controlled trial. JAMA 2010;303:333-40.
  21. Furlanello F, Lupo P, Pittalis M, et al. Radiofrequency catheter ablation of atrial fibrillation in athletes referred for disabling symptoms preventing usual training schedule and sport competition. J Cardiovasc Electrophysiol 2008;19:457-62.
  22. Koopman P, Nuyens D, Garweg C, et al. Efficacy of radiofrequency catheter ablation in athletes with atrial fibrillation. Europace 2011;13:1386-93.
  23. Calvo N, Mont L, Tamborero D,et al. Efficacy of circumferential pulmonary vein ablation of atrial fibrillation in endurance athletes. Europace 2010;12:30-6.

Keywords: Adrenergic Agents, Anti-Arrhythmia Agents, Atrial Fibrillation, Atrial Flutter, Athletes, Atrial Pressure, Catheter Ablation, Heart Atria, Heart Conduction System, Heart Rate, Pulmonary Veins, Risk Assessment, Sports


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