Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 1181 2023-05-29 20:00:43 |
2 format correction Meta information modification 1181 2023-05-31 02:33:57 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Petrungaro, M.; Fusco, L.; Cavarretta, E.; Scarà, A.; Borrelli, A.; Romano, S.; Petroni, R.; D’ascenzi, F.; Sciarra, L. Possible Mechanisms of Atrial Fibrillation in Athletes. Encyclopedia. Available online: https://encyclopedia.pub/entry/44982 (accessed on 21 June 2024).
Petrungaro M, Fusco L, Cavarretta E, Scarà A, Borrelli A, Romano S, et al. Possible Mechanisms of Atrial Fibrillation in Athletes. Encyclopedia. Available at: https://encyclopedia.pub/entry/44982. Accessed June 21, 2024.
Petrungaro, Mattia, Liuba Fusco, Elena Cavarretta, Antonio Scarà, Alessio Borrelli, Silvio Romano, Renata Petroni, Flavio D’ascenzi, Luigi Sciarra. "Possible Mechanisms of Atrial Fibrillation in Athletes" Encyclopedia, https://encyclopedia.pub/entry/44982 (accessed June 21, 2024).
Petrungaro, M., Fusco, L., Cavarretta, E., Scarà, A., Borrelli, A., Romano, S., Petroni, R., D’ascenzi, F., & Sciarra, L. (2023, May 29). Possible Mechanisms of Atrial Fibrillation in Athletes. In Encyclopedia. https://encyclopedia.pub/entry/44982
Petrungaro, Mattia, et al. "Possible Mechanisms of Atrial Fibrillation in Athletes." Encyclopedia. Web. 29 May, 2023.
Possible Mechanisms of Atrial Fibrillation in Athletes
Edit

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice, and it is an enormous burden worldwide because of its high morbidity, disability and mortality. It is generally acknowledged that physical activity (PA) is strongly associated with a significant reduction in the risk of cardiovascular (CV) disease and all-cause mortality. Moreover, it has been observed that moderate and regular physical activity has the potential to reduce the risk of AF, in addition to improving overall well-being.

atrial fibrillation arrhythmia physical activity

1. Introduction

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice, and it is an enormous burden worldwide because of its high morbidity, disability and mortality [1][2]. The prevalence of AF among the adult population is between 2% and 4%, with an increase in mortality between 1.5 and 3.5 times, and it has been associated with cardiovascular (CV) diseases such as heart failure, myocardial infarction, cerebral and ischemic events and all-cause mortality [3][4]. Its prevalence increases with age; indeed, more than 95% of AFs occur in those older than 60. AF is usually associated with cardiovascular and non-cardiovascular diseases [5]. However, this arrhythmia does not spare even young subjects with structurally normal hearts; this is the case of so-called lone AF [6].
It is generally recognized that physical activity (PA) is linked to a significant decrease in CV risk and all-cause mortality [7][8]. Moreover, it has been reported that moderate and regular physical activity has the potential to reduce the risk of AF [9][10].
Moderate and regular PA is considered a cornerstone in preventing AF by modifying many of its predisposing factors, which largely coincide with the classical CV disease risk factors [1][9][10][11][12][13]. Moderate, regular and aerobic physical activity improves many CV risk factors simultaneously, as opposed to drugs that are usually specific for a single factor [7]. Moderate PA can also be prescribed for subjects suffering from AF as part of their treatment because it improves muscular strength, ventricular rate control, 6 min walking test performance and quality of life [14][15]. The importance of PA in preventing AF seems to be further confirmed by the statistical correlation between a sedentary lifestyle and arrhythmia occurrence [16][17].
Nevertheless, some studies have associated intense physical activity with an increased risk of AF [18][19], reporting a higher incidence of AF in elite athletes [20][21][22] and suggesting a U-shaped dose–response curve [23][24]. These findings have raised doubts about the real beneficial effects of sports practice in arrhythmia prevention.

2. Electrophysiological Mechanisms of Atrial Fibrillation

Atrial fibrillation is a multifactorial arrhythmia. Its electrophysiology is complex and, even nowadays, not completely understood. Moreover, underlying arrhythmia mechanisms may differ depending on clinical scenarios and single patients [25][26], which can be crucial when considering athletes as “healthy” subjects.
Research on this topic is not new and dates back to the early twentieth century, but significant advances have been made in the last 30 years, leading to the contemporary knowledge about this arrhythmia. In particular, the “Coumel triangle” marked a cornerstone in the history of arrhythmology (Figure 1) [27]. The triangle’s three corners represent the factors needed to support any type of arrhythmia: triggers, arrhythmogenic substrate and modulating factors. In this simple, although dated, model, AF still seems to fit adequately. These mechanisms have been proposed to play a crucial role in the genesis and sustainment of AF, and all factors of the triangle may occur in the same patient [28]. Generally speaking, the “trigger” is mainly identified as premature ectopic beats, often originating from inside the pulmonary veins’ ostia [29][30], but it can also be constituted by other supraventricular arrhythmias [26][31] that may degenerate into AF. The term “substrate” is a generic definition including all the structural, morphological and functional alterations that may favor arrhythmia maintenance. The “modulating factors” are mainly represented by sympathetic and vagal tone modifications, which in different clinical scenarios may favor the development of AF [17]. Understanding how these factors may be directly influenced by physical activity is intuitive.
Figure 1. To support an arrhythmia, the presence of a trigger, a substrate and modulating factors is essential.

3. Importance of the Specific Arrhythmia Triggers in Athletes

In the case of AF in a young athlete with a structurally normal heart, an underlying synchronized tachycardia inducing AF might be present. In the absence of any structural heart disease, AF is often triggered by other tachyarrhythmias. It is well known that some re-entrant tachycardias can induce atrial flutter or AF noted as “tachycardia-induced tachycardia” or “tachycardia-induced AF” [32][33].
In the general population, the occurrence of premature atrial contractions, particularly pulmonary vein ectopic beats, are the main trigger in most episodes of paroxysmal AF [29]. It has been postulated that endurance athletes present a higher burden of premature atrial beats than sedentary individuals [34][35]. Nevertheless, currently available data are insufficient to demonstrate a clear relationship between atrial premature beats and PA and whether such a little increase is enough to contribute to the AF burden in athletes significantly. In fact, Baldesberger et al. [36] and Elliot et al. [37] did not find an increased incidence of atrial ectopy in their study on former professional cyclists. Therefore, the exact role of atrial premature beats in athletes as prevalent triggers of AF remains unclear.

4. Arrhythmogenic Substrate Modification in Athletes

Intensive training leads to morphological and functional remodeling of the heart and cardiovascular system, resulting in the so-called “athlete’s heart” [38], which may play a role in the induction of AF. These CV adaptations are particularly evident when induced by endurance exercise to cope with the increase in cardiac output required during exercise and include biatrial dilatation [34], left ventricular hypertrophy [39] and enlargement of the right ventricle [40][41]. Usually, all anatomical changes disappear with detraining, but the exact amount of time required remains unclear [40]. Several factors related to exercise-related AF include atrial enlargement, an increased stretch of the atrium wall during activity and electrolyte disturbances (sodium, potassium, calcium and magnesium). It is possible to speculate that intense physical activity, combined with non- optimal electrolytic replenishment, can lead to an electrolyte imbalance that could trigger AF. However, the extent to which this aspect really contributes to the prevalence of AF in professional athletes is yet to be completely understood.

5. Possible Modulating Factor Modifications in Athletes

Autonomic tone can be significantly modified in athletes. Established cardiovascular adaptation to regular exercise is enhanced parasympathetic activity [42] which may generate sinus bradycardia at rest in well-trained individuals and AV conduction disturbances [43]. This is induced by increased sympathetic tone during exercise and a consequent downregulation at rest, which makes the vagal tone dominant [44][45][46].
This condition is reversible after detraining. Enhanced vagal tone and reduced sympathetic tone, characteristic of endurance athletes, have been associated with the development of AF, as well as in normal hearts [20][29][47]. Clinically, several features suggest that vagal tone can modulate AF, for example, when AF arises during sleep or after heavy meals. High levels of acetylcholine increase the dispersion of atrial repolarization and shorten the atrial effective refractory periods and the wavelength of atrial excitation wavefronts [20][48]. Notably, most AF relapses in athletes occur in vagally dominant situations while, conversely, adrenergic-mediated AF is less frequent in this population [22]. In a selected population of patients with paroxysmal vagal AF, vagal atrial denervation by radiofrequency ablation of right atrial ganglionated plexi was also attempted using an anatomic approach [49][50].

References

  1. Hindricks, G.; Potpara, T.; Dagres, N.; Arbelo, E.; Bax, J.J.; Blomström-Lundqvist, C.; Boriani, G.; Castella, M.; Dan, G.A.; Dilaveris, P.E.; et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) Developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur. Heart J. 2021, 42, 373–498.
  2. Aggarwal, A.; Heslop, J.J.; Wigant, R.R.; Venkatapuram, S.; Hillis, S.J.; Parr, A.R.; Oral, H.; Baman, T. Occult atrial fibrillation in endurance athletes. Open Access J. Sport. Med. 2017, 8, 227–229.
  3. Colilla, S.; Crow, A.; Petkun, W.; Singer, D.E.; Simon, T.; Liu, X. Estimates of Current and Future Incidence and Prevalence of Atrial Fibrillation in the U.S. Adult Population. Am. J. Cardiol. 2013, 112, 1142–1147.
  4. Krijthe, B.P.; Kunst, A.; Benjamin, E.; Lip, G.Y.; Franco, O.; Hofman, A.; Witteman, J.C.; Stricker, B.H.; Heeringa, J. Projections on the number of individuals with atrial fibrillation in the European Union, from 2000 to 2060. Eur. Heart J. 2013, 34, 2746–2751.
  5. Ferreira, C.; Providência, R.; Ferreira, M.J.; Gonçalves, L.M. Atrial Fibrillation and Non-cardiovascular Diseases: A Systematic Review. Arq. Bras. Cardiol. 2015, 105, 519–526.
  6. Kopecky, S.L.; Gersh, B.J.; McGoon, M.D.; Whisnant, J.P.; Holmes, D.R.; Ilstrup, D.M.; Frye, R.L. The natural history of lone atrial fibril-lation. A population-based study over three decades. N. Engl. J. Med. 1987, 317, 669–674.
  7. Williams, P.T. Dose-response relationship of physical activity to premature and total all-cause and cardiovascular disease mortality in walkers. PLoS ONE 2013, 8, e78777.
  8. Malmo, V.; Nes, B.M.; Amundsen, B.H.; Tjonna, A.E.; Stoylen, A.; Rossvoll, O.; Wisloff, U.; Loennechen, J.P. Aerobic Interval Training Reduces the Burden of Atrial Fibrillation in the Short Term: A Randomized Trial. Circulation 2016, 133, 466–473.
  9. Santos-Lozano, A.; Sanchis-Gomar, F.; Barrero-Santalla, S.; Pareja-Galeano, H.; Cristi-Montero, C.; Sanz-Ayan, P.; Garatachea, N.; Fiuza-Luces, C.; Lucia, A. Exercise as an adjuvant therapy against chronic atrial fibrillation. Int. J. Cardiol. 2016, 207, 180–184.
  10. Abdulla, J.; Nielsen, J.R. Is the risk of atrial fibrillation higher in athletes than in the general population? A systematic review and meta-analysis. EP Eur. 2009, 11, 1156–1159.
  11. Du, X.; Dong, J.; Ma, C. Is atrial fibrillation a preventable disease? J. Am. Coll. Cardiol. 2017, 69, 19681982.
  12. Mozaffarian, D.; Furberg, C.D.; Psaty, B.M.; Siscovick, D. Physical activity and incidence of atrial fibrillation in older adults: The cardiovascular health study. Circulation 2008, 118, 800807.
  13. Elliott, A.D.; Maatman, B.; Emery, M.S.; Sanders, P. The role of exercise in atrial fibrillation prevention and promotion: Finding optimal ranges for health. Heart Rhythm 2017, 14, 17131720.
  14. Reed, J.L.; Mark, A.E.; Reid, R.D.; Pipe, A.L. The effects of chronic exercise training in individuals with permanent atrial fibrillation: A systematic review. Can. J. Cardiol. 2013, 29, 1721–1728.
  15. Osbak, P.S.; Mourier, M.; Kjaer, A.; Henriksen, J.H.; Kofoed, K.F.; Jensen, G.B. A randomized study of the effects of exercise training on patients with atrial fibrillation. Am. Heart J. 2011, 162, 1080–1087.
  16. Centurión, O.A.; Candia, J.C.; Scavenius, K.E.; García, L.B.; Torales, J.M.; Miño, L.M. The Association Between Atrial Fibrillation and Endurance Physical Activity: How Much is too Much? J. Atr. Fibrill. 2019, 12, 2167.
  17. D’Ascenzi, F.; Cameli, M.; Ciccone, M.M.; Maiello, M.; Modesti, P.A.; Mondillo, S.; Muiesan, M.L.; Scicchitano, P.; Novo, S.; Palmiero, P.; et al. The controversial relationship between exercise and atrial fibrillation: Clinical studies and pathophysiological mechanisms. J. Cardiovasc. Med. 2015, 16, 802–810.
  18. Merghani, A.; Malhotra, A.; Sharma, S. The U-shaped relationship between exercise and cardiac morbidity. Trends Cardiovasc. Med. 2016, 26, 232–240.
  19. Sanchis-Gomar, F.; Perez-Quilis, C.; Lippi, G.; Cervellin, G.; Leischik, R.; Löllgen, H.; Serrano-Ostáriz, E.; Lucia, A. Atrial fibrillation in highly trained endurance athletes-Description of a syndrome. Int. J. Cardiol. 2017, 226, 11–20.
  20. Karjalainen, J.; Kujala, U.M.; Kaprio, J.; Sarna, S.; Viitasalo, M. Lone atrial fibrillation in vigorously exercising middle aged men: Case-control study. BMJ 1998, 316, 1784–1785.
  21. Furlanello, F.; Bertoldi, A.; Dallago, M.; Galassi, A.; Fernando, F.; Biffi, A.; Mazzone, P.; Pappone, C.; Chierchia, S. Atrial fibrillation in elite athletes. J. Cardiovasc. Electrophysiol. 1998, 9, S63–S68.
  22. Mont, L.; Sambola, A.; Brugada, J.; Vacca, M.; Marrugat, J.; Elosua, R.; Paré, C.; Azqueta, M.; Sanz, G. Long-lasting sport practice and lone atrial fibrillation. Eur. Heart J. 2002, 23, 477–482.
  23. La Gerche, A.; Schmied, C.M. Atrial fibrillation in athletes and the interplay between exercise and health. Eur. Heart J. 2013, 34, 3599–3602.
  24. Jin, M.-N.; Yang, P.-S.; Song, C.; Yu, H.T.; Kim, T.-H.; Uhm, J.-S.; Sung, J.-H.; Pak, H.-N.; Lee, M.-H.; Joung, B. Physical Activity and Risk of Atrial Fibrillation: A Nationwide Cohort Study in General Population. Sci. Rep. 2019, 9, 1–9.
  25. Van Gelder, I.C.; Hobbelt, A.H.; Marcos, E.G.; Schotten, U.; Cappato, R.; Lewalter, T.; Schwieler, J.; Rienstra, M.; Boriani, G. Tailored treatment strategies: A new approach for modern management of atrial fibrillation. J. Intern. Med. 2016, 279, 457–466.
  26. Sciarra, L.; Rebecchi, M.; De Ruvo, E.; De Luca, L.; Zuccaro, L.M.; Fagagnini, A.; Corò, L.; Allocca, G.; Lioy, E.; Delise, P.; et al. How many atrial fibrillation ablation candidates have an underlying supraventricular tachycardia previously unknown? Efficacy of isolated triggering arrhythmia ablation. Europace 2010, 12, 1707–1712.
  27. Coumel, P.; Leenhardt, A. Mental Cardiac arrhytmias and the autonomic nervous system. J. Cardiovasc. Electrophysiol. 1993, 4, 338–355.
  28. Calò, L.; Sciarra, L. Heat or cold: Different questions, same doubts. Heart Rhythm 2017, 14, 17–18.
  29. Haïssaguerre, M.; Jaïs, P.; Shah, D.C.; Takahashi, A.; Hocini, M.; Quiniou, G.; Garrigue, S.; Le Mouroux, A.; Le Métayer, P.; Clémenty, J. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N. Engl. J. Med. 1998, 339, 659–666.
  30. Adragão, P.; Cavaco, D.; Aguiar, C.; Palos, J.; Morgado, F.; Ribeiras, R.; Abecasis, M.; Neves, J.; Bonhorst, D.; Seabra-Gomes, R. Ablation of pulmonary vein foci for the treatment of atrial fibrillation; percutaneous electroanatomical guided approach. Europace 2002, 4, 391–399.
  31. Brugada, J.; Mont, L.; Matas, M.; Navarro-Lopez, F. Atrial fibrillation induced by atrio-ventricular nodal reentrant tachycardia. Am. J. Cardiol. 1997, 79, 681–682.
  32. Prystowsky, E.N. Tachycardia-induced tachycardia: A mechanism of initiation of atrial fibrillation. In Atrial Arrhythmias; Di Marco, J., Prystowsky, E.N., Eds.; State of the art; Futura Publishing Company: Armonk, NY, USA, 1995; pp. 81–95.
  33. Delise, P.; Gianfranchi, L.; Paparella, N.; Brignole, M.; Menozzi, C.; Themistoclakis, S.; Mantovan, R.; Bonso, A.; Corò, L.; Vaglio, A.; et al. Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation. Am. J. Cardiol. 1997, 79, 1421–1423.
  34. Wilhelm, M.; Roten, L.; Tanner, H.; Wilhelm, I.; Schmid, J.-P.; Saner, H. Atrial remodeling, autonomic tone, and lifetime training hours in nonelite athletes. Am. J. Cardiol. 2011, 108, 580–585.
  35. Talan, D.A.; Bauernfeind, R.A.; Ashley, W.W.; Kanakis, C.; Rosen, K.M. Twenty-four hour continuous ECG recordings in long-distance runners. Chest 1982, 82, 19–24.
  36. Baldesberger, S.; Bauersfeld, U.; Candinas, R.; Seifert, B.; Zuber, M.; Ritter, M.; Jenni, R.; Oechslin, E.; Luthi, P.; Scharf, C.; et al. Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur. Heart J. 2008, 29, 71–78.
  37. Elliott, A.D.; Mahajan, R.; Linz, D.; Stokes, M.; Verdicchio, C.; Middeldorp, M.; La Gerche, A.; Lau, D.H.; Sanders, P. Atrial remodeling and ectopic burden in recreational athletes: Implications for risk of atrial fibrillation. Clin. Cardiol. 2018, 41, 843–848.
  38. Brosnan, M.J.; Rakhit, D. Differentiating Athlete’s Heart From Cardiomyopathies—The Left Side. Heart Lung Circ. 2018, 27, 1052–1062.
  39. Arbab-Zadeh, A.; Perhonen, M.; Howden, E.; Peshock, R.M.; Zhang, R.; Adams-Huet, B.; Haykowsky, M.J.; Levine, B.D. Cardiac remodeling in response to 1 year of intensive endurance training. Circulation 2014, 130, 2152–2161.
  40. Thompson, P. Exercise and the heart: The good, the bad and the ugly. Dialogues Cardiovasc. Med. 2002, 7, 140–158.
  41. Bhella, P.S.; Hastings, J.L.; Fujimoto, N.; Shibata, S.; Carrick-Ranson, G.; Palmer, M.D.; Boyd, K.N.; Adams-Huet, B.; Levine, B.D. Impact of lifelong exercise “dose” on left ventricular compliance and distensibility. J. Am. Coll. Cardiol. 2014, 64, 1257–1266.
  42. Okazaki, K.; Iwasaki, K.; Prasad, A.; Palmer, M.D.; Martini, E.R.; Fu, Q.; Arbab-Zadeh, A.; Zhang, R.; Levine, B.D. Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors. J. Appl. Physiol. 2005, 99, 1041–1049.
  43. Cooper, J.P.; Fraser, A.G.; Penny, W.J. Reversibility and benign recurrence of complete heart block in athletes. Int. J. Cardiol. 1992, 35, 118–120.
  44. Zeppilli, P.; Santini, C. L’elettrocardiogramma nell’atleta. In Cardiologia dello Sport; Zeppilli, P., Ed.; CESI: Roma, Italy, 1990; pp. 121–140.
  45. Zeppilli, P.; Manno, V. Vagotonia fisiologica e non fisiologica nell’atleta. G Ital. Cardiol. 1987, 17, 865–873.
  46. Werle, E.O.; Strobel, G.; Weicker, H. Decrease in rat cardiac beta1- and beta2-adrenoceptors by training and endurance exercise. Life Sci. 1990, 46, 9–17.
  47. 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, 415–421.
  48. Guasch, E.; Benito, B.; Qi, X.; Cifelli, C.; Naud, P.; Shi, Y.; Mighiu, A.; Tardif, J.C.; Tadevosyan, A.; Chen, Y.; et al. Atrial fibrillation promotion by endurance exercise: Demonstration and mechanistic exploration in an animal model. J. Am. Coll. Cardiol. 2013, 62, 68–77.
  49. Rebecchi, M.; Panattoni, G.; Edoardo, B.; de Ruvo, E.; Sciarra, L.; Politano, A.; Sgueglia, M.; Ricagni, C.; Verbena, S.; Crescenzi, C.; et al. Atrial fibrillation and autonomic nervous system: A translational approach to guide therapeutic goals. J. Arrhythm. 2021, 37, 320–330.
  50. Calò, L.; Rebecchi, M.; Sciarra, L.; De Luca, L.; Fagagnini, A.; Zuccaro, L.M.; Pitrone, P.; Dottori, S.; Porfirio, M.; de Ruvo, E.; et al. Catheter ablation of right atrial ganglionated plexi in patients with vagal paroxysmal atrial fibrillation. Circ. Arrhythm. Electrophysiol. 2012, 5, 22–31.
More
Information
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : , , , , , , , ,
View Times: 226
Revisions: 2 times (View History)
Update Date: 31 May 2023
1000/1000
Video Production Service