Atrial fibrillation (AF) is the most common arrhythmia in the athletic community and is more frequently observed in middle-aged than in young athletes. Recent studies have shown that the prevalence of AF is higher in individuals who are involved in intense short-term training and long-term sports participation compared to general population of the same age although clear evidence about the causal relation between these conditions is lacking. Anatomic adaptation, chronic systemic inflammation, and alterations in the autonomic system are all possible explanations for the increased prevalence of AF in athletes. AF associated with sports is usually paroxysmal with occasional crisis. Treatment of AF in this population can be challenging because of a lack of randomized trials and clear guidelines. Antiarrhythmic agents are usually the preferred choice of drugs. Several reports of catheter ablation have demonstrated encouraging results. Further studies are needed to understand the mechanism of autonomic hyperactivation and its interaction with the atrial substrate to develop new ablation strategies in this group of patients. Also, studies on the intensity and duration of exercise that would negate the proarrhythmic cardiac effects are also warranted.
Athletes are universally considered healthy individuals compared to the rest of the population. It is well known that athletes are more prone to sudden cardiac death and arrhythmias despite having structurally normal hearts compared to nonathletes of the same age. Atrial fibrillation (AF) is the most common clinically significant cardiac arrhythmia and is commonly associated with hypertension. The prevalence increases with age, ranging from 0.5% in young patients (aged <40 years) to >5% in patients aged >65 years. AF is also the most common arrhythmia in the athletic community and is more frequently observed in middle-aged than in young athletes. Recent studies have also shown that the prevalence of AF is higher in individuals who are involved in sports-related practices compared to the general population of same age. Intense short-term training and long-term sports participation can result in anatomic adaptation, chronic systemic inflammation, and alterations in the autonomic system, which can result in the initiation and maintenance of AF, although clear evidence about the causal relation between these conditions is lacking. Although AF is presumably the most common tachyarrhythmia in athletes and the general population, there are some differences in its cause, clinical presentation, and treatment strategies ( Table 1 ). In this review, we discuss the epidemiology, mechanism, clinical features, and treatment options in this special population.
| Athletes | Nonathletes | |
|---|---|---|
| Type | Vagal mediated | Adrenergic mediated |
| Presentation | Usually intermittent, paroxysmal | Paroxysmal, persistent, or permanent |
| Epidemiology | Variable, prevalence 0.2% to 60% | Mean prevalence of 0.5% to 5% (higher in older age group) |
| Clinical features | Palpitations are more common, chest discomfort, shortness of breath, diaphoresis, syncope | Palpitations, chest discomfort, shortness of breath, diaphoresis, syncope |
| Causes | Autonomic changes, cardiac adaptability, inflammation, fluid shifts, illicit drugs | Hypertension, valvular heart disease, myocardial infarction, pulmonary disease, hyperthyroidism, alcohol |
| Treatments | Sports abstinence, antiarrhythmic drugs, antiplatelet, ablation, anticoagulation (not preferred) | Rate-control medications, antiarrhythmic drugs, anticoagulation, ablation |
| Prognosis | Favorable for lone AF in the absence of underlying structural heart disease or risk factors | Not very favorable; risk for stroke and heart failure |
Epidemiology
Risk for AF in athletes
The incidence of AF in the general population is about 0.1% per year with a mean prevalence of 0.8 to 1% with older patients accounting for the greatest proportion of patients. Reports from epidemiologic studies demonstrating AF in athletes have been variable on the basis of age, years of training, and associated co-morbidities. Furlanello et al reported that AF accounted up to 0.2% in a population of 5,000 athletes. Pelliccia et al reported that the prevalence of AF was 0.3% in a study involving 1,776 subjects. However, a study by Mont et al found an AF prevalence of 63% in athletes with a mean age of 44 years. Coelho et al found that lone AF was the dominant arrhythmia and accounted for about 25% of athletes when presented with either palpitations or documented arrhythmia. It should be noted that the studies by Furlanello et al and Pelliccia et al had younger patients with relatively fewer years of training, unlike the later reports. Several other studies have shown an increased proportion of AF in athletes compared to the rest of the population ( Table 2 ). Several risk factors for lone AF such as current or former sports participation, duration of sports activity, accumulated lifetime activity, subject height, electrocardiographic findings such as long PQ, bradycardia, and echocardiographic findings such as enlargement of left atrium, left atrial inferosuperior diameter, and left atrial volume have been reported in various sports-related studies but not confirmed by prospective control studies. A recent meta-analysis by Abdulla et al demonstrated that the overall risk for AF was significantly higher in athletes than in controls (odds ratio 5.29, 95% confidence interval [CI] 3.57 to 7.85, p = 0.0001). Elosua et al reported that current practice of sports with lifetime practice >1,500 hours was associated with AF (odds ratio 5.06, 95% CI 1.35 to 19, p = 0.016), and lifetime sports practice of 1,561 to 5,668 hours was associated with a risk of 4.67 (95% CI 1.08 to 20, p = 0.039). The type of sports practiced was also a risk factor according to a few studies. As opposed to other causes of AF for which the risk for stroke and other cardiac events can be substantial, lone AF is generally benign. However, results reporting mortality data in athletes with AF is scarce and inconsistent. Interestingly, there are no studies eliciting the influence of race and gender on the risk and long-term outcomes of AF related to sports practices but past data indicate that men seem to be more prone to develop AF than women.
| Study | Type | Age (years) (Patients/Controls) | Sport Type (Patients/Controls) | Study Population (Patients/Controls) | Prevalence of AF (%) (Patients/Controls) | Relative Risk for AF |
|---|---|---|---|---|---|---|
| Karjalainen et al | Longitudinal | 47 ± 5/49 ± 5 | Orienteering/sedentary | 262/373 | 5.3/0.9 (p = 0.012) | 5.5 (95% CI 1.3–24.4 |
| Molina et al | Retrospective | 39 ± 9/50 ± 13 | Marathon running/sedentary | 252/305 | 5/0.7 (p = 0.013) | 8.80 (95% CI 1.2–61.2) |
| Baldesberger et al | Longitudinal | 66 ± 7/66 ± 6 | Cycling/golfing | 134/62 | 10/0(p = 0.028) | NR |
| Elosua et al | Retrospective (case-control) | 41 ± 13/44 ± 11 | Endurance sports: current practice and >1,500 accumulated hours of practice | 51/109 | 32/14 (p = 0.01) | 2.87 (95% CI 1.20–6.91) |
| Mont et al | Prospective | 48 ± 11 | Endurance sports | 107/107 | NR | 7.31 (95% CI 2.33–22.9) |
| Mont et al | Retrospective | 44 ± 13/49 ± 11 | Endurance sports >3 hours/week | 70 lone AF | 63/15 (p <0.05) | NR |
| Grimsmo et al | Prospective, 28- to 30-year follow up | Group I, 54–62; group II, 72–80; group III, 87–92 | Cross-country skiers | Group I, 33; group II, 37; group III, 8 | 12.8% of lone AF | Long PQ (rr = 0.38, p = 0.001 and rr = 0.27, p = 0.02), bradycardia (rr = 0.29, p = 0.012) were associated risk factors |
Athletes or vigorous exercise?
Although vigorous exercise has numerous health benefits, there are limited data on the role of vigorous exercise in the development of AF in subjects participating in exercise at a less competitive level or even exercising daily. A large 12-year prospective cohort study by Aizer et al found that middle-aged subjects (aged <50 years) who indulged in moderate exercise (5 to 7 times/week) had a significant risk (relative risk 1.53, 95% CI 1.12 to 2.09, p <0.01) for developing AF at 3-year follow-up compared to controls. Men who jogged ≥5 days per week had a 53% increased risk for developing AF compared to men who did not exercise. Data from the Grup Integrat de Recerca en Fibril·lació Auricular (GIRAFA) study support this theory. The results showed that the moderate and heavy physical activity, increased the risk for AF; intense physical activity of >564 hours was associated with a risk for the development of AF of 7.31 (95% CI 2.33 to 22.96, p = 0.0006), and 1 to 563 hours of activity was associated with a nonsignificant risk of 1.77 times (95% CI 0.22 to 14.26, p = 0.50) to develop AF. In contrast to the earlier reports, the Danish Diet Cancer and Health Study failed to demonstrate any association between physical activities during working hours and risk for hospitalization with a diagnosis of AF or atrial flutter. Further prospective controlled studies are essential regarding the degree of intensity of exercise and the risk for developing AF in various other cohorts.
Pathophysiology of Atrial Fibrillation in Athletes
The mechanism of AF in athletes is multifactorial ( Figure 1 ) .
Anatomic changes predisposing to AF
The atrial morphologic adaptations in athletes may be the consequence of long-standing volume and/or pressure overload due to long-term sports practice. Endurance sports increase preload which increases atrial pressure. Increasing atrial pressure experimentally shortens atrial refractory periods increasing dispersion of atrial refractoriness, which in turn correlates with new inducibility of AF. Some older studies reported increased left atrial diameters in athletes to be the cause for AF. Although the underlying mechanism for structural adaptation is not clear, recent echocardiographic data suggest that structural remodeling is often present in the atria of elite athletes without AF. Pelliccia et al reported that a significant proportion (>20%) of those involved in regular endurance practice had larger left atrial dimensions (>40 mm) compared to sedentary controls among 1,777 elite sport athletes without heart disease (mean age 24 ± 6 years, mean time of sports involvement 6 years). There have been conflicting data regarding increased atrial ectopy with physical activity. Baldesberger et al did not find an increased incidence of atrial ectopy, despite increases in ventricular ectopy in former professional cyclists. A review by Swanson showed that excessive endurance exercise can lead to chronic systemic inflammation which can modify the atrial substrate to favoring the onset and maintenance of AF. Another case-control study by Lindsay and Dunn involving 45 veteran athletes showed biochemical evidence of disruption of the collagen equilibrium that would favor fibrosis and increase in 3 collagen markers (plasma procollagen type I carboxy-terminal propeptide, C-telopeptide for type I collagen, and tissue inhibitor of metalloproteinase–1) compared to sedentary controls. This concept of fibrosis is also supported by experimental data from male Wistar rats. In this study, the experimental group was conditioned to run vigorously for 4, 8, and 16 weeks compared to time-matched sedentary rats that served as controls. At 16 weeks, exercise rats developed eccentric hypertrophy and diastolic dysfunction together with atrial dilation with collagen deposition in the right ventricle. Protein expression of fibrosis markers in both atria and right ventricle were significantly greater in exercise than in sedentary rats. The fibrotic changes caused by 16 weeks of intensive exercise were reversed after an 8-week exercise cessation. However, these findings are yet to be confirmed in humans.
Alteration in autonomic nervous system
There are some data suggesting that combined hyperactivation of parasympathetic and sympathetic system can be proarrhythmic. According to the GIRAFA study, vagal AF is a more common form of lone AF demonstrating that 70% of consecutive patients with lone AF had vagal AF. Experimental data also show that increased vagal tone shortens and increases the dispersion of the atrial refractory period creating the conditions required for reentry. Therefore, the increased vagal tone induced by sport practice may indeed facilitate the appearance of AF. In a review, Swanson suggested that gastroesophageal reflux may be a stimulus link between the autonomic system and exercise-induced AF. Further studies are indicated to determine the effect and interaction of the autonomic system on the atrial substrate in the initiation and maintenance of AF.
Inflammatory markers
Epidemiologic studies have noted an association between elevated C-reactive protein levels and the risk for developing AF. Regular moderate exercise training is known to reduce inflammatory markers, while high-intensity endurance training may transiently produce a sustained inflammatory response. Psychari et al found C-reactive protein to be an independent predictor of AF, and both CRP and interleukin-6 were positively related to left atrial diameter and negatively related to left ventricular function. Interleukin-6 was also positively related to the duration of AF. There are no data so far on the intensity of exercise, amount of inflammation, and risk for AF.
Fluid shifts and electrolyte abnormalities
Long and vigorous periods of training could generate substantial shifts in body fluids because of changes in volume regulation and electrolyte levels. Intense training can result in an hourly loss of up to 2 L of body fluids. Inappropriate fluid intake can lead to dehydration and electrolyte depletion (sodium, potassium, and magnesium), triggering atrial arrhythmias.
Illicit drugs
Several illicit drugs that have been banned by the World Anti-Doping Agency are commonly associated with AF ( Table 3 ). Stimulants such as amphetamines, ephedrine, and related substances that are used to enhance sports performance can cause AF. Although some isolated case reports have shown a link between AF and steroids, these have been reported in young athletes at the moment of maximal physical activity. Therefore, although anabolic steroids may have a role in the genesis of AF it is uncertain and is probably marginal.
