Atrial Fibrillation In Athletes Research Articles

Exercise-Dependent Modulation of Immunological Response Pathways in Endurance Athletes With and Without Atrial Fibrillation.

Atrial fibrillation (AF) is a common arrhythmia characterized by uncoordinated atrial electrical activity. Lone AF occurs in the absence of traditional risk factors and is frequently observed in male endurance athletes, who face a 2- to 5-fold higher risk of AF compared with healthy, moderately active males. Our understanding of how endurance exercise contributes to the pathophysiology of lone AF remains limited. This study aimed to characterize the circulating protein fluctuations during high-intensity exercise as well as explore potential biomarkers of exercise-associated AF. A prospective cohort of 12 male endurance cyclists between the ages of 40 and 65 years, 6 of whom had a history of exercise-associated AF, were recruited to participate using a convenience sampling method. The circulating proteome was subsequently analyzed using multiplex immunoassays and aptamer-based proteomics before, during, and after an acute high-intensity endurance exercise bout to assess temporality and identify potential markers of AF. The endurance exercise bout resulted in significant alterations to proteins involved in immune modulation (eg, growth/differentiation factor 15), skeletal muscle metabolism (eg, α-actinin-2), cell death (eg, histones), and inflammation (eg, interleukin-6). Subjects with AF differed from those without, displaying modulation of proteins previously known to have associations with incident AF (eg, C-reactive protein, insulin-like growth factor-1, and angiopoietin-2), and also with proteins having no previous association (eg, tapasin-related protein and α2-Heremans-Schmid glycoprotein). These findings provide insights into the proteomic response to acute intense exercise, provide mechanistic insights into the pathophysiology behind AF in athletes, and identify targets for future study and validation.

The effects of daily dose of intense exercise on cardiac responses and atrial fibrillation.

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia that is strongly associated with cardiovascular (CV) disease and sedentary lifestyles. Despite the benefits of exercise on overall health, AF incidence in high-level endurance athletes rivals that of CV disease patients, suggesting a J-shaped relationship with AF. To investigate the dependence of AF vulnerability on exercise, we varied daily swim durations (120, 180 or 240minday-1 ) in 7-week-old male CD1mice. We assessed mice after performing equivalent amounts of cumulative work during swimming (i.e. ∼700L O2 kg-1 ), as determined from O2 consumption rates ( ). The mean during exercise increased progressively throughout the training period and was indistinguishable between the swim groups. Consistent with similar improvements in aerobic conditioning induced by swimming, skeletal muscle mitochondria content increased (P=0.027) indistinguishably between exercise groups. Physiological ventricular remodelling, characterized by mild hypertrophy and left ventricular dilatation, was also similar between exercised mice without evidence of ventricular arrhythmia inducibility. By contrast, prolongation of daily swim durations caused progressive and vagal-dependent heart rate reductions (P=0.008), as well as increased (P=0.005) AF vulnerability. As expected, vagal inhibition prolonged (P=0.013) atrial refractoriness, leading to reduced AF vulnerability, although still inducible in the 180 and 240min swim groups. Accordingly, daily swim dose progressively increased atrial hypertrophy (P=0.003), fibrosis (P<0.001) and macrophage accumulation (P=0.006) without differentially affecting the ventricular tissue properties. Thus, increasing daily exercise duration drives progressively adverse atrial-specific remodelling and vagal-dependent AF vulnerability despite robust and beneficial aerobic conditioning and physiological remodelling of ventricles and skeletal muscle. KEY POINTS: Previous studies have suggested that a J-shaped dose-response relationship exists between physical activity and cardiovascular health outcomes, with moderate exercise providing protection against many cardiovascular disease conditions, whereas chronic endurance exercise can promote atrial fibrillation (AF). We found that AF vulnerability increased alongside elevated atrial hypertrophy, fibrosis and inflammation as daily swim exercise durations in mice were prolonged (i.e. ≥180minday-1 for 6weeks). The MET-hweek-1 (based on O2 measurements during swimming) needed to induce increased AF vulnerability mirrored the levels linked to AF in athletes. These adverse atria effects associated with excessive daily exercise occurred despite improved aerobic conditioning, skeletal muscle adaptation and physiological ventricular remodelling. We suggest that atrial-specific changes observed with exercise arise from excessive elevations in venous filling pressures during prolonged exercise bouts, which we argue has implications for all AF patients because elevated atrial pressures occur in most cardiovascular disease conditions as well as ageing which are linked to AF.

The Complex but Fascinating Relationship between Sport and Atrial Fibrillation: From Pathophysiology to the Clinical Scenario

Atrial fibrillation (AF) is the most common cause of hospital admission among all arrhythmias in the general population. Moreover, AF represents the most common arrhythmia in the athletic population as well. The complex but fascinating relationship between sport and atrial fibrillation has not yet been fully clarified. Although the benefits of moderate physical activity in controlling cardiovascular risk factors and in reducing the risk of atrial fibrillation have been widely demonstrated, some concerns have been raised about the potential adverse effects of physical activity. Endurance activity in middle-aged men athletes appears to increase the risk of AF. Several different physiopathological mechanisms may explain the increased risk of AF in endurance athletes, including the imbalance of the autonomic nervous system, changes in left atrial size and function and presence of atrial fibrosis. The goal of this article is to review the epidemiology, pathophysiology and clinical management for AF in athletes, including pharmacological and electrophysiological strategies.

Atrial fibrillation in athletes : Prevalence, diagnosis, and treatment

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 acombination of pulmonary vein ectopy as atrigger, 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. 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.

Atrial fibrillation and sport: need for monitoring.

Historically, regular exercise contributed to reduce the arrhythmic burden and improve cardiovascular outcomes in the general population. However, a heightened risk of atrial fibrillation (AF) seems to occur mainly amongst endurance athletes. The exact mechanisms are not fully elucidated, but dynamic interactions between electro-anatomical changes induced by exercise, the autonomic system, variable triggers, along individual genetic predisposition are the main contributors to AF development in athletes. The type and training load of sports are also crucial in determining the arrhythmogenic milieu predisposing to AF insurgence and perpetuation. Moreover, a sex difference seems to influence an increased risk of AF only in men undergoing strenuous exercise, whereas women appear protected even during more vigorous training. In the absence of solid evidence, the advent of modern technologies could help to monitor and deep investigate the peculiar aspects of AF in these athletes. This review aims to describe the pathophysiology, diagnosis, and management of AF in athletes, shedding light on possible future strategies to face AF in this population.

Ageing, comorbidities, and the complex determinants of atrial fibrillation in athletes.

Ageing, comorbidities, and the complex determinants of atrial fibrillation in athletes.

Hypertension and other risk factors of atrial fibrillation in athletes

Cardiovascular mortality in athletes in 50 % of cases is due to cardiovascular diseases (CVD). Among them heart arrhythmias, in particular atrial fibrillation (AF) comprise a significant part. Therefore, the assessment of risk factors for AF is extremely important in athletes. We summarize the data of recent experimental and clinical studies on the relationship of physical activity, hypertension, obesity, carbohydrate metabolism disorders, genetic aspects and AF. The diagnostic approaches to heart rhythm disorders in athletes are discussed. We also indicate the directions of further research. The pathogenetic rationale for diagnostic strategies for AF in athletes is developed.

Differing mechanisms of atrial fibrillation in athletes and non-athletes: alterations in atrial structure and function.

Atrial fibrillation (AF) is more common in athletes and may be associated with adverse left atrial (LA) remodelling. We compared LA structure and function in athletes and non-athletes with and without AF. Individuals (144) were recruited from four groups (each n = 36): (i) endurance athletes with paroxysmal AF, (ii) endurance athletes without AF, (iii) non-athletes with paroxysmal AF, and (iv) non-athletic healthy controls. Detailed echocardiograms were performed. Athletes had 35% larger LA volumes and 51% larger left ventricular (LV) volumes vs. non-athletes. Non-athletes with AF had increased LA size compared with controls. LA/LV volume ratios were similar in both athlete groups and non-athlete controls, but LA volumes were differentially increased in non-athletes with AF. Diastolic function was impaired in non-athletes with AF vs. non-athletes without, while athletes with and without AF had normal diastolic function. Compared with non-AF athletes, athletes with AF had increased LA minimum volumes (22.6 ± 5.6 vs. 19.2 ± 6.7 mL/m2, P = 0.033), with reduced LA emptying fraction (0.49 ± 0.06 vs. 0.55 ± 0.12, P = 0.02), and LA expansion index (1.0 ± 0.3 vs. 1.2 ± 0.5, P = 0.03). LA reservoir and contractile strain were decreased in athletes and similar to non-athletes with AF. Functional associations differed between athletes and non-athletes with AF, suggesting different pathophysiological mechanisms. Diastolic dysfunction and reduced strain defined non-athletes with AF. Athletes had low atrial strain and those with AF had enlarged LA volumes and reduced atrial emptying, but preserved LV diastolic parameters. Thus, AF in athletes may be triggered by an atrial myopathy from exercise-induced haemodynamic stretch consequent to increased cardiac output.

Atrial fibrillation in athletes

Large observational studies have shown that a sedentary lifestyle increases the risk of atrial fibrillation fivefold.[1][1],[2][2] However, high-intensity aerobic exercise, especially for men, also increases the risk of atrial fibrillation at a threshold of more than 1500–2000 lifetime hours.[3][3

P970 Significant differences in atrial structural and functional parameters leading to differing mechanisms of atrial fibrillation in athletes compared to non-athletes

Abstract Background/Introduction: There is an increased incidence of atrial fibrillation (AF) in endurance athletes. We sought to evaluate the likely mechanistic basis for this phenomenon. Methods 36 endurance athletes in sinus rhythm, with a previous history of AF (ATH-AF) were compared to age and gender matched endurance athletes with no prior history of AF (ATH), non athletes with paroxysmal AF (NONATH-AF) and age and gender matched healthy controls (CONTROL). A detailed transthoracic echocardiogram was performed with all groups in sinus rhythm, with detailed left atrial (LA) and left ventricular (LV) measurements, including strain analysis. Results All athletes had increased LA and LV size when compared with healthy controls (Table 1). Non athletes with paroxysmal AF had increased LA size when compared with controls. However, indexed LA/LV ratio was preserved in athletes and similar to healthy individuals, whilst AF patients had significantly increased LA/LV ratio. Athletes with AF had higher e’ velocity and lower E/e’, whereas e’ was reduced and E/e’ elevated in non-athlete AF patients. Athletes had impaired LA reservoir and contractile strain, and reduced LV global longitudinal strain (GLS) compared with healthy controls. Conclusions Compared to healthy controls, athletes have reduced LA and LV strain, with preserved LV diastolic function and LA/LV ratio. In contrast, altered diastolic function with differential increase in LA volume was observed in AF patients. The increased risk of AF in athletes is likely mediated by different mechanistic processes other than an atrial myopathy consequent to diastolic dysfunction as observed in non-athletes with AF. Table 1. LA and LV parameters Parameter ATH-AF ATH NONATH-AF CONTROL P value LVEDV indexed (ml/m2) 84 ± 12 79 ± 14 57 ± 10 51 ± 13 &amp;lt;0.001 LVESV indexed (ml/m2) 35 ± 6 34 ± 7 25 ± 8 27 ± 33 0.02 LV ejection fraction (%) 58 ± 4 56 ± 4 56 ± 10 58 ± 8 0.586 LV global longitudinal strain (%) 19.2 ± 1.7 18.9 ± 2.1 21 ± 3.1 21.7 ± 2.9 &amp;lt;0.001 e’ vel (cm/s) 10 ± 2 10 ± 3 8 ± 2 9 ± 2 0.007 E/e’ 5.7 ± 1.3 5.9 ± 1.8 9.1 ± 3.3 7.5 ± 1.5 &amp;lt;0.001 LAV max indexed (ml/m2) 45 ± 11 43 ± 12 38 ± 11 27 ± 8 &amp;lt;0.001 Indexed LAV/LVEDV ratio 0.5 ± 0.1 0.6 ± 0.2 0.7 ± 0.2 0.5 ± 0.1 &amp;lt;0.001 LA reservoir strain (%) 27.2 ± 4.8 28.2 ± 3.7 27.9 ± 8.4 33.2 ± 7.0 &amp;lt;0.001 LA conduit strain (%) 14.2 ± 4.5 14.4 ± 4.0 14.9 ± 5.5 16.6 ± 6.3 0.182 LA contractile strain (%) 13.0 ± 3.1 13.8 ± 3.6 13.0 ± 5.1 16.6 ± 3.1 &amp;lt;0.001 LV = left ventricular, LAV = left atrial volume, LA = left atrial

Atrial Fibrillation in Athletes-Features of Development, Current Approaches to the Treatment, and Prevention of Complications.

Atrial fibrillation (AF) is one of the most common types of cardiac arrhythmias. This review article highlights the problem of the development of atrial fibrillation in individuals engaged in physical activity and sports. Predisposing factors, causes, and development mechanisms of atrial fibrillation in athletes from the perspective of the authors are described. Methods of treatment, as well as prevention of thromboembolic complications, are discussed. Directions for further studies of this problem and prevention of complications are proposed.

P4421Increased circulating levels of VCAM-1 correlate with left atrial remodeling in highly trained athletes

Abstract Introduction Reports have shown increased risk of atrial fibrillation (AF) in athletes. Vascular cell adhesion molecule-1 (VCAM1) is associated with new onset AF in general population. VCAM1 and its relation with left atrial (LA) remodeling have not been investigated in athletes. Purpose To study VCAM1 and LA remodeling in marathon runners. Methods Study of 36 male marathon runners in the training period previous to race (42 km) and 18 sedentary controls with no risk factors. Athletes were divided in two groups according to highest training intensity reached (group 1, &gt;100 km/week; group 2, 50–100 km/week). Previous to race in all subjects, VCAM1 serum levels were measured by ELISA and an echocardiogram was performed. In athletes, VCAM1 was measured immediately post-race. Wilcoxon and Spearman were used. Results See table. Group 1 showed a significant increment in VCAM1 post-race (651±350 to 905±373 ng/mL; p=0.002) as compared to group 2 with no increment (533±133 to 651±138 ng/mL; p=0.117). In athletes, a moderate correlation between LA volume and VCAM1 was found (rho: 0.483; p=0.007). Baseline characteristics Group 1 (n=18) Group 2 (n=18) Controls (n=18) p value Age (years) 37±6 38±5 36±4 0.373 Heart rate (bpm) 53±8 57±7 69±6 * 0.001 Body surface area (m2) 1.8±0.1 1.8±0.1 1.9±0.1 0.075 LV diastolic diameter (mm) 49±5 48±5 46±4 0.404 LV systolic diameter (mm) 29±5 30±5 30±4 0.879 Septal wall (mm) 9.1±1.2† 8.2±1.1 8.1±0.8 0.005 Posterior wall (mm) 9.3±2.1† 8.5±1.2 7.6±0.8 0.001 Ejection fraction (%) 55±3 55±6 57±4 0.110 LV mass index (g/m2) 106±27† 78±18 58±11 0.001 LA volume (mL/m2) 42±8† 30±11 25±9 0.001 E wave (cm/sec) 78±13 84±12 77±15 0.217 A wave (cm/sec) 50±12 53±10 48±16 0.438 DT (msec) 233±65 229±65 221±66 0.184 VCAM1 (ng/mL) 651±350† 533±133 440±98 0.022 Mean ± SD. *p&lt;0.05 vs group 1 and 2 post Kruskall-Wallis; †p&lt;0.05 vs other groups post Kruskall-Wallis. LV, left ventricle; LA, left atrium; DT, deceleration time. Conclusions Most trained athletes had increased levels of VCAM1 as compared to controls and less trained athletes. They also showed an increment post-effort. VCAM1 is related to LA remodeling in athletes. VCAM1 could be a potential biomarker of AF in athletes which should be confirmed. Acknowledgement/Funding FONDECYT 1170963 (LG); FONDAP 15130011 (LG,SL)

Atrial fibrillation in athletes and general population: A systematic review and meta-analysis.

Background:Atrial fibrillation (AF) is the most common type of heart arrhythmia, but the impact of long-term, high-intensity endurance exercise on the risk of AF remains uncertain.Methods:PubMed, EMBASE, and Cochrane library databases were searched till Nov 2017 to retrieve the articles. The included studies were summarized, pooled odds ratio (OR) and its 95% confidence interval (CI) were calculated. Both fixed and random effects models were used to combine the data. Stratified and logistic meta-regression analyses were performed to explore the sources of heterogeneity across studies.Results:Nine studies including 2308 athletes and 6593 controls were eligible. Our results showed that the risk of AF was significantly higher in athletes than in general population (OR = 2.34, 95% CI = 1.04–5.28, Pheterogeneity<.001, I2 = 92.3%). Subgroup analysis based on gender and mean age demonstrated a significantly increased risk in men (OR = 4.03, 95% CI = 1.73–9.42, Pheterogeneity<.001, I2 = 82.7%) and participants with mean age <60 (OR = 3.24, 95% CI = 1.23–8.55, Pheterogeneity<.001, I2 = 84.3%). Furthermore, subgroup analysis based on type of athletes demonstrated a significantly increased risk of AF in participants with single type of sport (OR = 3.97, 95% CI = 1.16–13.62, Pheterogeneity = .018, I2 = 70.4%). Results remained unchanged after performing sensitivity analysis. Meta-regression showed that gender, age, type of study, sample size, and sports mode were unrelated to heterogeneity.Conclusion:Our study confirmed that the risk of AF was significantly higher in athletes than in general population, especially among men and participants aged <60.

Competitive Endurance Activities of Middle-aged Athletes as a Risk Factor for Atrial Fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia in athletes. Epidemiological studies have documented a greater prevalence of AF in athletes engaged in long-term endurance sports. Several mechanisms were proposed to underlie the association between exercise and AF, but the exact pathophysiology remains unclear. The studies up to now have been concentrated on the competitive middle-aged endurance athletes, but there is no evidence of AF prevalence among highly active noncompetitive athletes of the same age. Endurance athletes who do not compete might be at a lower risk for AF than their competitive peers. This hypothesis is theoretically examined, and the current evidence summarized in this article.

52Atrial remodeling and ectopic burden in recreational athletes: Implications for risk of atrial fibrillation in athletes

52Atrial remodeling and ectopic burden in recreational athletes: Implications for risk of atrial fibrillation in athletes

Age modifies the risk of atrial fibrillation among athletes: A systematic literature review and meta-analysis

BackgroundThe relationship between competitive sports and atrial fibrillation (AF) is controversial. We aimed to systematically evaluate and summarize all published observational data on the association between competitive sports and AF. Methods and resultsWe searched PubMed, EMBASE, Scopus and SportDiskus for all observational studies that assessed the risk of AF among athletes involved in competitive sports. Data were extracted and pooled odds ratios (OR) were calculated using random effects models. Six cohort studies and 2 case-control studies with a total of 9113 subjects were included in our meta-analysis. Pooled analyses showed an increased risk of incident and prevalent AF among athletes compared to the general population (OR = 1.64 [95% confidence interval (CI): 1.10–2.43]). Age-stratified analysis revealed an effect modification with age. Studies enrolling younger adults (<54 years) had an increased risk of AF among athletes compared to controls (OR = 1.96 [95% CI: 1.06–3.65]), but this association was not seen among older adults ≥54 years (OR = 1.41 [95% CI: 0.81–2.44], p = 0.23). ConclusionAthletes have an increased risk of AF compared to the general population. Age appears to modify the risk of AF in athletes.

Mechanisms of atrial fibrillation in athletes: what we know and what we do not know.

Exercise is an emerging cause of atrial fibrillation (AF) in young individuals without coexisting cardiovascular risk factors. The causes of exercise-induced atrial fibrillation remain largely unknown, and conclusions are jeopardised by apparently conflicting data. Some components of the athlete’s heart are known to be arrhythmogenic in other settings. Bradycardia, atrial dilatation and, possibly, atrial premature beats are therefore biologically plausible contributors to exercise-induced AF. Challenging findings in an animal model suggest that exercise might also prompt the development of atrial fibrosis, possibly due to cumulative minor structural damage after each exercise bout. However, there is very limited, indirect data supporting this hypothesis in athletes. Age, sex, the presence of comorbidities and cardiovascular risk factors, and genetic individual variability might serve to flag those athletes who are at the higher risk of exercise-induced AF. In this review, we will critically address current knowledge on the mechanisms of exercise-induced AF.

Atrial Fibrillation in Athletes: A Lesson in the Virtue of Moderation.

Although the cardiovascular benefits of moderate exercise are well established, there is growing epidemiological support for the notion that high-intensity endurance athletics increases the risk of atrial fibrillation (AF). There are many gaps in evidence related to epidemiology and mechanisms of AF in endurance athletes. The proposed pathophysiological mechanisms include alterations of autonomic tone, electrical remodeling, anatomical remodeling, fibrosis, and inflammation. Clinical management of the athlete with AF often includes a period of decreased frequency, intensity, and duration of exercise with assessment for improvement in AF recurrence. Based on symptoms, a strategy of rate or rhythm control should be selected; however, due to side effects and intolerance of medications, ablation may be a preferred approach. The risks and benefits of anticoagulation for stroke prevention must be carefully assessed in the athlete with AF. All patients should be encouraged to be physically active with moderation; however, men should be advised of the higher risk of AF with long-term, high-intensity endurance training.

State of the Art Review: Atrial Fibrillation in Athletes.

Exercise has substantial health benefits with pleomorphic vascular, metabolic, psychological and anti-neoplastic actions resulting in improved quality of life and longevity. Despite these many benefits, numerous studies have shown that endurance athletes are more likely to develop atrial fibrillation (AF) than non-athletes. The type, intensity and amount of sport appears to influence the risk of developing AF. Several endurance sport activities have been shown to increase the risk of developing AF but an excess in AF has not been shown in non-endurance sports. Furthermore, lifetime hours of participation appear to increase the risk of developing AF. Intriguingly, women appear relatively protected and an association between endurance sport and AF has not been clearly demonstrated amongst female endurance athletes. The mechanisms by which endurance sport promotes the development of AF are unclear. There are, however, a number of pathophysiological mechanisms which are known to increase the risk of AF in non-athletes which have correlates in athletes. These include structural remodelling of the left atrium, elevated left atrial pressure, inflammation, myocardial fibrosis, vagal tone, sinus bradycardia and genetic predisposition. In this article, we explore how some of these mechanisms may contribute to the development of AF in endurance athletes.

Atrial Fibrillation in Athletes.

Atrial fibrillation is the most common arrhythmia in athletes and may be associated with endurance sport practice. Atrial ectopic beats, chronic systemic inflammation, autonomic system alterations, anatomic adaptation, myocardial injury and illicit drugs seem to be implicated in the increased prevalence of atrial fibrillation in athletes, but clear evidence is lacking. Treatment of the arrhythmia is a challenging issue, as atrial fibrillation may impair athletic performances and deteriorate athletes' quality of life. This review focuses on the epidemiology, possible pathophysiological mechanisms, and management of atrial fibrillation in athletes.