Fibrillation In Athletes Research Articles

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 <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 <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 <0.001 LAV max indexed (ml/m2) 45 ± 11 43 ± 12 38 ± 11 27 ± 8 <0.001 Indexed LAV/LVEDV ratio 0.5 ± 0.1 0.6 ± 0.2 0.7 ± 0.2 0.5 ± 0.1 <0.001 LA reservoir strain (%) 27.2 ± 4.8 28.2 ± 3.7 27.9 ± 8.4 33.2 ± 7.0 <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 <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.

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.

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

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.

Athletes with channelopathy may be eligible to play.

The European and Bethesda recommendations roughly state that any athlete with channelopathy is not eligible to participate in sports on a presumed risk of potentially life-threatening ventricular tachycardia or fibrillation. However, eligibility decision-making on a presumed risk of ventricular tachycardia or fibrillation is debatable. Channelopathies are primary electrical cardiac disorders and are usually transmitted as an autosomal dominant trait. Some of the channelopathies are potentially fatal in relation to exercise and predispose to life-threatening cardiac arrhythmias including ventricular tachycardia or fibrillation. Exercise, swimming, body heating and electrolyte depletion can all act as a trigger of ventricular tachycardia or fibrillation in channelopathy. However, new research mentioned a very low incidence of ventricular tachycardia or fibrillation in athletes with channelopathy challenging the decision of disqualification. Recently, the American recommendations for sports participation in athletes with a cardiovascular disorder have updated their eligibility decision-making.In this manuscript we describe the signature features of the electrocardiogram changes in channelopathies and we argue that new research data should allow for the introduction of more liberal eligibility decision-making for sports participation in athletes with channelopathy, not only in the United States but also in European countries.

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.

Atrial fibrillation and the athletic heart.

Endurance exercise, despite a plethora of proven health benefits, is increasingly recognized as a potential cause of lone atrial fibrillation. Moderate exercise reduces all-cause mortality and protects against developing atrial fibrillation. However, more intense exercise regimes confer modest incremental health benefits, induce cardiac remodelling and negate some of the cardiovascular benefits of exercise. The implications of endurance exercise and athletic heart are becoming increasingly relevant as the popularity of endurance exercise has increased 20-fold within a generation. An apparent dose-response relationship exists between endurance exercise and left atrial dilatation. Repeated strenuous endurance exercise overloads atria, resulting in stretch-induced 'microtears', inflammation and endocardial scarring. Although these findings are observational in humans, similar mechanisms have recently been confirmed in animal models suggesting causation. Currently, it is not known whether a ceiling for endurance exercise exists, and, if so, what factors determine the threshold of harm. Although preliminary research is promising, much work remains if we are to understand the mechanisms underpinning atrial fibrillation in athletes.

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the “cardiac fatigue” caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. Methods: We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. Results: When comparing triathletes with LVM <220g and athletes with LVM >220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2max) 57.3 ±7.5ml/min/kg vs. 59.8±9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Conclusion: Significant left ventricular hypertrophy with LVM >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the "cardiac fatigue" caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. When comparing triathletes with LVM <220g and athletes with LVM >220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2± 21.5 mmHg vs. 198.8 ±22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2max) 57.3 ±7.5ml/min/kg vs. 59.8±9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP >170 mmHg at the aerobic threshold and the probability of LVM >220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM >220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Significant left ventricular hypertrophy with LVM >220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.

Exercise-induced arterial hypertension - an independent factor for hypertrophy and a ticking clock for cardiac fatigue or atrial fibrillation in athletes?

Background : Exercise-induced arterial hypertension (EIAH) leads to myocardial hypertrophy and is associated with a poor prognosis. EIAH might be related to the “cardiac fatigue” caused by endurance training. The goal of this study was to examine whether there is any relationship between EIAH and left ventricular hypertrophy in Ironman-triathletes. Methods: We used echocardiography and spiroergometry to determine the left ventricular mass (LVM), the aerobic/anaerobic thresholds and the steady-state blood pressure of 51 healthy male triathletes. The main inclusion criterion was the participation in at least one middle or long distance triathlon. Results : When comparing triathletes with LVM &lt;220g&nbsp; and athletes with LVM &gt;220g there was a significant difference between blood pressure values (BP) at the anaerobic threshold (185.2&plusmn; 21.5 mmHg vs. 198.8 &plusmn;22.3 mmHg, p=0.037). The spiroergometric results were: maximum oxygen uptake (relative VO 2 max) 57.3 &plusmn;7.5ml/min/kg vs . 59.8&plusmn;9.5ml/min/kg (p=ns). Cut-point analysis for the relationship of BP &gt;170 mmHg at the aerobic threshold and the probability of LVM &gt;220g showed a sensitivity of 95.8%, a specificity of 33.3%, with a positive predictive value of 56.8 %, a good negative predictive value of 90%. The probability of LVM &gt;220g increased with higher BP during exercise (OR: 1.027, 95% CI 1.002-1.052, p= 0.034) or with higher training volume (OR: 1.23, 95% CI 1.04 -1.47, p = 0.019). Echocardiography showed predominantly concentric remodelling, followed by concentric hypertrophy. Conclusion : Significant left ventricular hypertrophy with LVM &gt;220g is associated with higher arterial blood pressure at the aerobic or anaerobic threshold. The endurance athletes with EIAH may require a therapeutic intervention to at least prevent extensive stiffening of the heart muscle and exercise-induced cardiac fatigue.

Atrial fibrillation in athletes and the interplay between exercise and health

This editorial refers to ‘Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study’[†][1], by K. Andersen et al. , on page 3624 Exercise is one of the most powerful lifestyle intervention strategies for the primary and secondary prevention of cardiovascular disease. There is a wealth of evidence regarding the lower ranges of the exercise dose–response relationship providing concrete evidence for the current recommendations of at least 30 min of moderate intensity exercise on most days as a means of reducing cardiovascular events.1 However, there is an increasing proportion of today's society engaging in sports practices which vastly exceed these guidelines, and there has been very limited study of the upper ranges of the exercise dose–response relationship.2 On the one hand are studies suggesting that long-term health and life expectancy of well-trained athletes is superior to that of the general population,3−5 while, on the other, there is evidence suggesting an increased prevalence of arrhythmias and chronic structural remodelling of the athletic heart.6−9 Atrial fibrillation (AF) may therefore represent the most intriguing and best evidenced example of the interplay between exercise and cardiac health. AF can be diagnosed in ∼1% of the population by age 60 and in >10% when older than 80 years,10 making it the most prevalent sustained arrhythmia in adults. In cohorts of young or middle-aged subjects, AF is relatively uncommon, thus implying that large cohorts would be required to provide sufficient power to identify any excess in prevalence due to sports practice. In this context, it is not surprising that Pelliccia et al . found only very few cases of AF despite significant left atrial enlargement in a fairly large ( n = 1777) athletic cohort aged 24 ± 6 years.11 In contrast, Baldesberger et al . … [1]: #fn-2

Atrial Fibrillation in Athletes

Many studies have shown a relationship between long-term endurance sport practice and atrial fibrillation. Inflammation, anatomic remodelling, alterations in the autonomic system and neurohormonal activation are all possible explanations for the increased prevalence of this arrhythmia in athletes. Atrial fibrillation may determine disabling symptoms like palpitations and impaired physical performance, compromising eligibility for competitive activities, but exclusion from sport is not necessary for all athletes. Limited data are available on drug therapy and recently ablation resulted to be a particularly attractive option for young athletes with paroxysmal atrial fibrillation. The purpose of this review is to discuss mechanisms, clinical features, management of atrial fibrillation in competitive athletes, including criteria for eligibility and disqualification in sport practice.

Prevalence, mechanism and management of atrial fibrillation in athletes

Prevalence, mechanism and management of atrial fibrillation in athletes