Athletes with arrhythmias: Treatment and returning to athletic participation

INTRODUCTION — As with the population in general, arrhythmias are commonly documented in athletes. Rarely are arrhythmias fatal; however, sudden cardiac death (SCD) resulting from malignant ventricular tachyarrhythmias can occur in young and apparently healthy persons. In addition, athletes treated with a permanent pacemaker or implantable cardioverter-defibrillator (ICD) are at increased risk of damage to the device during sport participation.

This topic will discuss the approach to returning to competition or participation in athletes with arrhythmias.

The clinical manifestations and diagnostic evaluation of athletes with specific arrhythmias or arrhythmia-related syndromes are discussed in detail separately. (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation" and "Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances".)

Additionally, the risk of SCD in athletes and the approach to screening to prevent SCD in athletes are discussed elsewhere. (See "Screening to prevent sudden cardiac death in competitive athletes".)

The approach to evaluation of syncope is discussed separately (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation", section on 'Syncope and presyncope' and "Syncope in adults: Management and prognosis".)

In select diseases, the decision to return to sport participation may be determined more by the disease than by the specific rhythm or treatment. The decision on sport participation in such diseases is covered separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation", section on 'Hypertrophic cardiomyopathy'.)

AV CONDUCTION ABNORMALITIES — Altered atrioventricular (AV) nodal conduction (eg, first-degree AV block and Mobitz type I second-degree AV block) can result from increased vagal tone, which is normally seen as an adaptive response to certain types of athletic conditioning, particularly endurance training (table 1).

First-degree AV block — First-degree AV block, characterized by prolongation of the PR interval (waveform 1), is commonly seen in athletes and has no important implications. Often, it is accompanied by resting sinus bradycardia.

Athletes with isolated first-degree AV block who are asymptomatic and have no evidence for structural heart disease can participate in all sports [1,2]. The nature and severity of underlying heart disease, if present, can independently dictate other restrictions. (See "First-degree atrioventricular block", section on 'Management'.)

Second-degree AV block: Mobitz type I (Wenckebach) — Mobitz type I (Wenckebach) second-degree AV block, especially at rest or sleep, is often present in normal, well-conditioned athletes due to enhanced vagal tone (waveform 2). The approach to Mobitz type I (Wenckebach) second-degree AV block depends on the presence of symptoms and the response to exercise:

●Asymptomatic patients – The approach to asymptomatic patients depends on the characteristics of the rhythm:

•Resolution of type I second-degree AV block – Asymptomatic athletes with Mobitz type I (Wenckebach) second-degree AV block that resolves (ie, disappears) with exercise can participate in all competitive sports (figure 1) [1,2].

•Type I second-degree AV block that worsens with exertion – Asymptomatic athletes in whom Mobitz type I (Wenckebach) second-degree AV block initially appears or worsens with exercise may need further evaluation, as worsening of Mobitz type I (Wenckebach) second-degree AV block with exercise is highly suspicious for a structural pathologic condition affecting the AV node or His-Purkinje system (figure 1).

●Symptomatic type I second-degree AV block – Though Mobitz type I (Wenckebach) second-degree AV block rarely causes symptoms, symptomatic athletes may need ventricular pacing and should undergo treatment of any associated potentially reversible causes (eg, myocardial ischemia, Lyme disease). The development of Mobitz type I (Wenckebach) second-degree AV block during exercise should prompt referral to an electrophysiologist. (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)", section on 'Management'.)

Second-degree AV block: Mobitz type II — In patients who have a reversible cause of Mobitz type II AV block that resolves, return to sport is permissible, while patients who require a permanent pacemaker should follow guidance appropriate for that device. Most patients with Mobitz type II second-degree AV block (waveform 3) require a permanent pacemaker unless a reversible cause (eg, Lyme disease) is identified. (See 'Athletes with permanent pacemakers' below.)

Third-degree (complete) AV block — The approach to patients with third-degree AV block depends on the cause:

●Acquired third-degree AV block – Third-degree (complete) AV block (waveform 4 and waveform 5) is uncommon in athletes and, when present, usually is due to disease in the His-Purkinje system. Acquired third-degree (complete) AV block without a reversible cause is treated with a pacemaker. The approach to return to sport is determined by the cause of acquired third-degree heart block and by issues related to the permanent pacemaker. (See "Third-degree (complete) atrioventricular block" and 'Athletes with permanent pacemakers' below.)

●Congenital third-degree AV block – A subset of patients with third-degree (complete) AV block have congenital third-degree (complete) AV block, which usually is present at birth, but may develop later in childhood. Congenital third-degree (complete) AV block may go unnoticed because of the higher junctional escape rate and lack of symptoms. Evaluation of these cases should preferentially be performed by expert electrophysiologists. (See "Congenital third-degree (complete) atrioventricular block", section on 'Treatment'.)

•Asymptomatic patients – Asymptomatic athletes with congenital AV block, a structurally normal heart and normal cardiac function, a narrow QRS complex, ventricular rates at rest greater than 40 to 50 beats per minute increasing appropriately with exertion (>120 beats per minute), no history of syncope or near syncope, and no ventricular tachycardia (VT) during exertion can selectively participate in competitive sports [1,2].

•Symptomatic patients – By contrast, athletes with congenital third-degree AV block complicated by ventricular arrhythmias, or those with symptoms of fatigue, near-syncope, or syncope, should have a pacemaker implanted before they participate in competitive sports. In patients with congenital third-degree AV block and a permanent pacemaker, return to sport depends on issues related to the pacemaker. (See 'Athletes with permanent pacemakers' below.)

Bundle branch block — Athletes with left bundle branch block (LBBB) should undergo an echocardiogram or cardiovascular magnetic resonance (CMR) imaging to rule out structural heart disease. While complete right bundle branch block (RBBB) (waveform 6) is occasionally observed among athletes and may be seen with or without underlying structural heart disease, complete LBBB (waveform 7) is more likely to reflect an underlying pathologic condition [3]. (See "Right bundle branch block" and "Left bundle branch block".)

Management depends on the type of block:

●Right bundle branch block – Athletes with asymptomatic RBBB and no evidence of underlying cardiac disease have no restriction for sport participation [2].

●Left bundle branch block – Athletes with LBBB and no ventricular arrhythmias who do not develop AV block with exercise can participate in all competitive sports, consistent with the limitations due to the underlying cardiac condition and the existing recommendations [1,2].

Periodic follow-up is suggested for all individuals with complete LBBB to assess for new symptoms or evidence for cardiac disease. There are no expert consensus or guideline recommendations regarding the frequency of follow-up, but we feel that in the absence of symptoms, one annual follow-up with repeat electrocardiogram (ECG) and echocardiography is appropriate, with additional follow-up after one year to generally be determined by the development of symptoms.

●Bifascicular block – The presence of bifascicular block (LBBB, RBBB and left anterior fascicular block, RBBB and left posterior fascicular block) in a young, otherwise healthy athlete also raises the possibility of an inherited conduction system disease such as Lenègre disease, an autosomal dominant disorder that results in progressive conduction system dysfunction or cardiomyopathy. First-degree relatives of an athlete with bifascicular block should be screened with an ECG to search for any evidence of conduction system disease [4]. (See "Etiology of atrioventricular block", section on 'Familial disease'.)

SINUS NODE DYSFUNCTION — Most well-trained endurance athletes have resting sinus bradycardia (heart rate <60 beats per minute) (table 1) [5,6]. This has traditionally been attributed to increased vagal tone induced by exercise conditioning. However, there is some evidence that this may be due in part to alteration of the intrinsic properties of the sinoatrial and AV nodes [7].

●Sinus bradycardia with symptoms or structural abnormalities – Athletes with symptoms including impaired consciousness or fatigue resulting from bradycardia should be restricted from competitive sports until appropriately evaluated and treated. If the subject remains asymptomatic for two to three months during treatment, participation in all competitive sports is permitted, consistent with the recommendation inherent to the cardiac condition responsible for symptoms.

●Sinus pauses – Asymptomatic sinus pauses or sinus arrest of less than three seconds duration are not uncommonly seen in Holter ECG monitoring in normal athletes and are of no clinical significance [8]. They often occur in association with sinus bradycardia. However, longer pauses, sinoatrial exit block, sinus node dysfunction, or symptoms caused by any of these rhythms are abnormal [2,9]. (See "Sinus node dysfunction: Treatment".)

SUPRAVENTRICULAR ARRHYTHMIAS

Atrial or junctional premature beats — Premature atrial complexes (also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) are common (junctional premature beats being less common) in the general population and in athletes and are not generally associated with underlying structural heart disease but may cause symptoms. (See "Supraventricular premature beats".)

●Without structural heart disease – Athletes with a structurally normal heart who have isolated atrial or junctional premature beats, regardless of frequency, can participate in all competitive sports [2,10].

●With structural heart disease – Athletes with underlying structural heart disease who have atrial or junctional premature beats can participate in competitive sports consistent with the limitations of the structural heart disease. The details on structural heart disease in adults is discussed separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation".)

Atrial fibrillation — Atrial fibrillation (AF) is an arrhythmia that may be present intermittently or persistently. In young athletes, AF may occur in the absence of any structural heart disease or other provoking condition and is often termed lone AF, although many patients will have some underlying risk factors for AF. In older athletes, hypertension and coronary artery disease are common underlying conditions. As with any patient with AF, athletes with AF should be evaluated for potential underlying causes and risk (eg, thyroid disease, alcohol use, etc). (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation", section on 'Triggers'.)

●Rhythm management

•Paroxysmal AF without structural heart disease – Athletes with self-terminating AF who do not have structural heart disease can participate in all competitive sports. Beta blockade or calcium channel blockade are appropriate for therapy if heart rates during exercise are greater than expected for the level of exercise. (See "Management of atrial fibrillation: Rhythm control versus rate control" and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".)

•Persistent or permanent AF – If symptoms of AF limit athletic performance, a rhythm control strategy is the preferred method of treatment in athletes with AF, though athletes with minimal symptoms or infrequent episodes may not require a rhythm control strategy and can be managed with rate control. Rhythm control can be achieved with antiarrhythmic agents or ablation procedures. Ablation can provide a sustained benefit, particularly in those with paroxysmal AF in the presence of a normal or nearly normal heart, which is the most common scenario in athletes.

Athletes without structural heart disease who have had successful AF ablation, including surgical ablation, may participate in all competitive sports (figure 1) after four to six weeks.

Athletes who do not undergo ablation who have recurrent or persistent AF can selectively participate in competitive sports if the ventricular rate increases and slows appropriately and is comparable with that of a normal sinus response in relation to the level of activity. In this case, evaluation should be individualized, and regular follow-up is advised. (See "Management of atrial fibrillation: Rhythm control versus rate control".)

●Anticoagulation – In athletes with AF, the decision to anticoagulate is the same as in patients who are not athletes. Most athletes will have a low risk of systemic thromboembolism as manifested by a low CHA₂DS₂-VASc score (calculator 1). The details on anticoagulation for AF are discussed separately. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation".)

Athletes who require anticoagulation should not participate in sports with danger of severe bodily collision (eg, football, basketball, skiing, hockey, boxing, wrestling, taekwondo, other martial arts, rugby, basketball, handball) (figure 1).

Atrial flutter — Athletes with typical atrial flutter either in the presence or in the absence of structural heart disease should be offered therapeutic resolution by radiofrequency catheter ablation, given the high likelihood of successfully curing atrial flutter [2]. In addition, if atrial flutter is cured, anticoagulation can be discontinued after four weeks. Athletes who have had atrial flutter resolved by ablation can participate in sports according to the limitation of any concurrent underlying cardiac disease (if present) after four weeks have elapsed without recurrences of atrial flutter. (See "Overview of atrial flutter".)

If curative ablation is not possible, drug therapy is advised. Antiarrhythmic agents may be effective in maintaining sinus rhythm, but patients should be treated with a rate-controlling agent in addition to an antiarrhythmic agent. Individuals who maintain a ventricular rate that increases and slows appropriately comparable with that of a normal sinus response in relation to the level of activity, while receiving therapy with AV nodal blocking drugs, can selectively participate in skill-based sports (figure 1) with the warning that rapid 1:1 conduction could occur [2].

Athletes who are anticoagulated cannot participate in competitive sports where the danger of bodily collision is present. (See "Atrial flutter: Maintenance of sinus rhythm", section on 'Anticoagulation'.)

Atrioventricular nodal reentrant tachycardia — Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia in young athletes and is usually associated with symptoms resulting from a rapid heart rate. Patients with infrequent episodes of AVNRT, or those with minimal or well-tolerated symptoms, may opt for a conservative management approach with either no specific therapy or pharmacologic suppression. If pharmacologic therapy fails or if the side effects result from chronic medical therapy, catheter ablation remains the preferred option. (See "Atrioventricular nodal reentrant tachycardia".)

●Prior to treatment – Athletes who have syncope, presyncope, or other manifestations of hemodynamic impairment secondary to the AVNRT, and do not have structural heart disease in addition to the arrhythmia, should not participate in competitive sports until they have been adequately treated.

●After ablation – Following catheter ablation, athletes without structural heart disease who are asymptomatic and have no recurrence of arrhythmia for four weeks thereafter can participate in all competitive sports [2,10].

●Management without ablation – When ablation is not performed, athletes who do not have exercise-induced AVNRT but who experience only sporadic, brief, and self-limited episodes without hemodynamic impairment during the episode can participate in all sports. In such cases, individual evaluation and regular follow-up is advised.

Atrial tachycardia — Atrial tachycardia (AT) may be due to an automatic focus or reentry; these arrhythmias are less common than AVNRT or atrioventricular reentrant tachycardia (AVRT) (table 1). (See "Focal atrial tachycardia" and "Sinoatrial nodal reentrant tachycardia (SANRT)" and "Intraatrial reentrant tachycardia".)

●After ablation, structurally normal heart – Athletes with AT in the absence of structural heart disease who have elimination of the AT by an ablation technique may participate in all competitive sports (figure 1) after four weeks without a recurrence [2,10].

●Medical therapy alone – If ablation is not performed, athletes who receive appropriate medical therapy can participate in competitive sports if the ventricular rate increases and slows appropriately and is comparable with that of a normal sinus response in relation to the level of activity. In this case, evaluation should be individualized, and regular follow-up is advised.

●Structural heart disease – In patients with AT due to structural heart disease, the decision to return sport is determined by the type of structural heart disease, as discussed separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation".)

Wolff-Parkinson-White syndrome — Patients with Wolff-Parkinson-White (WPW) pattern manifest ventricular preexcitation on the surface ECG (table 1). When this pattern is associated with documented tachycardia or symptoms referable to tachycardia, the patient is said to have the WPW syndrome. The most common arrhythmia occurring in patients with WPW is AVRT. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)

●Asymptomatic patients – The optimal approach to asymptomatic athletes with a WPW ECG pattern who have no history of palpitations or tachycardia and no evidence of structural heart disease is debated. The minimum diagnostic approach includes exercise ECG or Holter ECG monitoring to assess the abrupt reversibility of the abnormal conduction pathway with increasing heart rate (considered expression of low conduction capability and benign outcome). Abrupt loss of preexcitation during an increasing sinus rate argues for a benign bypass tract, while gradual loss or no loss of preexcitation does not prove that a bypass tract is benign (although this is not diagnostic of a malignant bypass tract) (algorithm 1).

Asymptomatic athletes without structural heart disease, without a history of palpitations, or without tachycardia, and who have a stress test documenting benign bypass tract behavior (abrupt reversibility to normal conduction), particularly those >20 to 25 years old, can participate in all competitive sports. Asymptomatic athletes undergoing electrophysiology studies with induced AV reciprocating tachycardia or AF in whom the shortest cycle length is less than 250 ms should undergo ablation of the accessory pathway [10]. Athletes with episodes of AF and syncope or near syncope whose maximal ventricular rate at rest (without therapy) as a result of conduction over the accessory pathway is >240 beats per minute should be advised for catheter ablation therapy of the accessory pathway prior to continuing competition.

●Symptomatic patients – Athletes with ventricular preexcitation on the ECG and symptoms of palpitations, presyncope, or syncope, or with documented arrhythmia (ie, WPW syndrome) should be offered radiofrequency catheter ablation of the abnormal pathway (table 2) [2,10,11]. The success rate of ablation for WPW is >95 percent, with a reasonably low risk of complications.(See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Catheter ablation'.)

●After ablation – Athletes with no structural heart disease who have had successful ablation of the accessory pathway, who remain asymptomatic, and who have normal AV conduction and no evidence of preexcitation on a 12-lead ECG can participate in all competitive sports after four weeks (figure 1).

VENTRICULAR ARRHYTHMIAS

Ventricular premature beats — Premature ventricular complexes/contractions (PVCs; also referred to as premature ventricular beats or premature ventricular depolarizations) are common in athletes of all age groups and occur in those with or without structural heart disease.

The evaluation of athletes with PVCs should initially assess for the presence of underlying pathologic substrate (ie, arrhythmogenic cardiomyopathies, coronary heart disease, inflammatory cardiac diseases, etc). Evaluation should include exercise testing (Holter ECG) to assess for inducibility or worsening of PVCs during exercise. In patients with exercise-induced PVCs or those with either a right bundle branch block or left bundle branch block pattern that originates from the left ventricle or right ventricle wall or apex (ie, superior axis deviation), CMR is required to exclude an underlying arrhythmogenic substrate.

Management depends on the specific scenario:

●Asymptomatic, no structural heart disease, and PVCs regardless of exertion – Athletes without documented evidence of structural heart disease who have PVCs at rest and during exercise (ie, during exercise testing at a level comparable with the sport in which they compete), and who are asymptomatic or minimally symptomatic, can participate in all competitive sports [2].

●Symptomatic PVCs that increase with exertion – If the PVCs increase in frequency during exercise or exercise testing to the extent that the athlete develops symptoms of impaired consciousness, significant fatigue, or dyspnea, the athlete should be thoroughly evaluated, including CMR, to exclude an underlying pathologic condition. In the presence of an underlying cardiac abnormality, the athlete should be treated accordingly. If no cardiac abnormality is found, the athlete should be treated for any symptoms and should have close follow-up. In both cases, the athlete is advised to only participate in skill-based competitive sports (figure 1) [2].

Catheter ablation should be offered to athletes with symptoms or frequent PVCs (>15 percent) that persist over time, are associated with a drop in left ventricular ejection fraction, and are not reduced by medical treatment. (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation", section on 'Additional testing'.)

●PVCs associated with structural heart disease – Athletes with structural heart disease who are in high-risk groups and have PVCs should be properly treated before returning to competitive sports, but this is largely dependent on the type of underlying heart disease (figure 1) [2].

Nonsustained ventricular tachycardia — In asymptomatic athletes with brief (generally <8 to 10 consecutive ventricular beats) episodes of nonsustained monomorphic VT, rates generally <150 beats per minute, and no documented evidence of structural heart disease established by noninvasive tests (eg, echocardiography, CMR), there is no apparent increased risk for SCD. If exercise testing (preferably by ambulatory ECG recording during the specific competitive activity) demonstrates suppression of the VT or no significant worsening compared with baseline, participation in all competitive sports is permissible with regular follow-up (figure 1) [2].

Further details on nonsustained VT can be found separately. (See "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management" and "Nonsustained VT in the absence of apparent structural heart disease".)

Sustained ventricular tachycardia — In the athlete with sustained VT, a search for underlying heart disease is paramount. In the presence of underlying heart disease, these arrhythmias are potentially life-threatening. Athletes should be advised to immediately cease participation until further evaluation can be completed.

●Structurally normal heart – The decision to return to play is influenced by the approach to treatment and whether the rhythm recurs:

•Management with ablation – Athletes with a structurally normal heart and monomorphic nonsustained or sustained VT that can be localized to a specific site(s) in the heart are candidates for a catheter ablation procedure that may potentially offer a cure. Following a successful ablation procedure, the athlete can resume full competitive activity within four weeks if there is no recurrence despite provocative testing (eg, stress ECG) [2].

•Management without ablation – A more conservative approach is recommended for the athlete with a structurally normal heart, not undergoing ablation, who chooses drug suppression, because catecholamines released during athletic activity can counter the suppressive effects of the drug, and the VT can reemerge. In this setting, the athlete should generally not compete in any sports for at least two to three months after the last VT episode and should undergo evaluation (eg, stress ECG) before returning to play [2].

●Structurally abnormal heart – For the athlete with structural heart disease, genetic or inflammatory disease, and VT, moderate- and high-intensity competition is contraindicated regardless of whether the VT is suppressed or ablated (figure 1).

Additional details on nonsustained VT and VT can be found separately. (See "Nonsustained VT in the absence of apparent structural heart disease" and "Ventricular tachycardia in the absence of apparent structural heart disease".)

Ventricular flutter and fibrillation — Athletes with conditions that result in cardiac arrest in the presence or absence of structural heart disease generally are treated with an ICD and have traditionally been counselled against participation in moderate- or high-intensity competitive sports (figure 1) [2]. (See 'Athletes with ICDs' below.)

Recommendations in the section on VT also apply. (See 'Sustained ventricular tachycardia' above.)

ATHLETES WITH A CARDIAC IMPLANTABLE ELECTRONIC DEVICE (CIED)

Athletes with permanent pacemakers — Athletes with permanent pacemakers should not participate in competitive sports in which the danger of bodily collision exists because such trauma may damage the pacemaker system and lead to bradycardia-induced syncope or other fatal arrhythmia [2,12]. This restriction generally applies to activities where direct blows to the chest are a part of the sport, such as football, rugby, boxing, martial arts, hockey, motorcycling, downhill skiing, and lacrosse. Protective padding for the device is advisable for other sports where trauma to the device is less likely (eg, soccer, basketball, baseball, softball).

In addition, activities in which there is extensive arm movement (volleyball, climbing, golf) increase the risk of lead damage, which may result in loss of pacing or premature lead replacement; patients should be counseled about these risks prior to resuming participation in such activities.

Athletes with ICDs — We advise patients with ICDs not to participate in sports; the main risks of participation include a higher risk of arrhythmic events and damage to the ICD. The risks of participation should be communicated during a shared decision-making process; the clinician's role in this process is to identify the cause of ventricular arrhythmias and estimate the likelihood that participation in the specific sport will provoke ventricular arrythmias (figure 1) or damage the ICD.

In some conditions, such as arrhythmogenic right VT, the participation in sport is not specifically limited by the presence of the ICD but rather by the effects on the heart.

The optimal approach to ICD programming in athletes is uncertain, but likely similar to the approach to programming in nonathletes. However, if the athlete has the potential to raise the sinus rate to near the ICD VT detection level, a history of AF with rapid ventricular rate, or a need for relatively low tachyarrhythmia detection rates, we recommend that the athlete undergo formal exercise testing to guide ICD programming. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions".)

This approach to return to sport is consistent with the 2015 American Heart Association/American College of Cardiology scientific statement and 2020 European Society of Cardiology guidelines on sports and exercise in patients with cardiovascular disease [2,12].

The available evidence suggests wide variation in the risk of subsequent arrhythmic events or ICD damage in highly selected patients who return to sport:

●One study from a single center assessed the risk of adverse outcomes (ie, arrhythmic syncope or seizures, symptomatic nonsustained VT, appropriate ICD shock, sudden cardiac arrest, or sustained VT) in patients with genetically determined heart disease (eg, hypertrophic cardiomyopathy, long-QT syndrome) who were at risk of sudden death and who underwent a shared decision-making process [13]. Of note, 32 percent of patients had an ICD (primary prevention indication in 66 percent) and the shared decision-making process was unstructured. In this cohort, there were four arrhythmic events during 200 patient-years of observation.

●Among a cohort of 440 persons with ICDs (201 of whom had ventricular fibrillation [VF]/VT prior to ICD implantation) who participated in organized sports and were followed for a median of 44 months, there were no deaths or VF/VT requiring external defibrillation [14]. However, there was an increased risk of shocks with exercise; 46 patients (10 percent) received an appropriate shock during participation in sports. Of those experiencing a shock during sports, 14 percent quit all sports and 25 percent reduced sporting activity. In addition, another 44 patients (10 percent) experienced definite or possible lead malfunctions.

●In a post-hoc analysis from the ICD Sports Safety Registry, which reviewed the data from 129 young athletes (≤21 years of age; mean age 16 years) followed for a median of 42 months, 35 athletes (27 percent) received a total of 49 shocks (29 appropriate, 20 inappropriate) [15]. No deaths or injuries occurred during sport participation, although lead malfunction occurred in 20 percent of patients over 10 years.

●Among the same 440 patient cohort from the ICD Sports Safety Registry, 62 percent of participants were programmed with a high-rate cutoff (≥200 beats per minute) and 30 percent with a long-detection interval (defined as ">nominal" or standard programming intervals) [16]. Patients programmed with a high-rate cutoff received significantly fewer total and inappropriate shocks, and those with long-detection interval had fewer total shocks. A full discussion of the approach to optimal ICD programming is presented separately. (See "Implantable cardioverter-defibrillators: Optimal programming".)

SUMMARY AND RECOMMENDATIONS

●General considerations – As with the population in general, arrhythmias are commonly documented in athletes. Rarely are arrhythmias fatal; however, sudden cardiac death (SCD) resulting from malignant ventricular tachyarrhythmias can occur in young and apparently healthy persons. In addition, athletes treated with a permanent pacemaker or implantable cardioverter-defibrillator (ICD) are at increased risk of damage to the device during sport participation.

●Specific arrhythmias – The approach to management and return to sport typically includes an evaluation for the cause of the arrhythmia (eg, structural heart disease), appropriate treatment, and a discussion of the risk of exertion on recurrence of the arrhythmia. We address the athlete-specific issues for the following broad groups of arrhythmias:

•Atrioventricular (AV) conduction abnormalities (see 'AV conduction abnormalities' above)

•Sinus node dysfunction (see 'Sinus node dysfunction' above)

•Supraventricular arrhythmias (see 'Supraventricular arrhythmias' above)

•Ventricular arrhythmias (see 'Ventricular arrhythmias' above)

●Athletes with a pacemaker – Athletes with a permanent pacemaker should not participate in competitive sports when the danger of bodily collision exists; such trauma may damage the pacemaker system and lead to bradycardia-induced syncope or other fatal arrhythmia. This restriction generally applies to activities where direct blows to the chest are a part of the sport, such as football, rugby, boxing, martial arts, hockey, motorcycling, downhill skiing, and lacrosse. Protective padding for the device is advisable for other sports such as soccer, basketball, baseball, and softball where trauma is possible but less likely.

In addition, activities in which there is extensive arm movement (volleyball, climbing, golf) increase the risk of lead damage, which may result in loss of pacing or premature lead replacement; patients should be counseled about these risks prior to resuming participation in such activities.

●Athletes with an implantable cardioverter-defibrillator – We advise patients with ICDs not to participate in sports; the main risks of participation include a higher risk of arrhythmic events and damage to the ICD. (See 'Athletes with ICDs' above.)