INTRODUCTION — As with the population in general, arrhythmias are not infrequently documented in athletes. Arrhythmias in athletes may present clinically with a variety of symptoms most commonly including palpitations or syncope. Occasionally reduced performance or general malaise may also be reported. Of critical relevance is the syncope induced by exercise. Rarely are arrhythmias fatal; however, sudden cardiac death (SCD) resulting from a malignant ventricular tachyarrhythmia is a devastating event in young and apparently healthy persons.
This topic will discuss the treatment of arrhythmias in athletes, along with the discussion of returning to competition/participation. The clinical manifestations and diagnostic evaluation of athletes with specific arrhythmias or arrhythmia-related syndromes are discussed in detail separately. Additionally, the risk of sudden death in athletes and the approach to screening to prevent sudden death in athletes are discussed elsewhere. (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation" and "Athletes: Overview of sudden cardiac death risk and sport participation" and "Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances" and "Screening to prevent sudden cardiac death in athletes".)
SYNCOPE — Syncope that occurs during exertion suggests a potentially life-threatening arrhythmic etiology (eg, aortic stenosis, hypertrophic cardiomyopathy, ventricular arrhythmia, etc) and should be evaluated urgently. On the other hand, syncope occurring after exertion (eg, during cooling off period) is more likely reflex in origin, similar to the vasovagal faint. (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation", section on 'Syncope and presyncope'.)
Therapies to prevent recurrent syncope in athletes are highly variable depending upon the suspected etiology of the syncope. The diagnostic approach and management of syncope in athletes is similar to that in non-athletes and is discussed in detail separately. (See "Syncope in adults: Management and prognosis".)
Athletes with concerning syncope should have a full evaluation to ascertain the presence of underlying cardiac disease responsible for the syncope. Return to sport is permitted after the cause has been determined and, if necessary, treated. When any underlying cardiac disease has been reasonably excluded, the athlete can safely return to sport without restriction [1]. However, athletes with syncope or presyncope with a high risk of recurrence should not participate in sports where the likelihood of even a momentary loss of consciousness may be hazardous and/or potentially responsible for adverse events (such as scuba diving, rock climbing, automobile racing, etc).
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). No specific limitations are necessary in this setting as long as the athlete is asymptomatic and the conduction abnormalities improve (ie, disappear) with exertion. However, higher degrees of AV conduction abnormality will require attention prior to participation in athletics.
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). In general, Mobitz type I (Wenckebach) second degree AV block has no important clinical implications.
Asymptomatic athletes with Mobitz type I (Wenckebach) second degree AV block and improvement of AV block with exercise can participate in all competitive sports (figure 1) [1,2]. 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/His-Purkinje system (figure 1). 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). 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 — Mobitz type II second degree AV block (waveform 3) is uncommon in athletes and, when present, usually is due to disease in the His-Purkinje system. Mobitz type II second degree AV block is by nature unstable and frequently progresses to third degree (complete) AV block. In the absence of a potentially reversible condition (ie, Lyme disease), Mobitz II AV block generally requires a pacemaker before permitting resumption of regular physical activity or sport activity [1]. The development of Mobitz II heart block should prompt referral to an electrophysiologist. (See "Second-degree atrioventricular block: Mobitz type II" and "Lyme carditis".)
Third degree (complete) 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. Nearly all athletes with third degree (complete) AV block will present with some degree of symptoms (eg, lightheadedness, presyncope, syncope, fatigue, dyspnea, chest pain, sudden cardiac arrest), though the severity of the symptoms can be quite variable. In the absence of a potentially reversible condition (ie, Lyme carditis), acquired third degree (complete) AV block should be treated with a pacemaker before permitting resumption of regular physical or sport activity [1]. The development of complete heart block should prompt referral to an electrophysiologist. (See "Third-degree (complete) atrioventricular block" and "Lyme carditis".)
A subset of patients with third degree (complete) AV block is the group with 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.
Asymptomatic athletes with congenital heart 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 during exertion can selectively participate in competitive sports [1,2]. Evaluation of these cases should preferentially be performed by expert electrophysiologists. By contrast, athletes with ventricular arrhythmia, or those with symptoms of fatigue, near-syncope, or syncope, should have a pacemaker implanted before they participate in competitive sports. (See "Congenital third degree (complete) atrioventricular block", section on 'Treatment'.)
Bundle branch block — While complete right bundle branch block (RBBB) (waveform 6) is not uncommon among athletes and may be seen with or without underlying structural heart disease, complete left bundle branch block (LBBB) (waveform 7) is rarely seen and often reflects an underlying pathologic condition [3]. (See "Right bundle branch block" and "Left bundle branch block".)
Athletes with asymptomatic RBBB and no evidence of underlying cardiac disease have no restriction for sport participation [1]. 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 ascertain a possible incidence of symptoms or evidence for cardiac disease. There is 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 ECG and echocardiography is appropriate, with additional follow-up after one year to generally be determined by the development of symptoms.
Screening of family members in the presence of fascicular block(s) — 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. First degree relatives of an athlete with bifascicular block on his/her ECG 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 atrioventricular (AV) nodes [7].
Athletes with a normal heart and sinus bradycardia in whom the heart rate increases appropriately during physical activity have no restriction for sport participation [1]. 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 bradycardia and sinus tachycardia that are appropriate for the clinical situation are not considered abnormal, and further testing is not necessary. (See "Sinus bradycardia" and "Sinus tachycardia: Evaluation and management".)
●Sinus arrhythmia and a wandering atrial pacemaker are frequent in well-trained individuals due to increased vagal tone. No testing is necessary unless the arrhythmia results in inappropriately slow heart rates associated with symptoms.
Asymptomatic sinus pauses or sinus arrest of less than three seconds duration are not uncommonly seen in Holter electrocardiogram (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, and sinus node dysfunction are abnormal [9]. Athletes with a symptomatic tachycardia/bradycardia (sick sinus) syndrome should be restricted from participating in competitive sports. These patients should be treated and if they have no structural heart disease, the cause of inappropriate bradycardia (sick sinus) syndrome has been resolved, and they have remained asymptomatic for three months, they can participate in all competitive sports [1]. (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 or symptoms. (See "Supraventricular premature beats".)
Athletes with a structurally normal heart who have atrial or junctional premature beats, regardless of frequency, can participate in all competitive sports [1,10]. 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. (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 patent 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 (table 1). As with any patient with AF, athletes with AF should be evaluated for potential underlying causes and risk (eg, thyroid disease, binge alcohol use, etc). (See "New onset atrial fibrillation", section on 'Possible predisposing cause'.)
Athletes with self-terminating AF and no associated structural heart disease can participate in all competitive sports. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation", section on 'Classification and terminology'.)
Generally, because of symptoms, a rhythm control strategy is the preferred method of treatment in athletes with AF, although there may be athletes with minimal symptoms or such infrequent episodes that a rhythm control strategy is not necessary. Rhythm control can be achieved with antiarrhythmic agents or ablation procedures. Increasingly, ablation provides 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 with recurrent/persistent AF (not undergoing ablation) 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 "Rhythm control versus rate control in atrial fibrillation".)
The other component of management is anticoagulation. Most athletes will have a low risk of systemic thromboembolism as manifested by a low CHA2DS2-VASC score (calculator 1). Therefore, the decision to anticoagulate should be individually considered. However, athletes who require anticoagulation should not participate in sports with danger of severe bodily collision (for example, football, basketball, or hockey) (figure 1).
Atrial flutter — Sustained atrial flutter is uncommon in athletes. Typical atrial flutter is relatively easily cured with radiofrequency catheter ablation procedures. 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 [1]. 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", section on 'Maintenance of normal sinus rhythm'.)
Only when 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 participate in class IA competitive sports (figure 1) with the warning that rapid 1:1 conduction still may occur [1]. However, full participation in all competitive sports generally should not be allowed.
Athletes in whom anticoagulation is deemed necessary 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 — 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".)
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 any competitive sports until they have been adequately treated. Following catheter ablation, athletes without structural heart disease who are asymptomatic and have no recurrence of arrhythmia for four weeks after the procedure can participate in all competitive sports [1,10]. 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 this case, 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 atrioventricular nodal reentrant tachycardia (AVNRT) or atrioventricular reentrant tachycardia (AVRT) (table 1). (See "Focal atrial tachycardia" and "Sinoatrial nodal reentrant tachycardia (SANRT)" and "Intraatrial reentrant tachycardia".)
Patients with recurrent or refractory symptomatic AT are candidates for medical therapy or catheter ablation. Athletes with atrial tachycardia in the absence of structural heart disease who have elimination of the atrial tachyarrhythmia by an ablation technique, may participate in all competitive sports (figure 1) after four weeks without a recurrence [1,10]. When ablation is not performed, athletes 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, with appropriate therapy. In this case, evaluation should be individualized and regular follow-up is advised.
Wolff-Parkinson-White syndrome — Patients with Wolff-Parkinson-White (WPW) pattern manifest ventricular pre-excitation on the surface electrocardiogram (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 an AVRT. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)
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 and/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 pre-excitation during an increasing sinus rate argues for a benign bypass tract, while gradual loss or no loss of pre-excitation does not prove that a bypass tract is benign (although this is not diagnostic of a malignant bypass tract) (algorithm 1).
Athletes with ventricular pre-excitation 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 tract (table 2) [1,10,11]. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Catheter ablation'.)
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 EP studies with induced AV reciprocating tachycardia or atrial fibrillation in whom the shortest cycle length is less than 250 ms should undergo ablation of the accessory pathway [10]. Athletes with episodes of atrial fibrillation and syncope or near syncope whose maximal ventricular rate at rest (without therapy) as a result of conduction over the accessory pathway >240 beats per minute should be considered for catheter ablation therapy of the accessory pathway prior to continuing competition.
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 pre-excitation 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 the presence of underlying pathologic substrate (ie, arrhythmogenic cardiomyopathies, coronary heart disease, inflammatory cardiac diseases, etc).
●Athletes without 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 [1].
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 further evaluated. 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 relief of symptoms and have close follow-up. In both of these cases, the athlete can participate in class IA competitive sports only (figure 1) [1].
Catheter ablation should be offered to athletes with particularly frequent PVCs (>15 percent) that persist over time and are not reduced by medical treatment. (See "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation", section on 'Additional testing'.)
●Athletes with structural heart disease who are in high-risk groups and have PVCs should be properly treated and can participate in class IA competitive sports only (figure 1) [1].
Nonsustained ventricular tachycardia — In asymptomatic athletes with brief (generally <8 to 10 consecutive ventricular beats) episodes of nonsustained monomorphic ventricular tachycardia (VT), rates generally <150 beats per minute, and no structural heart disease established by noninvasive and invasive tests, there is no apparent increased risk for sudden cardiac death. If exercise testing (preferably by ambulatory electrocardiogram [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) [1].
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.
●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 [1]. 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 re-emerge. In this setting, the athlete should generally not compete in any sports for at least two to three months after the last VT episode [1].
●If there have been no clinical recurrences and the VT is not inducible by exercise or exercise testing, and the athlete has no structural heart disease, all competitive sports may be permitted under periodical follow-up [1]. Because deconditioning can result in the loss or lessening of ventricular arrhythmias, a short period of deconditioning and retesting can be selectively advised. (See "Nonsustained VT in the absence of apparent structural heart disease" and "Ventricular tachycardia in the absence of apparent structural heart disease".)
●For the athlete with structural heart disease, molecular or inflammatory disease, and VT, moderate- and high-intensity competition is contraindicated regardless of whether the VT is suppressed or ablated. Only class IA competitive sports are permitted (figure 1).
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 to not participate in any moderate- or high-intensity competitive sports (figure 1) [1]. However, in today's shared decision making approach, athletes with ICDs and who have had no episodes of ventricular flutter or ventricular fibrillation requiring device therapy for three months may engage in competitive sports, with an understanding of the potential risks involved. (See 'Athletes with ICDs' below.)
Recommendations in the section on VT also apply. (See "Pathophysiology and etiology of sudden cardiac arrest".)
ATHLETES WITH A CARDIAC IMPLANTABLE ELECTRONIC DEVICE (CIED)
Athletes with permanent pacemakers — Athletes with permanent pacemakers should not participate in competitive sports when the danger of bodily collision exists because such trauma may damage the pacemaker system [1]. This restriction should generally exclude 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.
Before allowing athletes to engage in the other sport activities, an exercise test should be conducted at the level of activity demanded by the particular sport so as to be certain that the paced heart rate increases appropriately.
Athletes with ICDs — Although athletes with implantable cardioverter-defibrillators (ICDs) have been restricted to low-impact, low-static and dynamic sports (type IA) by previous ESC and ACC/AHA guidelines (figure 1), the 2015 ACC/AHA Scientific Statement and 2018 ESC recommendation loosened that restriction [1,12,13]. In contemporary practice, participation in sports with higher static and dynamic components may be selectively considered if the patient has been free of arrhythmias for three months and, after appropriate information of the risks, he/she accepts the higher risk of sports-related arrhythmias and ICD appropriate and inappropriate discharge [1]. The decision regarding athletic participation should also be made with consideration of the underlying arrhythmogenic condition. Any sport in which there is a risk of traumatic injury to the device or lead system should be discouraged (figure 1).
The best available data about outcomes among athletes with ICDs come from the ICD Sports Safety Registry.
●Among a cohort of 440 persons with ICDs (201 of whom had ventricular fibrillation [VF]/ventricular tachycardia [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 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.
The optimal approach to ICD programming in athletes is uncertain, but likely similar to the approach to programming in non-athletes. 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".)
Furthermore, it is advised for athletes with an ICD to undergo exercise testing if there is a history of atrial fibrillation with a potentially rapid ventricular rate, a need for low tachyarrhythmia detection rates, or the potential to raise the sinus rate to near the ICD VT detection level. (See "Implantable cardioverter-defibrillators: Overview of indications, components, and functions".)
SUMMARY AND RECOMMENDATIONS
●Arrhythmias are not infrequently documented in athletes and can result in significant symptoms and impaired athletic performance. Rarely are supraventricular arrhythmias fatal; however, sudden cardiac death resulting from a malignant ventricular tachyarrhythmia is a devastating event in young and apparently healthy persons. (See 'Introduction' above.)
●Syncope that occurs during exertion suggests a potentially life-threatening arrhythmic etiology (eg, aortic stenosis, hypertrophic cardiomyopathy, ventricular arrhythmia, etc) and should be evaluated urgently. On the other hand, syncope occurring after exertion (eg, during cooling off period) is more likely reflex in origin, similar to the vasovagal faint. (See 'Syncope' above.)
●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 and is generally not a cause for concern. However, higher degrees of AV conduction abnormality (eg, Mobitz type II second degree AV block and third degree AV block) will require attention prior to participation in athletics. (See 'AV conduction abnormalities' above.)
●Sinus bradycardia and sinus tachycardia that are appropriate for the clinical situation are not considered abnormal, and further testing is not necessary. Asymptomatic sinus pauses or sinus arrest of less than three seconds duration are not uncommonly seen in normal athletes and are of no clinical significance. However, longer pauses, sinoatrial exit block, and sinus node dysfunction are abnormal. (See 'Sinus node dysfunction' above.)
●Atrial premature beats are common in the general population and in athletes, and are not generally associated with underlying structural heart disease or symptoms. Premature ventricular complexes (PVCs) are also common in athletes of all age groups and occur in those with or without structural heart disease; the identification of PVCs should prompt an evaluation for the presence of underlying pathologic substrate. (See 'Atrial or junctional premature beats' above and 'Ventricular premature beats' above.)
●Sustained atrial fibrillation and/or atrial flutter are uncommon in athletes. A full cardiac evaluation, should be performed and referral to an arrhythmia specialist for any patient with one of these arrhythmias. (See 'Atrial fibrillation' above and 'Atrial flutter' above.)
●Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia in young athletes and is often 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' above.)
●Patients with Wolff-Parkinson-White (WPW) pattern manifest ventricular pre-excitation on the surface electrocardiogram (ECG). 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 an atrioventricular reentrant tachycardia (AVRT), although atrial fibrillation and other arrhythmias may arise. Athletes with ventricular pre-excitation on the ECG and symptoms of palpitations, presyncope, or syncope, or with documented arrhythmia (ie, WPW syndrome) should undergo invasive electrophysiologic testing for both diagnostic and potential therapeutic (ie, catheter ablation of the accessory pathway) purposes. (See 'Wolff-Parkinson-White syndrome' above.)
●Most individuals with sustained or nonsustained symptomatic monomorphic or polymorphic ventricular tachycardia have underlying structural heart disease. Since these arrhythmias are potentially life-threatening, further evaluation is essential prior to the resumption of athletic activity. (See 'Nonsustained ventricular tachycardia' above and 'Sustained ventricular tachycardia' above.)
●Recommendations regarding the ability to participate in competitive athletics or intense athletic training are discussed in the relevant sections of the text.
●In general, athletes with symptomatic supraventricular arrhythmias, WPW, ventricular arrhythmias, and symptomatic bradyarrhythmias should be referred to a cardiac electrophysiologist.
