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Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation

Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation
Literature review current through: Jan 2024.
This topic last updated: Jan 18, 2024.

INTRODUCTION — As in the general population, athletes can have atrial and ventricular arrhythmias. Atrial arrhythmias are rarely fatal; however, sudden cardiac death resulting from a malignant ventricular tachyarrhythmia is a devastating event in young and apparently healthy persons.

This topic will discuss the clinical manifestations and diagnostic evaluation of athletes with specific arrhythmias or arrhythmia-related syndromes. The treatment of arrhythmias in athletes, along with the discussion of returning to competition/participation, is 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: Treatment and returning to athletic participation" 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 competitive athletes".)

EPIDEMIOLOGY — Supraventricular arrhythmias, such as atrioventricular nodal reentrant tachycardia, atrioventricular tachycardia, atrial tachycardia, atrial fibrillation (AF), and atrial flutter, are generally symptomatic, and, when diagnosed, these conditions require investigation. These arrhythmias are rarely seen on screening electrocardiograms (ECGs). In one study of 32,561 young athletes who underwent ECG screening, only six patients had an atrial tachyarrhythmia, four with ectopic atrial tachycardia and two with AF [1]. Supraventricular arrhythmias are not thought to be more common in the athlete or caused by sports activity, with the possible exception of AF in master athletes. Some epidemiologic data demonstrate a higher than expected prevalence of AF in athletes at the extreme of training/exercise [2-4]. However, premature atrial complex (also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) can be seen in athletes and these may fall under a variant of normal.

Ventricular arrhythmia (ie, >2 premature ventricular complexes/contractions [PVCs; also referred to as premature ventricular beats or premature ventricular depolarizations]; in the standard 12-lead ECG) is uncommon in athletes, and not different from the general population, being present in <1 percent of athletes screened with ECGs [5]. If more frequent PVCs are recorded on a standard (10-second) ECG, it is likely that the athlete has a high 24-hour PVC burden. While PVCs are most likely benign in a highly trained athlete, their presence may nevertheless be the hallmark of an underlying heart disease and require careful evaluation [6-8].

CLINICAL PRESENTATION — When present, symptoms should be evaluated to determine whether any action needs to be taken. Arrhythmic symptoms may be related to the arrhythmia itself (eg, palpitations) or due to the hemodynamic consequences of the arrhythmias (eg, dyspnea, dizziness). Patients with an arrhythmia can present with a variety of symptoms, including:

Palpitations

Syncope or presyncope

Lightheadedness or dizziness

Unexplained, transient impairment in physical performance

Chest pain

Shortness of breath

Sudden cardiac arrest (SCA)

Patients with a tachyarrhythmia most commonly present with palpitations, the sensation of a rapid or irregular heartbeat felt in the anterior chest or neck. Usually, the symptoms are abrupt in onset, although this may vary depending on the specific arrhythmia. Palpitations may be associated with diaphoresis, lightheadedness, or dizziness. Patients with a tachyarrhythmia may also report shortness of breath or chest discomfort, with syncope and SCA being less common presentations.

Patients with a bradyarrhythmia most commonly present with fatigue and/or exertional dyspnea, although patients may present with lightheadedness, dizziness, or syncope if the heart rate is significantly slower or if there is a prolonged pause or period of asystole. Patients with a bradyarrhythmia may also report palpitations (ie, the feeling of irregular heart beating), though less commonly than in patients with a tachyarrhythmia. Chest pain is rare in patients with a bradyarrhythmia.

Asymptomatic — Athletes frequently have asymptomatic benign sinus bradycardia, due to high vagal tone. In some, the high vagal tone at rest or while asleep may even cause Mobitz type 1 (Wenckebach) second-degree atrioventricular (AV) block. When the vagal tone is removed, as is seen with exercise, AV conduction normalizes, and peak heart rate attained is normal.

Although unusual, athletes may remain asymptomatic with a tachyarrhythmia typically when the resulting ventricular rate is in the normal range and is adequate to maintain the required cardiac output. In such cases, the arrhythmia is identified incidentally when the athlete is seeking medical attention for another reason or when the athlete undergoes preparticipation screening. (See "Screening to prevent sudden cardiac death in competitive athletes".)

Palpitations — Palpitations are a sensory symptom defined as an unpleasant awareness of the forceful, rapid, or irregular beating of the heart. Patients may at times describe the sensation as a rapid fluttering in the chest, flip-flopping in the chest, or a pounding sensation in the chest or neck, and these descriptions may help elucidate the cause of the palpitations. (See "Evaluation of palpitations in adults".)

Syncope and presyncope — Syncope (and presyncope, with lightheadedness or dizziness) in an athlete is an important symptom that requires a thorough evaluation. Syncope that occurs during exertion suggests a potentially life-threatening arrhythmic etiology (eg, aortic stenosis, hypertrophic cardiomyopathy [HCM], ventricular arrhythmia, etc) and should be evaluated very seriously and urgently. On the other hand, syncope in the recovery phase after exertion (eg, during cooling off period) is generally not arrhythmic and is more likely due to a vagal reflex.

A common cause of syncope and presyncope in young athletes is neurally mediated (vasovagal) syncope, which is generally unassociated with cardiac disease and conveys a benign clinical outcome [9-13]. This type of syncope is due to neurally mediated mechanisms; however, hypovolemia from unreplaced fluid losses may contribute in athletes. Athletes (especially those engaged in endurance disciplines) may be more susceptible to neurally mediated syncope by nature of their increased vagal tone [14]. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies".)

Athletes with classic reflex (neurally mediated) syncope do not require further workup. However, if there are concerning features for structural heart disease or cardiac cause of syncope, further evaluation is necessary.

Among the pathologic cardiac causes of exertional syncope are ventricular tachycardia associated with arrhythmogenic cardiomyopathies or obstruction resulting from HCM or aortic stenosis, and hypotension due to vagally-mediated vasodepression in patients with HCM. Exercise-associated syncope may also be related to hyponatremia or hyperthermia as a result of intense or prolonged exercise. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation" and "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Syncope'.)

The prevalence and nature of syncope in athletes was evaluated in a report on 7568 young athletes (mean age 16 years), 474 of whom (6.2 percent) reported a syncopal spell in the preceding five years [11]. Syncope was unrelated to exercise in 411 patients (87 percent), postexertional in 57 (12 percent), and exertional in six (1 percent). All episodes of nonexertional or postexertional syncope were diagnosed as vasovagal (neurally mediated syncope), situational, or postexertional postural hypotension based upon the clinical history. In the six patients with exertional syncope, further testing identified one case of HCM, one case of right ventricular outflow tract tachycardia, and four cases of neurocardiogenic syncope. At six years of follow-up, the rate of syncope recurrence was 2 per 100 patient-years. There were no other adverse cardiovascular events in follow-up.

Chest discomfort and/or shortness of breath — Chest discomfort and/or shortness of breath are not infrequent symptoms in patients with either a tachyarrhythmia or a bradyarrhythmia. Chest discomfort (not all patients will describe "pain" but instead a sensation that is different than normal) is more commonly seen in patients with a tachyarrhythmia, often in association with palpitations. Shortness of breath is typically exertional and may result from either a tachyarrhythmia, likely resulting in increased pulmonary vascular pressures and/or congestion, or from a bradyarrhythmia, usually due to inadequate cardiac output to meet the body’s oxygen demands during exercise. (See "Outpatient evaluation of the adult with chest pain" and "Approach to the patient with dyspnea".)

Sudden cardiac arrest — SCA as the initial presentation of arrhythmia in an athlete is a rare and devastating event. Malignant arrhythmias, usually ventricular tachycardia (VT) or ventricular fibrillation (VF), are responsible for SCA in athletes. Usually, such arrhythmias occur in the setting of underlying structural cardiac disease (eg, HCM, arrhythmogenic cardiomyopathy, etc), although previously undiagnosed primary electrical disease (eg, Brugada syndrome, long QT syndrome, etc) may also be the cause of VT/VF. Preparticipation screening of athletes is largely directed at identifying underlying cardiac conditions, which would increase the risk of SCA for athletes. (See "Screening to prevent sudden cardiac death in competitive athletes" and "Approach to sudden cardiac arrest in the absence of apparent structural heart disease".)

DIAGNOSIS AND DIAGNOSTIC EVALUATION — The initial evaluation of the athlete with an arrhythmia consists of a complete history (aimed at defining the type of symptoms, the timing of the arrhythmia, and potential underlying diseases), physical examination (with an emphasis on assessing hemodynamic stability if the patient is actively experiencing an arrhythmia), and 12-lead ECG. If possible, the ECG is obtained both during sinus rhythm and with symptoms. For patients in whom the initial ECG is normal or unrevealing, additional ambulatory ECG, particularly prolonged (two to four weeks) monitoring, is useful in the evaluation of athletes. The diagnosis cannot usually be made until there is an ECG obtained during the symptom, as correlation between the ECG and the particular symptom is necessary [15].

Following the initial evaluation (and stabilization of the patient, if necessary), additional cardiac testing is warranted to assess for underlying structural heart disease, which may influence subsequent diagnostic and therapeutic decision making. (See 'Additional testing' below.)

Assessing the patient for hemodynamic stability — The most important clinical determination when an arrhythmia is noted is whether the patient is experiencing signs and symptoms related to the arrhythmia. The appropriate evaluation and treatment will depend upon whether the patient is actively experiencing a tachyarrhythmia or bradyarrhythmia. The approach to assessing hemodynamic stability of both tachyarrhythmias and bradyarrhythmias is discussed in detail separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Assessing the patient for hemodynamic stability' and "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Assessment of hemodynamic stability' and "Third-degree (complete) atrioventricular block", section on 'Unstable patients'.)

Evaluation of the ECG — For most patients, a probable diagnosis may be made by reviewing an ECG obtained during the time of symptoms or arrhythmia. Without a simultaneous ECG at the time of symptoms, definitive diagnosis is not generally possible. Whenever possible, a previous ECG when the patient was in normal sinus rhythm may be helpful for comparison and for identifying potential underlying pathology (eg, preexisting conduction delays, accessory pathways with a delta wave, Q waves suggesting a prior myocardial infarction, etc). (See "Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances".)

Key features to review on the ECG of a patient with a tachyarrhythmia include:

Regular versus irregular QRS complexes

Narrow versus wide QRS complexes

Rate of the tachycardia

Initiation and termination of the tachycardia

The presence and pattern of atrial activity and its relationship to the QRS complexes

P wave and QRS complex morphologies

Key features to review on the ECG of a patient with a bradyarrhythmia include:

The relationship between P waves and QRS complexes

QRS complex morphology and the likely origin of any escape rhythms

The approach to evaluation of the ECG in patients with suspected tachyarrhythmias and bradyarrhythmias is discussed in detail separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Evaluation' and "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram' and "Third-degree (complete) atrioventricular block", section on 'Electrocardiographic findings'.)

Additional testing — For athletes with a confirmed arrhythmia diagnosis (based on ECG results), as well as for those in whom an arrhythmia is highly suspected based upon the presenting signs and symptoms but without ECG documentation, additional cardiac testing is typically performed, including cardiac imaging in all patients, stress testing and ambulatory ECG monitoring in symptomatic patients, and selected additional testing on a case-by-case basis. The primary focus of any additional testing is to document the presence (or absence) of underlying structural heart disease. In some cases, additional testing may be performed with the intent of identifying the arrhythmia with prolonged ambulatory monitoring or with testing to provoke the arrhythmia.

Cardiac imaging — All athletes with a known arrhythmia, or those with a high suspicion for an arrhythmia, should have a transthoracic echocardiogram performed. Echocardiography is readily available and, in most patients, provides adequate visualization of the heart. However, if echocardiographic imaging is deemed to be nondiagnostic, additional imaging with cardiovascular magnetic resonance (CMR) should be performed. CMR is mandatory when the clinical suspicion for underlying cardiomyopathies (HCM, arrhythmogenic right ventricular cardiomyopathy [ARVC]) is high.

Stress testing — For athletes with symptoms suggestive of an arrhythmia during exertion, exercise stress testing is warranted. Exercise testing in patients with symptoms of arrhythmic origin is intended to assess the athlete's hemodynamic behavior during exercise (ie, the heart rate and blood pressure response to exercise) and the reproducibility of symptoms, as well as the potential recording of the arrhythmia. Cardiac monitoring during the test will allow the determination of whether the symptoms, if reproduced, are due to an arrhythmia. Moreover, the exercise test may be part of the diagnostic evaluation for underlying cardiac disease (ie, coronary heart disease, hypertrophic or dilated cardiomyopathy, channelopathies, etc).

Ideally, the stress test optimally should mimic the exertion, which brings on the symptoms. While a standard Bruce protocol may be acceptable for some athletes, this protocol (and other standard protocols used in the diagnosis of obstructive coronary heart disease) is often not optimal for competitive athletes with symptoms. For example, if the athlete has symptoms only with sprints, then sprints should be performed during the treadmill test. Alternatively, both symptomatic endurance athletes and lab personnel should be forewarned that a long duration test might be necessary to reproduce the type of endurance exercise in which symptoms have occurred. Arrhythmias may not always be reproducible in the exercise lab, and thus ambulatory ECG monitoring is relevant to the identification of the nature of arrhythmic event.

Ambulatory ECG monitoring — For athletes in whom an arrhythmia is highly suspected based upon the presenting signs and symptoms, but whose initial ECG is unrevealing, we perform ambulatory ECG monitoring. Ambulatory ECG, especially the long-term (two to four weeks) recording, significantly increases the likelihood of capturing abnormal heart rhythms and confirming the diagnosis. Ambulatory ECG monitoring is generally performed during normal routine activity as well as during exercise. The choice of a particular monitoring device and duration of monitoring depends primarily on the frequency and duration of symptoms. The approach to choosing an ambulatory ECG monitor is discussed in detail separately. For athletes with daily symptoms, a 24-hour monitor may be sufficient. However, most will need longer-term monitors. Continuous monitoring is possible with devices that attach to the skin with electrodes. Some of these devices store the entire ECG while others only store abnormally slow or fast arrhythmias or when the patient triggers a recording. Some will instantly alert the health care provider with abnormal results while others do not have this wireless capability. The ability to obtain a single-lead, real-time ECG by portable devices is rapidly expanding. These devices typically collect a lead I (right arm to left arm) ECG, which can be of very high quality. Some of these devices are linked to a cell phone while others stand alone. They are very valuable for individuals whose symptoms persist long enough to activate the device (typically around 30 seconds), while they are not valuable for those with very short episodes or to evaluate syncope and presyncope. (See "Ambulatory ECG monitoring", section on 'Our approach to choosing an ambulatory ECG monitoring strategy'.)

Electrophysiology studies — Invasive electrophysiologic studies (EPS) are not generally indicated in the work-up of the athlete’s arrhythmias, which is mostly based on either ECG or ambulatory monitoring. If a tachyarrhythmia has been diagnosed by an ECG, then an EPS and ablation may be indicated, with an aim to cure the arrhythmia. EPS is rarely indicated in the absence of an ECG diagnosis of tachyarrhythmia with the exception being those individuals with concerning syncope/presyncope or palpitations and a surface ECG documenting preexcitation (Wolff-Parkinson-White syndrome). In these individuals, an EPS with electrophysiologic mapping can be used to identify and/or treat causes of sudden cardiac death. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrophysiology studies (EPS)'.)

Other studies — In select patients, when a particular diagnosis is being investigated, additional testing may provide helpful information to confirm or exclude the diagnosis of the disease-causing arrhythmias. As examples:

Brugada syndrome – The presence of Brugada syndrome is suggested by the presence of sudden death in the family or by the presence of ECG abnormalities at rest or with provocative drug challenge (eg, repolarization abnormalities in the anterior leads ) [16]. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'Drug challenge for type 2 or equivocal ECG'.)

Long QT syndrome – The presence of long QT syndrome (LQTS) is suggested by family history of LQTS, syncope associated with various stimuli (eg, swimming, loud noises), or QTc prolongation at rest or with provocation [16]. (See "Congenital long QT syndrome: Diagnosis", section on 'Exercise testing'.)

Hypertrophic cardiomyopathy – The presence of HCM is suggested by an abnormal ECG, cardiac murmur, or family history of HCM and confirmed with additional diagnostic testing (eg, echocardiography, CMR testing) [17]. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Diagnostic evaluation'.)

Arrhythmogenic right ventricular cardiomyopathy – The presence of ARVC is suggested by family history (eg, sudden death, syncope), incomplete or complete right bundle branch block, and/or repolarization abnormalities in V1 to V3. (See "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Supraventricular arrhythmias" and "Society guideline links: Ventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – Arrhythmias are not infrequently documented in athletes and can result in significant cardiac symptoms and occasional impaired athletic performance. Rarely are 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.)

Clinical presentation – Patients with an arrhythmia can present with a variety of symptoms, including palpitations, syncope/presyncope, lightheadedness/dizziness, chest pain, shortness of breath, and rarely sudden cardiac arrest (SCA). Arrhythmic symptoms may be related to the arrhythmia itself (eg, palpitations) or due to the hemodynamic consequences of the arrhythmias (eg, dyspnea, dizziness). Patients with a tachyarrhythmia most commonly present with palpitations. Patients with a bradyarrhythmia most commonly present with fatigue and/or exertional dyspnea, although patients may present with lightheadedness, dizziness, or syncope. (See 'Clinical presentation' above.)

Evaluation of the ECG – The initial evaluation of the athlete with an arrhythmia consists of a complete history, physical examination, and 12-lead ECG. If possible, the ECG is obtained both during sinus rhythm and the symptoms, and a previous ECG when the patient was in normal sinus rhythm may be helpful for comparison and for identifying potential underlying pathology. (See 'Evaluation of the ECG' above.)

Additional testing – For athletes with a confirmed arrhythmia diagnosis (based on ECG results), as well as for those in whom an arrhythmia is highly suspected based upon the presenting signs and symptoms but without ECG documentation, additional cardiac testing is typically performed, including cardiac imaging and ambulatory ECG monitoring, and stress testing and selected additional testing on a case-by-case basis. (See 'Additional testing' above.)

Diagnosis and diagnostic testing – The arrhythmic diagnosis is often confirmed using the ECG obtained during the arrhythmia, as the correlation can be made between the type of arrhythmia and particular symptom(s), but may require additional ECG monitoring if the initial ECG is unrevealing. (See 'Diagnosis and diagnostic evaluation' above.)

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