7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances : Mark S Link, MD, Antonio Pelliccia, MD : Peter J Zimetbaum, MD, Ary L Goldberger, MD : Todd F Dardas, MD, MS All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Dec 12, 2022. INTRODUCTION As with the population in general, apparent electrocardiographic (ECG) abnormalities, including conduction disturbances and arrhythmias, are often documented in athletes. ECG findings in athletes may be benign, physiologic consequences of cardiovascular adaptation to regular exercise training or may be the expression of pathologic conditions. Therefore, there is a need for appropriate knowledge of what is normal and physiologic versus nonphysiologic and abnormal in an athlete's ECG. These abnormalities can impact eligibility for participation and lead to a costly and sometimes invasive work-up, even when they are not associated with significant symptoms or impaired athletic performance. Rarely are arrhythmias fatal; however, sudden cardiac death (SCD) resulting from a malignant ventricular tachyarrhythmia is a devastating event, particularly in young and apparently healthy persons. Thus, appropriate assessment of ECG anomalies in athletes is of major importance. The two primary and interrelated goals when evaluating athletes for apparent ECG abnormalities are: To document the presence of ECG abnormalities that may be due to underlying structural heart disease that place the athlete at risk for SCD. To evaluate the importance of an arrhythmia in assessing the athlete's eligibility for competition. https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 1/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate This topic will discuss ECG abnormalities, including conduction disturbances and their importance in athletes. The clinical manifestations, diagnostic evaluation, and treatment of athletes with arrhythmias, along with the discussion of returning to athletic participation, are discussed separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Athletes with arrhythmias: Clinical manifestations and diagnostic evaluation" and "Athletes with arrhythmias: Treatment and returning to athletic participation".) The approach to pre-participation evaluation and screening of athletes is also discussed separately. (See "Screening to prevent sudden cardiac death in competitive athletes" and "Sports participation in children and adolescents: The preparticipation physical evaluation".) PREVALENCE A broad range of ECG abnormalities can be seen in trained athletes ( table 1) [1-3]. The type of sport appears to impact the resulting changes, with endurance athletes more likely to have ECG abnormalities than non-endurance athletes [3]. The type of abnormality and whether the abnormality is related or unrelated to training impacts the decision regarding further evaluation and participation in athletics [1]. In one report of 1005 athletes who were evaluated with ECG and echocardiography, the ECG was found to be abnormal in 14 percent, while echocardiographic abnormalities were found in 5 percent [2]. Apparently abnormal ECG patterns were associated with a larger left ventricular (LV) end-diastolic dimension and wall thickness and were more common in: Males Younger athletes Endurance athletes (eg, cycling, rowing, cross-country skiing) These findings would suggest a causative role of exercise in physiologic LV remodeling [3]. Notably, the vast majority of the ECG abnormalities were composed of increased R/S wave voltages, suggestive of LV hypertrophy (LVH). Other major abnormalities such as repolarization abnormalities and primarily negative T waves were relatively rare (3 percent) and unrelated to cardiac dimensions. The negative T waves should raise suspicion for underlying structural cardiac diseases, and these ECG abnormalities may have clinical or pathologic implications [4]. Subsequent reports have confirmed that a large proportion of the ECG changes in athletes are likely a consequence of the physiologic cardiac remodeling and characterized by a benign clinical significance. Thus, the proportion of abnormal ECG patterns with clinical relevance has substantially decreased. As an example, the proportion of abnormal ECG patterns was found to https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 2/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate be about 5 percent in a large population of White athletes [5], but up to 16 percent in Afro- Caribbean and Black athletes [6]. CLINICAL APPROACH TO READING THE ECG IN ATHLETES A clinical approach to the ECG reading (ie, distinguishing the few ECGs that may be the expression of an underlying pathologic condition from the majority of ECG changes that are simply a consequence of the athletic conditioning) was suggested in 2010 [7] and subsequently refined in 2017 by an international group [7-9]. For practical purposes, ECG changes in athletes can be classified into two groups ( figure 1): one related to whether the ECG abnormality is likely a result of chronic training (normal ECG changes in athletes); the other related to whether the ECG finding occurs independently of training and thus may be expression of a pathologic condition (borderline or abnormal ECG changes in athletes) [7]. Common ECG abnormalities ("normal" in athletes) are frequent and are not associated with an increased risk of underlying cardiac disease and incidence of adverse events during exercise ( table 1). These include, among others, sinus bradycardia, sinus arrhythmia, ectopic atrial rhythm, junctional rhythm, first degree atrioventricular (AV) block, incomplete right bundle branch block (RBBB), isolated voltage meeting standard criteria for LVH or right ventricular hypertrophy (RVH), and early repolarization. Athletes with these ECG abnormalities do not require additional evaluation and can continue to participate safely in athletics. In contrast, uncommon ECG abnormalities are unrelated to training and often occur secondary to an underlying pathologic disease process (eg, hypertrophic cardiomyopathy, arrhythmogenic RV cardiomyopathy, Wolff-Parkinson-White syndrome, long QT syndrome, and other ion channelopathies) ( table 1). These abnormalities are associated with an increased risk of SCD. Persons with uncommon ECG abnormalities should undergo additional cardiovascular testing and evaluation for clinically important cardiac pathology. However, there is a potential overlap between training-related versus training-unrelated ECG changes. In addition, in some athletes, the distinction between an athlete's heart and a pathologic condition is difficult, and gray areas will exist. As a result, the international criteria also include a third category of borderline ECG changes, comprehensive of left or right axis deviation, left or right atrial enlargement, and complete RBBB. The presence of a single, borderline abnormality is likely unrelated to structural cardiac abnormalities, while the combination of two or more of these borderline changes https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 3/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate increases the probability of finding an underlying structural cardiac abnormality and requiring additional investigations. NORMAL ECG FINDINGS There are multiple ECG findings in athletes that represent normal (physiologic) variants. In asymptomatic persons with no family history of inherited cardiac disease or SCD, no further evaluation is required, and patients are not restricted from activity [9]. These include: Increased QRS voltage meeting standard criteria for LVH or RVH found in isolation (ie, without other ECG abnormalities). Incomplete right bundle branch block. Early repolarization variants/ST-segment elevation. (See "Early repolarization".) ST-segment elevation followed by terminal T-wave inversion in leads V1 to V4 in Afro- Caribbean and Black athletes. T-wave inversion in leads V1 to V3 in children <16 years of age. Sinus bradycardia. (See "Sinus bradycardia".) Sinus arrhythmia. (See "Normal sinus rhythm and sinus arrhythmia", section on 'Sinus arrhythmia'.) Ectopic atrial rhythm. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Ectopic atrial rhythm'.) Junctional rhythm. (See "ECG tutorial: Atrial and atrioventricular nodal (supraventricular) arrhythmias", section on 'Junctional ectopic rhythm'.) First degree AV conduction delay (block). (See "First-degree atrioventricular block".) Second degree AV block: Mobitz type I (Wenckebach). (See "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)".) BORDERLINE ECG FINDINGS Borderline ECG findings may represent pathology or innocent ECG alterations. If one of the borderline ECG findings is present alone in an asymptomatic person with no family history of https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 4/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate inherited cardiac disease or SCD, no further evaluation is required, and the patient is not restricted from activity. In contrast, if two or more of the borderline ECG findings are present, further evaluation is required. Right/left axis deviation and right/left atrial enlargement Axis deviation and atrial abnormality (the latter as defined by ECG voltage criteria) are not uncommonly seen in both athletes and non-athletes. Among a cohort of over 2500 athletes and nearly 10,000 non-athletes, axis deviation or findings consistent with atrial enlargement were seen in 5.5 and 4.4 percent of persons, respectively [10]. Among 579 patients with identified ECG abnormalities who underwent follow-up testing with echocardiography, none of the 579 persons had an identified major structural or functional cardiac abnormality. These observations suggested that right axis deviation and right atrial enlargement occurring in isolation or in association with other electrical markers of "athlete's heart" are probably normal variants, whereas left axis deviation and left atrial enlargement may reflect a relative increase in LV dimensions in some athletes (but not pathologic conditions). Complete right bundle branch block Complete right bundle branch block (RBBB) ( waveform 1) is not uncommon among athletes and nonathletic young individuals and generally is not a sign of underlying structural heart disease [11]. Complete RBBB is detected in approximately 1 percent of the general population and large data sets in young adult athletes reveal a prevalence of 0.5 to 2.5 percent. In a study of 510 United States collegiate athletes, RBBB was reported in 13 (2.5 percent) athletes. The athletes with complete RBBB exhibited larger RV dimensions and a lower RV ejection fraction, but preserved fractional area change. None of the athletes with complete or incomplete RBBB had pathological structural cardiac disease, suggesting that this particular ECG pattern may be an adaptation to exercise that manifests as only an electrical change in the absence of any RV morphological change [11]. (See "Right bundle branch block" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Bundle branch block'.) ABNORMAL ECG FINDINGS Abnormal ECG findings are significantly more likely to represent pathology rather than a normal response to training. As such, patients with an abnormal ECG finding should undergo further evaluation to search for cardiac pathology. T-wave inversion T-wave inversion of at least 1 mm in two or more contiguous leads is generally abnormal and should prompt additional evaluation. In contrast, however, ST-segment elevation followed by terminal T-wave inversion in leads V1 to V4 in Afro-Caribbean and Black https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 5/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate athletes, as well as T-wave inversion in leads V1 to V3 in children <16 years of age, is considered normal ECG findings. T-wave inversion is more commonly seen in patients with structural heart disease, notably hypertrophic cardiomyopathy and arrhythmogenic RV cardiomyopathy (ARVC), among others. In HCM, T-wave inversion is usually prevalent in inferolateral leads and is associated with other abnormalities (eg, ST-segment depression, Q waves, left axis deviation, or left atrial enlargement). In one study of 100 healthy athletes who were age- and sex-matched with 100 patients with ARVC, those with ARVC were significantly more likely to have T-wave inversion extending beyond lead V3, inferior T-wave inversions, often associated with premature ventricular beats, and/or lower LVH voltage scores [12]. Moreover, ARVC patients do not usually present with ST-segment elevation preceding the inverted T-wave, in contrast to normal young subjects [9]. The finding of T-wave inversion on the ECG should prompt additional evaluation, usually beginning with echocardiography. Serial imaging may be required if the initial imaging evaluation is unrevealing but the ECG findings persist. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Electrocardiography' and "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis", section on 'Electrocardiography' and 'Normal ECG findings' above.) ST-segment depression ST-segment depression can be seen in a variety of cardiomyopathic conditions, and is not considered a normal response to exercise training. This finding on the ECG should prompt additional evaluation. Echocardiography is the minimum evaluation for athletes with ST-segment depression to investigate for underlying cardiomyopathy. Cardiovascular magnetic resonance (CMR) imaging should be considered based on the echocardiographic findings and/or level of clinical suspicion. Pathologic Q waves Contemporary practice considers pathologic Q waves present if the Q/R ratio 0.25 or a duration 40 milliseconds (again in two or more contiguous leads). Q waves can be seen in a variety of cardiomyopathic conditions as well as in the setting of an accessory pathway. The presence of possibly pathologic Q waves should prompt close scrutiny of the ECG for other evidence of an accessory pathway, along with echocardiography to evaluate for cardiomyopathy. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Electrocardiographic findings'.) Left bundle branch block In contrast to right bundle branch block (RBBB), left bundle branch block (LBBB) ( waveform 2) is rarely seen (in athletes or nonathletes) and often reflects underlying structural heart disease, mandating careful investigation for underlying cardiac https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 6/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate abnormality. LBBB is generally not associated with symptoms but when identified should prompt further evaluation. Athletes with complete LBBB require a thorough investigation for myocardial disease, typically beginning with echocardiography. CMR imaging should be considered based on the echocardiographic findings and/or level of clinical suspicion. (See "Left bundle branch block" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Bundle branch block'.) QRS duration 140 milliseconds While the exact implications in athletes are uncertain, a prominent intraventricular conduction delay ( 140 milliseconds) that does not meet criteria for LBBB or RBBB has been associated with increased risk of death or cardiomyopathy in general populations [13]. In asymptomatic athletes with profound non-specific intraventricular conduction delay, an echocardiogram is recommended to evaluate for myocardial disease. Other testing may be indicated depending on echocardiographic findings and/or clinical suspicion. Epsilon wave An epsilon wave is defined as a distinct low-amplitude signal (appearing as small positive deflections or notches) localized between the end of the QRS complex and onset of the T wave in leads V1 to V3. Epsilon waves are among the more subtle ECG abnormalities, and, not surprisingly, subject to high interobserver variability [14]. The presence of epsilon waves is a highly specific ECG marker and represents one of the diagnostic criteria for arrhythmogenic RV cardiomyopathy. However, epsilon waves are typically a manifestation of more advanced disease and unlikely to be an isolated ECG finding, especially in young asymptomatic athletes. Ventricular preexcitation 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. (See 'Supraventricular tachyarrhythmias' below and "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis".) The WPW pattern occurs in approximately 1/1000 to 4/1000 athletes. The presence of an accessory pathway can predispose an athlete to sudden death because rapid conduction of atrial fibrillation (AF) across the accessory pathway can result in ventricular fibrillation (VF). SCD due to VF in patients with WPW is a risk but is quite rare (<1 percent of the WPW patients). This complication appears to be confined to patients with AF or atrial flutter and rapid conduction to the ventricles over a bypass tract, which has a particularly short functional refractory period [15- 17]. 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 uncertain, but Pediatric https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 7/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate Society Guidelines recommend that symptomatic athletes with WPW pattern should be investigated for the presence of a low- or high-risk accessory pathway. Noninvasive risk stratification begins with an exercise stress test in which abrupt, complete loss of preexcitation as the heart rate increases suggests a low-risk accessory pathway. However, as a practical matter, this determination may be difficult at high heart rates due to shortening PR intervals; therefore, if noninvasive testing cannot confirm a low-risk pathway or is inconclusive, electrophysiology testing should be considered to determine the shortest preexcited RR interval during AF. If the shortest preexcited RR interval is 250 ms (240 bpm) and when multiple pathways exist, then the accessory pathway is deemed to be at high risk, and prophylactic treatment (typically catheter ablation) is advised. Ablation of the accessory pathway is recommended in competitive and recreational athletes with preexcitation and documented arrhythmias. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Treatment to prevent recurrent arrhythmias' and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Wolff-Parkinson- White syndrome'.) Long QT syndrome Overall, the average QTc in healthy persons after puberty is 420 20 milliseconds, while during infancy the average QTc is 400 20 milliseconds. The calculation of the QT interval in athletes has limitations due to sinus arrhythmia, slightly widened QRS complexes, and T-U complexes. To properly perform a manual QT measurement, it is critical to identify the end of the T wave since the onset of the QRS is typically seen easily. Leads II and V5 usually provide the best delineation of the T wave. Corrections for heart rates are usually made with the Bazett formula, although it may be inaccurate at heart rates 40 beats per minute and >120 beats per minute [18]. Consensus statements on ECG interpretation in athletes have recommended that male athletes with a QTc >470 milliseconds and female athletes with a QTc >480 milliseconds undergo further evaluation for long QT syndrome (LQTS) to better balance false-positive and false-negative findings [1,9]. Recording QTc intervals beyond the normal cutoff values should raise the suspicion of either acquired or congenital LQTS. The most frequent cause is congenital LQTS, a potentially lethal ventricular arrhythmia syndrome with the hallmark ECG feature of QT prolongation. Symptoms, if present, include arrhythmic syncope, seizures, or aborted cardiac arrest/sudden death stemming from torsades de pointes and VF. Athletes with an occasional finding of a QTc interval above the normal limits should have repeated ECG evaluations. Indeed, personal symptoms, family history, the scoring systems, the QTc changes during exercise, and recovery and genetic testing are needed to clarify the https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 8/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate diagnosis. Since the risk of cardiac events during sports activities is largely gene specific, genetic testing and cascade screening of family members should be performed following a clinical diagnosis of LQTS. Individuals with LQT1 are at highest risk during stressful exercise. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations".) Brugada pattern and syndrome Clinical concern for this syndrome is based primarily on the presence of the so-called type 1 Brugada pattern, which is defined as coved-type ST-segment elevation 2 mm followed by a negative T wave in 1 of the right precordial leads positioned in the fourth, third, or second intercostal space, noted either spontaneously or following provocation by a sodium ion channel blocker ( waveform 3). Confirmation of proper precordial lead placement is paramount, as high placement of the V1 and V2 electrodes in the second and/or third intercostal spaces (rather than the fourth intercostal space) can accentuate a type 1 Brugada ECG pattern and result in a false diagnosis. Patients with typical ECG features who are asymptomatic and have no other clinical criteria are said to have Brugada pattern, whereas patients with typical ECG features who have experienced SCD or a sustained ventricular tachyarrhythmia, or who have one or more of the other associated clinical criteria, are said to have Brugada syndrome. (See "Brugada syndrome: Epidemiology and pathogenesis", section on 'Brugada pattern versus Brugada syndrome'.) Although Brugada syndrome is associated with an increased risk of SCD, such events in patients with the Brugada pattern type 1 are typically not related to exercise, and Brugada syndrome has not been noted as a cause of SCD in athletes [19-21]. The type 1 Brugada ECG pattern is not a recognized variant of athlete's heart and should raise the possibility of a sodium ion channelopathy. Patients with a type 1 ECG pattern should be referred to a cardiac electrophysiologist for further evaluation, regardless of symptoms. There is general agreement that type 2 Brugada pattern should not be considered diagnostic for the pathologic variant, and should not prompt any testing, unless in the presence of the disease in the family or suspicious symptoms (ie, syncope). (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation" and "Athletes: Overview of sudden cardiac death risk and sport participation", section on 'Brugada syndrome'.) Profound sinus bradycardia Well-conditioned athletes, particularly endurance athletes, frequently exhibit some degree of sinus bradycardia with PR interval prolongation and even Mobitz type I (Wenckebach) second-degree AV block due to physiologically enhanced cardiac vagal tone. This is more likely when the patient is at rest or asleep. However, profound sinus bradycardia <30 beats per minute and/or PR prolongation >400 milliseconds are unusual in athletes and may be a marker of underlying cardiac disease. https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 9/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate In most athletes, a formal or informal exercise test documenting an appropriate response of HR and PR interval with exercise is satisfactory. However, if there are concerns of an inadequate chronotropic response to exercise, additional testing (eg, echocardiogram, ambulatory ECG monitoring) should be pursued. Advanced AV block Second degree AV block: Mobitz type II Mobitz type II second degree atrioventricular (AV) block ( waveform 4) is usually due to disease in the His-Purkinje system. Mobitz type II AV block is identified by consistent unchanging PR intervals (which are usually normal in duration but may be prolonged) followed by the block of one or more P waves that fail to conduct to the ventricles. Mobitz type II second degree AV block is by nature unstable and requires prompt evaluation. (See "Second-degree atrioventricular block: Mobitz type II" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Second degree AV block: Mobitz type II'.) Acquired third degree (complete) AV block Patients with third degree (complete) AV block will have evidence of atrial (P waves) and ventricular (QRS complexes) activity that are independent of each other on the surface ECG. When acquired and in the AV node, complete AV block ( waveform 5) escape rhythms are often junctional with a narrow QRS complex. By contrast, the escape rhythm is ventricular with a wide QRS complex when complete AV block is due to structural disease of the His-Purkinje system ( waveform 6). Regardless of the etiology, third degree (complete) AV block requires prompt evaluation. (See "Third-degree (complete) atrioventricular block" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Third degree (complete) AV block'.) Congenital third degree (complete) AV block Congenital complete AV block is due to disease in the AV node, often occurring in the absence of other structural cardiac abnormalities. Most patients have a narrow complex and junctional escape rhythm. These patients will also require cardiac evaluation. (See "Congenital third-degree (complete) atrioventricular block".) Evaluation of athletes with advanced AV block In athletes with evidence of advanced AV block (either Mobitz type II second degree AV block or third degree [complete] AV block), further evaluation typically includes an echocardiogram, ambulatory ECG monitoring, and an exercise ECG test. Based on these results, laboratory testing and CMR imaging may be considered. Referral to a heart rhythm specialist is essential. Atrial fibrillation and atrial flutter AF, which may be present intermittently or persistently, is the most common arrhythmia in clinical practice, increasing in incidence with age, including older athletes. Among younger athletes, AF is relatively rare, with an incidence of approximately https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 10/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate 3 in 1000 athletes in one study [22]. Atrial flutter is uncommon in athletes. AF and atrial flutter are rarely life-threatening and usually lead to symptoms like palpitations, shortness of breath, chest pressure, dizziness, neck pounding, or syncope from rapid heart rates. In young athletes, AF may occur in the absence of any structural heart disease or other provoking condition and is termed "lone AF." However, in older athletes, hypertension and coronary artery disease are common underlying conditions. Moreover, AF or flutter can be associated with other conditions that can lead to SCD, including WPW, Brugada syndrome, myocarditis, congenital heart disease, and any form of cardiomyopathy. When AF or flutter is found, a comprehensive clinical evaluation is advised, including echocardiogram to assess for structural heart disease. Anticoagulation is considered based on standard guidelines (CHA DS - 2 2 VASc score). Subsequent investigation should be directed as needed based on the clinical findings. (See "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Atrial fibrillation' and "Overview of atrial flutter" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Atrial flutter' and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation", section on 'Evaluation'.) Supraventricular tachyarrhythmias AV nodal reentrant tachycardia (AVNRT) is a common arrhythmia in young people and is often associated with symptoms resulting from a rapid heart rate. (See "Atrioventricular nodal reentrant tachycardia" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Atrioventricular nodal reentrant tachycardia'.) AV reentrant tachycardia (AVRT) occurs in patients with manifest WPW syndrome or a concealed (ie, not seen on 12-lead ECG) bypass tract. This arrhythmia may have a narrow QRS complex when ventricular activation is via the normal AV node-His Purkinje system (orthodromic AVRT) or, less commonly, a wide QRS complex when ventricular activation is via the accessory pathway (antidromic AVRT). It should be noted, however, that a wide complex tachycardia with an orthodromic AVRT may also be observed if there is aberrant conduction. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Wolff-Parkinson-White syndrome'.) Atrial tachycardia may be due to an automatic focus or reentry; these arrhythmias are not commonly seen in athletes ( table 1). (See "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Atrial tachycardia'.) Detection on ECG (or suspicion from history) of supraventricular tachyarrhythmias should prompt evaluation, including an echocardiogram, ambulatory ECG monitor, and exercise https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 11/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate treadmill test, and referral to a heart rhythm specialist is generally indicated for consideration of electrophysiology study and ablation. Individuals with proven supraventricular tachycardia without preexcitation should be educated on how to perform vagal maneuvers (such as carotid sinus massage or, preferably, Valsalva maneuver) to facilitate termination of the arrhythmia. Ventricular premature beats Ventricular premature beats (VPBs) are common in athletes of all age groups and occur in those with or without structural heart disease. VPBs may be idiopathic or secondary to the cardiomyopathies, ion channelopathies, or other diseases such as myocarditis, myocardial infarction, or sarcoidosis. The presence of two or more VPBs in a 10- second ECG tracing is considered abnormal and warrants further investigation. Largely, their prognostic importance is based upon the possible association with underlying structural heart disease ( table 1). Exclusion of underlying cardiac disease is the first step in these individuals and should be performed with echocardiography. With regard to the ECG characteristics, the morphology of the VPBs is relevant, with those presenting with an RBBB or LBBB, wide QRS, and superior axis (originating from the left ventricle or RV free wall) and those exacerbating during effort having high index of suspicion for underlying cardiac disease. Additional features associated with higher probability of cardiac disease are the high frequency (>2000 VPBs in 24- hour ECG monitoring) and the complexity (couplets, or nonsustained ventricular tachycardia [VT] associated to VPBs) [9]. Athletes with VPBs who do not have structural heart disease do not appear to have an increased risk of cardiovascular events [23,24]. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Ventricular premature beats'.) Ventricular tachycardia Monomorphic VT may be idiopathic (eg, RV outflow tract VT or left anterior fascicular [Belhassen-type]) or secondary to underlying cardiac disease. Most otherwise fit individuals who present with polymorphic VT have underlying structural heart disease. Further evaluation is essential for either of these presentations. The evaluation should include a thorough family history, an echocardiogram to evaluate for structural heart disease, ambulatory ECG monitoring, and an exercise ECG test. Depending on the results, further evaluation may be indicated, including CMR imaging to assess for arrhythmogenic RV cardiomyopathy or other cardiomyopathies, or genetic testing. All individuals with sustained monomorphic or polymorphic VT should be referred to a heart rhythm specialist. (See "Cardiac evaluation of the survivor of sudden cardiac arrest" and "Ventricular tachycardia in the absence of apparent structural heart disease" and "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Ventricular arrhythmias'.) https://www.uptodate.com/contents/athletes-with-arrhythmias-electrocardiographic-abnormalities-and-conduction-disturbances/print 12/27 7/5/23, 10:33 AM Athletes with arrhythmias: Electrocardiographic abnormalities and conduction disturbances - UpToDate SUMMARY AND RECOMMENDATIONS Prevalence A broad range of ECG abnormalities can be seen in trained athletes, particularly increased QRS voltage and repolarization abnormalities ( table 1). (See 'Prevalence' above.) Clinical approach to reading the ECG in athletes For practical purposes, ECG changes in athletes can be classified into three main groups ( figure 1): one related to whether the ECG abnormality is likely to be a physiologic result of chronic training (normal ECG changes in athletes), one in which the ECG finding is borderline abnormal, and the third related to whether the ECG finding occurs independently of training and thus may be an expression of a pathologic condition (borderline or abnormal ECG changes in athletes). (See 'Clinical approach to reading the ECG in athletes' above.) Normal ECG findings Common ECG abnormalities ("normal" in athletes) are frequent and are not associated with an increased risk of underlying cardiac disease and incidence of adverse events during exercise. (See 'Normal ECG findings' above.) Borderline ECG findings Borderline ECG findings may represent pathologic or innocent ECG alterations. (See 'Borderline ECG findings' above.) Abnormal ECG findings Abnormal ECG findings are significantly more likely to represent pathology rather than a normal response to training. As such, patients with an abnormal ECG finding should undergo further evaluation to search for cardiac pathology. (See 'Abnormal ECG findings' above.) Sport participation The approaches to risk stratification and returning to participation/competition in athletes who have an abnormal ECGs or a cardiovascular disease are discussed in detail separately. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Athletes with arrhythmias: Treatment and returning to athletic participation".) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Maron BJ, Levine BD, Washington RL, et al. 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