Electrocardiographic right and left bundle branch block patterns in athletes: Prevalence, pathology, and clinical significance

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ScienceDirect Journal of Electrocardiology 48 (2015) 380 – 384 www.jecgonline.com

Review

Electrocardiographic right and left bundle branch block patterns in athletes: Prevalence, pathology, and clinical significance☆ Jonathan H. Kim, MD, a Aaron L. Baggish, MD b,⁎ a

Emory Clinical Cardiovascular Research Institute, Atlanta, GA, USA b Cardiovascular Performance Program, Boston, MA, USA

Abstract

Differentiating benign electrocardiographic (ECG) patterns in athletes from those representative of underlying cardiac pathology is both clinically relevant and challenging. Complete right (RBBB) and left (LBBB) bundle branch block are relatively rare in asymptomatic athletic populations, and current expert consensus guidelines recommend further clinical investigation upon detection of either ECG pattern. However, present data suggest that typical RBBB is not associated with structural cardiac pathology and may alternatively represent an ECG marker of exercise-induced right ventricular remodeling. In accordance with current guidelines, the presence of asymptomatic LBBB in athletes is not associated with normal exercise physiology and more likely indicative of underlying cardiac pathology. While long-term outcomes for asymptomatic athletes with RBBB or LBBB remain unknown, current evidence regarding these ECG patterns should be considered to improve the specificity of future athlete-specific ECG interpretation guidelines. © 2015 Elsevier Inc. All rights reserved.

Keywords:

Bundle branch block; Athlete; ECG; Screening

Introduction Tragically, the first manifestation of cardiac disease in athletes is often sudden cardiac death (SCD). The 12-lead electrocardiogram (ECG) may enhance the ability to detect occult structural and electrical cardiac pathology in athletes. Accordingly, various governing bodies within sport and the European Society of Cardiology have recommended mandatory utilization of 12-lead ECG during the pre-participation evaluation of young athletes [1–3]. Accurately differentiating benign ECG patterns from those indicative of underlying cardiac pathology in athletes may be challenging. Despite several expert consensus documents carefully outlining “training related” versus “training unrelated” athletic ECG patterns [2,4,5], false positive rates, defined as the absence of direct ECG correlation with underlying structural cardiac pathology, remain between 4% and 15% [4–7]. While the American Heart Association endorses a targeted pre-participation evaluation comprised of only medical history and physical examination [8], a significant number of US professional ☆

Disclosures: The authors have no relevant disclosures or conflicts of interest to report. ⁎ Corresponding author at: Cardiovascular Performance Program, Massachusetts General Hospital, 55 Fruit Street, Yawkey Suite 5B, Boston, MA 02114, U.S.A. E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2015.03.015 0022-0736/© 2015 Elsevier Inc. All rights reserved.

sporting teams and universities employ ECG-inclusive preparticipation protocols. In addition, a growing number of private organizations offer screening ECGs to communitybased athletes. As such, refining the specificity and decreasing the rate of false positive ECG interpretations in athletes remains a high priority. Recent data have advanced our understanding of what constitutes both adaptive ECG patterns and those that are unrelated to athletic training [9], and therefore emphasize the need for critical reappraisal of contemporary athlete ECG interpretation criteria. Currently, the specific ECG patterns of complete right bundle branch block (RBBB) and left bundle branch block (LBBB) in athletes are considered training unrelated patterns that warrant further clinical investigation [2,4,5]. This review provides an overview of the anatomy and physiology of bundle branch block and an up-to-date summary of the data evaluating both RBBB and LBBB in athletes and their differential relationships with underlying cardiac pathology.

Anatomy and physiology of the bundles In the early 1900s, Eppinger and Tothberger first discovered the classic bundle branch block ECG patterns upon injecting canine myocardium with silver nitrate [10]. At present, the electrogenesis of RBBB and LBBB continue

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to be further elucidated in humans. Anatomically, it is known that electrical conduction originates from the sinoatrial (SA) node, spreads through both atria and specialized tissue at the atrioventricular (AV) junction (including the AV node and His bundle), and then separates into the bundle branches activating both the right (RV) and left ventricle (LV). The bundle that supplies the LV further separates into a narrow anterior fascicle, broad posterior fascicle, and a third septal segment that originates from smaller branches from each of the fascicles [11]. Ultimately, conduction spreads within the ventricular myocardium via specialized Purkinje fibers. Normal electrical activation of the ventricles originates from the left side of the interventricular septum, which under normal physiology manifests as a small septal r wave in lead V1 and Q-wave in lead V6. Propagation of this stimulus then travels through both ventricles with the LV maintaining electrical predominance on surface recordings of electrical conduction. In RBBB, only the third sequence of ventricular depolarization (RV depolarization) is delayed with septal and LV activation unaffected. In the presence of LBBB, ventricular depolarization initiates on the right side of the interventricular septum with subsequent delayed activation of the LV. Although the exact electrical activation sequence in LBBB is highly complex with variability in the location and length of block, LV depolarization propagates in a non-homogeneous and dyssynchronous fashion, previously described as a “U-shaped” activation pattern [12]. The disruption in the conduction system imparted by both RBBB and LBBB manifests on the 12-lead ECG. The diagnosis of RBBB is established based on the following findings: (1) QRS duration N 120 ms in the presence of normal sinus or other supraventricular rhythm, (2) R-wave or RSR′ complex in lead V1, and (3) an R-complex with a prolonged, shallow S-wave in lead V5, V6, aVL or I [13]. Incomplete right bundle branch block (IRBBB) is defined by a QRS duration b 120 ms and an R′ or r′ wave in either lead V1 or V2[13]. The benefits of cardiac resynchronization therapy in clinical heart failure management have led to renewed interest in defining the exact electrical activation patterns of morphologic LBBB [14]. Consequently, controversy has arisen in accurately defining electrocardiographic LBBB [14]. Although several criteria in the literature now exist [14], previous studies focused on athletic ECG interpretation of LBBB have utilized: (1) QRS-complex duration N 120 ms in the presence of normal sinus or other supraventricular rhythm, (2) QS- or RS-complex in lead V1, (3) broad or notched R-waves in leads V5 and V6, or an RS pattern, and (4) the absence of Q-wave in lead V5, V6 or I [13]. Incomplete left bundle branch block is defined by a QRS duration ≥ 100 ms and b 120 ms in leads I, aVL, and V5 or V6[13]. Right bundle branch block Prevalence Although mostly cross-sectional in design, there have been many studies evaluating the presence of ECG abnormalities in

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athletes [7,15–27]. It has been well established that IRBBB is common, particularly among endurance athletes [21]. More recent studies inclusive of large cohorts of athletes have demonstrated IRBBB in 10–20% of athletes [16,20]. In the largest observational cohort of 32,652 amateur Italian athletes, Pelliccia et al. reported that IRBBB was present in 7% of the cohort [28]. Complete RBBB is far less common and has a reported incidence ranging from 0.2% to 3% of athletes [7,15–27]. Compared to healthy members of the general population, the prevalence of RBBB in athletes appears increased. In the largest study evaluating the prevalence and outcomes of those in the general population with RBBB and free of cardiovascular disease, Bussink et al. reported that RBBB was present in approximately 1% of a cohort of 18,441 subjects. On closer inspection, in the 1866 subjects who were 30 years or younger, RBBB was observed in approximately 0.5% [29]. Significance RBBB in endurance athletes may be a marker of physiologic adaptations that accompany the repetitive volume challenge inherent in isotonic/dynamic exercise. We conducted a study analyzing 510 collegiate, primarily endurance, athletes with both 12-lead ECG and 2-D echocardiography with Doppler and found that athletes with IRBBB and RBBB demonstrated increased biventricular chamber dimensions, relative reductions in RV systolic function, and interventricular dyssynchrony compared to those athletes with normal QRS duration [21]. Moreover, the degree of change in RV size and function correlated with increasing QRS duration and previously quantified exercise exposure. It is therefore plausible that exercise-induced RV enlargement may lead to stretching of RV Purkinje fibers, resultant delayed RV depolarization, and the development of RBBB as an ECG marker of physiologic right ventricular adaptation. Although recent data have challenged asymptomatic RBBB as a benign finding in the general population [29], prior evidence has supported that asymptomatic RBBB is not associated with future cardiovascular events and does not require further diagnostic evaluation [30,31]. Specific to athletes, McClaskey et al. recently reviewed prior longitudinal studies (1966 to present) of outcomes among athletes with ECG abnormalities [32]. Although adverse cardiovascular outcomes were noted in two studies inclusive of athletes with bundle branch block (combined total of 279 athletes at longitudinal mean follow-up of 5 years; 4 athletes with angina and 1 with acute myocardial infarction) [33,34], it was not specified in either study if the respective adverse outcomes occurred in the athletes with bundle branch block [33,34]. Pathologic correlations In the absence of clinical symptoms or associated right precordial repolarization abnormalities suggestive of arrhythmogenic right ventricular cardiomyopathy (ARVC), the presence of IRBBB should not be considered representative of underlying cardiac pathology [29]. No previous work examining asymptomatic athletes with RBBB has

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demonstrated an association between RBBB and underlying cardiac pathology [7,15–27]. However, “atypical” RBBB as characterized by extensive repolarization abnormalities (ST-segment elevation, markedly prolonged R′ associated with wide QRS duration, and epsilon waves) should not be interpreted as a benign ECG finding. In a clinicopathologic study, Corrado et al. studied 96 cases of SCD in which a previous 12-lead ECG was available. In 4% of cases, RBBB associated with ST elevation in the right precordial leads, consistent with the Brugada Type I pattern, was present with post-mortem evidence of ARVC [35]. In addition, epsilon waves may be present in 30% of cases of ARVC [36]. Detection of these significant repolarization abnormalities in any asymptomatic patient with RBBB warrants further investigation. Left bundle branch block Prevalence The detection of LBBB in asymptomatic adults, including athletes, is rarer with an estimated prevalence ranging between 0.1% and 0.8% [19,23,25,37]. Notably, in a substantial number of studies documenting benign ECG abnormalities in athletic cohorts, no cases of LBBB were identified [15–18,20,22,24,26,27]. Significance and pathologic correlations As a consequence of the low prevalence of LBBB reported in athletic cohorts, data regarding LBBB clinical correlations and outcomes are limited. Previous cross-sectional data have provided some insight regarding pathologic correlations of LBBB in athletes. Pelliccia et al. studied 1005 elite Italian athletes and observed 2 with LBBB. In this landmark study, ECG patterns were correlated with cardiac anatomy as visualized by echocardiography. Although the majority of athletes categorized as demonstrating “distinctly abnormal”

ECG patterns (including LBBB) exhibited no underlying cardiac pathology, it was not specifically disclosed whether those athletes with LBBB had evidence of cardiovascular abnormalities [25]. In a separate study by our group designed to examine ECG patterns and underlying structural cardiac parameters in US collegiate athletes, LBBB was identified in 2 athletes, one of which was ultimately diagnosed with impaired left ventricular function secondary to post-viral myocarditis [23]. Finally, in a non-athletic study analyzing ECG features of patients with sarcomere mutation carriers with and without the phenotype of hypertrophic cardiomyopathy, LBBB was present in 1 (1/57, 2%) patient who was gene positive and also with pathologic LV hypertrophy [38]. Previous population-based epidemiologic studies have provided additional insight into the prognosis of patients with asymptomatically detected LBBB. In a large sample of 3983 subjects with 29 year follow-up, Rabkin et al. reported that subjects with LBBB were associated with increased cardiovascular morbidity and mortality compared to subjects without LBBB [39]. SCD was frequently the first manifestation of cardiovascular disease in those with LBBB [39]. In the Framingham study cohort of 5209 patients, 50% cardiovascular mortality occurred in those subjects (N = 55) who developed LBBB [40]. Clinical implications There are several important clinical implications regarding the detection of RBBB and LBBB in asymptomatic athletes. First, asymptomatic endurance athletes found to have isolated RBBB with QRS duration b 140 ms and without repolarization abnormalities aside from concordant T wave inversions in V1 and V2 are unlikely to harbor significant cardiovascular disease. In contrast, “atypical” RBBB, or RBBB associated with extensive repolarization abnormalities, is more likely representative of underlying structural cardiac disease. As shown in Table 1, the

Table 1 Studies among athletes utilizing both 12-lead electrocardiography and 2-D trans-thoracic echocardiography. Prevalence of incomplete right bundle branch block, complete right bundle branch block, left bundle branch block and correlation with structural cardiac disease. Year

Study

Total N

Athlete Cohort

IRBBB %

RBBB %

LBBB %

Structural Cardiac Diseasea

2014 2014 2014 2014 2013 2012 2011 2011 2011 2010 2007 2000 1997 1987

Brosnanet al.[15] Chandraet al.[16] Fudgeet al.[17] Brosnanet al.[7] Kervioet al.[18] Wilsonet al.[19] Papadakiset al.[20] Kimet al.[21] Noseworthyet al.[22] Baggishet al.[23] Maet al.[24] Pellicciaet al.[25] Fulleret al.[26] Maronet al.[27]

1261 4081 1339 1197 282 1355 2723 510 879 510 351 1005 146 501

Professional endurance Athletes 14–35 years-old Athletes 13–24 years-old Athletes 16–35 years-old Professional soccer National level Athletes 14–35 years-old Collegiate Collegiate Collegiate National level National level High school Collegiate

34 13 N/A 29 43 45 16 9 11 N/A 4 12 N/A 3

0.7 0.4 0.5 0.4 0.4 0.1 1 3 1.3 3 0 0.2 0–10d 0.2

0 0 0 N/A 0 0.1 0 N/A 0 0.4 0 0.2 0 0

No No Unknown No No LBBBb No No No LBBBc No Unknown No No

IRBBB: incomplete right bundle branch block; LBBB: left bundle branch block; RBBB: complete right bundle branch block. a Cardiac pathology resulting in sport restriction and related to IRBBB, RBBB, or LBBB. b One athlete with LBBB detected and found to have hypertrophic cardiomyopathy. c One athlete (out of 2) with LBBB diagnosed with myocarditis. d RBBB grouped with those with pre-excitation, ventricular premature beats, supraventricular tachycardia.

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compilation of evidence to date (specifically studies incorporating both ECG and echocardiographic data) supports isolated RBBB as a normal, training related ECG pattern. Second, RBBB appears to be a physiologic consequence of dynamic exercise and represents an ECG marker of exercise-induced cardiac remodeling. Confirmatory work is required, however, particularly given recent controversial and observational data that have implicated an association between endurance exercise and the development of an “exercise-induced” RV cardiomyopathy [41]. In contrast, the presence of LBBB in an athlete does not appear to represent a physiologic response to exercise. Although data are sparse, LBBB is more likely representative of structural heart disease, and there are several compelling epidemiologic studies that implicate LBBB as a marker of future cardiovascular morbidity and mortality. Therefore, in concurrence with the current guidelines, further work-up is warranted upon the detection of an asymptomatic athlete with LBBB. Future directions Although our understanding and interpretation of both RBBB and LBBB in the asymptomatic athlete has progressed over the last two decades, several unanswered questions and issues remain. First, given the paucity of longitudinal and gender-specific data for both RBBB and LBBB, the analysis of long-term outcomes in athletes, both male and female, with bundle branch block represents an important area of future study. For athletes continuing to engage in competitive sport with either RBBB or LBBB, the association of these ECG patterns with the development of cardiac disease and all-cause mortality has not been fully elucidated. Such study will require a longitudinal design and careful subject selection within large cohorts of athletes given the rare prevalence of both ECG patterns. Second, incorporation of endurance athletes with RBBB as a selection criterion should be implemented in future work assessing the long-term impact of endurance exercise on RV function. Whether RBBB is purely a healthy and physiologic consequence of exercise versus a predictor of future cardiomyopathy or arrhythmia is unknown and worthy of future longitudinal study. Finally, with current evidence supportive of RBBB as unrelated to underlying structural heart disease, addressing this in future ECG guidelines may improve the specificity of athlete-specific ECG interpretation.

Conclusions Refining the interpretation of 12-lead ECG in athletes remains clinically relevant and challenging. RBBB is unlikely to represent cardiac disease and may be an ECG marker of isotonic exercise physiology. In contrast, LBBB is significantly less common, does not appear to be related to normal physiology, and therefore warrants comprehensive investigation. The association between both RBBB and LBBB and long-term cardiovascular outcomes in athletes are not well known and is an important area of future study.

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References [1] Ljungqvist A, Jenoure P, Engebretsen L, Alonso JM, Bahr R, Clough A, et al. The International Olympic Committee (IOC) Consensus Statement on periodic health evaluation of elite athletes March 2009. Br J Sports Med 2009;43:631–43. [2] Pelliccia A, Fagard R, Bjørnstad HH, Anastassakis A, Arbustini E, Assanelli D, et al. Recommendations for competitive sports participation in athletes with cardiovascular disease: a consensus document from the Study Group of Sports Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J 2005;26:1422–45. [3] Borjesson M, Dellborg M. Is there evidence for mandating gram as part of the pre-participation examination? Clin J Sport Med 2011;21:13–7. [4] Drezner JA, Ackerman MJ, Anderson J, Ashley E, Asplund CA, Baggish AL, et al. Electrocardiographic interpretation in athletes: the “Seattle criteria”. Br J Sports Med 2013;47:122–4. [5] Sheikh N, Papadakis M, Ghani S, Zaidi A, Gati S, Adami PE, et al. Comparison of electrocardiographic criteria for the detection of cardiac abnormalities in elite black and white athletes. Circulation 2014;129:1637–49. [6] Wasfy MM, DeLuca J, Wang F, Berkstresser B, Ackerman KE, Eisman A, et al. ECG findings in competitive rowers: normative data and the prevalence of abnormalities using contemporary screening recommendations. Br J Sports Med 2014;49:200–6. [7] Brosnan M, La Gerche A, Kalman J, Lo W, Fallon K, MacIsaac A, et al. The Seattle Criteria increase the specificity of preparticipation ECG screening among elite athletes. Br J Sports Med 2014;48:1144–50. [8] Maron BJ, Friedman RA, Kligfield P, Levine BD, Viskin S, Chaitman BR, et al. Assessment of the 12-lead electrocardiogram as a screening test for detection of cardiovascular disease in healthy general populations of young people (12–25 years of age): a scientific statement from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol 2014;64:1479–514. [9] Gati S, Sheikh N, Ghani S, Zaidi A, Wilson M, Raju H, et al. Should axis deviation or atrial enlargement be categorised as abnormal in young athletes? The athlete's electrocardiogram: time for re-appraisal of markers of pathology. Eur Heart J 2013;34:3641–8. [10] Eppinger H, Rothberger CJ. Zur analyse des elektroardiogramms. Wien Klin Wochenschr 1909;22:1091–8. [11] Massing GK, James TN. Anatomical configuration of the His bundle and bundle branches in the human heart. Circulation 1976;53:609–21. [12] Auricchio A, Fantoni C, Regoli F, Carbucicchio C, Goette A, Geller C. Characterization of left ventricular activation in patients with heart failure and left bundle-branch block. Circulation 2004;109:1133–9. [13] Prineas RJ, Crow RS, Blackburn H. The Minnesota Code Manual of Electrocardiographic Findings. Standards and Procedures for Measurement and Classification. London: John Wright/PSG Inc.; 1982. [14] Strauss DG. Importance of defining left bundle branch block. J Electrocardiol 2012;45:505–7. [15] Brosnan M, La Gerche A, Kalman J, Lo W, Fallon K, MacIsaac A, et al. Comparison of frequency of significant electrocardiographic abnormalities in endurance versus nonendurance athletes. Am J Cardiol 2014;113:1567–73. [16] Chandra N, Bastiaenen R, Papadakis M, Panoulas VF, Ghani S, Duschi J, et al. Prevalence of electrocardiographic anomalies in young individuals: relevance to a nationwide cardiac screening program. J Am Coll Cardiol 2014;63:2028–34. [17] Fudge J, Harmon KG, Owens DS, Prutkin JM, Salerno JC, Asif IM, et al. Cardiovascular screening in adolescents and young adults: a prospective study comparing the Pre-participation Physical Evaluation Monograph 4th Edition and ECG. Br J Sports Med 2014;48:1172–8. [18] Kervio G, Pelliccia A, Nagashima J, Wilson MG, Gauthier J, Murayama M, et al. Alterations in echocardiographic and electrocardiographic features in Japanese professional soccer players: comparison to African-Caucasian ethnicities. Eur J Prev Cardiol 2013;20:880–8. [19] Wilson MG, Chatard JC, Carre F, Hamilton B, Whyte GP, Sharma S, et al. Prevalence of electrocardiographic abnormalities in West-Asian and African male athletes. Br J Sports Med 2012;46:341–7. [20] Papadakis M, Carre F, Kervio G, Rawlins J, Panoulas VF, Chandra N, et al. The prevalence, distribution, and clinical outcomes of

384

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

J.H. Kim, A.L. Baggish / Journal of Electrocardiology 48 (2015) 380–384 electrocardiographic repolarization patterns in male athletes of African/Afro-Caribbean origin. Eur Heart J 2011;32:2304–13. Kim JH, Noseworthy PA, McCarty D, Yared K, Weiner R, Wang F, et al. Significance of electrocardiographic right bundle branch block in trained athletes. Am J Cardiol 2011;107:1083–9. Noseworthy PA, Weiner R, Kim J, Keelara V, Wang F, Berkstresser B, et al. Early repolarization pattern in competitive athletes: clinical correlates and the effects of exercise training. Circ Arrhythm Electrophysiol 2011;4:432–40. Baggish AL, Hutter AM, Wang F, Yared K, Weiner RB, Kupperman E, et al. Cardiovascular screening in college athletes with and without electrocardiography: A cross-sectional study. Ann Intern Med 2010;152:269–75. Ma JZ, Dai J, Sun B, Ji P, Yang D, Zhang JN. Cardiovascular preparticipation screening of young competitive athletes for prevention of sudden death in China. J Sci Med Sport 2007;10:227–33. Pelliccia A, Maron BJ, Culasso F, Di Paolo FM, Spataro A, Biffi A, et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 2000;102:278–84. Fuller CM, McNulty CM, Spring DA, Arger KM, Bruce SS, Chryssos BE, et al. Prospective screening of 5,615 high school athletes for risk of sudden cardiac death. Med Sci Sports Exerc 1997;29:1131–8. Maron BJ, Bodison SA, Wesley YE, Tucker E, Green KJ. Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. J Am Coll Cardiol 1987;10:1214–21. Pelliccia A, Culasso F, Di Paolo FM, Accettura D, Cantore R, Castagna W, et al. Prevalence of abnormal electrocardiograms in a large, unselected population undergoing pre-participation cardiovascular screening. Eur Heart J 2007;28:2006–10. Bussink BE, Holst AG, Jespersen L, Deckers JW, Jensen GB, Prescott E. Right bundle branch block: prevalence, risk factors, and outcome in the general population: results from the Copenhagen City Heart Study. Eur Heart J 2013;34:138–46. Thrainsdottir IS, Hardarson T, Thorgeirsson G, Sigvaldason H, Sigfusson N. The epidemiology of right bundle branch block and its

[31]

[32]

[33]

[34] [35]

[36] [37]

[38]

[39] [40]

[41]

association with cardiovascular morbidity–the Reykjavik Study. Eur Heart J 1993;14:1590–6. Aro AL, Anttonen O, Tikkanen JT, Junttila MJ, Kerola T, Rissanen HA, et al. Intraventricular conduction delay in a standard 12-lead electrocardiogram as a predictor of mortality in the general population. Circ Arrhythm Electrophysiol 2011;4:704–10. McClaskey D, Lee D, Buch E. Outcomes among athletes with arrhythmias and electrocardiographic abnormalities: implications for ECG interpretation. Sports Med 2013;43:979–91. Lie H, Erikssen J. Five-year follow-up of ECG aberrations, latent coronary heart disease and cardiopulmonary fitness in various age groups of Norwegian cross-country skiers. Acta Med Scand 1984;216:377–83. Serra-Grima R, Puig T, Doñate M, Gich I, Ramon J. Long-term followup of bradycardia in elite athletes. Int J Sports Med 2008;29:934–7. Corrado D, Basso C, Buja G, Nava A, Rossi L, Thiene G. Right bundle branch block, right precordial ST-segment elevation, and sudden death in young people. Circulation 2001;103:710–7. Gemayel C, Pelliccia A, Thompson PD. Arrhythmogenic right ventricular cardiomyopathy. J Am Coll Cardiol 2001;38:1773–81. Hardarson T, Arnason A, Elíasson GJ, Pálsson K, Eyjólfsson K, Sigfússon N. Left bundle branch block: prevalence, incidence, follow-up and outcome. Eur Heart J 1987;8:1075–9. Lakdawala NK, Thune JJ, Maron BJ, Cirino AL, Havndrup O, Bundgaard H, et al. Electrocardiographic features of sarcomere mutation carriers with and without clinically overt hypertrophic cardiomyopathy. Am J Cardiol 2011;108:1606–13. Rabkin SW, Mathewson FA, Tate RB. Natural history of left bundlebranch block. Br Heart J 1980;43:164–9. Schneider JF, Thomas HE, Kreger BE, McNamara PM, Kannel WB. Newly acquired left bundle-branch block: the Framingham study. Ann Intern Med 1979;90:303–10. Heidbüchel H, Hoogsteen J, Fagard R, Vanhees L, Ector H, Willems R, et al. High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification. Eur Heart J 2003;24:1473–80.