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Domenico Corrado, Antonio Pelliccia, Hein Heidbuchel, Sanjay Sharma, Mark Link, Cristina Basso, Alessandro Biffi, Gianfranco Buja, Pietro Delise, Ihor Gussac, Aris Anastasakis, Mats Borjesson, Hans Halvor Bjørnstad, François Carrè, Asterios Deligiannis, Dorian Dugmore, Robert Fagard, Jan Hoogsteen, Klaus P. Mellwig, Nicole Panhuyzen-Goedkoop, Erik Solberg, Luc Vanhees, Jonathan Drezner, N.A. Mark Estes, Sabino Iliceto, Barry J. Maron, Roberto Peidro, Peter J. Schwartz, Ricardo Stein, Gaetano Thiene, Paolo Zeppilli, William J. McKenna, on behalf of the Sections of Sports Cardiology of the European Association of Cardiovascular Prevention and Rehabilitation; and the Working Group of Myocardial and Pericardial Disease of the European Society of Cardiology, Recommendations for interpretation of 12-lead electrocardiogram in the athlete, European Heart Journal, Volume 31, Issue 2, January 2010, Pages 243–259, https://doi.org/10.1093/eurheartj/ehp473
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Abstract
Cardiovascular remodelling in the conditioned athlete is frequently associated with physiological ECG changes. Abnormalities, however, may be detected which represent expression of an underlying heart disease that puts the athlete at risk of arrhythmic cardiac arrest during sports. It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential cardiac pathology. The present article represents the consensus statement of an international panel of cardiologists and sports medical physicians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and management of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. The aim of the present position paper is to provide a framework for this distinction. For every ECG abnormality, the document focuses on the ensuing clinical work-up required for differential diagnosis and clinical assessment. When appropriate the referral options for risk stratification and cardiovascular management of the athlete are briefly addressed.
Comments
We have read the excellent report by Corrado et al. (1) regarding ECG changes in athletes and how we can differentiate them from the Brugada ECG pattern, especially the QRS-T pattern in V1-V2.
The review is full of excellent advice and recommendations, but we would like to point out some areas that we think need to be commented on and clarified.
1) According to this report (1), the index ST elevation at J point / ST elevation after 80 ms measured in V1 distinguishes Brugada pattern presenting a ratio > 1 from athletes with a ratio < 1. Corrado et al. believe that the high take-off of QRS-ST in V1 coincides with the J point, as seen in Figure 8 in the report (1). This is not true, however. In general, when the ECG recording is performed simultaneously in various leads, as is well known and recently clearly demonstrated by Postema (2), the J point, that coincides with the end of QRS, appears later than the high take-off of QRS-ST, not only in Brugada syndrome but also in athletes. Therefore, in order to compare the ECG patterns of Brugada patients and athletes, or even other cases with rSr' in V1-V2, such as patients with pectus excavatum, the measurement of the index J point/80 msec. must not be made starting at high take-off of QRS in V1, but to the end of QRS. To determine exactly where the J point is, we have to record several leads simultaneously. This is not required for athletes and pectus excavatum patients because in these cases the end of QRS in V1- V2 is usually very visible but it is not at high take-off. The index measured according to what we have now exposed (ST elevation at end of QRS/80 msec.) will most probably also be useful for the differential diagnosis, but it will be necessary to confirm this.
2) The fact that QRS ends later than the high take-off of QRS-ST, and therefore the J point does not coincide with this high take-off, favours the hypothesis that the changes in V1-V2 in Brugada syndrome are due, at least partially, to a depolarization delay.
3) We agree with the comment that "the prevalence of incomplete right bundle branch block (RBBB) (QRS duration <120 ms) has been estimated to range from 35 to 50% in athletes compared with less than 10% in young, healthy controls. The ECG pattern is more often noted in athletes engaged in endurance sports, with a striking male preponderance. It has been suggested that the right ventricular (RV) conduction delay is not within the specialized conduction system, but is caused by the enlarged RV cavity size/increased cardiac muscle mass and the resultant increased conduction time". However, later in the paper when the topic right ventricular hypertrophy (RVH) is discussed, the authors mention that "electrocardiogram evidence of right atrial enlargement and/or RV hypertrophy are uncommon findings in athletes". There are some discrepancies in these two affirmations. The authors should state that very often incomplete RBBB is seen in athletes as a marker of RVH, even in the absence of classical ECG criteria for RVH (3).
Antonio Bayes de Luna
Javier Garcia Niebla
Diego Goldwasser
References
1. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J. 2010;31:243.
2. Postema PG, van Dessel PF, Kors JA, et al. Local depolarization abnormalities are the dominant pathophysiologic mechanism for type 1 electrocardiogram in Brugada syndrome: a study of electrocardiograms, vectorcardiograms, and body surface potential maps during ajmaline provocation. J Am Coll Cardiol 2010;55:789.
3. Bayes de Luna A. Clinical electrocardiography: A textbook. Futura publishing. New York 1993. Page 476.
Conflict of Interest:
None declared