Does early repolarization in the athlete have analogies with the Brugada syndrome?

Bianco, Massimiliano; Bria, Serena; Gianfelici, Antonio; Sanna, N.; Palmieri, Vincenzo; Zeppilli, Paolo

doi:10.1053/euhj.2000.2247

Cited by 84 publications

(52 citation statements)

References 15 publications

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“…11 In order to distinguish the normal ST segment elevation observed in athletes from that of Brugada syndrome, the magnitude of the ST elevation and the QRS duration may be useful. 8 Therefore, not only ST segment elevation, but also the S wave width should be measured to detect high-risk patients and we propose an S wave width in V1 ≥0.08 s and ST segment elevation ≥0.18 mV as new criteria for high-risk Brugada syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…4 On the other hand, symptomatic patients often need an implantable cardioverter defibrillator (ICD) because of a high incidence of recurrence. 5,6 Recent reports 7,8 have suggested an important contribution of intraventricular conduction delay to the onset of lethal ventricular arrhythmias and so we hypothesized that there might be some findings on the standard 12-lead electrocardiogram (ECG) reflecting intraventricular conduction delay that could be used to distinguish highand low-risk patients. In order to clarify the ECG characteristics that could be useful for the diagnosis of high-risk Brugada syndrome, we reviewed 12-lead ECGs from the Japanese Brugada syndrome registry.…”

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confidence: 99%

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New ECG Criteria for High-Risk Brugada Syndrome.

Atarashi

Ogawa

2003

Circ J

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ince Brugada and Brugada 1 reported a unique electrocardiographic syndrome that is predominantly diagnosed in males and often associated with ventricular fibrillation (VF), much attention has been paid to the detection of a right bundle branch block pattern associated with bizarre ST elevation in the right precordial leads (V1-3). In clinical practice, it is very important to identify patients who have a high risk of developing VF and sudden death, and for this purpose, ST elevation in the precordial leads is not very useful because it varies in shape and amplitude day by day 2 and is also dependent on electrode positioning. 3 We have investigated the prevalence of Brugada syndrome in the working Japanese population, and our 3-year follow-up data demonstrated a very low cardiac event rate in asymptomatic patients. 4 On the other hand, symptomatic patients often need an implantable cardioverter defibrillator (ICD) because of a high incidence of recurrence. 5,6 Recent reports 7,8 have suggested an important contribution of intraventricular conduction delay to the onset of lethal ventricular arrhythmias and so we hypothesized that there might be some findings on the standard 12-lead electrocardiogram (ECG) reflecting intraventricular conduction delay that could be used to distinguish highand low-risk patients. In order to clarify the ECG characteristics that could be useful for the diagnosis of high-risk Brugada syndrome, we reviewed 12-lead ECGs from the Japanese Brugada syndrome registry. MethodsWe reviewed standard 12-lead ECGs that were on file at the Japanese Brugada syndrome registry 2,4 and selected 60 from 60 patients because their quality was sufficient for accurate measurement of the QRS width and ST amplitude in the right precordial leads. All ECGs were recorded at a paper speed of 25 mm/s. The ECGs were from 17 patients with a history of VF, 9 patients with episodes of syncope, and 34 asymptomatic patients (Table 1). We measured the width of the S wave and ST segment elevation in leads V1 and V2 because there is usually a prominent r' in Brugada syndrome and either of these 2 leads shows the maximum ST segment elevation. We thought that conduction delay might be detected at the terminal portion of the QRS deflection, so the S wave of V1 and V2 was measured from the tip of r to the tip of r', and the amplitude of the ST segment was measured at 0.08 s from the J point. These measurement were made by 2 cardiologist who were unaware of the clinical information about the patients. Magnification was used to minimize the measuring error. When the measured values were not identical, the mean value of the 2 measurements was calculated. Data AnalysisAll variables are reported as the mean ± SD for each group. The nonparametric Mann-Whitney U test was used to assess the significance of differences between the groups. Correlations between the presence or absence of Circ J 2003; 67: 8 -10 (Received August 21, 2002; revised manuscript received October 3, 2002; accepted October 15, 2002) Department of Internal Med...

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Section: Discussionmentioning

confidence: 99%

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New ECG Criteria for High-Risk Brugada Syndrome.

Atarashi

Ogawa

2003

Circ J

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“…Between 40 and 80% of endurance athletes exhibit abnormal resting 12-lead echocardiograms (ECGs). [74][75][76] Abnormal ECGs were found to be more common in male than female athletes. 77,78 Of the abnormalities detected in athletes of both sexes, the most common findings were Q waves, T-wave inversions, left-axis deviation, ST depression, and prolonged QTc.…”

Section: Sudden Cardiac Deathmentioning

confidence: 99%

Gender- and Sex-specific Sports-related Injury Research in Emergency Medicine: A Consensus on Future Research Direction and Focused Application

et al. 2014

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Title IX, the commercialization of sports, the social change in sports participation, and the response to the obesity epidemic have contributed to the rapid proliferation of participation in both competitive organized sports and nontraditional athletic events. As a consequence, emergency physicians are regularly involved in the acute diagnosis, management, disposition, and counseling of a broad range of sports-related pathology. Three important and highly publicized mechanisms of injury in sports relevant to emergency medicine (EM) include concussion, heat illness, and sudden cardiac death. In conjunction with the 2014 Academic Emergency Medicine consensus conference "Gender-specific Research in Emergency Care: Investigate, Understand, and Translate How Gender Affects Patient Outcomes," a consensus group consisting of experts in EM, emergency neurology, sports medicine, and public health convened to deliberate and develop research questions that could ultimately advance the field of sports medicine and allow for meaningful application in the emergency department (ED) clinical setting. Sex differences in injury risk, diagnosis, ED treatment, and counseling are identified in each of these themes. This article presents the consensus-based priority research agenda.

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“…Sharma et al (1999) found that almost half of elite junior athletes had voltage criteria for left ventricular hypertrophy. ST segment elevation soon after the QRS complex, known as 'early repolarization', appears to be a normal feature of the ECG in athletes (Bianco et al 2001). In a study of repolarization in over 1200 athletic students, Bjornstad et al (1994) found that the mean QRS-T angle was significantly greater in athletes, and U waves were more prominent.…”

Section: Ecg Abnormalities In Athletesmentioning

confidence: 99%

Physiological Society Symposium – the Athlete's Heart

Hart¹

2003

Experimental Physiology

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Exercise training is accompanied by hypertrophy of the heart, both in man and in experimental animals (Schaible & Scheuer, 1985;Moore & Korzick, 1995). The aim of this brief review is to summarize what is known about the electrophysiology of exercise-induced hypertrophy, and to relate the cellular data to the cardiac changes that are seen in trained athletes. Relatively little work has been carried out on the electrophysiology of exercise-induced hypertrophy in comparison with cardiac hypertrophy from other causes. Therefore it is necessary to begin by summarizing the principal cellular features of cardiac hypertrophy in general. What is cardiac hypertrophy?Cardiac hypertrophy means a relative increase in cardiac mass, and it represents the principal long-term response of the heart to increased wall stress. In experimental studies, the most commonly used index of the presence and severity of hypertrophy is the heart : body weight ratio (Hart, 1994). This may increase by 10-15 % in mild hypertrophy, and by more than 50 % in severe hypertrophy associated with Cardiac hypertrophy is a general term signifying an increase in cardiac mass in response to applied stress. In mild, early hypertrophy, cardiac myocyte contractile performance may be normal or enhanced, whereas in severe hypertrophy associated with cardiac failure, myocyte contraction is reduced in amplitude and increased in duration. In contrast to the varied contractile response, the duration of electrical excitation shows similar changes in both mild and severe hypertrophy. Action potential duration in mid-myocardial and sub-epicardial layers is increased, which is associated with ventricular arrhythmias (in a similar manner to the long QT syndromes from other causes), based on afterdepolarizations and enhanced automaticity. Single-cell studies following exercise training in animal models show that exercise-induced cardiac hypertrophy displays features similar to mild, compensated hypertrophy from other causes. Developed shortening of unloaded single cells is increased or unchanged, and developed force in single myocytes is enhanced. Action potential duration is increased, apart from in the sub-endocardial layer. As with mild hypertrophy from other causes, this will be pro-arrhythmic because of altered dispersion of repolarization and enhanced automaticity. Major abnormalities of the ECG in man include frequent and complex ventricular ectopy, ST segment changes and prolongation of repolarization. In this review a case is presented for regarding exercise-induced cardiac hypertrophy as being no different from mild cardiac hypertrophy resulting from other, pathological causes. The cellular electrophysiological changes are sufficient to account for many of the abnormalities of the ECG, including high-grade ventricular ectopy. Sudden death in trained athletes who have no evidence of specific heart disease may be a direct consequence of cardiac hypertrophy and altered repolarization. Experimental Physiology (2003) 88.5, 639-644.

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Does early repolarization in the athlete have analogies with the Brugada syndrome?

Cited by 84 publications

References 15 publications

New ECG Criteria for High-Risk Brugada Syndrome.

New ECG Criteria for High-Risk Brugada Syndrome.

Gender- and Sex-specific Sports-related Injury Research in Emergency Medicine: A Consensus on Future Research Direction and Focused Application

Physiological Society Symposium – the Athlete's Heart

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