- Email: [email protected]
A Long Lasting Electrocardiographic History
LETTER TO THE EDITOR To the Editor: A Long Lasting Electrocardiographic History The syndrome of right bundle branch block and STsegment elevation, now called the Brugada syndrome, was initially described in 19881 and 1989.2 The first patient presented in both of these publications (in Martini et al,2 this patient is number 3) was a 44-year-old man (now age 69) who had cardiac arrest while talking with his postman. He was successfully defibrillated. His initial electrocardiogram (ECG) suggested ischemic heart disease because of STsegment elevation, but coronary angiography showed no obstructive lesion. Right ventricular angiography and magnetic resonance imaging study were not performed. An electrophysiologic study showed conduction delay at the right ventricular outflow tract.1 Neither ventricular tachycardia nor ventricular fibrillation was induced at the electrophysiological study. In the subsequent years, a 2-dimensional echocardiogram showed moderate enlargement of the right ventricular outflow tract. However, neither arrhythmogenic right ventricular cardiomyopathy nor a channelopathy could be confirmed at genetic study. He was treated with amiodarone for 2 years and then with acebutolol, which he is still taking. Six years ago he received an implantable cardioverter-defibrillator (ICD) because of ventricular fibrillation induced during an electrophysiological study. The ICD has never delivered any therapy. He remains alive and well.
Figure 2 E: Coved ST-segment elevation accentuated during stress test. F: Saddle-back ST-segment elevation. G: Epsilon wave in V2, which is best seen in the larger magnification at H (arrow).
Many reports have discussed the pathophysiology and ECGs3 of the Brugada syndrome. As illustrated in Figures 1 and 2, the ECGs of this patient showed different patterns over the years, ranging from normal, to a dome-shaped, saddle-back, and coved ST-segment elevation, and in the last few years (Figures 2G and 2H), the presence of an epsilon wave. Although the latter is usually found in patients with a right ventricular cardiomyopathy,4,5 conduction delay in the right ventricular outflow tract, as proposed in the first publication of this phenomenon, is possible.1 Bortolo Martini, M.D. [email protected] Andrea Nava, M.D. Boldrini Hospital Thiene, Vicenza, Italy
References 1.
2. 3. 4.
Figure 1 The ECG tracings in Figures 1 and 2 were not taken consecutively but were recorded in different years. A: Normal ECG. B, C: Dome-shaped ST-segment elevation. These traces were recorded when the patient was taking amiodarone. D: Coved ST-segment elevation.
5.
1547-5271/$ -see front matter © 2010 Heart Rhythm Society. All rights reserved.
Nava A, Canciani B, Schiavinato ML, Martini B. La repolarisation precoce dans le precordiales droites: trouble de la conduction intraventriculaire droite? Correlations de l’electrocardiographie- vectorcardiographie avec l’electrophysiologie. Mises a Jour Cardiologiques 1988;17:157–159. Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989;118:1203–1209. Wilde AAM, Antzelevitch C, Borggrefe M, et al. Proposed diagnostic criteria for the Brugada syndrome. Circulation 2002;106:2514 –2519. Coronel R, Casini S, Koopmann TT. Right ventricular fibrosis and conduction delay in a patient with clinical signs of Brugada syndrome: a combined electrophysiological, genetic, histopathologic, and computational study. Circulation 2005;112:2769 –2777. Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome. Circulation 2005;112:3680 – 3687.
Figure 2 E: Coved ST-segment elevation accentuated during stress test. F: Saddle-back ST-segment elevation. G: Epsilon wave in V2, which is best seen in the larger magnification at H (arrow).
Many reports have discussed the pathophysiology and ECGs3 of the Brugada syndrome. As illustrated in Figures 1 and 2, the ECGs of this patient showed different patterns over the years, ranging from normal, to a dome-shaped, saddle-back, and coved ST-segment elevation, and in the last few years (Figures 2G and 2H), the presence of an epsilon wave. Although the latter is usually found in patients with a right ventricular cardiomyopathy,4,5 conduction delay in the right ventricular outflow tract, as proposed in the first publication of this phenomenon, is possible.1 Bortolo Martini, M.D. [email protected] Andrea Nava, M.D. Boldrini Hospital Thiene, Vicenza, Italy
References 1.
2. 3. 4.
Figure 1 The ECG tracings in Figures 1 and 2 were not taken consecutively but were recorded in different years. A: Normal ECG. B, C: Dome-shaped ST-segment elevation. These traces were recorded when the patient was taking amiodarone. D: Coved ST-segment elevation.
5.
1547-5271/$ -see front matter © 2010 Heart Rhythm Society. All rights reserved.
Nava A, Canciani B, Schiavinato ML, Martini B. La repolarisation precoce dans le precordiales droites: trouble de la conduction intraventriculaire droite? Correlations de l’electrocardiographie- vectorcardiographie avec l’electrophysiologie. Mises a Jour Cardiologiques 1988;17:157–159. Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J 1989;118:1203–1209. Wilde AAM, Antzelevitch C, Borggrefe M, et al. Proposed diagnostic criteria for the Brugada syndrome. Circulation 2002;106:2514 –2519. Coronel R, Casini S, Koopmann TT. Right ventricular fibrosis and conduction delay in a patient with clinical signs of Brugada syndrome: a combined electrophysiological, genetic, histopathologic, and computational study. Circulation 2005;112:2769 –2777. Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in patients with clinical phenotype of Brugada syndrome. Circulation 2005;112:3680 – 3687.