Abstract
A 69-year-old man without structural heart disease was admitted for syncope. His electrocardiogram displayed complete right bundle branch (CRBBB). A coved type ST elevation was observed with transient normalization of CRBBB giving rise to a normal QRS. These findings suggest that Brugada syndrome can be masked by CRBBB.
Keywords: Brugada syndrome, Coved type ST elevation, Right bundle-branch block
Introduction
Brugada syndrome (BrS) is characterized by an ST elevation in the precordial leads and by ventricular tachyarrhythmias.1 The debate continues as to whether the BrS electrocardiographic (ECG) pattern is best explained by a repolarization2 or depolarization3 disorder.
We present a case of a patients presenting with syncope. His ECG showed a typical CRBBB; however, when the complete right bundle branch (CRBBB) resolved, the QRS narrowed, and the typical BrS ECG pattern was observed.
Case
The patient was a 69-year-old man with an uneventful medical history until 2 months ago, when he developed syncope that recurred twice. His history and his family history were noncontributory. At the time of admission to another hospital, his physical and routine laboratory examinations were normal. His ECG showed a CRBBB. He was referred to our hospital for the further evaluation. After obtaining a written informed consent, we attempted catheterization, which included an electrophysiologic study followed by the implantation of an implantable cardioverter and defibrillator (ICD).
Electrocardiographic findings
After admission, the patient was placed under ECG monitoring, and 12-lead ECGs were repeatedly recorded. His ECG showed normal sinus rhythm with a normal P-R interval and an undetermined frontal electrical axis. The QRS showed a typical CRBBB: late R in V1 and V2 with slurred S in V6. The width of the QRS duration was 140 milliseconds (Fig. 1).
Fig. 1.
The 12-lead ECG. The 12-lead ECG showed a typical CRBBB: late R in V1 and slurred S in V6. The QRS duration was wide: 140 milliseconds. This pattern was consistently recorded.
Electrocardiographic at catheterization
The patient underwent cardiac catheterization, and the pressure tracings, ventriculography, and coronary angiography were normal. A provocation test for a coronary spasm using acetylcholine was also negative. An electrophysiologic study was performed in a standardized manner. His ECG showed a CRBBB, and the P-R, A-H, and H-V intervals were normal. Triple extrastimuli from the outflow tract of the right ventricle (RV) were able to induce ventricular fibrillation. During the catheterization, it was noted that the CRBBB resolved spontaneously resulting in a narrow QRS complex, which displayed the typical pattern for BrS (Fig. 2A). The J point was isoelectric in V1 and distinctly elevated in V2 (Fig. 2A, arrows). The cause of the CRBBB normalization is not apparent, but this interesting manifestation was reproduced twice. A further provocation test using a class IC drug was not attempted.
Fig. 2.
The 12-lead ECG with spontaneous normalization of the CRBBB. A, The ECG shows a CRBBB in the first and last 2 beats. The third beat shows a loss of CRBBB and the normalized QRS complex (asterisk), and in this beat, the type 1 pattern (coved type) of Brugada syndrome is evident. The J point is slightly lowered in V1 and elevated in V2 including the initial part of the ST segment (arrows). B, Spontaneous resolution of the CRBBB during the12-lead Holter recording (asterisk). The normalized QRS complex was associated with a slightly shorter RR and PR interval, and an ST-segment elevation in V1 and V2 was evident. The QRS with CRBBB showed distinct downward displacement of the J point and the ST segment (arrows).
Follow-up
The patient was diagnosed to have symptomatic BrS, and an ICD was implanted 1 week later. During the remaining hospitalization period, a 12-lead Holter ECG was recorded, and spontaneous resolution of the CRBBB was observed 3 times. The cause of normalization of the QRS complexes was not evident, but a slightly shorter RR and PR interval may suggest either premature beat or development of first-degree left bundle-branch block as the cause of normalization. This time, V1 or V2 showed a ST-segment elevation in the normalized QRS. In the QRS complexes with CRBBB, the J point and the initial part of the ST segment were clearly depressed below the isoelectric line, indicating secondary ST-T changes (Fig. 2B, arrows). Two weeks later, he received an ICD shock that was shown to be an appropriated shock for ventricular fibrillation.
Discussion
Very recently, Chiale et al4 reported a case of a 51-year-old man with BrS complicated by a CRBBB pattern. Ajmaline accentuated the ST elevation in V1 to V3, and pacing form the RV disclosed coved-type ST-segment elevation typical of BrS.4 However, the current article is the first report of a patient with BrS that was concealed by a CRBBB and unmasked when the CRBBB spontaneously normalized. The CRBBB pattern of the patient was similar to the classical pattern, consisting of a prolonged QRS complex, late R in V1 to V2, and wide S in V6 and other leads. However, the J point and the ST segment in the normalized QRS complexes were different on the 2 occasions, suggesting that CRBBB is also affected by the underlying BrS ECG pattern (Fig. 2A and B). The ECG alterations typical for BrS have long been considered to be due to a repolarization defect giving rise to an accentuation of the epicardial action potential notch in the right ventricular epicardium and the development of a transmural gradient during the early phases of the action potential, resulting in the inscription of an accentuated J wave or ST-segment elevation.2 Some investigators have proposed that the BrS ECG pattern is the result of a localized conduction delay in the outflow tract of the RV3,5,6 and that the J wave–like deflection in V1 is produced by a simulation.5 In the present case, the BrS ECG pattern is masked by conduction impairment in the RV, and unmasked when conduction is transiently normalized. Although CRBBB is a conduction disturbance at the central part in the right bundle, depolarization abnormality suggested as the etiologic mechanism is assumed to be at more periphery in the localized area, the RV outflow tract.5 Therefore, our observation is likely to favor the repolarization abnormality, but we cannot exclude other possibility.5,6
References
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