© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
CASE REPORT
Cibenzoline induced Brugada ECG pattern
aCardiovascular Research and Teaching Institute, Aalst Cardiovascular Center OLV Hospital, Moorselbaan 164, 9300 Aalst, Belgium; bA.Z.H. Familie Reet, Belgium
Manuscript submitted 11 February 2005. Accepted after revision 25 June 2005.
*Corresponding author. Tel.: +32 499221329; fax: +32 53 72 41 85. E-mail address: andreasarkozy{at}yahoo.ca
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Abstract |
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We report a case of a 61-year-old female patient who presented with palpitations. The baseline electrocardiogram showed incomplete right bundle branch block with saddle back pattern of the ST segment in one precordial lead, but without any significant ST elevation. She was treated with oral cibenzoline. The subsequent ECG showed a coved Brugada ECG (type I) pattern, which resolved following the discontinuation of cibenzoline. An ajmaline test reproduced the coved type Brugada ECG pattern. Our case is the first report of oral cibenzoline therapy unmasking the diagnostic coved Brugada ECG pattern in a patient with a baseline normal ECG. Cibenzoline, a class I sodium channel blocker antiarrhythmic drug, should probably be avoided in the treatment of patients with Brugada syndrome.
Key Words: Brugada syndrome, cibenzoline, sudden death
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Case report |
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A 61-year-old female consulted us because of paroxysmal palpitations. The episodes, each lasting a few minutes, had abrupt start and finish. The cardiac evaluation revealed a structurally normal heart. The family history was negative for sudden death. There was no history of syncope or presyncope. The baseline ECG, in the absence of any ST elevation, showed incomplete right bundle branch block with a saddle back ST pattern in lead V2 and left anterior fascicular block (Fig. 1A). Holter monitoring revealed frequent supraventricular extrasystoles and short runs of a narrow QRS complex tachycardia. Given the bothersome symptoms, she was started on oral cibenzoline 2 × 130 mg/day.
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The resting ECG at next follow-up showed triangular type ST elevation with increased J point elevation, corresponding to the diagnostic type I Brugada ECG pattern (Fig. 1B). Both renal and liver functions were within the normal range. Following the discontinuation of cibenzoline the ECG returned to baseline with incomplete right bundle branch block and no significant ST segment elevation or other T wave abnormalities (Fig. 1C). Subsequent evaluation included an ajmaline test. At the time of the test the baseline ECG showed incomplete right bundle branch block without any ST segment abnormality (Fig. 2A). The administration of 0.7 mg/kg intravenous ajmaline reproduced the diagnostic coved type ST elevation (type I Brugada ECG pattern) (Fig. 2B). During the electrophysiological study neither supraventricular nor ventricular arrhythmias were induced.
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Discussion |
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The Brugada syndrome is characterized by an electrocardiogram (ECG) with coved type ST elevation in the right precordial leads (V1–V3) and ventricular arrhythmias [1]
. However, the ECG may be normal in patients with Brugada syndrome. The role of sodium channel blockers, more specifically class I/a and class I/c antiarrhythmic drugs, in unmasking the typical ECG is well established [2]. These drugs exaggerate the coved type ST and J point elevation (type I ECG pattern) and convert a normal baseline saddle back type ST elevation (type II, type III pattern) to coved (type I). They can also unmask the coved (type I) ECG pattern, when the initial ECG is completely normal. Ajmaline is used in our centre for this purpose. Flecainide and procainamide are also used, although less data are available about the sensitivity and specificity of these drugs [3].
Cibenzoline is a class I sodium channel blocker antiarrhythmic drug available in a limited number of countries. Cibenzoline produces a dose-dependent increase in QRS duration (up to 33%), QTc (up to 12%), A-H (up to 14%) and H-V (up to 47%) intervals and ventricular effective refractory period (up to 9%) [4]. In conjunction with the pronounced decrease in the maximum upstroke velocity of the action potential, this profile indicates a predominantly class I/c effect [4]. Cibenzoline also has moderate calcium channel blocking (class IV) effects and prolongs the action potential duration through its potassium channel blocking (class III) effect [4]. It is used for the treatment of supraventricular and ventricular arrhythmias [5], and in obstructive hypertrophic cardiomyopathy [6].
In the literature, few case reports have been published describing the worsening of the Brugada type ECG pattern following the intravenous administration of cibenzoline [7–9]. Our case report is the first case, describing the effect of oral cibenzoline unmasking the coved (type I) Brugada ECG pattern in a patient with a previously normal ECG. In our case the baseline ECG showed only incomplete right bundle branch block and intermittent saddle back ST segment pattern without any ST elevation or T wave abnormality. Following oral cibenzoline administration, the ECG showed the diagnostic coved Brugada ECG pattern (type I). This was also reproducible with ajmaline administration, supporting the diagnosis of Brugada ECG pattern. Since the patient had only minor symptoms, the baseline ECG was nearly normal and ventricular arrhythmias during the electrophysiological study were not inducible, we estimated a low future risk of sudden death.
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References |
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[1] Brugada P and Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome: a multicenter report. J Am Coll Cardiol 1992; 20: 1391–1396.[Abstract]
[2] Brugada R, Brugada J, Antzelevitch C, et al. Sodium channel blockers identify risk for sudden death in patients with ST segment elevation and right bundle branch block but structurally normal heart. Circulation 2000; 101: 510–515.
[3] Wilde AAM, Antzelevich C, Borggrefe M, et al. Proposed diagnostic criteria for the Brugada syndrome. Eur Heart J 2002; 23: 1648–1654.
[4] Harron DWG, Brogden RN, Faulds D, et al. Cibenzoline. A review of its pharmacological properties and therapeutic potential in arrhythmias. Drugs 1992; 43: 734–759.[Web of Science][Medline]
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[6] Hamada M, Shigematsu Y, Ikeda S, et al. Class I/a antiarrhythmic drug cibenzoline: a new approach to the medical treatment of hypertrophic obstructive cardiomyopathy. Circulation 1997; 96: 1520–1524.
[7] Tada H, Nogami A, Shimizu W, et al. ST segment and T wave alternans in a patient with Brugada syndrome. Pacing Clin Electrophysiol 2000; 23: 413–415.[CrossRef][Medline]
[8] Ohkubo K, Watanabe I, Okumura Y, et al. Wolff-Parkinson-White Syndrome concomitant with asymptomatic Brugada syndrome. Pacing Clin Electrophysiol 2004; 27: 109–111.[Medline]
[9] Furuhashi M, Uno K, Tsuchihashi K, et al. Prevalence of asymptomatic ST segment elevation in right precordial leads with right bundle branch block (Brugada type ST shift) among the general Japanese population. Heart 2001; 86: 161–166.
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