CLINICAL RESEARCH
Ventricular arrhythmia induced by sodium channel blocker in patients with Brugada syndrome
Hiroshi Morita, MD*,*,
Shiho Takenaka Morita, MD*,
Satoshi Nagase, MD*,
Kimikazu Banba, MD*,
Nobuhiro Nishii, MD*,
Yoshinori Tani, MD*,
Atsuyuki Watanabe, MD*,
Kazufumi Nakamura, MD*,
Kengo Fukushima Kusano, MD*,
Tetsuro Emori, MD*,
Hiromi Matsubara, MD*,
Kazumasa Hina, MD ,
Toshimasa Kita, MD and
Tohru Ohe, MD, FACC*
* Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Okayama, Japan
Department of Cardiovascular Medicine, Cardiovascular Center Sakakibara Hospital, Okayama, Japan Okayama, Japan
Manuscript received February 24, 2003;
revised manuscript received April 23, 2003,
accepted June 3, 2003.
* Reprint requests and correspondence: Dr. Hiroshi Morita, Department of Cardiovascular Medicine, Okayama University Graduate School, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
hmorita{at}cc.okayama-u.ac.jp
OBJECTIVES: We administered pilsicainide chloride, a class Ic pure sodium channel blocker, to patients with Brugada syndrome (BS) and evaluated the occurrence of ventricular arrhythmia (VA) and T-wave alternans (TWA).
BACKGROUND: Ventricular arrhythmia and TWA are sometimes induced by a sodium channel blocker challenge test in BS patients, but the significance of the induced VA and TWA is not known.
METHODS: Pilsicainide was administered to 65 patients with BS (10 symptomatic and 55 asymptomatic patients), and the occurrence of VA, TWA, and change of electrocardiogram were evaluated. Electrophysiologic study was performed in 57 patients, and the induction of VA by programmed electrical stimulation (PES) was evaluated.
RESULTS: Ventricular arrhythmia was not induced by administration of pilsicainide in 55 patients (no-VA group). Administration of pilsicainide-induced VA in 10 patients (Pil-VA group) and polymorphic ventricular tachycardia in four patients. Pilsicainide-induced VA in 60% of the symptomatic patients but in only 7% of asymptomatic patients (p < 0.01). ST level, QTc, and indexes of cardiac conduction in the Pil-VA group were not different from those in the no-VA group. Ventricular fibrillation was induced by PES in 67% of the patients in the Pil-VA group and in 33% of the patients in the no-VA group. In six cases, macroscopic TWA occurred in association with pilsicainide-induced VA, but TWA occurred in only one patient without pilsicainide-induced arrhythmia.
CONCLUSIONS: Administration of a sodium channel blocker results in induction of not only ST-elevation but also VA and TWA in patients with BS.
|
Abbreviations and Acronyms
| | HV | = His-ventricle | | PES | = programmed electrical stimulation | | PVC | = premature ventricular contraction | | TWA | = T-wave alternans | | VA | = ventricular arrhythmia | | VF | = ventricular fibrillation | | VT | = ventricular tachycardia |
|
This article has been cited by other articles:
|
|
|
|
 
H. Morita, K. F. Kusano, D. Miura, S. Nagase, K. Nakamura, S. T. Morita, T. Ohe, D. P. Zipes, and J. Wu
Fragmented QRS as a Marker of Conduction Abnormality and a Predictor of Prognosis of Brugada Syndrome
Circulation,
October 21, 2008;
118(17):
1697 - 1704.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Nagase, K. F. Kusano, H. Morita, N. Nishii, K. Banba, A. Watanabe, S. Hiramatsu, K. Nakamura, S. Sakuragi, and T. Ohe
Longer Repolarization in the Epicardium at the Right Ventricular Outflow Tract Causes Type 1 Electrocardiogram in Patients With Brugada Syndrome
J. Am. Coll. Cardiol.,
March 25, 2008;
51(12):
1154 - 1161.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. F. Kusano, M. Taniyama, K. Nakamura, D. Miura, K. Banba, S. Nagase, H. Morita, N. Nishii, A. Watanabe, T. Tada, et al.
Atrial Fibrillation in Patients With Brugada Syndrome: Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds
J. Am. Coll. Cardiol.,
March 25, 2008;
51(12):
1169 - 1175.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Ueyama, A. Shimizu, M. Esato, Y. Yoshiga, A. Sawa, S. Suzuki, N. Sugi, and M. Matsuzaki
Pilsicainide-induced Brugada-type ECG and ventricular arrhythmias originating from the left posterior fascicle in a case with Brugada syndrome associated with idiopathic left ventricular tachycardia
Europace,
January 1, 2008;
10(1):
86 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Watanabe, K. Fukushima Kusano, H. Morita, D. Miura, W. Sumida, S. Hiramatsu, K. Banba, N. Nishii, S. Nagase, K. Nakamura, et al.
Low-dose isoproterenol for repetitive ventricular arrhythmia in patients with Brugada syndrome
Eur. Heart J.,
July 1, 2006;
27(13):
1579 - 1583.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Morita, D. P. Zipes, J. Lopshire, S. T. Morita, and J. Wu
T wave alternans in an in vitro canine tissue model of Brugada syndrome
Am J Physiol Heart Circ Physiol,
July 1, 2006;
291(1):
H421 - H428.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. M. Narayan
T-Wave Alternans and the Susceptibility to Ventricular Arrhythmias
J. Am. Coll. Cardiol.,
January 17, 2006;
47(2):
269 - 281.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. G. Meregalli, A. A.M. Wilde, and H. L. Tan
Pathophysiological mechanisms of Brugada syndrome: Depolarization disorder, repolarization disorder, or more?
Cardiovasc Res,
August 15, 2005;
67(3):
367 - 378.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. P. Zipes
The year in electrophysiology
J. Am. Coll. Cardiol.,
April 7, 2004;
43(7):
1306 - 1314.
[Full Text]
[PDF]
|
|
|
|
