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Intravenous Administration of Class I Antiarrhythmic Drugs Induced T Wave Alternans in a Patient with Brugada Syndrome
Author(s) -
CHINUSHI MASAOMI,
WASHIZUKA TAKASHI,
OKUMURA HIROSHI,
AIZAWA YOSHIFUSA
Publication year - 2001
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2001.00493.x
Subject(s) - medicine , brugada syndrome , procainamide , cardiology , t wave alternans , ventricular fibrillation , j wave , st segment , sudden cardiac death , anesthesia , myocardial infarction
T Wave Alternans in Brugada Syndrome. A 71‐year‐old man who experienced aborted sudden death was referred to our hospital. Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12‐lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V 1 to V 3 . Double ventricular extrastimuli at coupling intervals > 180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V 1 to V 3 , and visible T wave alternans was induced in leads V 2 and V 3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V 2 and V 3 . Class I antiarrhythmic drug‐related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.