ST segment elevation induced by class IC antiarrhythmic agents: underlying electrophysiologic mechanisms and insights into drug-induced proarrhythmia.
Three patients in whom Class IC sodium channel blockers induced ST segment elevation in leads V1 through V3 are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of idiopathic ventricular fibrillation are discussed.
Krishnan
S C
SC
Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Hospital, Boston, Massachusetts 02215, USA.
Josephson
M E
ME
D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000503:physiopathology; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D004562:Electrocardiography / Q000187:drug effects*; D004594:Electrophysiology; D016700:Encainide / Q000494:pharmacology; D005424:Flecainide / Q000494:pharmacology; D006801:Humans; D008297:Male; D008875:Middle Aged; D026941:Sodium Channel Blockers; D014693:Ventricular Fibrillation / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents; D026941:Sodium Channel Blockers; D005424:Flecainide; D016700:Encainide