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Role of Early Afterdepolarization in Familial Long QTU Syndrome and Torsade de Pointes
Author(s) -
ZHOU JINTAI,
ZHENG LIANGRONG,
LIU WEIYU
Publication year - 1992
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1992.tb03041.x
Subject(s) - medicine , afterdepolarization , verapamil , propranolol , epinephrine , cardiology , lidocaine , long qt syndrome , anesthesia , sinus rhythm , delta wave , qt interval , electrophysiology , electroencephalography , calcium , repolarization , slow wave sleep , psychiatry , atrial fibrillation
Torsade de pointes (TdP) syncopal episodes were almost invariably precipitated by emotional stress or menstruation in a 17‐year‐old girl. V wave accentuation occurred during sinus rhythm without pauses in periods of heightened sympathetic tone. To examine the role of early afterdepolarization (EAD), monophasic action potentials were recorded during ventricular extrasystoles and TdP occurring spontaneously and induced by ventricular pacing. The effects of lidocaine, verapamil, propranolol, and epinephrine were assessed. Our data show that: (1) EAD plays a significant role in the genesis of familial long QTU syndrome and TdP; (2) rapid ventricular pacing causes postpause‐dependent EADs, U waves, and TdP; and (3) EAD is enhanced by epinephrine infusion in the absence of pause, whereas EAD‐triggered firing is inhibited by verapamil and propranolol but not by lidocaine.