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Brady Cardie‐Dependent Early Afterdepolarizations in a Patient with QTU Prolongation and Torsade de Pointes in Association with Marked Bradycardia and Hypokalemia
Author(s) -
SHIMIZU WATARU,
TANAKA KOUICHI,
SUENAGA KENJI,
WAKAMOTG ATSUO
Publication year - 1991
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.1540-8159.1991.tb02841.x
Subject(s) - medicine , hypokalemia , afterdepolarization , bradycardia , prolongation , cardiology , qt interval , sinus bradycardia , repolarization , electrocardiography , anesthesia , u wave , heart rate , electrophysiology , blood pressure
Endocardial monophasic action potentials (MAPs) were recorded at the right ventricular apex in a patient with QTU prolongation and torsade de poinles (TdP) in association with marked bradycardia and hypokalemia. There was a distinct hump on phase 3 repolarization of the MAPs characteristic of early afterdepolarizations (EADs), which was associated with marked prolongation of the QTU interval on the surface electrocardiogram. EAD amplitude was bradycardia dependent, and there was a strong correlation (r = 0.91) between the preceding RR interval and the amplitude of the EAD (percent of MAP amplitude). Intravenous administration of lidocaine or right ventricular pacing suppressed the ventricular premature complexes and TdP in association with the suppression of the EADs on the MAPs. Furthermore, these EADs were not recorded on the MAPs 1 month Iater when the QTU prolongation and TdP had disappeared. These findings suggest that the TU abnormality and QTU prolongation responsible for TdP were due to bradycardia‐dependent EADs.