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Epinephrine-induced ventricular premature complexes due to early afterdepolarizations and effects of verapamil and propranolol in a patient with congenital long QT syndrome.

作者信息

Shimizu W, Ohe T, Kurita T, Tokuda T, Shimomura K

机构信息

Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan.

出版信息

J Cardiovasc Electrophysiol. 1994 May;5(5):438-44. doi: 10.1111/j.1540-8167.1994.tb01183.x.

DOI:10.1111/j.1540-8167.1994.tb01183.x
PMID:7519951
Abstract

We report a patient with congenital long QT syndrome in whom early afterdepolarizations (EADs) were demonstrated on monophasic action potential (MAP) recordings in the left ventricular mid-base inferior wall. Epinephrine infusion at 5 micrograms/min increased the amplitude of the EADs and the late component of the T(U) wave. Epinephrine also induced ventricular premature complexes (VPCs) with right bundle branch block morphology and left-axis deviation that occurred from the peak of the EADs. Verapamil injection (5 mg) during continuous epinephrine infusion abolished all VPCs with a slight reduction in the amplitude of the EADs. Propranolol injection (5 mg) in addition to verapamil further reduced the amplitude of the EADs and the late component of the T(U) wave. These findings suggest that the epinephrine-induced VPCs were closely related to triggered rhythm arising from the EADs, and that both verapamil and propranolol were effective for the suppression of VPCs and EADs.

摘要

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