Suppression of erythromycin-induced early afterdepolarizations and torsade de pointes ventricular tachycardia by mexiletine.
Pacing Clin Electrophysiol
; 21(1 Pt 2): 147-50, 1998 Jan.
Article
em En
| MEDLINE
| ID: mdl-9474662
ABSTRACT
Erythromycin is a selective IKr-blocking, action potential duration (APD)-prolonging drug, which may induce early afterdepolarizations (EADs) and torsade de pointes ventricular tachycardia. The successful termination of an erythromycin-induced clinical torsades de pointes by the authors with mexiletine prompted them to investigate in vitro whether erythromycin is able to induce EADs in Purkinje fibers and, if so, whether EADs are suppressible or not by mexiletine. Electrically stimulated canine Purkinje fibers (n = 9) were superfused with erythromycin (200 mg/l) and action potentials were recorded by an intracellular microelectrode technique. Erythromycin induced a pronounced prolongation of APD and the appearance of EADs in all Purkinje preparations (9/9). After the addition of mexiletine (10 mM), a marked shortening of APD and the disappearance of EADs (7/9) were observed. Mexiletine, an inhibitor of the tetrodotoxin-sensitive window Na(+)-current, may prevent IKr-blocking drug-induced torsade de pointes ventricular tachycardia by abolishing APD prolongation and EADs.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ramos Subendocárdicos
/
Eritromicina
/
Torsades de Pointes
/
Mexiletina
/
Antiarrítmicos
/
Antibacterianos
Limite:
Animals
/
Female
/
Humans
/
Middle aged
Idioma:
En
Revista:
Pacing Clin Electrophysiol
Ano de publicação:
1998
Tipo de documento:
Article
País de afiliação:
Hungria