作者: S.Cora Verduyn , Marc A Vos , Jolanda van der Zande , Atilla Kulcsàr , Hein J.J Wellens
DOI: 10.1016/S0735-1097(97)00333-1
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摘要: Abstract Objectives. We sought to further elucidate the role of early afterdepolarizations (EADs) and interventricular dispersion repolarization (ΔAPD) in genesis acquired torsade de pointes (TdP) arrhythmias. Background. Administration class III agents can be associated with TdP. developed a dog model which TdP reproducibly induced by pacing after d-sotalol. This shows reproducible results over weeks. Methods. In 14 anesthetized dogs chronic complete atrioventricular block, two separate experiments were performed d-sotalol (2 mg/kg body weight) or almokalant (0.12 mg/kg) was administered. Monophasic action potentials simultaneously recorded from endocardium right left ventricle register EADs measure potential duration (APD). ΔAPD defined as APD minus that ventricle. Results. Baseline conditions identical serially experiments. The cycle length QT time increased 16% 26% 15% 31% almokalant, respectively. After both drugs prolonged more than ventricle, thereby increasing (almokalant [mean ± SD]: 110 60 ms; d-sotalol: 80 45 ms, p Conclusions. same dog, delay repolarization, EADs, multiple EBs ventricular inhomogeneity These changes related higher incidence confirm strong association occurrence findings also show possible value our for evaluating proarrhythmic different drugs.