Why the study?
Does intravenous ibutilide increase the risk of torsades de pointes and alter ventricular repolarization in a canine model of pacing-induced cardiomyopathy compared to acute AV block?
Does intravenous ibutilide increase the risk of torsades de pointes and alter ventricular repolarization in a canine model of pacing-induced cardiomyopathy compared to acute AV block?
In a canine model, ibutilide demonstrates significant proarrhythmic effects, including an increased risk of torsades de pointes, particularly in the setting of pacing-induced cardiomyopathy.
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Ibutilide may amplify TdP risk in cardiomyopathy; animal findings leave human translation and risk stratification open.
The authors developed a canine model of pacing induced cardiomyopathy to study the possible mechanisms of ibutilide induced torsades de pointes (TP) in heart failure. Thirteen dogs received intravenous ibutilide after acute AV block for 60 minutes, and after implantation of a VVI pacemaker, with a rate of 270 beats/min for 2-3 weeks. Twelve-lead ECG and right and left ventricle monophasic action potentials were recorded at different right ventricle pacing cycle lengths from 600 ms to 1200 ms during the study. The results showed ibutilide could significantly prolong ventricular repolarization and increase the dispersion in a dose dependent and reverse use dependent manner. Furthermore, after ibutilide administration, cardiomyopathic dogs had a greater dispersion of ventricular repolarization, and also had higher incidences of early afterdepolarizations and spontaneous or pacing induced TP than acute AV block dogs.
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HSIEH et al. (2000) studied this question.
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