Key result
Terfenadine at 10 µM caused a 100% incidence of non-Torsades de Pointes-like ventricular tachycardia/fibrillation in experimental models, driven by I(Na) blockade rather than QT prolongation.
Why the study?
Does terfenadine induce ventricular tachycardia/fibrillation through QT prolongation and Torsades de Pointes or via other mechanisms in in vitro cardiac models?
Population
In vitro models including rabbit isolated hearts, left ventricular wedge preparations, HEK293 cells…
Design
Preclinical
Authors
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Terfenadine cardiotoxicity may primarily involve sodium channel blockade; challenges hERG/QT-centric models and leaves open human translation.
Does terfenadine induce ventricular tachycardia/fibrillation through QT prolongation and Torsades de Pointes or via other mechanisms in in vitro cardiac models?
Terfenadine-induced cardiac death may be primarily driven by non-TdP-like VT/VF caused by sodium channel blockade and conduction slowing, rather than hERG blockade and QT prolongation.
Lu et al. (2012) studied Terfenadine-induced pro-arrhythmia. Terfenadine was evaluated on Incidence of non-Torsades de Pointes-like ventricular tachycardia/fibrillation. Terfenadine at 10 µM caused a 100% incidence of non-Torsades de Pointes-like ventricular tachycardia/fibrillation in experimental models, driven by I(Na) blockade rather than QT prolongation.
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