Abstract
Trazodone has been associated with prolonged QT-interval and increased risk of polymorphous ventricular tachycardias clinically and has demonstrated in vitro inhibition of hERG (human ether-á-go-go-related gene) channel current. This study attempts to put the effects of trazodone into perspective by comparing its hERG inhibition to that of three agents known to inhibit I Kr, and comparing the effects of trazodone and cisapride on action potential duration and the QT-interval in the rabbit Langendorff heart preparation. Trazodone inhibited hERG channel current in a concentration-dependent manner with an IC 50 of 0.69 μM. Like astemizole, terfenadine and cisapride, trazodone inhibits hERG channel current at clinically relevant concentrations. Like cisapride, trazodone increased both the QT-interval and APD 90 in the Langendorff heart preparation in a reverse frequency-dependent manner at clinically relevant concentrations. These data strongly suggest that trazodone prolongs the QT-interval through inhibition of hERG channel current.
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