Key result
Trazodone dose-dependently decreased maximum upstroke velocity, prolonged action potential duration, and inhibited major cardiac ion channels, especially hERG, in hiPSC-CMs.
Why the study?
Does trazodone alter cardiac action potentials and inhibit ion channels in human-induced pluripotent stem cell-derived cardiomyocytes?
Does trazodone alter cardiac action potentials and inhibit ion channels in human-induced pluripotent stem cell-derived cardiomyocytes?
Trazodone exhibits cardiotoxic effects by inhibiting hERG and sodium channels, leading to prolonged action potential duration and decreased upstroke velocity, which explains its arrhythmogenic potential.
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Trazodone's multi-channel inhibition warrants ECG vigilance in vulnerable patients; extends mechanistic evidence for cardiotoxicity in hiPSC-CM models.
Lee et al. (2015) studied Trazodone-induced cardiotoxicity. Trazodone was evaluated on Cardiac action potentials and ion channel inhibition. Trazodone dose-dependently decreased maximum upstroke velocity, prolonged action potential duration, and inhibited major cardiac ion channels, especially hERG, in hiPSC-CMs.
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