Key result
Antipsychotics and other non-cardiovascular drugs can block HERG potassium channels, leading to QT prolongation and potentially lethal torsade de pointes arrhythmias.
Why the study?
Do antipsychotics cause QT prolongation and torsade de pointes arrhythmias via HERG potassium channel blockade?
Do antipsychotics cause QT prolongation and torsade de pointes arrhythmias via HERG potassium channel blockade?
Antipsychotics and other non-cardiovascular drugs can block HERG potassium channels, leading to QT prolongation and potentially lethal torsade de pointes arrhythmias.
Supports QT monitoring with antipsychotics; confirms HERG mechanism while leaving open real-world arrhythmia incidence.
The prolongation of the cardiac repolarization process, a result of the blocking of the Human Ether-ago-go Related Gene potassium channel, is an undesired accessory property shared by many pharmacological classes of non-cardiovascular drugs. Often the delayed cardiac repolarization process can be identified by a prolongation of the QT interval of the electrocardiograph. In these conditions, premature action potentials can trigger a dangerous polymorphic ventricular tachyarrhythmia, known as torsade de pointes, which occasionally can result in lethal ventricular fibrillation. In this work, brief descriptions of the electrophysiological basis of torsade de pointes and of the several pharmacological classes of torsadogenic drugs are given. Attention is focused on antipsychotics, with a deeper overview on the experimental and clinical reports about their torsadogenic properties.
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Calderone et al. (2005) conducted a review in Drug-induced torsade de pointes arrhythmias. Antipsychotics was evaluated. Antipsychotics and other non-cardiovascular drugs can block HERG potassium channels, leading to QT prolongation and potentially lethal torsade de pointes arrhythmias.
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