Isoproterenol enhancement of IKs current in Amiodarone-induced Long QT Syndrome

The response over time of the QT interval and the Transmural Dispersion of Repolarization (TDR) to Isoproterenol infusion (ISO) in an 85 year-old-man with severe and syntomatic bradycardia, in the setting of an Amiodarone-induced Long QT Syndrome (LQTS) is the subject of this communication. ISO shortened the QT and decreased the TDR. We propose that ISO increased the generation of signals from the β-Adrenergic Receptor (β-AR) restoring the components of the hKCNQ1 macromolecular complex, thereby enhancing the IKs function; shortening of the QT interval, reduction of the TDR and normalization of the T wave morphology was then possible. In Amiodarone-induced LQTS, the increase in IKs activity promoted by β-AR stimulation is prominent; at the same time, during IKr block, IKs activation limits excessive QT prolongation. Clinically, severe and syntomatic bradycardia was the main concern: ISO activation of the β-AR proved useful both to increase heart rate and to reduce QT prolongation. A slow heart rate, associated to a prolonged QT interval and to a big TDR, are not sufficient to develop Torsades de Pointes in Amiodarone-induced LQTS.