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 beta-Adrenergic Receptor (beta-AR) restoring the components of the hKCNQ1 macromolecular complex, thereby enhancing the I(Ks) 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 I(Ks) activity promoted by beta-AR stimulation is prominent; at the same time, during I(Kr) block, I(Ks) activation limits excessive QT prolongation. Clinically, severe and syntomatic bradycardia was the main concern: ISO activation of the beta-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.