Alterations in ECG QT intervals correlate with the risk of potentially fatal arrhythmias, for which transgenic mouse hearts are becoming increasingly useful experimental models. However, QT intervals are poorly defined in murine ECGs owing to the short cardiac action potential (AP) waveforms. Previous studies have determined the QT interval as the times from the beginning of the QRS complex to (1) 95% recovery of the ECG deflection to baseline [1]; (2) the point at which recovery of the T wave deviates from the tangent to the steepest slope of its recovery [2]; (3) the return of the QT segment to the isoelectric baseline [3]; or (4) the point of convergence of T waves and their first derivative on a signal-averaged ECG recording [4] (Fig. 1). The present work develops a consistent measure of murine QT interval that correlates with changes in the duration of ventricular myocyte APs. All procedures were performed in accordance with the UK Animals (Scientific Procedures) Act (1986). Volume-conducted ECGs were compared with simultaneously-recorded APs obtained using floating intracellular microelectrodes in Langendorff-perfused mouse hearts. QT intervals were measured from the onset of the QRS complex. The interval, Q-APR90, measured to the time at 90% AP recovery was compared with two measures of QT interval. QT1 was measured to the recovery of the ECG trace to the isoelectric baseline for entirely positive T-waves, or to the trough of any negative T-wave undershoot. QT2, extensively used in previous studies, was measured to the return of any ECG trough to the isoelectric baseline. QT1, but not QT2, closely correlated with changes in Q-APR90 (Fig. 2). These findings were confirmed in Scn5a+/ΔKPQ hearts used to model human long QT syndrome. Application of this method in whole, avertin anaesthetized mice (2.4 mg/10g body weight intraperitoneal) similarly demonstrated a prolonged corrected QT interval, QTc, in Scn5a+/ΔKPQ hearts, and normal values in RyR2+/S and RyR2S/S hearts containing the RyR-P2328S modification. Thus, we achieve a simple approach for the determination of QT and QTc intervals that correlates with the duration of ventricular myocyte action potentials in murine hearts.