Torsade de pointes (TdP) represents a complex polymorphic ventricular tachycardia. While the triggering mechanisms of early afterdepolarization and increased dispersion of repolarization are well investigated, the sudden self-limiting termination remains poorly understood. Analysis of TdP to investigate factors causing spontaneous termination. We used a large data set of Langendorff experiments in isolated rabbit hearts in which drug-induced QT prolongation, bradycardia and hypokalemia provoke TdP. We included 427 episodes with typical TdP characteristics of polymorphic, self-terminating beats and twisting QRS complexes occurring in the presence of abnormal QT prolongation due to various different QT prolonging agents. The use of eight monophasic action potential catheters allowed the characterization of action potential duration, configuration, and dispersion of repolarization beyond the capabilities of the surface ECG. To identify possible mechanisms of arrhythmia termination, the initial, midpoint, and terminal three ventricular complexes were analyzed for each episode. An abrupt decrease in spatial dispersion over the course of a TdP episode was identified as a precursor for termination of TdP. Within the last three beats, a sudden significant decrease in dispersion of repolarization was observed as a predictor of termination. In parallel, there was a decrease in action potential duration (APD90) before termination. Also, a change in action potential configuration (APD90/50 ratio) in terms of loss of action potential dome with restitution of action potential triangulation was observed. In more than 400 TdP episodes homogenization of myocardial repolarization with the recovery of action potential configuration determines the termination of TdP episodes.