Torsades de pointes (TDP) is a polymorphic ventricular tachycardia with a peculiar electrocardiographic pattern of continuously changing morphology of the QRS complex twisting around an imaginary baseline. The clinical setting under which TDP develops covers many clinico-pathologic conditions, including the long QT syndrome (LQTS). In the present review, we analyze the evolution of the hypotheses for the mechanisms underlying TDP and we discuss some of the experimental models used and their related clinico-pathologic counterparts. Together with the hypothesis that TDP represents a form of reentrant arrhythmia, recent evidence has suggested the possibility that triggered activity may indeed be responsible for TDP. Data collected in vitro are presented that demonstrate a role for catecholamines in the development of afterpotentials in ventricular tissue. Whether adrenergic-mediated afterdepolarizations are the mechanism responsible for TDP in the clinical setting of LQTS has not yet been proven and remains an important area of investigation.