It’s another genetic cause of ventricular arrhythmias and sudden death. It’s not Torsades---the QT interval is not prolonged and the tachycardia morphology is typically a bidirectional alternans type of tachycardia rather than twisting about an isoelectric point. It’s reviewed here in the Journal of Cardiovascular Electrophysiology, via Medscape. The mechanism is believed to relate to excessive myocardial cytosolic calcium.
An analogous situation is seen in digitalis toxic ventricular ectopy, classically presenting as bidirectional tachycardia, also believed related to intracellular calcium excess. Digitalis exerts its inotropic effect by increasing the delivery of calcium to the contractile proteins.
By the way, UpToDate has an excellent discussion of CPVT in a section on the polymorphic VTs with normal QT intervals which, for obvious reasons, I can’t link here.