ABSTRACT
Since the inception of the molecular cardiology era, cloning and molecular analysis of ion channels have shown that several clinical disorders primarily presenting with arrhythmia and sudden death (e.g., long-QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), familial atrial fibrillation) are due to genetically determined alterations of ionic fluxes (www.fsm.it/cardmoc). Hence, inherited arrhythmogenic diseases have become a sort of natural model that scientists exploit to investigate the molecular bases of cardiac excitability.
