text: The anti-arrhythmic drugs are a class of pharmacological compounds whose action is that of restore the normal sinus rhythm when a patient is affected by an arrhythmia, so their action is that of performing a pharmacological cardioversion.
  Indeed, the pharmacological cardiotoxicity of anti-arrhythmic compounds is related to the action of these drugs to induce potential fatal arrhythmias such as torsade de pointes or ventricular fibrillation. The anti-arrhythmic drugs directly act on the opening/closing of ion channels, thus modifying the ion currents.
  In treating arrhythmias, the pharmacological therapeutic action is related to the generation of a new combination of the blockage/opening of ion channels. Nevertheless, this new pharmacologically induced configuration may lead to an unbalance in ionic currents and as a consequence causing a modification in the action potential morphology which increases the risk of inducing an arrhythmia.
  Over the years, it has been studied how the change of the action potential shape, i.e. prolongation of the repolarization phase or early after depolarizations, is bonded to the likelihood of inducing fatal arrhythmias, such as torsade de pointes. Thus, the risk of inducing a fatal arrhythmias has to be prevented assessing the pharmacological cardiotoxicity at the early stages of the manufacturing of a new drug.