In patients with SCN5A mutations, the use of lacosamide may cause the augmentation of slow inactivation of cardiac sodium channels, potentially leading to re-entrant arrhythmias and early afterdepolarizations in ventricular cardiac tissue (1, 21), which greatly increases the risk of refractory ventricular tachyarrhythmias and sudden cardiac arrest. This evidence concerns the gene SCN5A and sudden cardiac arrest.