**1. Introduction**

Concomitant cardiac pathology, including arrhythmogenic channelopathies, can complicate the course of a normal pregnancy and could be related to additional risks for both fetus and mother, including sudden cardiac death (SCD). Long QT syndrome (LQTS) is a cardiac channelopathy, characterized by the prolongation of ventricular repolarization and polymorphic ventricular tachycardia (VT) known as "Torsades de pointes", leading to syncope or SCD. The prevalence of LQTS is approximately 1 in 2000 individuals and can be inherited (approximately 90%) or occur de novo (10%) [1]. LQTS is caused by mutations in several ion-channel genes. The commonest mutations are located in the potassium-channel KCNQ1 (LQT1) and hERG (LQT2) genes, and in the sodium-channel SCN5A (LQT3) gene [2]. These three major genetic subtypes account for approximately 80% of all LQTS cases [3]. There are various subtype-specific triggers for cardiac events in LQTS. Patients with LQT1 experience most of their cardiac incidents as the result of increased adrenergic activity during exercise, especially swimming, or emotional stress. Audible stimulation, such as a ringing telephone or an alarm clock, may provoke LQT2 onset, whereas patients with LQT3 are more likely to have events while resting or sleeping [4]. Women with congenital or acquired LQTS have longer QT intervals and are more likely to develop polymorphic ventricular arrhythmia (VA) or SCD than men [5]. These differences may exist due to alterations of sex hormone levels, dependent on the various menstrual cycle periods, gestation, and the postnatal period, which are related to alterations in QT duration and frequency of cardiac events [6,7].
