The ECG QT interval measures the length of ventricular systole. Its prolongation is essentially caused by a delayed repolarization phase, and is associated with an increased risk of ventricular arrhythmias and sudden death in several congenital and acquired conditions. Abnormalities in cardiac electrophysiology are well documented in patients with liver cirrhosis, and the prolonged QT interval has emerged as the electrophysiological hallmark of cirrhotic cardiomyopathy. This article will focus on: first, the epidemiology of QT interval prolongation in cirrhosis; second, the potential molecular mechanisms responsible for the pathogenesis of this electrophysiological abnormality and the putative role of circulating cardiotoxins; third, its prognostic meaning; and fourth, its clinical relevance, in terms of the association between the presence of a long QT interval and the occurrence of ventricular arrhythmias in cirrhotic patients treated with drugs known to increase the QT length or exposed to stressful conditions, such as liver transplantation, gastrointestinal bleeding and shock.