Electrophysiological abnormalities in cirrhosis, such as the prolongation of the QT interval, are associated with higher risk of ventricular arrhythmias. Holter monitoring offers a full picture of these during 24 hour. Our study aimed to evaluate the extent of the QT interval prolongation, identify etiological and biochemical elements linked with it, and investigate the correlation with ventricular arrhythmic events related to etiology and severity of liver cirrhosis. We included 43 patients with cirrhosis and evaluated the maximal QT interval (maxQT), corrected QT interval (QTc) and its maximum (maxQTc), and ventricular arrhythmic events during 24 hour Holter monitoring. All parameters were prolonged and significantly increased in alcoholic cirrhosis when compared to viral C or B etiology (P<0.05). MaxQT and QTc moderately correlated with serum proteins (r=0.402; P<0.01 and r=0.308; P<0.05) and triglycerides (r=-0.357; P<0.05 and r=-0.344; P<0.05). Viral C etiology associated significantly more premature ventricular contractions than viral B (P<0.01), toxic (P<0.01), and mixed etiology (P<0.05). The ventricular arrhythmic events did not differentiate groups based on Child class or gender (P=NS). In liver cirrhosis, Holter monitoring confirms. QT interval prolongation particularly correlated with moderate severity, alcoholic etiology, and plasmatic level of total proteins and triglycerides but not with a higher incidence of ventricular arrhythmic events, except for hepatitis C virus etiology, supporting the novel hypothesis of a direct cardiac arrhythmic effect of this virus.