P ortal hypertension (PH), defined by a hepatic venous pressure gradient (HVPG) greater than 6 mmHg, 1 is a common complication of cirrhosis. The presence and the development of esophageal varices (EV) is a clinical manifestation of PH, 2,3 with a prevalence that can range from 40% to 80% in patients with cirrhosis. This prevalence increases progressively in relation to the severity of liver damage. 4,5 The presence of EV is also a clear indicator of a certain stage of cirrhosis. 6 The development of EV in patients with cirrhosis occurs when the HVPG is greater than 10 mmHg, 3,7 with an incidence of approximately 5% per year and a yearly rate of progression to larger varices of 5% to 15%. 4,5,8 The clinical relevance of EV is linked to the risk of bleeding that occurs when HVPG is greater than 12 mmHg, 7-9 with a mortality rate that exceeds 20% within 6 weeks from the bleeding episode, despite aggressive treatment. 10 The Baveno IV 2005 Consensus Workshop 11 and the American Association for the Study of Liver Diseases 2007 single-topic symposium on portal hypertension 12 recommended that endoscopic screening for esophageal and gastric varices should always be performed when a diagnosis of cirrhosis is made. Upper endoscopy should be repeated at 2-year to 3-year intervals in patients without varices, and at 1-year to 2-year intervals in those with small varices, to evaluate their development or progression. 11,12 These guidelines might not be ideal for clinical