Noninvasive measurements of variceal pressure adequately reflect the hemodynamic effects of propranolol on portal hypertension. However, the prognostic value of variceal pressure responses during continued propranolol therapy has not been evaluated, and it is unclear whether this may substitute invasive measurements of portal pressure response. Fifty-five portal hypertensive patients with cirrhosis were studied before and at 4 months of continued propranolol therapy. Variceal pressure was measured using an endoscopic pressure gauge. Portal pressure was evaluated as the hepatic venous pressure gradient (HVPG). Over a 28 ؎ 11 month follow-up, 16 patients experienced variceal bleeding. Baseline characteristics were similar in bleeders and nonbleeders. At 4 months, reduction in variceal pressure was less marked in bleeders than in nonbleeders (5% ؎ 20% vs. ؊15% ؎ 24%; P ؍ .03). A fall in variceal pressure 20% or greater of baseline was an independent predictor of absence of variceal bleeding; which occurred in 5% of patients with a 20% or greater fall in variceal pressure versus 42% of patients with less than a 20% reduction (P ؍ .004). The HVPG response had similar independent prognostic value (decrease H20%: 6% bleeding; decrease F20%: 45% bleeding; P ؍ .004) but identified different patients. Achieving a 20% decrease in either variceal pressure or HVPG was highly sensitive (85%) and specific ( Variceal bleeding is the most frequent and severe complication of portal hypertension in patients with cirrhosis. 1 Several treatment options are available to prevent recurrent variceal bleeding, including pharmacological therapy, endoscopic banding ligation, and surgical or transjugular intrahepatic portosystemic shunts (TIPS). 1,2 It has been recently shown that pharmacological treatment with propranolol offers almost optimal protection from bleeding and rebleeding when the portal venous pressure (estimated by the hepatic venous pressure gradient [HVPG]), achieves a target reduction. 3,4 The risk of bleeding or rebleeding is virtually abolished when the HVPG decreases to 12 mm Hg or below, 3-5 and the actuarial risk of rebleeding at 2 years is only 9% when the HVPG is reduced by at least 20% of the baseline value. 4 This has been thereafter confirmed by other studies, 6 emphasizing the concept that pharmacological treatment represents the optimal therapy in the subgroup of patients achieving such a pronounced decrease in HVPG. [1][2][3][4] Unfortunately, there is no adequate noninvasive way of assessing the HVPG response to treatment, which calls for repeated invasive hemodynamic studies.Several endoscopic findings, such as the size of the varices and the presence of red color signs (which are thought to reflect a reduced thickness of variceal wall) show a significant correlation with the risk of bleeding. 1,7,8 These are some of the main determinants of variceal wall tension, 7 which is believed to play a key role in determining variceal rupture. 7,9 According to Laplace' s law, variceal wall tension is directly re...