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Carvedilol is a potent noncardioselective β-blocker, with weak vasodilating properties because of α 1 blockade. A reduction in both intrahepatic and portocollateral resistance contribute to enhanced effects on portal pressure. There are 10 published hemodynamic studies involving 168 patients investigating the role of carvedilol in portal hypertension. A reduction in the hepatic venous pressure gradient of up to 43% (range 10–43%) has been reported, particularly after chronic administration. However, tolerability at doses greater than 12.5 mg/day was comprised because of a fall in mean arterial pressure (MAP), particularly in ascitic patients. Carvedilol was more effective than propranolol in reducing hepatic venous pressure gradient in two of three studies, albeit with a greater decrease in MAP. One study showed deterioration of pre-existing ascites with carvedilol. The addition of nitrates to propranolol was less effective than carvedilol monotherapy in another study. A large multicentre, randomized controlled trial comparing carvedilol with variceal band ligation for the prevention of variceal bleeding has been published. Carvedilol resulted in fewer episodes of bleeding, although there was no difference in survival. Carvedilol was well tolerated. Carvedilol is a promising agent, and seems to be more effective than propranolol in hemodynamic studies. The efficacy in primary prevention of variceal bleeding suggests that carvedilol has a role in the management of clinically significant portal hypertension.