Author information
1Tinsley Harrison Internal Medicine Residency Program, University of Alabama at Birmingham, 1720 2(nd) Ave South, BDB 461, Birmingham, AL 35294. Electronic address: markcromer@uabmc.edu.
2Digestive Health Institute, Orlando Health, 1720 S. Orange Ave. Suite 200, Orlando, FL 32806. Electronic address: charles.wilcox@orlandohealth.com.
3Division of Gastroenterology & Hepatology, Department of Medicine, University of Alabama at Birmingham, 1720 2(nd) Ave South, BDB 321, Birmingham, AL 35294. Electronic address: mshoreibah@uabmc.edu.
Abstract
Decompensated cirrhosis is associated with a significantly increased risk of mortality. Variceal hemorrhage (VH) further increases the risk of mortality, and of future variceal bleed events. Non-selective beta-blockers (NSBBs) are effective therapy for primary and secondary prophylaxis of VH and have become the cornerstone of pharmacologic therapy in cirrhosis. Beta-blockers are associated with a reduced overall mortality and GI-bleeding related mortality; they may also confer hemodynamically independent beneficial effects in patients with decompensated cirrhosis. Long-term treatment with beta-blockers may improve decompensation-free survival in compensated cirrhosis with clinically significant portal hypertension (CSPH). Carvedilol more effectively lowers the hepatic vein portal gradient than traditional NSBBs and has been shown to improve survival in compensated cirrhosis. Treatment goals in compensated cirrhosis with CSPH should focus on early utilization of beta-blockers to prevent decompensation and reduce mortality.