Background 9-week TAA: -17%, p = 0.0038), decreased liver fibrosis area (-26.8%, p = 0.0013 vs. -23.1%, p = 0.0047), and reduced α-SMA expression (-22.7%, p = 0.0018 vs. -17.4%, p = 0.0455). Additionally, carvedilol improved endothelial dysfunction and reduced oxidative stress and inflammation. Propranolol did not exert these beneficial effects and produced a smaller, non-significant reduction in PP (-7%, p = 0.4029). Conclusions The greater reduction in PP achieved with carvedilol is mediated not only by its non-selective β-blocker effects but, more importantly, by its ability to reverse hepatic endothelial dysfunction, reduce fibrosis, enhance antioxidant activity, and exert moderate anti-inflammatory effects. These findings support extending the use of carvedilol even to patients without overt signs of portal hypertension. Impact And Implications Carvedilol is considered the best β-blocker for treating portal hypertension. In this study we show that carvedilol, unlike traditional β-blockers such as propranolol, downregulates the factors that lead to increased portal pressure in cirrhosis: it lowers the hepatic vascular tone by counteracting hepatic sinusoidal endothelial dysfunction, and decreases liver fibrosis by deactivating hepatic stellate cells and inhibiting their proliferation. On top of decreasing portal vein inflow via its non-selective β-blocker effect. Moreover, through its antioxidant and anti-inflammatory activity, it may contribute to improving liver function. These effects are noted both in early and in advanced cirrhosis, suggesting that it can be effective in slowing/reversing disease progression when associated with etiological therapy.
Nulan et al. (Wed,) studied this question.