Do β-blockers pose more harm than good in decompensated cirrhosis?

In patients with decompensated cirrhosis, β-blockers trigger a stronger systemic haemodynamic response and exert a weaker portal pressure-lowering effect, a recent study has found.

Of the 403 patients included, 190 and 213 had decompensated and compensated cirrhosis, respectively. Baseline active alcohol consumption was higher in decompensated patients, as was alcohol-related cirrhosis. Liver function, platelet count, and portal flow velocity were also worse in decompensated cirrhosis, and liver stiffness was greater.

Portal hypertension was more severe in decompensated patients at baseline, and they had a more developed hyperdynamic circulatory state.

Under treatment with β-blockers, portal pressure decrease was lower in decompensated patients (10±18 percent vs 15±12 percent; p<0.05), while reductions in heart rate (p<0.001) and cardiac output (p<0.01) were greater.

The probability of mortality was higher in decompensated, both at 3 years (14 percent vs 30 percent) and at 5 years (22 percent vs 41 percent; p<0.001 for both). Competing-risk regression analysis showed that cardiac output under β-blocker treatment was a good and independent predictor of mortality in decompensated patients (C-index, 0.74, 95 percent confidence interval, 0.66–0.83).

“β-blockers are often used to reduce the risk of variceal bleeding in patients with cirrhosis,” researchers said. “Herein, we show that in patients with decompensated cirrhosis the potentially detrimental systemic effects of β-blockers are greater than in compensated patients, while the beneficial pressure lowering effects are reduced.”