Nonselective β-blockers are useful to prevent
bleeding in patients with
cirrhosis and large
varices but not to prevent the development of
varices in those with compensated
cirrhosis and
portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to β-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated
cirrhosis and the response to β-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated
cirrhosis before and after intravenous
propranolol (0.15 mg/kg): 194 patients had an HVPG ≥10 mm Hg (clinically significant PHT [
CSPH]), with either no
varices (n = 80) or small
varices (n = 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with
CSPH had higher liver stiffness (P < 0.001), worse Model for
End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P = 0.01) and
splenomegaly (P = 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with
CSPH had lower systemic vascular resistance (1336 ± 423 versus 1469 ± 335 dyne · s · cm(-5) , P < 0.05) and higher cardiac index (3.3 ± 0.9 versus 2.8 ± 0.4 L/min/m(2) , P < 0.01). After
propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with
CSPH (-16 ± 12% versus -8 ± 9%, P < 0.01). The HVPG decreased ≥10% from baseline in 69% of patients with
CSPH versus 35% with subclinical PHT (P < 0.001) and decreased ≥20% in 40% versus 13%, respectively (P = 0.001).
CONCLUSION: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute β-blockade than those with
CSPH, suggesting that β-blockers are more suitable to prevent decompensation of
cirrhosis in patients with
CSPH than in earlier stages.