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SVR reduces hepatic venous pressure gradient, portal hypertension persists

Sustained virologic response correlated with reduced hepatic venous pressure gradient in patients with HCV-associated cirrhosis, according to a recently published study. However, clinically significant portal hypertension continued to persist in most patients.

“Development of [clinically significant portal hypertension] is a hallmark in the natural history of cirrhosis because it is associated with a higher risk of hepatic decompensation, and increased risk of hepatocellular carcinoma and death,” Sabela Lens, MD, from the Universidad de Barcelona, and colleagues wrote. “Our study was performed in [a] large cohort of patients with cirrhosis and CSPH, most of them with esophageal varices and/or previous clinical decompensation. The results clearly show that [hepatic venous pressure gradient] is significantly reduced when evaluated 24 weeks after obtaining SVR with the use of interferon-free regimens.”

Inclusion criteria for the multicenter prospective study of patients with HCV-related cirrhosis included presence of clinically significant portal hypertension within 6 months before treatment and SVR by 24 weeks after treatment.

All 226 patients included had a hepatic venous pressure gradient of 10 mmHg or higher (range, 12-18 mmHg). Hepatic venous pressure gradient values increased with the presence of varices and their size (P < .001) and were higher among patients with decompensated cirrhosis (P < .01).

Following SVR, 140 patients had a hepatic venous pressure gradient reduction of 10% or more from baseline and 90 patients had a reduction of 20% or more, while 176 patients had persistent clinically significant portal hypertension including 142 with hepatic venous pressure gradient of 12 mmHg or higher and 57 with a gradient of 16 mmHg or higher. Thirty-nine patients had an increase in hepatic venous pressure gradient.

On multivariate analysis, lower baseline levels were an independent negative predictor of a 10% or more reduction (OR = 0.52; 95% CI, 0.27-0.59). Baseline hepatic venous pressure gradient and liver stiffness measure were significantly lower among those with a 20% or more reduction (OR = 0.92; 95% CI, 0.85-0.98).

Patients with persistent clinically significant portal hypertension despite SVR had higher baseline hepatic venous pressure gradient (OR = 1.9; 95% CI, 1.5-2.5) and the presence of esophageal varices (OR = 3.2; 95% CI, 1.2-8.3). Those whose hepatic venous pressure gradient values increased had significantly higher previous instances of acute variceal bleeding (OR = 2.7; 95% CI, 1.1-6.7) and lower platelet count (OR = 0.99; 95% CI, 0.98-0.99).

“In spite of a significant [hepatic venous pressure gradient] reduction at 6 months after the end of therapy, [clinically significant portal hypertension] persisted in a high proportion of patients (78%), implying that these patients remain at high risk of developing complications of portal hypertension and hepatocellular carcinoma,” the researchers concluded. “It is relevant to closely monitor patients with [clinically significant portal hypertension] despite a relevant [liver stiffness measurement] reduction after SVR.” – by Talitha Bennett

Disclosure: Lens reports she received speaker and consultant fees from Gilead, AbbVie and Janssen. Please see the full study for the other researchers’ relevant financial disclosures.