Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension

BACKGROUND Portal hypertension(PHT)in patients with alcoholic cirrhosis causes a range of clinical symptoms,including gastroesophageal varices and ascites.The hepatic venous pressure gradient(HVPG),which is easier to measure,has replaced the portal venous pressure gradient(PPG)as the gold standard for diagnosing PHT in clinical practice.Therefore,attention should be paid to the correlation between HVPG and PPG.METHODS Between January 2017 and June 2020,134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures.Correlations were assessed using Pearson’s correlation coefficient to estimate the correlation coefficient(r)and determination coefficient(R^(2)).Bland-Altman plots were constructed to further analyze the agreement between the measurements.Disagreements were analyzed using paired t tests,and P values<0.05 were considered statistically significant.RESULTS In this study,the correlation coefficient(r)and determination coefficient(R2)between HVPG and PPG were 0.201 and 0.040,respectively(P=0.020).In the 108 patients with no collateral branch,the average wedged hepatic venous pressure was lower than the average portal venous pressure(30.65±8.17 vs.33.25±6.60 mmHg,P=0.002).Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography(19.4%),while the average PPG was significantly higher than the average HVPG(25.94±7.42 mmHg vs 9.86±7.44 mmHg;P<0.001).The differences between HVPG and PPG<5 mmHg in the collateral vs no collateral branch groups were three cases(11.54%)and 44 cases(40.74%),respectively.CONCLUSION In most patients,HVPG cannot accurately represent PPG.The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Portal Hypertension in Nonalcoholic Fatty Liver Disease: Challenges and Paradigms

Portal hypertension in cirrhosis is defined as an increase in the portal pressure gradient(PPG)between the portal and hepatic veins and is traditionally estimated by the hepatic venous pressure gradient(HVPG),which is the difference in pressure between the free-floating and wedged positions of a balloon catheter in the hepatic vein.By convention,􀀫HVPG≥10mmHg indicates clinically significant portal hypertension,which is associated with adverse clinical outcomes.Nonalcoholic fatty liver disease(NAFLD)is a common disorder with a heterogeneous clinical course,which includes the development of portal hypertension.There is increasing evidence that portal hypertension in NAFLD deserves special considerations.First,elevated PPG often precedes fibrosis in NAFLD,suggesting a bidirectional relationship between these pathological processes.Second,HVPG underestimates PPG in NAFLD,suggesting that portal hypertension is more prevalent in this condition than currently believed.Third,cellular mechanoresponses generated early in the pathogenesis of NAFLD provide a mechanistic explanation for the pressurefibrosis paradigm.Finally,a better understanding of liver mechanobiology in NAFLD may aid in the development of novel pharmaceutical targets for prevention and management of this disease.