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≥10 mmHg 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 pressure-fibrosis 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.

OBJECTIVE: To assess the correlation and agreement between hepatic venous pressure gradient (HVPG) and portal pressure gradient (PPG) in patients with autoimmune liver diseases (ALD) and portal hypertension, and to investigate the extent to which hepatic vein collateralization affects the accuracy of this assessment.
METHODS: Ninety-eight patients with ALD between 2017 and 2021 who underwent transjugular intrahepatic portosystemic shunt with conventional and innovative 15 mL pressurized contrast were selected to measure wedged hepatic venous pressure (WHVP) and portal venous pressure and to calculate the HVPG and PPG. Pearson\'s correlation was used for correlation analysis between the two groups. Bland-Altman plots were plotted to estimate the agreement between paired pressures.
RESULTS: The r values of PPG and HVPG in the early, middle, late, and portal venous visualization were 0.404, 0.789, 0.807, and 0.830, respectively, and the R2 values were 0.163, 0.622, 0.651, and 0.690, respectively. The p value for the r and R2 values in the early group was 0.015, and the p values in the remaining groups were less than 0.001. Bland-Altman plots showed that patients in the portal venous visualization group had the narrowest 95% limits of agreement. The mean value of the difference was close to the zero-scale line.
CONCLUSIONS: In patients with ALD, the correlation between the HVPG and PPG was good, and the later the collateral development, the better the correlation. Hepatic vein collateral was an essential factor in underestimating WHVP and HVPG, and the earlier the collateral appeared, the more obvious the underestimation.

BACKGROUND: The hemodynamics of patients with cirrhosis and portal hypertension are complex and variable. We aimed to investigate differences in venous pressures determined by innovative angiography and conventional angiography using balloon occlusion of the hepatic veins in patients with alcoholic cirrhosis and portal hypertension.
METHODS: A total of 134 patients with alcoholic cirrhosis who fulfilled the inclusion criteria from June 2017 to June 2020 were included. During transjugular intrahepatic portosystemic shunt, conventional and innovative angiography were performed, and venous pressures were measured. A paired t-test and Pearson\'s correlation coefficient were used for analysis.
RESULTS: Conventional and innovative hepatic angiography detected lateral branches of the hepatic vein in 26 (19.4%) and 65 (48.5%) cases, respectively (P < 0.001). Innovative angiography detected a total of 65 patients with lateral shunts, of whom 37 (56.9%) had initial shunts. The average wedged hepatic venous pressure and portal venous pressure of the initial lateral branches were 21.27 ± 6.66 and 35.84 ± 7.86 mmHg, respectively, with correlation and determination coefficients of 0.342 (P < 0.05) and 0.117, respectively. The mean hepatic venous pressure gradient and portal pressure gradient were 9.59 ± 7.64 and 26.86 ± 6.78 mmHg, respectively, with correlation and determination coefficients of 0.292 (P = 0.079) and 0.085, respectively.
CONCLUSIONS: Innovative angiography reveals collateral branches of the hepatic veins more effectively than conventional angiography. Hepatic vein collateral branches are the primary factors leading to underestimation of wedged hepatic venous pressures and hepatic venous pressure gradients, with the initial hepatic vein collateral branches resulting in the most severe underestimations.

BACKGROUND: Iodine concentrations measured using dual-energy spectral CT (DESCT) have been recently proposed as providing good performance for examining tissues hemodynamics.
OBJECTIVE: To evaluate the diagnostic efficacy of DESCT-derived parameters in evaluating portal venous pressure in patients with liver cirrhosis.
METHODS: A total of 71 patients with liver cirrhosis who underwent percutaneous transhepatic portal vein puncture procedures were included in this study. All participants underwent DESCT and gastrointestinal endoscopy within one month before the operation. The direct portal venous pressure of each participant was measured preoperatively.
RESULTS: Stepwise multivariate linear regression analysis showed that the iodine concentrations in the portal vein and hepatic parenchyma during the portal venous phase and the platelet count were independently correlated with the direct portal venous pressure (P < 0.001, P < 0.001, and P = 0.030, respectively). Receiver operating characteristic analysis revealed that the normalized iodine concentration of the hepatic parenchyma had the best performance for identifying clinically significant portal hypertension (≥10 mmHg), esophageal varices, and high-risk esophageal varices (the area under the curve values were 0.951, 0.932, and 0.960, respectively).
CONCLUSIONS: The normalized iodine concentration of the hepatic parenchyma is a reliable parameter to non-invasively assess portal venous pressure in patients with liver cirrhosis.

OBJECTIVE: To evaluate the impact of intraoperatively measured portal vein pressure (PVP) on mortality in non-cirrhotic bilharzial patients undergoing splenectomy.
METHODS: The present study is a prospective study that was conducted in Egypt from April 2014 to April 2018. Adult patients with non-cirrhotic bilharziasis who were scheduled to undergo splenectomy were included. Studied cases were divided into a survival cohort and a non-survival cohort. The main objective was the correlation between the incidence of mortality and intraoperative PVP.
RESULTS: The present work comprised 130 cases with a mean age of 51.8 ± 6.4 years old. The in-hospital mortality rate was 22.3%, with sepsis as a major cause of death (37.9%). In term of the association between preoperative variables and mortality, survivors had statistically significant lower portal vein diameter (13.6 ± 1.8 versus 15.2 ± 1.8mm; p<0.001) and higher portal vein velocity (14.2 ± 1.8 versus 10.4 ± 2.3 cm/sec; p<0.001) than nonsurvivors. The survived patients had significantly lower PVP (13.9 ± 1.1 versus 17.7 ± 2.7; p<0.001). A cut-off value of ≥14.5 mmHg, the PVP yielded a sensitivity of 86.2% and a specificity of 69% for the prediction of mortality. The association analysis showed a statistically significant association between mortality and postoperative liver function parameters.
CONCLUSIONS: High intraoperative PVP is linked to early postoperative death in non-cirrhotic cases undergoing splenectomy. Our study showed that PVP > 14.5mmHg was an independent predictor of death and showed good diagnostic performance for the detection of early postoperative mortality.

Cirrhosis caused by viral and alcoholic hepatitis is an essential cause of portal hypertension (PHT). The incidence of PHT complication is directly proportional to portal venous pressure (PVP), and the clinical research of PVP and its hemodynamic indexes is of great significance for deciding the treatment strategy of PHT. Various techniques are currently being developed to decrease portal pressure but hemodynamic side effects may occur. In this article, the hemodynamic indexes of cirrhotic PHT patients were studied to explore the correlation between the index and PVP and to evaluate the clinical value of Doppler ultrasound in measuring PVP in patients with PHT. This was achieved by selecting 90 cirrhotic PHT patients who underwent transjugular intrahepatic portosystemic shunt in our hospital from June 2015 to September 2019. Fifty healthy people who had a physical examination in the hospital in the same period were selected as the control group. The liver hemodynamic parameters of two groups were measured by Doppler ultrasound, and the cirrhotic PHT patients were graded by the Child-Pugh grading method to evaluate the liver function and measure the PVP value. The results showed that both the central portal vein velocity (PVV) and splenic vein velocity (SVV) of the PHT group were lower than those of the control group. Also, the portal vein diameter (PVD), portal venous flow and splenic vein diameter (SVD) were higher than those of the control group (all Ps < 0.05). Among liver function graded PHT patients, the PVD, PVV, SVD and SVV were significantly different (all Ps < 0.05). Furthermore, the PVP of patients with liver function grades A, B and C was 38.9 ± 1.4, 40.6 ± 5.1 and 42.5 ± 4.8 cmH2O, respectively, with a significant difference. It can be concluded from this study that Doppler ultrasound can be used as a tool for clinical assessment of PHT in cirrhosis patients. Doppler ultrasound showed a good prospect in noninvasive detection of PHT in cirrhosis; however, this technique needs application on large sample population study to validate the results.

Nonalcoholic fatty liver disease (NAFLD) is a substantial and growing problem worldwide and has become the second most common indication for liver transplantation as it may progress to cirrhosis and develop complications from portal hypertension primarily caused by advanced fibrosis and erratic tissue remodeling. However, elevated portal venous pressure has also been detected in experimental models of fatty liver and in human NAFLD when fibrosis is far less advanced and cirrhosis is absent. Early increases in intrahepatic vascular resistance may contribute to the progression of liver disease. Specific pathophenotypes linked to the development of portal hypertension in NAFLD include hepatocellular lipid accumulation and ballooning injury, capillarization of liver sinusoidal endothelial cells, enhanced contractility of hepatic stellate cells, activation of Kupffer cells and pro-inflammatory pathways, adhesion and entrapment of recruited leukocytes, microthrombosis, angiogenesis and perisinusoidal fibrosis. These pathological events are amplified in NAFLD by concomitant visceral obesity, insulin resistance, type 2 diabetes and dysbiosis, promoting aberrant interactions with adipose tissue, skeletal muscle and gut microbiota. Measurement of the hepatic venous pressure gradient by retrograde insertion of a balloon-tipped central vein catheter is the current reference method for predicting outcomes of cirrhosis associated with clinically significant portal hypertension and guiding interventions. This invasive technique is rarely considered in the absence of cirrhosis where currently available clinical, imaging and laboratory correlates of portal hypertension may not reflect early changes in liver hemodynamics. Availability of less invasive but sufficiently sensitive methods for the assessment of portal venous pressure in NAFLD remains therefore an unmet need. Recent efforts to develop new biomarkers and endoscopy-based approaches such as endoscopic ultrasound-guided measurement of portal pressure gradient may help achieve this goal. In addition, cellular and molecular targets are being identified to guide emerging therapies in the prevention and management of portal hypertension.

OBJECTIVE: Portal venous pressure (PVP) measurement is of clinical significance, especially in patients with portal hypertension. However, the invasive nature and associated complications limits its application. The aim of the study is to propose a noninvasive predictive model of PVP values based on CT-extracted radiomic features.
METHODS: Radiomics PVP (rPVP) models based on liver, spleen and combined features were established on an experimental cohort of 169 subjects. Radiomics features were extracted from each ROI and reduced via the LASSO regression to achieve an optimal predictive formula. A validation cohort of 62 patients treated for gastroesophageal varices (GOV) was used to confirm the utility of rPVP in predicting variceal recurrence. The association between rPVP and response to treatment was observed.
RESULTS: Three separate predictive formula for PVP were derived from radiomics features. rPVP was significantly correlated to patient response to endoscopic treatment for GOV. Among which, the model containing both liver and spleen features has the highest predictability of variceal recurrence, with an optimal cut-off value at 29.102 mmHg (AUC 0.866). A Kaplan Meier analysis further confirmed the difference between patients with varying rPVP values.
CONCLUSIONS: PVP values can be accurately predicted by a non-invasive, CT derived radiomics model. rPVP serves as a non-invasive and precise reference for predicting treatment outcome for GOV secondary to portal hypertension.

It has been reported that variceal pressure can predict the occurrence of variceal bleeding. However, the majority of methods presently used to measure variceal pressure are either invasive or inconvenient. In the present study, a fiber-optic pressure sensor was constructed to detect variceal pressure. The prospective study focused on the in vitro accuracy of a fiber-optic pressure sensor and investigated the clinical reliability and feasibility of this method. The fiber-optic pressure sensor covered a pressure-sensitive probe containing a fiber-optic pressure sensor and a workstation to record the pressure tracing. It was hypothesized that the endoscopic fiber-optic pressure sensor can effectively predict the risk of variceal bleeding. To test this hypothesis, 80 patients who suffered from cirrhosis and who had a history of variceal bleeding were included in the present study. The fiber-optic pressure sensor was guided through the biopsy channel using an endoscope in the patient cohort. Transjugular intrahepatic stent-shunt (TIPS) was subsequently performed within 24 h after measuring variceal pressure. A comparison of the results of the 80 patients was made between variceal pressure measured by the endoscopic fiber-optic pressure sensor and the portal pressure gradient (PPG) measured by a TIPS. The variceal pressure measurements with the fiber-optic pressure sensor were technically satisfactory in 78 patients. The results indicated that there was a linear correlation between the variceal pressure measured by the endoscopic fiber-optic pressure sensor and the PPG (r=0.940, P<0.001). These observations suggest that the fiber-optic pressure sensor is an accurate and feasible measurement technique. Therefore, the results of the present study indicate that the endoscopic fiber-optic pressure sensor is effective in predicting the risk of variceal bleeding.

BACKGROUND: Graft inflow modulation (GIM) during adult-to-adult living donor liver transplantation (LDLT) is a common strategy to avoid small-for-size syndrome, and some transplant surgeons attempt small size graft strategy with frequent GIM procedures, which are mostly performed by splenectomy, in LDLT. However, splenectomy can cause serious complications such as portal vein thrombosis and overwhelming postsplenectomy infection.
METHODS: Forty-eight adult-to-adult LDLT recipients were enrolled in this study and retrospectively reviewed. We applied the graft selection criteria, which routinely fulfill graft-to-recipient weight ratio ≥ 0.8%, and consider GIM as a backup strategy for high portal venous pressure (PVP).
RESULTS: In our current strategy of LDLT, splenectomy was performed mostly due to hepatitis C and splenic arterial aneurysms, but splenectomy for GIM was intended to only one patient (2.1%). The final PVP values ≤ 20 mmHg were achieved in all recipients, and no significant difference was observed in patient survival or postoperative clinical course based on whether splenectomy was performed or not. However, 6 of 18 patients with splenectomy (33.3%) developed postsplenectomy portal vein thrombosis (PVT), while none of the 30 patients without splenectomy developed PVT after LDLT. Splenectomy was identified as a risk factor of PVT in this study (P < 0.001). Our study revealed that a lower final PVP could be risk factor of postsplenectomy PVT.
CONCLUSIONS: Using sufficient size grafts was one of the direct solutions to control PVP, and allowed GIM to be reserved as a backup procedure. Splenectomy should be avoided as much as possible during LDLT because splenectomy was found to be a definite risk factor of PVT. In splenectomy cases with a lower final PVP, a close follow-up is required for early detection and treatment of PVT.