A high portal pressure gradient (PPG) is associated with an increased risk of failure to control esophagogastric variceal hemorrhage and refractory ascites in patients with decompensated cirrhosis. However, direct measurement of PPG is invasive, limiting its routine use in clinical practice. Consequently, there is an urgent need for non-invasive techniques to assess PPG.

To develop and validate a deep learning model that predicts PPG values for patients with decompensated cirrhosis and identifies those with high-risk portal hypertension (HRPH), who may benefit from early transjugular intrahepatic portosystemic shunt (TIPS) intervention.

Data of 520 decompensated cirrhosis patients who underwent TIPS between June 2014 and December 2022 were retrospectively analyzed. Laboratory and imaging parameters were used to develop an artificial neural network model for predicting PPG, with feature selection via recursive feature elimination for comparison experiments. The best performing model was tested by external validation.

After excluding 92 patients, 428 were included in the final analysis. A series of comparison experiments demonstrated that a three-parameter (3P) model, which includes the international normalized ratio, portal vein diameter, and white blood cell count, achieved the highest accuracy of 87.5%. In two distinct external datasets, the model attained accuracy rates of 85.40% and 90.80%, respectively. It also showed notable ability to distinguish HRPH with an AUROC of 0.842 in external validation.

The developed 3P model could predict PPG values for decompensated cirrhosis patients and could effectively distinguish HRPH.

To evaluate the differences in the agreement between wedged hepatic venous pressure (WHVP) and portal venous pressure (PVP) at different hepatic venous pressure gradient (HVPG) levels to identify specific HVPG thresholds where WHVP can reliably estimate PVP, thus enhancing the accuracy of risk stratification and treatment decision-making for portal hypertension (PHT) patients. A multicenter study of 616 patients with PHT from three centers was stratified into five groups by their HVPG: HVPG < 12 (group A), 12 ≤ HVPG < 16 mmHg (group B), 16 ≤ HVPG < 20 mmHg (group C), 20 ≤ HVPG < 24 mmHg (group D), HVPG ≥ 24 mmHg (group E). Concordance was analyzed using Pearson's correlation coefficient (R), the intraclass correlation coefficient (ICC), and Bland‒Altman analysis in each HVPG stratum. Correlation and agreement between WHVP and PVP varied by HVPG group. Highest agreement was observed in the range of 20 ≤ HVPG < 24 mmHg. (R = 0.55, ICC = 0.68). The proportion of patients with a discrepancy between WHVP and PVP that was greater than 10% of the PVP value was highest in group A (95.7%) and lowest in group D (48.4%). Overestimation of PVP was more common in group E (44.5%), and underestimation of PVP was more common in group A (94.6%). This study does not confirm the usefulness of hepatic vein pressure measurements to predict the PVP and PPG. The means of WHVP and PVP were significantly different in ranges A, B, C, and E.

The measurement of portal venous pressure (PVP) has been extensively studied, primarily through indirect methods. However, the potential of ultrasound-guided percutaneous transhepatic PVP measurement as a direct method has been largely unexplored. This study aimed to investigate the accuracy, safety, and feasibility of this approach.

In vitro, the experiment aimed to select a needle that could accurately transmit pressure, had a small inner diameter and was suitable for liver puncture, and performed on 20 healthy New Zealand white rabbits. An ultrasound-guided percutaneous transhepatic portal vein puncture was undertaken to measure PVP. Additionally, free hepatic venous pressure (FHVP) and wedged hepatic venous pressure (WHVP) were measured under digital subtraction angiography (DSA). The correlation between the two methods was assessed. Enroll study participants from October 18, 2023 to November 11, 2023 with written informed consent. Five patients were measured the PVP under ultrasound guidance before surgery to determine the feasibility of this measurement method.

There was no significant difference in the results obtained using 9 different types of needles (P > 0.05). This demonstrated a great repeatability (P < 0.05). The 22G chiba needle with small inner diameter, allowing for accurate pressure transmission and suitable for liver puncture, was utilized for percutaneous transhepatic PVP measurement. There were positive correlations between PVP and HVPG (r = 0.881), PVP and WHVP (r = 0.709), HVPG and WHVP (r = 0.729), IVCP and FHVP (r = 0.572). The PVP was accurately and safely measured in 5 patients with segmental hepatectomy. No complications could be identified during postoperative ultrasound.

Percutaneous transhepatic portal venous puncture under ultrasound guidance is accurate, safe and feasible to measure portal venous pressure.

This study has been registered in the Chinese Clinical Trial Registry with registration number ChiCTR2300076751.

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.

To explore the correlation between HVPG and PPG in patients with alcoholic cirrhosis and PHT.

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 (R2). 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.

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.

In most patients, HVPG cannot accurately represent PPG. The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Hepatic venous pressure gradient (HVPG) has a strong predictive value for variceal rebleeding in cirrhotic patients, but the accuracy of HVPG may be compromised in nonalcoholic steatohepatitis (NASH) cirrhosis. This study aimed to evaluate the accuracy of HVPG and portal pressure gradient (PPG) for predicting rebleeding in NASH cirrhosis after acute variceal bleeding.

Thirty-eight NASH cirrhosis patients and 82 hepatitis B virus (HBV) cirrhosis patients with acute variceal bleeding were included in this study. All patients recived transjugular intrahepatic portalsystemic shunt (TIPS). The prognostic value of HVPG and PPG for variceal rebleeding was evaluated.

Compared with HBV cirrhosis, NASH cirrhosis demonstrated a lower HVPG (15.3 ± 3.8 vs. 18.0 ± 4.8; p = 0.003) and lower PPG (18.0 ± 3.7 vs. 20.0 ± 3.4; p = 0.005). HVPG (AUC = 0.82; p = 0.002) and PPG (AUC = 0.72; p = 0.027) had promising prognostic value among NASH cirrhosis patients. The optimal threshold of HVPG and PPG for predicting rebleeding in NASH cirrhosis was 17 mmHg and 20 mmHg. At multivariate analysis, HVPG ≥17 mmHg was a significant predictor of variceal rebleeding (HR 9.40; 95% CI 1.85-47.70; p = 0.007).

In the patients with cirrhosis and vairceal bleeding, the levels of HVPG and PPG were found to be low in NASH cirrhosis than HBV cirrhosis. However, the prevalence of rebleeding was similar between two groups. HVPG measurement is still an accurate way to assess the risk of variceal rebleeding in NASH cirrhosis.

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.

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.

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.

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.

The hepatic venous pressure gradient (HVPG) has been employed as the gold standard for indicating the portal venous pressure gradient (PPG) in the diagnosis of portal hypertension (PHT). However, little has been reported on whether the HVPG can accurately estimate the PPG in patients with hepatic vein collateral shunts. We aimed to explore the correlation between the HVPG and the PPG in hepatitis B cirrhosis patients with different hepatic vein anatomies.

A total of 461 hepatitis B cirrhosis patients with portal hypertension (PHT) who were treated with a transjugular intrahepatic portosystemic shunt (TIPS) between January 2016 and June 2020 were included. All patients underwent various venous pressure measurements and balloon-occluded compression hepatic venography during the TIPS operation. Agreements were evaluated by Pearson's correlation and the Bland-Altman method. Disagreements were assessed by paired t tests.

The correlation coefficient (r) values (P < 0.001) between the HVPG and the PPG of the early (151 patients, 32.8 %), middle (73 patients, 15.8 %), late (46 patients, 10.0 %), portal vein (151 patients, 32.8 %), and no lateral branch development groups (40 patients, 8.7 %) were 0.373, 0.487, 0.569, 0.690, and 0.575, respectively; the determination coefficient (R2) values were 0.139, 0.238, 0.323, 0.475, and 0.330, respectively. According to the Bland-Altman method, agreement was the greatest in the portal vein development group, with the 95 % limits of agreement (95 % LoA, mean differences ± 1.96 SD) being the smallest. The differences were statistically significant (P < 0.05).

The correlation between the HVPG and the PPG is the worst in early lateral branch development, followed by middle development, and the influence of lateral branches becomes significantly reduced in late development. Hepatic venous collateral formation is a vital factor for underestimation of the HVPG, which is the most accurate predictor of PPG in patients with portal vein development. Patients with no collateral channel development in the hepatic vein have a higher HVPG than PPG, which is an important reason for overestimation of the HVPG.

The liver is one of the most important organs in the human body, with functions such as detoxification, digestion, and blood coagulation. In terms of vascular anatomy, the liver is divided into the left and the right liver by the main portal vein, and there are three hepatic efferent veins (right, middle, and left) and two portal branches. Patients with impaired liver function have increased intrahepatic vascular resistance and splanchnic vasodilation, which may lead to an increase in the portal pressure gradient (PPG) and cause portal hypertension (PHT). In order to measure the increased pressure gradient of portal vein, the hepatic venous pressure gradient (HVPG) can be measured to reflect it in clinical practice. The accuracy of PPG measurements is directly related to patient prognosis.

To analyze the correlation between HVPG of three hepatic veins and PPG in patients with PHT.

From January 2017 to December 2019, 102 patients with PHT who met the inclusion criteria were evaluated during the transjugular intrahepatic portosystemic shunt procedure and analyzed.

The mean HVPG of the middle hepatic vein was 17.47 ± 10.25 mmHg, and the mean HVPG of the right and left hepatic veins was 16.34 ± 7.60 and 16.52 ± 8.15 mmHg, respectively. The average PPG was 26.03 ± 9.24 mmHg. The correlation coefficient and coefficient of determination of the right hepatic vein, middle hepatic vein, and left hepatic vein were 0.15 and 0.02 (P = 0.164); 0.25 and 0.05 (P = 0.013); and 0.14 and 0.02 (P = 0.013), respectively. The mean wedged hepatic vein/venous pressure (WHVP) of the middle and left hepatic veins was similar at 29.71 ± 12.48 and 29.1 ± 10.91 mmHg, respectively, and the mean WHVP of the right hepatic vein was slightly lower at 28.01 ± 8.95 mmHg. The mean portal vein pressure was 34.11 ± 8.56 mmHg. The correlation coefficient and coefficient of determination of the right hepatic vein, middle hepatic vein, and left hepatic vein were 0.26 and 0.07 (P = 0.009); 0.38 and 0.15 (P < 0.001); and 0.26 and 0.07 (P = 0.008), respectively. The average free hepatic venous pressure (FHVP) of the right hepatic vein was lowest at 11.67 ± 5.34 mmHg, and the average FHVP of the middle and left hepatic veins was slightly higher at 12.19 ± 4.88 and 11.67 ± 5.34 mmHg, respectively. The average inferior vena cava pressure was 8.27 ± 4.04 mmHg. The correlation coefficient and coefficient of determination of the right hepatic vein, middle hepatic vein, and left hepatic vein were 0.30 and 0.09 (P = 0.002); 0.18 and 0.03 (P = 0.078); and 0.16 and 0.03 (P = 0.111), respectively.

Measurement of the middle hepatic vein HVPG could better represent PPG. Considering the high success rate of clinical measurement of the right hepatic vein, it can be the second choice.

Hepatic venous pressure gradient (HVPG) is a hemodynamic index widely used for evaluating the severity of portal hypertension. Theoretically, HVPG can be measured in any of the three major (i.e., right, middle and left) hepatic veins (HVs); however, it remains unclear whether HVPGs measured in different HVs are exchangeable, and if not, what factors cause inter-HV HVPG differences? In consideration of the potential limitations of invasive in vivo measurements, we employed a computational model implemented in conjunction with stochastic parameter sampling to simulate and compare HVPG measurements in multiple HVs under various sinusoidal portal hypertensive conditions. Results demonstrated that HVPGs measured in the right and middle HVs were basically exchangeable, whereas those in the left HV were relatively lower due primarily to the smaller proportion of hepatic venous flow through the left HV compared with that through the right or middle HV. Moreover, it was found that hepatic vein-to-vein shunts (HVVS) led to a marked augmentation of inter-HV HVPG differences and significant underestimation of portal pressure gradient with HVPG. These findings suggest that understanding the distribution of hepatic venous flow and status of HVVS is essential for selecting a proper HV for implementing HVPG measurement in clinical practice.

Background: To examine the incidence of cirrhosis patients with high-risk esophageal varices (EV) who show hepatic venous pressure gradient (HVPG) < 10 mmHg and to identify their hemodynamic features. Methods: This prospective study consisted of 110 cirrhosis patients with EV, all with the candidate for primary or secondary prophylaxis. Sixty-one patients had red sign, and 49 patients were bleeders. All patients underwent both Doppler ultrasound and HVPG measurement. Results: There were 18 patients (16.4%) with HVPG < 10 mmHg. The presence of venous-venous communication (VVC) was more frequent in patients with HVPG < 10 mmHg (10/18) than in those with HVPG ≥ 10 mmHg (19/92; p = 0.0021). The flow volume in the left gastric vein (LGV) and the incidence of red sign were higher in the former (251.9 ± 150.6 mL/min; 16/18) than in the latter (181 ± 100.5 mL/min, p = 0.02; 45/92; p = 0.0018). The patients with red sign had lower HVPG (13.3 ± 4.5) but advanced LGV hemodynamics (velocity 13.2 ± 3.8 cm/s; flow volume 217.5 ± 126.6 mL/min), whereas those without red sign had higher HVPG (16.2 ± 4.6, p = 0.001) but poorer LGV hemodynamics (10.9 ± 2.3, p = 0.002; 160.1 ± 83.1, p = 0.02). Conclusion: Patients with high-risk EV with HVPG < 10 mmHg showed 16.4% incidence. Although low HVPG may be underestimated by the presence of VVC, the increased LGV hemodynamics compensates for the severity of portal hypertension, which may contribute to the development of red sign.

Hepatic venous pressure gradient (HVPG) measurement correlates with staging of liver fibrosis. Patients with nonalcoholic steatohepatitis (NASH) have a different pattern of fibrosis compared with hepatitis C virus (HCV) with possible alterations in pressures.

The aim of this study was to compare portal pressures with the stage of fibrosis in NASH in comparison with other liver diseases.

Records of all patients who had undergone transjugular liver biopsy with pressure measurements between January 2001 and June 2013 were reviewed. Wedge hepatic venous pressure (WHVP) and HVPG were compared with stages of fibrosis in liver diseases of different etiologies.

Among 142 patients included in this study, the liver disease etiology was as follows: HCV (26.6%) and NASH (24.6%), with the remaining (38.7%) grouped under other categories. The mean age of the patients was 51.2±11.5 years, with more men with HCV (73.1%) compared with NASH (51.4%) in terms of etiology (P=0.046). There were strong correlations between the stage of fibrosis with both the HVPG (r=0.64; P<0.0001) and the WHVP (r=0.63; P<0.0001) in NASH patients. Compared with HCV patients, NASH patients had a lower HVPG (3.4±2.4 vs. 7.5±11 mmHg/stage; P=0.01) with a coefficient estimate of -0.24 (P=0.017) and WHVP (9.6±5.5 vs. 14.6±15.2 mmHg/stage; P=0.03) for the stage of fibrosis.

HVPG and WHVP measurements were strongly correlated with stages of fibrosis in NASH. Patients with NASH had lower HVPG and WHVP for each stage of fibrosis compared with HCV patients. This raises the concern of underestimation of pressures by HVPG in NASH etiology for the stage of disease or increased fibrosis despite lower pressures in them.

The aim of this study was to explore the underlying pathophysiological mechanism for portal hypertension in primary biliary cirrhosis (PBC) using radiological findings.

The study included 10 patients with PBC (Scheuer stage I, one patient; stage II, two patients; and cirrhosis, seven patients) and 29 patients with viral cirrhosis. Both groups underwent Doppler ultrasound and hepatic venous catheterization. The Doppler data, pressure data, and vascular enhancement findings were compared between the groups.

Hemodynamics in the portal trunk and hepatic vein upon Doppler sonography did not differ between patients with viral cirrhosis, cirrhotic PBC, and noncirrhotic PBC. The hepatic venous pressure gradient (mean±SD) was 225.5±77.1 mmH2O (range 125-445 mmH2O) in viral cirrhosis, 224.6±39.5 mmH2O (range 170-262 mmH2O) in cirrhotic PBC, and 41.3±7.4 mmH2O (range 33-47 mmH2O) in noncirrhotic PBC, being significantly higher in viral cirrhosis and cirrhotic PBC than noncirrhotic PBC (P=0.0005). The intrahepatic portal vein was detected in a retrograde manner on the hepatic venogram in 29/29 (100%) patients with viral cirrhosis (all with gastroesophageal varices), 7/7 (100%) patients with cirrhotic PBC (5/7 with gastroesophageal varices), and 3/3 (100%) patients with noncirrhotic PBC (none with gastroesophageal varices). The presence of veno-venous communication was found in 15/29 (51.7%) patients with viral cirrhosis, 6/7 (85.7%) patients with cirrhotic PBC, and 3/3 (100%) patients with noncirrhotic PBC.

The study suggested that sinusoidal blockage is the underlying pathophysiology even in the early-stage PBC, proved by the visible intrahepatic portal vein in three noncirrhotic PBC patients, and veno-venous communication in the liver is responsible for alleviated hepatic venous pressure gradient.

To examine the efficacy of saline-enhanced ultrasound (US) in predicting the X-ray appearance of hepatic venography.

This prospective study consisted of 50 cirrhosis patients (31 males and 19 females; mean age, 64.2±11.1 years). US patterns in the liver, after injection of agitated saline via balloon-occluded catheter, were evaluated with respect to the findings of CO2-enhanced hepatic venogram.

US demonstrated two patterns: type I showing positive parenchymal enhancement (40 patients) and type II showing negative parenchymal enhancement with detection of hepatic vein (10 patients). There were also two patterns shown by hepatic venography: type A showing retrograde detection of intrahepatic portal vein (41 patients) and type B showing hepatic venous enhancement via intrahepatic venous-venous communications with no detection of intrahepatic portal vein (9 patients). All patients with type I showed retrograde detection of intrahepatic portal vein via hepatic sinusoid on X-ray venograms (type A). Of the 10 patients with type II, nine showed type B and one showed type A. Sensitivity and specificity of type I US pattern to predict the detection of intrahepatic portal vein on the venogram were 100% and 90%, respectively. There was no significant difference in hepatic venous pressure gradient or wedged hepatic venous pressure between patients with type I and type II.

Saline-enhanced US is effective in predicting the findings of hepatic venogram. As type II strongly suggests the shunt-modified venogram, image taking in these cases would be superfluous with the added advantage of avoiding unnecessary radiation exposure.

Idiopathic portal hypertension is a rare cause of portal hypertension, frequently misdiagnosed as cryptogenic cirrhosis. This study evaluates specific findings at hepatic vein catheterisation or liver stiffness in idiopathic portal hypertension.

39 cases of idiopathic portal hypertension patients were retrospectively reviewed. Hepatic vein catheterisation and liver stiffness measurements were compared to matched patients with cirrhosis and portal hypertension, and non-cirrhotic portal vein thrombosis, included as controls.

Hepatic vein-to-vein communications were found in 49% idiopathic portal hypertension patients precluding adequate hepatic venous pressure gradient measurements in 12. In the remaining 27 patients, mean hepatic venous pressure gradient (HVPG) was 7.1 ± 3.1 mm Hg. Only 5 patients had HVPG≥10mmHg. HVPG was markedly lower than in cirrhosis (17 ± 3 mm Hg, p<0.001). Mean liver stiffness in idiopathic portal hypertension was 8.4 ± 3.3 kPa; significantly higher than in non-cirrhotic portal vein thrombosis (6.4 ± 2.2 kPa, p=0.009), but lower than in cirrhosis (40.9 ± 20.5 kPa, p=0.005). Only 2 idiopathic portal hypertension patients had liver stiffness >13.6 kPa.

Patients with idiopathic portal hypertension frequently have hepatic vein-to-vein communications and, despite unequivocal signs of portal hypertension, HVPG and liver stiffness values much lower than the cut-off for clinical significant portal hypertension in cirrhosis. These findings oblige to formally rule-out idiopathic portal hypertension in the presence of signs of portal hypertension.

To prospectively correlate spleen elasticity and degree of portal hypertension estimated with the hepatic venous pressure gradient (HVPG) and to evaluate splenic elasticity as a predictor of gastroesophageal varices.

The institutional review board approved this study, and patients provided written informed consent. In a pilot study of 60 patients with chronic liver damage, the authors measured liver and spleen elasticity with real-time tissue elastography (RTE), obtained serum markers related to fibrosis, examined hepatic and splenic blood flow with duplex Doppler ultrasonography, estimated HVPG, and performed upper gastrointestinal endoscopy. Then, with use of thresholds determined in the pilot study, the authors conducted a validation trial with another 210 patients, performing all studies except the measurement of HPVG. The relationship between HVPG and the other parameters was analyzed. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) in the diagnosis of gastroesophageal varices were calculated by using cutoff values obtained from receiver operating characteristic curves.

Among the parameters associated with HVPG, correlation was closest with splenic elasticity (R = 0.854, P < .0001). When 8.24 was selected as the cutoff of splenic elasticity for predicting HVPG of more than 10 mm Hg, the accuracy of diagnosing gastroesophageal varix was 90% (sensitivity, 96%; specificity, 85%; PPV, 83%; NPV, 97%). The results of the validation trial showed that the 8.24 cutoff for splenic elasticity was associated with a diagnostic accuracy of 94.8% (sensitivity, 98%; specificity, 93.8%; PPV, 82.1%; NPV, 99.4%) for gastroesophageal varices.

Splenic elasticity determined with RTE is the most closely associated parameter for evaluating HVPG and is useful as a clinical marker of portal hypertension and a predictive marker of gastroesophageal varices.