The Baveno VII workshop held in October 2021 was featured by the subject of personalized care in portal hypertension. The workshop focused on the following 9 topics including: the relevance and indications for measuring the hepatic venous pressure gradient as a gold standard; the use of non-invasive tools for the diagnosis of compensated advanced chronic liver disease and clinically significant portal hypertension; the impact of etiological and of non-etiological therapies in the course of cirrhosis; the prevention of the first episode of decompensation; the management of the acute bleeding episode; the prevention of further decompensation; as well as the diagnosis and management of splanchnic vein thrombosis and other vascular disorders of the liver. This essay provides a compilation and summary of recommendations regarding the abovementioned topics, and presents the most recent research proceedings and the corresponding consensus to our readers.
Consensus ; Esophageal and Gastric Varices ; Humans ; Hypertension, Portal/therapy* ; Liver Cirrhosis/therapy* ; Portal Pressure

The liver is abundant in blood supply and receives 25% of the cardiac output via the hepatic artery and portal vein. Circulatory disorders may cause hepatic injury, resulting in congestive hepatopathy(CH) and ischemic hepatitis(IH). Hepatic congestion arising from increased hepatic venous pressure and decreased cardiac output is the common pathophysiological basis of both CH and IH. In addition, extensive arteriovenous shunts affect portal pressure and cardiac function, leading to alterations of hepatic blood supply. The current review summarizes the pathophysiology, clinical manifestations and therapeutic interventions of the above diseases, in order to provide reference for clinical practice.
Cardiovascular Diseases ; Hepatic Artery ; Humans ; Liver ; Liver Diseases ; Portal Pressure ; Portal Vein

BACKGROUND/AIMS: In recent years, greater assessment accuracy after transjugular intrahepatic portosystemic shunt (TIPS) to ascertain prognosis has become important in decompensated cirrhosis due to portal hypertension. The aim of this study was to assess the ratio of the portal pressure gradient (PPG) pre-TIPS (pre-PPG) to albumin (PPA), which influence ascites formation in cirrhotic patients in the 6-months after TIPS placement, and is a metric introduced in our study. METHODS: This was a retrospective cohort study of 58 patients with decompensated cirrhosis admitted to an academic hospital for the purpose of TIPS placement. We collected the following data: demographics, laboratory measures, and PPG during the TIPS procedure. Then we analyzed the association between the above data and ascites formation post-TIPS in cirrhosis patients. RESULTS: Twenty-two patients with ascites and 28 without ascites were evaluated. Univariate and binary logistic regression analysis were adjusted for the following variables: to determine prognosis; Child-Pugh scores, lymphocyte count, platelet count, hemoglobin level, albumin level and pre-PPG or PPA. The outcome showed that PPA was better than pre-PPG and albumin for predicting ascites according to area under receiver operating characteristic curves and a statistical model that also showed PPA’s influence 6-months post-TIPS. CONCLUSIONS: The combined measurement of pre-PPG and albumin, defined as PPA, may provide a better way to predict post-TIPS ascites in decompensated cirrhosis, which underlines the need for a large clinical trial in the future.
Ascites ; Cohort Studies ; Demography ; Fibrosis ; Humans ; Hypertension, Portal ; Logistic Models ; Lymphocyte Count ; Models, Statistical ; Platelet Count ; Portal Pressure ; Portasystemic Shunt, Surgical ; Prognosis ; Retrospective Studies ; ROC Curve ; Serum Albumin

BACKGROUND: This study aimed to determine the prognostic role of the categorized hemodynamic stage (HS) based on the hepatic venous pressure gradient (HVPG) in patients with portal hypertension. METHODS: Of 1,025 cirrhotic patients who underwent HVPG measurement, data on 572 non-critically-ill patients were collected retrospectively between 2008 and 2013. The following two HS categorizations were used: HS-1 (6–9, 10–12, 13–16, 17–20, and > 20 mmHg; designated as groups 1–5, respectively) and HS-2 (6–12, 13–20, and > 20 mmHg). Clinical characteristics, mortality rates, and prognostic predictors were analyzed according to the categorized HS. RESULTS: During the mean follow-up period of 25 months, 86 (15.0%) patients died. The numbers of deaths in HS-1 groups were 7 (6.3%), 7 (6.9%), 30 (18.0%), 20 (15.6%), and 22 (34.4%), respectively (P < 0.001). However, the traditional HVPG cutoffs of 10 and 16 mmHg did not improve the discrimination of mortality. In contrast, the mortality rates did differ significantly between the three HS-2 groups (P < 0.05). In the multivariate analysis, all models revealed that HS-2 was a common prognostic factor in predicting mortality. The mortality rates increased significantly according to HS-2 in patients with hypoalbuminemia (HVPG, 13–20 mmHg; hazard ratio [HR], 2.54 and HVPG > 20 mmHg; HR, 5.45) and intermediate model for end-stage liver disease (MELD) score (HVPG, 13–20 mmHg; HR, 3.86 and HVPG > 20 mmHg; HR, 8.77; P < 0.05). CONCLUSION: Categorizing HVPG values according to HS-2 is a useful prognostic modality in patients with portal hypertension and can play an independent role in predicting the prognosis in patients with hypoalbuminemia and an intermediate MELD score.
Discrimination (Psychology) ; Fibrosis ; Follow-Up Studies ; Hemodynamics ; Humans ; Hypertension, Portal ; Hypoalbuminemia ; Liver Diseases ; Mortality ; Multivariate Analysis ; Prognosis ; Retrospective Studies ; Venous Pressure

PURPOSE: Posthepatectomy liver failure is a serious complication and considered to be caused by increased portal pressure and flow. Splanchnic vasoactive agents and propranolol are known to decrease portal pressure. The aim of this study was to identify optimal candidates with potential for clinical use among somatostatin, terlipressin, and propranolol using rats with 90% hepatectomy. METHODS: Rats were divided into 5 groups: sham operation (n = 6), control (n = 20), propranolol (n = 20), somatostatin (n = 20), and terlipressin group (n = 20). Seven-day survival rates and portal pressure change were measured, and biochemical, histologic, and molecular analyses were performed. RESULTS: Portal pressure was significantly decreased in all 3 treatment groups compared to control. All treatment groups showed a tendency of decreased liver injury markers, and somatostatin showed the most prominent effect at 24 hours postoperatively. Histologic liver injury at 24 hours was significantly decreased in propranolol and terlipressin groups (P = 0.016, respectively) and somatostatin group showed borderline significance (P = 0.056). Hepatocyte proliferation was significantly increased after 24 hours in all treatment groups. Median survival was significantly increased in terlipressin group compared to control group (P < 0.01). CONCLUSION: Terlipressin is considered as the best candidate, while somatostatin has good potential for clinical use, considering their effects on portal pressure and subsequent decrease in liver injury and increase in liver regeneration.
Animals ; Hepatectomy* ; Hepatocytes ; Liver Failure ; Liver Regeneration* ; Liver* ; Portal Pressure ; Propranolol ; Rats* ; Somatostatin ; Survival Rate ; Vasoconstrictor Agents*

A growing number of studies have explored endoscopic ultrasound (EUS)-guided vascular catheterization. Potential clinical applications of EUS-guided portal venous access include angiography, measurement of the portosystemic pressure gradient, EUS-guided transhepatic intrahepatic portosystemic shunt creation and portal vein sampling for the evaluation in gastrointestinal cancer. The following article reviews the different devices and techniques employed in these applications.
Angiography ; Endosonography ; Gastrointestinal Neoplasms ; Portal Pressure* ; Portal Vein ; Portasystemic Shunt, Surgical ; Ultrasonography ; Vascular Access Devices

Pathologic increase in portal pressure can be caused by increased resistance to blood flow at the level of the portal vein (pre-hepatic), hepatic sinusoids (hepatic) or hepatovenous outflow (post-hepatic). This results in recruitment and dilatation of tiny portosystemic collateral pathways, diverting portal venous blood flow to low pressure systemic veins. Based on the location of the causative factor of portal venous resistance, different collateral pathways and shunts may develop, resulting in unique syndromes of portal hypertension and in-turn requiring unique treatment options. Knowledge of the common and less-common portosystemic collateral pathways have important implication for clinicians and interventionalists. The objective of this pictorial review is to illustrate the various collateral pathways using diagrammatic and conventional non-invasive and invasive radiologic examples. Additionally, we will briefly address minimally invasive interventional techniques used to treat the sequelae of portal hypertension.
Dilatation ; Hypertension, Portal ; Portal Pressure ; Portal Vein ; Radiology, Interventional ; Varicose Veins ; Veins

Idiopathic non-cirrhotic portal hypertension (INCPH) is a disease with an uncertain etiology consisting of non-cirrhotic portal hypertension and portal pressure increase in the absence of liver cirrhosis. In INCPH, patients exhibit normal liver functions and structures. The factors associated with INCPH include the following: Umbilical/portal pyremia, bacterial diseases, prothrombic states, chronic exposure to arsenic, vinyl chloride monomers, genetic disorders, and autoimmune diseases. Approximately 70% of patients present a history of major variceal bleeding, and treatment relies on the prevention of complications related to portal hypertension. Autoimmune disorders associated with INCPH are mainly systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis. To the best of our knowledge, a case of ankylosing spondylitis (AS) associated with INCPH has not been reported thus far. Therfore, we report our experience of a patient with AS accompanied by INCPH, who showed perisplenic varices with patent spleno-portal axis and hepatic veins along with no evidence of cirrhosis on liver biopsy, and provide a brief literature review.
Arsenic ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Biopsy ; Esophageal and Gastric Varices ; Fibrosis ; Hepatic Veins ; Humans ; Hypertension, Portal ; Liver ; Liver Cirrhosis ; Lupus Erythematosus, Systemic ; Portal Pressure ; Scleroderma, Systemic ; Spondylitis, Ankylosing ; Varicose Veins ; Vinyl Chloride

Portal hypertension is a major pathophysiology in patients with cirrhosis. Portal pressure is the gold standard to evaluate the severity of portal hypertension, and radiological intervention is the only procedure for pressure measurement. Ultrasound (US) is a simple and noninvasive imaging modality available worldwide. B-mode imaging allows broad applications for patients to detect and characterize chronic liver diseases and focal hepatic lesions. The Doppler technique offers real-time observation of blood flow with qualitative and quantitative assessments, and the application of microbubble-based contrast agents has improved the detectability of peripheral blood flow. In addition, elastography for the liver and spleen covers a wider field beyond the original purpose of fibrosis assessment. These developments enhance the practical use of US in the evaluation of portal hemodynamic abnormalities. This article reviews the recent progress of US in the assessment of portal hypertension.
Contrast Media ; Elasticity Imaging Techniques ; Fibrosis ; Hemodynamics ; Humans ; Hypertension, Portal* ; Liver ; Liver Diseases ; Portal Pressure ; Spleen ; Ultrasonography* ; Ultrasonography, Doppler

BACKGROUND/AIMS: Non-selective beta blockers (NSBBs) are currently the only accepted regimen for preventing portal hypertension (PHT)-related complications. However, the effect of NSBBs is insufficient in many cases. Bacterial translocation (BT) is one of the aggravating factors of PHT in cirrhosis; therefore, selective intestinal decontamination by rifaximin is a possible therapeutic option for improving PHT. We investigated whether the addition of rifaximin to propranolol therapy can improve hepatic venous pressure gradient (HVPG) response. METHODS: Sixty-four cirrhosis patients were randomly assigned to propranolol monotherapy (n=48) versus rifaximin and propranolol combination therapy (n=16). Baseline and post-treatment HVPG values, BT-related markers (lipopolysaccharide [LPS], LPS-binding protein [LBP], interleukin-6 [IL-6], and tumor necrosis factor α [TNF-α]), serological data, and adverse event data were collected. HVPG response rate was the primary endpoint. RESULTS: Combination therapy was associated with better HVPG response rates than monotherapy (56.2% vs 87.5%, p=0.034). In combination therapy, posttreatment BT-related markers were significantly decreased (LPS, p=0.005; LBP, p=0.005; IL-6, p=0.005; TNF-α, p=0.047). CONCLUSIONS: Rifaximin combination therapy showed an additive effect in improving PHT compared to propranolol monotherapy. These pilot data suggest that the addition of rifaximin to NSBBs could be a good therapeutic option for overcoming the limited effectiveness of NSBBs.
Bacterial Translocation ; Decontamination ; Fibrosis ; Humans ; Hypertension, Portal ; Interleukin-6 ; Pilot Projects* ; Portal Pressure* ; Propranolol* ; Tumor Necrosis Factor-alpha ; Venous Pressure