Hepatic Vein Pressure Research Articles

Combination of carvedilol with variceal band ligation in prevention of first variceal bleed in Child-Turcotte-Pugh B and C cirrhosis with high-risk oesophageal varices: the ‘CAVARLY TRIAL’

ObjectivesBeta-blockers and endoscopic variceal band ligation (VBL) have been preferred therapies for primary prophylaxis of variceal bleeding. However, the choice of therapy in patients with advanced liver disease with high-risk...

Persistent varices in cured patients: Understanding the role of hepatic venous pressure gradient

Background & AimsEtiologic factor removal (ER) drives recompensation and improves portal hypertension in cirrhosis. Esophageal varices (EV) and portosystemic shunts (PSS) have been found in patients despite hepatic vein pressure gradient (HVPG) dropping below 10mmHg after ER, questioning HVPG accuracy in reflecting true portal pressure in the setting of ER. We aim to evaluate the correlation of HVPG with direct portal pressure (DPP) in patients with persistence of EV after ER despite HVPG < 10mmHg. MethodsBicentric "proof of concept" study evaluating HVPG and ultrasound guided percutaneous DPP in patients with HCV or alcohol related cirrhosis with persistent varices, and HVPG<10mmHg after at least 5 years of ER. Results7 patients with HCV and 3 with alcohol-related cirrhosis with persistent varices, and HVPG <10mmHg after at least 5 years of ER were included. At evaluation, all patients had a patent portal vein and were compensated. Median platelet counts were 129.5 (95-145) 10ˆ9/ml, and LSM 16.15 (14.4-22.3) kPa. In 5 patients, EV remained the same size (2 large and 3 small), and 5 downsized to small after ER. Wedge hepatic vein pressure [Median 19 (16.5-20) mmHg] and portal pressure [Median 18 (15-19.5) mmHg] had an excellent correlation (R =0.93, p<0.0001). Portal pressure gradient (PPG) confirmed the absence of clinically significant portal hypertension as identified by HVPG across all the patients. ConclusionHVPG accurately reflects PPG in the context of HCV and alcohol-related cirrhosis regression. After ER, EV may persist despite HVPG <10mmHg. The benefit of prophylaxis in patients with EV and HVPG <10mmHg is unknown. Future studies with clinical endpoints are needed to validate our findings. Impact and implicationsDespite a favorable evolution after removal of the etiological factor, varices persist in some patients and there is a lack of concise guidelines for the evaluation and management of portal hypertension in this population. Our research underscores the persistence of varices in absence of clinically significant portal hypertension, and significantly, demonstrates the accuracy of hepatic venous pressure gradient (HVPG) in reflecting portal vein pressure in this specific patient group. These findings emphasize the crucial role of HVPG in the assessment of portal hypertension after etiological factor removal and lay the groundwork for further investigation into clinical outcomes and the necessity of non-selective beta-blockers (NSBB) in individuals with persistent varices after the removal of etiologic factor.

Dissociation in hepatic vein pressure gradient, liver stiffness measurement and complications in histological subtypes of porto-sinusoidal vascular disease

Background and aimsPortosinusoidal vascular disease (PSVD) is a broad term encompassing varied histological patterns with changes in portal tracts and sinusoids without cirrhosis. We aimed to assess whether there is...

Assessing the Severity of Portal Hypertension: Is Liver or Spleen Stiffness Measurement an Alternative to the Gold Standard, Hepatic Vein or Porto-Systemic Pressure Gradient?

Introduction: Liver stiffness measurement (LSM) and spleen stiffness measurement (SSM) are increased in patients with cirrhosis and portal hypertension (PH). However, increased SSM values are associated with presence of esophageal varices. Currently, the gold standard for risk stratification in patients with compensated advanced chronic liver disease (cACLD) is by measurement of portal pressure through assessment of hepatic vein or porto-systemic pressure gradient (HVPG and PSPG). However, these procedures are invasive, and either LSM or SSM may be a non-invasive alternative.&#x0D; Aim: We aimed to investigate the relationship between LSM or SSM and HVPG/PSPG and examined the diagnostic accuracy for identification of clinically significant PH (≥10 mm Hg) or severe PH (≥12 mm Hg).&#x0D; Methods: A retrospective study (IRB Protocol #19230) allowed us to identify patients who had who undergone portal pressure measurements (HVPG or PSPG). A total of 36 patients also had SSM values. Of these, 29 patients carried a hepatic cause of PH, while the remaining had pre-hepatic (n=4) and post-hepatic (n=3) etiology.&#x0D; Results: The median age was 58 years (range: 25-71) with 52% male and 83% with cirrhosis. The median LSM and SSM were 35.7 kPa (range:7.4-75.0, normal ≤7.0 kPa) and 43.8 kPa (range: 20.7-100, normal ≤ 21.0 kPa). Both LSM (r = 0.42, P-value = 0.02) and SSM (r = 0.45, P-value: 0.01) correlated significantly with HVPG/PSPG. The diagnostic accuracy for both LSM and SSM for clinically significant PH was good for LSM (AUROC 0.76, 95% CI:0.58-0.94) and excellent for SSM (AUROC: 0.81, 95% CI:0.65-0.98). The diagnostic accuracy of LSM and SSM was lower for severe PH [AUROC 0.71 (P-value = 0.06) and 0.67 (P-value = 0.1) for LSM and SSM, respectively].&#x0D; Conclusion: Both LSM and SSM correlate with portal pressure measurements and provide diagnostic accuracy to identify patients with clinically significant, but not severe, PH.

Endohepatology in clinical practice: EUS-guided portal pressure measurement combined with EUS-guided liver biopsy and variceal screening and treatment in outpatients.

EUS-guided portal pressure gradient (PPG) is a novel technique that permits a true, direct measure of portal vein pressure and hepatic vein pressure. This article details our experience and lessons learned from 20 consecutive outpatient EUS-PPG procedures performed at a single center, along with simultaneous EUS-guided liver biopsy, variceal screening, and variceal banding. Data on the first 20 patients who underwent EUS-PPG at a single center were retrospectively viewed and analyzed. The effects of various liver diseases or other patient-related factors on the clinical and technical success of EUS-PPG measurements, as well as EUS-guided liver biopsy (EUS-LB), were evaluated. During the procedure, if esophageal varices were encountered, they were assessed, and if felt to be clinically indicated, endoscopic variceal ligation was performed. The 20 patients included 10 male and 10 female patients. All procedures were technically successful. In all patients, the portal vein and hepatic veins could be easily identified. One adverse event of bleeding occurred during the EUS-PPG measuring procedure. All 20 EUS-LBs were technically successful and yielded adequate samples for histological evaluations, with an average of 25 complete portal tracts per sample. Among patients with esophageal varices, 40% of patients underwent banding. The mean EUS-PPG among 5 patients with esophageal varices was 11.6 mm Hg, compared with 3.2 mm Hg among 15 patients without esophageal varices. This study demonstrates that EUS-PPG is a novel, safe, reproducible, and effective technique. Also, the fact that EUS-PPG, EUS-LB, variceal screening, and variceal banding could be performed in 1 session and on an outpatient basis speaks to the growing relevance and impact of the nascent field of endohepatology.

Impact of catheter tip to hepatic vein ostium distance on the validity and prognostication of hepatic venous pressure gradient in cirrhosis

Hepatic venous pressure gradient (HVPG) is an accurate measure of portal hypertension in cirrhosis. However, the effect of catheter tip distance from hepatic vein ostium (HVO) on HVPG is unknown. We performed a retrospective study on 228 patients with 307 HVPGs in our institution. The objectives of this study were to assess the effect of catheter position on the validity of HVPG and its prognostication in cirrhosis. In this study, free hepatic vein pressure (FHVP) was considered optimal when difference between FHVP and inferior vena cava pressure was ≤ 2 mmHg. HVPG progressively decreased (p < 0.001) when measured at increasing distance from HVO due to an increasing FHVP (p = 0.036) but an unchanged wedged hepatic vein pressure (p = 0.343). Catheter tip distance > 5 to ≤ 8 cm [odds ratio {OR} 0.16 (95% CI 0.05–0.47), p = 0.001] and > 8 cm [OR 0.14 (95% CI 0.04–0.47), p = 0.002] compared to ≤ 3 cm from HVO were independent predictors of not achieving optimal FHVP. Baseline HVPG ≥ 16 mmHg was strongly associated with deaths due to cirrhosis and liver transplantation for end-stage liver disease compared to HVPG < 16 mmHg when FHVP was optimal (p < 0.001) but not when it was suboptimal (p = 0.359). Our study showed that FHVP is spuriously elevated when measured at > 5 cm from HVO, resulting in inaccurately low HVPG.

Predictive value of liver and spleen stiffness measurement based on two-dimensional shear wave elastography for the portal vein pressure in patients with compensatory viral cirrhosis.

This study aimed to explore the predictive value of liver and spleen stiffness measurement based on two-dimensional shear wave elastography for the portal vein pressure in patients with compensatory viral cirrhosis. From January 2017 to August 2019, 107 patients with compensatory viral cirrhosis and 76 patients with viral hepatitis were enrolled as cirrhosis group and hepatitis group, respectively. Patient data were obtained during admission, and this study was a review and analysis of patient data. Liver stiffness measurement (LSM), spleen stiffness measurement (SSM), portal vein diameter and spleen thickness were compared between the two groups, and their diagnostic value for compensatory viral cirrhosis was analyzed. According to the hepatic vein pressure, the cirrhosis group patients were divided into non-hypertensive group (no portal hypertension, hepatic venous pressure gradient (HVPG) < 5 mmHg), mild group (mild portal hypertension, 5 mmHg ≤ HVPG ≤ 10 mmHg) and severe group (clinically significant portal hypertension group, HVPG > 10 mmHg). LSM, SSM, portal vein diameter and spleen thickness of the three groups were compared, and the correlation between SSM and hepatic vein pressure was analyzed. LSM, SSM, portal vein diameter and spleen thickness in the cirrhosis group were higher than those in hepatitis group (all P<0.05). The area under the curve (AUC) of combined detection was larger than that of LSM, SSM and spleen thickness detection alone in liver cirrhosis diagnosis (all P<0.05). LSM, SSM, portal vein diameter and spleen thickness increased with the increase of hepatic vein pressure in patients with liver cirrhosis (all P<0.05). LSM, SSM, portal vein diameter and spleen thickness were all positively correlated with hepatic vein pressure (P<0.05). ROC curve showed that AUC of combined detection was greater than that of LSM, SSM, portal vein diameter and spleen thickness alone detection in the diagnosis of clinically significant portal hypertension (all P<0.05). The increase of LSM, SSM, portal vein diameter and spleen thickness were the influencing factors for hepatic vein pressure rising (all P<0.05). There was an increase of LSM and SSM in patients with compensatory viral cirrhosis, which were positively correlated with hepatic venous pressure, and combined index detection has diagnostic and predictive value for the change of portal venous pressure.

Impact of the inferior vena cava morphology on fluid dynamics of the hepatic veins.

We reported previously that a large vertical interval between the hepatic segment of the inferior vena cava (IVC) and right atrium (RA), referred to as the IVC-RA gap, was associated with more intraoperative bleeding during hemi-hepatectomy. We conducted a computational fluid dynamics (CFD) study to clarify the impact of fluid dynamics resulting from morphologic variations around the liver. The subjects were 10 patients/donors with a large IVC-RA gap and 10 patients/donors with a small IVC-RA gap. Three-dimensional reconstructions of the IVC and hepatic vessels were created from CT images for the CFD study. Median pressure in the middle hepatic vein was significantly higher in the large-gap group than in the small-gap group (P = 0.008). Differences in hepatic vein pressure caused by morphologic variation in the IVC might be one of the mechanisms of intraoperative bleeding from the hepatic veins.

The incidence and natural history of ascites after liver transplantation.

Ascites is common in cirrhosis but uncommon after liver transplant. We aimed to characterize the incidence, natural history, and current management strategies of post-transplant ascites. We performed a retrospective cohort study of patients who underwent liver transplantation at 2 centers. We included patients who underwent deceased donor whole graft liver transplants between 2002 and 2019. Chart review identified patients with post-transplant ascites, requiring a paracentesis between 1 and 6-month post-transplants. Detailed chart review identified clinical and transplant characteristics, evaluation of ascites etiology, and treatments. Of 1591 patients who successfully underwent a first-time orthotopic liver transplant for chronic liver disease, 101 (6.3%) developed post-transplant ascites. Only 62% of these patients required large volume paracentesis for ascites before transplant. 36% of patients with post-transplant ascites had early allograft dysfunction. Most patients with post-transplant ascites (73%) required a paracentesis within 2 months of transplant, but 27% had delayed ascites onset. From 2002 to 2019, ascites studies were obtained less often, and hepatic vein pressure measurement was performed more often. Diuretics were the mainstay of treatment (58%). The use of albumin infusion and splenic artery embolization to treat post-transplant ascites increased over time. Larger pre-transplant spleen size was associated with a greater number of post-transplant paracenteses (r=0.32 and p=0.003). For patients who underwent splenic intervention, paracentesis frequency was significantly reduced (1.6-0.4 paracenteses/month, p=0.0001). The majority (72%) of patients had clinical resolution of their ascites at 6-month post-transplant. Persistent or recurrent ascites continues to be a clinical issue in the modern era of liver transplantation. Most had clinical resolution within 6 months, some requiring intervention.

Computed tomography imaging features to evaluate the severity of portal hypertension and predict the rebleeding risk after endoscopic treatment in cirrhotic patients with variceal hemorrhage

PurposeTo investigate the association of computed tomography (CT) imaging features and severity of portal hypertension (PH) and develop a nomogram to predict high-risk PH in cirrhotic patients with gastroesophageal variceal hemorrhage (GVH). MethodsThe study retrospectively enrolled 158 cirrhotic patients with a history of endoscopic treatment for GVH. Hepatic vein pressure gradient (HVPG) was measured and the patients were classified into high-risk (HVPG > 16 mmHg) or low-risk (HVPG ≤ 16 mmHg) PH group. Pre-treatment CT features, including cavernous transformation of portal vein (CTPV), hilar periportal space (a distance between right portal vein and posterior edge of segment IV of the liver), and depth of right posterior hepatic notch sign (a sharp indentation in the right medial posterior liver surface), were evaluated. Risk factors associated with high-risk PH were analyzed, and a nomogram based on the imaging features was developed. ResultsHigh-risk PH group showed a higher rebleeding rate after treatment than that of the low-risk (P = 0.029). Multivariate analysis indicated that larger hilar periportal space (P < 0.001), less frequencies of CTPV (P = 0.044) and deeper right posterior hepatic notch (P < 0.001) were independent risk factors associated with high-risk PH. A nomogram based on the three CT imaging features was established to predict high-risk PH with an excellent discrimination (c-statistic 0.854). ConclusionThe nomogram based on CT features of hilar periportal space, depth of right posterior hepatic notch and CTPV can help to distinguish cirrhotic patients with high-risk PH, who are more vulnerable of variceal rebleeding after endoscopic treatment.

Noninvasive diagnosis of liver fibrosis in schistosomiasis japonica: Opportunities and challenges

Noninvasive diagnosis of liver fibrosis in schistosomiasis japonica: Opportunities and challenges

An Unusual Manifestation of Elevated Liver Enzymes and Architecture

Question: A 68-year-old woman with a past medical history of cerebral vascular accident and chronic kidney disease underwent an outpatient anorectal examination under anesthesia for evaluation of a 6-month history of rectal bleeding and constipation. She was found to have a rectal mass involving the posterior vaginal wall. Biopsy specimens from the rectal and vaginal lesions showed invasive squamous cell carcinoma (SCC) with venous invasion (Figures A and B). The carcinoma was p16+ representing a high-risk human papilloma virus–induced SCC (Figure C). Computed tomography of the chest, abdomen, and pelvis showed the vaginal mass and a nodular liver suggestive of cirrhosis. With regard to the patient’s risk factors for liver disease, the patient had remote social alcohol consumption in her 20s without a history of intravenous drug use, family history of liver disease, autoimmune diseases, or hepatitis. In preparation for palliative chemotherapy, blood work was obtained, which was pertinent for white blood cell count of 8.8 103/μL, hemoglobin of 12.7 g/dL, platelets 257 103/μL, aspartate aminotransferase 127 U/L, alanine aminotransferase 65 U/L, alkaline phosphatase 1133 U/L, bilirubin 4.8 mg/dL, prothrombin time of 15.3 seconds, and international normalized ratio of 1.2. Serologic work-up was unremarkable for viral, autoimmune, or metabolic etiologies of liver disease, so magnetic resonance cholangiopancreatography was obtained (Figure D). Subsequently, the patient underwent transjugular hepatic hemodynamic pressure measurements with results as follows: right atrial pressure = 7 mm Hg, free hepatic vein pressure = 15 mm Hg, wedged hepatic vein pressure = 27 mm Hg, and corrected sinusoidal pressure = 12 mm Hg, followed by nontargeted liver biopsy (Figure E).

EUS-Guided Portal Pressure Gradient Measurement in Patients with Portal Hypertension: Evidence-Based Case Report

Aim: This evidence-based case report aims to assess the accuracy of EUS-PPG measurement in patients with portal hypertension.Method: A literature search was performed using PubMed, Cochrane, ProQuest, and EBSCO. A total of 2 articles were selected after meeting the inclusion and exclusion criteria. Critical study assessment was conducted to assess the validity, importance, and applicability of the study.Results: As a result, the first study found higher EUS-PPG measurement values in patients with clinical parameters of portal hypertension and the second study found a good correlation between EUS-PPG measurement values with hepatic vein pressure gradient (HVPG) and transjugular intrahepatic portosystemic shunt (TIPS) portal pressure gradient (PPG).Conclusion: From these two studies, it can be concluded that EUS-PPG measurement is a safe, effective, and feasible method to be performed on patients.

Agreement between Wedged Hepatic Venous Pressure and Portal Pressure in Hepatic Sinusoidal Obstruction Syndrome.

Wedge hepatic vein pressure (WHVP) accurately estimates the portal pressure (PP) in chronic sinusoidal portal hypertension patients. Whether this applies to patients with acute portal hypertension due to hepatic sinusoidal obstruction syndrome (HSOS) is unclear. Our aim was to assess the agreement between WHVP and PP in patients with HSOS by comparing them to decompensated cirrhosis patients. From December 2013 to December 2021, patients with pyrrolidine alkaloid-induced HSOS (PA-HSOS) receiving hepatic venous pressure gradient (HVPG) measurement and transjugular intrahepatic portosystem shunt (TIPS) were retrospectively collected and matched with those of patients with virus- or alcohol-related cirrhosis as a cirrhosis group. Pearson's correlation (R), intraclass correlation coefficient (ICC), scatter plots, and the Bland-Altman method were performed for agreement evaluation. A total of 64 patients were analyzed (30 PA-HSOS and 34 cirrhosis groups). The correlation between WHVP and PP was moderate in the PA-HSOS group (R: 0.58, p = 0.001; ICC: 0.68, p = 0.002) but good in the cirrhosis group (R: 0.81, p &lt; 0.001; ICC: 0.90, p &lt; 0.001). The percentage of patients with inconsistent WHVP and PP in the two groups was 13 (43.3%) and 15 (26.5%) (p = 0.156), respectively, and an overestimation of PP was more common in the PA-HSOS group (33.3% vs. 2.9%, p = 0.004). HVPG and portal pressure gradient (PPG) consistency was poor in both groups (R: 0.51 vs. 0.26; ICC: 0.65 vs. 0.41; p &lt; 0.05). WHVP in patients with PA-HSOS did not estimate PP as accurately as in patients with virus- or alcohol-related cirrhosis, which was mainly due to PP overestimation.

Quantification of exceedingly high levels of von Willebrand factor in cirrhosis: Next upgrading of the MELD-Na score?

That Von Willebrand factor antigen (VWF Ag) levels predict clinical outcome in patients with cirrhosis and portal hypertension was firstly stated by La Mura et al. [1] who described the relation of this (and other) markers of endothelial dysfunction with systemic and hepatic haemodynamics [1]. They found that VWF levels significantly correlated with the Hepatic Vein Pressure Gradient (HVPG), Child–Pugh score and the model for end-stage liver disease (MELD), but independently predicted clinical outcome.

S3143 Rare Case of Plasma Cell Infiltration-Induced Cirrhosis

Introduction: Multiple myeloma (MM) is a type of malignancy that arises from the unorganized replication of plasma cells within the bone marrow. The overproduction of these cells damages systems throughout the body leading to early asymptomatic symptoms that can rapidly progress to systemic signs of disease. Liver involvement with MM is less common and generally occurs through plasma cell infiltration, light chain/amyloid deposition, and biliary obstruction. Though it can occur, the probability of it presenting near the time of diagnosis of MM is very rare and associated with poorer outcomes. Case Description/Methods: A 59-year-old male presented with generalized weakness, shortness of breath and weight gain. Physical exam showed sign of ascites and hepatomegaly. PMH was significant for esophageal cancer and a recent diagnosis of MM. No history of acute or chronic liver disease or cirrhosis risk factors. CT scan showed cardiomegaly, bilateral pleural effusions, pulmonary edema, and cirrhosis with abdominal ascites. Labs was unremarkable other than normocytic anemia. An echocardiogram showed mild reduced ejection fraction (47%) with speckle tracking suggestive of cardiac amyloidosis. Abdominal ultrasound confirmed appearance of cirrhosis, ascites, and right pleural effusion. Cirrhosis work up revealed negative hepatitis panel, normal alpha-1 antitrypsin, and normal ceruloplasmin. EGD was performed and ruled out extracellular vesicles (EV) but noted type I isolated gastric varices. Liver biopsy confirmed cirrhosis and showed portal tract damage with severe extensive plasma cell infiltration. Additionally, fragments of hepatic parenchymal showed disrupted lobular architecture by septal fibrosis and nodular formation. Immunohistochemistry was positive for CD3, CD20, CD5, BCL2, CD79a, and CD138 as well as increased lambda light chain compared to free kappa light chain. Despite extensive treatment including repeated thoracentesis and paracentesis, patient eventually developed in to decompensating liver cirrhosis (Figure 1). Discussion: In previous studies, plasma cell infiltration of the liver was seen in about 40% of cases of MM, but rarely lead to cirrhosis. This case is unique in that the patient had liver failure caused by cirrhosis and that it was some of the presenting symptoms. Whether due to masked signs or aggressive onset, the outcome for this diagnosis is poor and more specific factors observing liver function could have provided a more favorable outcome.Figure 1.: Cirrhosis secondary to plasma cell infiltration. Table 1. - Total Protein 5.0 g/dL Serum Ascites Albumin Gradient (SAAG) 1.9 g/dL Left Hepatic Vein Pressure 25 Hg Left Portal Vein Pressure 29 Hg Portosystemic Pressure Gradient 5 Hg EUS Guided Shear Wave Elastography of Liver 27 kPa

Study on the correlation between PPG and HVPG in patients with portal hypertension

Objective: To explore the correlation between portal vein pressure gradient (PPG) and hepatic vein pressure gradient (HVPG) in patients with portal hypertension (PHT). Methods: 752 cases with portal hypertension (PHT) who underwent transjugular intrahepatic portosystemic shunt (TIPS) and met the enrollment criteria between January 2016 to December 2019 were analyzed for hepatic vein, inferior vena cava and portal vein pressure. Paired t-test was used for analysis. Pearson correlation test was used to estimate correlation coefficient and coefficient of determination. P<0.05 were considered statistically significant. Results: Wedged hepatic vein pressure (WHVP), portal vein pressure (PVP), correlation coefficient, and coefficient of determination were 27.98±8.95 mmHg, 33.85±7.33 mmHg, 0.329 (P<0.001), and 0.108, respectively. HVPG, PPG,correlation coefficient, and coefficient of determination were 16.84±7.97 mmHg, 25.11±6.95 mmHg (P<0.001), 0.145, and 0.021 (P<0.001), respectively. The difference between HVPG and PPG was greater than 5 mmHg in 524 cases, accounting for 69.7%. The difference between HVPG and PPG was within 5 mmHg or basically equal in 228 cases, accounting for 30.3%. The correlation coefficient between free hepatic venous pressure (FHVP) and inferior vena cava pressure (IVCP) was 0.568 (P<0.001), and the coefficient of determination was 0.323. According to the presence or absence of hepatic venous collaterals after balloon occluded hepatic angiography, they were divided into two groups: 157 (20.9%) cases in the group with hepatic venous collaterals, and 595 (79.1%) cases in the group without hepatic venous collaterals. The parameters of the two groups were compared: WHVP (15.73±3.63) mmHg vs. (31.22±6.90) mmHg, P<0.001; PVP (31.69±8.70) mmHg vs. (34.42±6.81) mmHg, P<0.001; HVPG (7.18±4.40) mmHg vs. (19.40±6.62) mmHg, P<0.001; PPG (24.24±8.11) mmHg vs. (25.34±6.60) mmHg, P<0.001; free hepatic venous pressure (FHVP) (8.58±3.37) mmHg vs. (11.82±5.07) mmHg , P<0.001; inferior vena cava pressure (IVCP) (7.45±3.29) mmHg vs. (9.09±4.14) mmHg, P<0.001. Conclusion: The overall correlation is poor between HVPG and PPG. HVPG of most patients is not an accurate representation of PPG, and the former is lower than the latter. Hepatic venous collateral formation is one of the important reasons for the serious underestimation of HVPG values.

Intrahepatic Portosystemic Shunt In Cardiac Amyloidosis: Turning Off The Faucet Leads To Resolution Of Hepatic Encephalopathy And Improvement In Heart Failure Symptoms

<h3>Introduction</h3> Spontaneous portosystemic shunts (SPSS) are extremely rare and usually extrahepatic due to portal hypertension in the setting of cirrhosis. Current knowledge regarding SPSS in adults in the absence of cirrhosis is limited. The implications of SPSS in patients with transthyretin amyloid cardiomyopathy (ATTR-CM) are unknown. <h3>Case</h3> A 76-year-old man with a history of HTN, CAD and systolic dysfunction (EF 45%) presented to the hospital with symptoms of HF exacerbation and cognitive dysfunction. Initial cardiac labs were notable for a borderline elevated troponin and high natriuretic peptic level. Hepatic labs were notable for mild elevation in transaminases, thrombocytopenia and an elevated ammonia level. Transthoracic echocardiogram (TTE) revealed that the EF was stable at 45%, but there was biatrial enlargement and progression of concentric LVH to 1.8cm and resultant small LV cavity (EDV index 39ml/m²), suspicious for infiltrative cardiomyopathy (Fig A). SPEP/UPEP with immunofixation and serum free light chains were normal and Tc-99m PYP study was consistent with ATTR-CM (Fig B). Abdominal US revealed a large intrahepatic venous shunt from the right portal vein to the right hepatic vein. Right heart catheterization, portal venogram and liver biopsy revealed a right atrial pressure of 14mmHg, cardiac output of 6.2L/min, normal pulmonary vascular resistance, hepatic vein pressure of 14mmHg, portal vein pressure of 15mmHg, confirmation of the large SPSS (Fig C) and no evidence of cirrhosis. The patient underwent embolization of the SPSS with a 22mm vascular plug (Fig D). Following closure, the patient's HF symptoms and HE improved dramatically and his abnormal hepatic labs normalized. He was started on a stabilizer for the treatment of his ATTR-CM. At one year, he has not had recurrent symptoms of HE, nor repeat hospitalization for HF exacerbation. <h3>Discussion</h3> This patient most likely had a SPSS that only manifested clinically in the setting of elevated right atrial and hepatic pressures due to the development of ATTR-CM. Ultimately, the decision was made to close the SPSS for two reasons. The first was to treat HE—in the same way that transjugular intrahepatic portosystemic shunt (TIPS) procedure can cause HE and subsequent TIPS closure can be an effective treatment for refractory HE. The second was to improve HF symptoms. Although this patient's cardiac output was "normal", it was likely actually high in the context of the severe LVH and small LV cavity due to ATTR-CM and the increased venous return was poorly tolerated given the underlying restrictive cardiomyopathy.

A110 FEASIBILITY OF EUS-GUIDED PORTAL PRESSURE GRADIENT MEASUREMENT WITHOUT DEEP SEDATION: A PATH TO ACCURATE PORTAL PRESSURE DETERMINATION

AimsHepatic venous pressure gradient (HVPG) is the gold standard for the diagnosis and staging of portal hypertension. Previous studies have shown that it underestimates pre-sinusoidal portal hypertension. Endoscopic ultrasound-guided portal pressure gradient (EUS-PPG) can safely measure direct portal vein pressure (PVP) and bridge this diagnostic gap. However, EUS-PPG has so far been performed with patients under deep sedation which can alter HVPG measurement and lead to misclassification of portal hypertension. Ketamine, a conscious sedation agent, has minimal effect on portal hemodynamics. We present our center’s experience with EUS-PPG under ketamine and low dose midazolam.MethodsWe retrospectively reviewed consecutive patients undergoing EUS-PPG with conscious sedation using ketamine and low-dose midazolam (<0.02 mg/kg) at the McGill University Health Centre from February to May 2021. Patients were placed in the left lateral position. Hepatic vein and portal vein were located through EUS via a trans-gastric/hepatic approach. A through the scope 25-gauge needle attached to a manometer was advanced through the liver to measure hepatic vein pressure (HVP) and portal vein pressure (PVP). Three measurements were sampled per vessel and mean pressure differences calculated to obtain PPG. PPG was considered reliable if the differences between the values was no more than 1mmHg.ResultsThree patients underwent EUS-PPG for evaluation of pre-sinusoidal portal hypertension. Cirrhosis was excluded in all patients based on recent liver biopsy or transient elastography. The first patient is a 69-year-old man with splenomegaly and recanalization of the paraumbilical vein on imaging. He received 80 mg of ketamine and no midazolam. HVPG measured was 1 mmHg. EUS-PPG was successful with PPG of 6 mmHg (HVP= 7 mmHg, and PVP= 13 mmHg). The second patient is a 42-year-old woman with previous sleeve gastrectomy and known with portal cavernoma. She received 120 mg of ketamine and 1 mg of midazolam. EUS-PPG was technically difficult due to respiratory movements. The measurement was not considered reliable as differences in PPG were as high as 2mmHg. In this case, PPG was 0mmHg (HVP= 15mmHg, and PVP= 15mmHg). The third patient, a 74-year-old man with hepatic steatosis and splenomegaly received 70 mg of ketamine and 1 mg of midazolam. EUS-PPG was successful (HVP= 3mmHg, PVP= 3mmHg) yielding a PPG 0mmHg. All patients tolerated the procedure well with no procedural or sedation-related complicationsConclusionsOur early experience suggests that EUS-PPG can be successfully and safely performed in patients under conscious sedation with ketamine and low-dose midazolam. This combination may avoid deep sedation with high dose midazolam or propofol which are known to alter accuracy of HVPG. Measurement of HVP (left) and PVP (right)Funding AgenciesNone

Endoscopic Ultrasound-guided Portal Pressure Gradient Measurement Is Technically Successful and Safe Without Deep Sedation: A Proof-of-Concept Case Series

The hepatic venous pressure gradient (HVPG), which is the difference between the wedged (WHVP) and free hepatic vein pressures (FHVP), is the gold standard to evaluate portal hypertension in patients with cirrhosis 1 Bosch J Abraldes JG Berzigotti A et al. The clinical use of HVPG measurements in chronic liver disease. Nat Rev Gastroenterol Hepatol. 2009; 6: 573-582 Crossref PubMed Scopus (436) Google Scholar . Unfortunately, there currently exists a gap in the evaluation of patients with pre-sinusoidal portal hypertension, where HVPG is known to underestimate portal pressure. Endoscopic ultrasound-guided portal pressure gradient measurement (EUS-PPG) has recently brought back the possibility of safely obtaining direct portal vein pressure (PVP) and represents a long-awaited less-invasive diagnostic tool for patients with suspected pre-sinusoidal portal hypertension.