Hepatic Venous Pressure Gradient Levels Research Articles

The clinical value of the hepatic venous pressure gradient in patients undergoing hepatic resection for hepatocellular carcinoma with or without liver cirrhosis.

The role of hepatic venous pressure gradient (HVPG) measurement in risk stratification before liver resection is an ongoing area of debate. This study examines the impact of preoperative HVPG levels on overall survival (OS)/time to recurrence (TTR) and postoperative complications after hepatic resection of hepatocellular carcinoma (HCC). Thirty-eight HCC patients undergoing HVPG measurement before liver resection at Cambridge University Hospitals NHS Foundation Trust between January 2014 and April 2022 were retrospectively analysed. Statistical analysis comprised univariable/multivariable Cox/logistic regression to identify risk factors of reduced OS/TTR or 90-day post-resection complications and Kaplan-Meier estimator, log-rank, chi-squared, Fisher's exact, and Mann-Whitney U test, or Student's t-test for survival/subgroup analysis. The median HPVG was 6 (range: 0-14) mmHg. The HVPG was an independent risk factor for poorer TTR in the overall cohort (cut-off: ≥7.5 mmHg (17.18/43.81 months; P = 0.009)). In the subgroup analysis of cirrhotic patients (N = 29 (76%)), HVPG was additionally an independent risk factor for lower OS (cut-off: ≥8.5 mmHg [44.39/76.84 months; P = 0.012]). The HVPG had no impact on OS/TTR in non-cirrhotic patients (N = 9 (24%)), nor was it associated with postoperative complications in any cohort. In conclusion, preoperative HVPG levels are useful predictors for TTR and OS in cirrhotic HCC patients undergoing hepatic resection.

Correlation of Hepatic Venous Pressure Gradient Level With Clinical and Endoscopic Parameters in Decompensated Chronic Liver Disease.

The amount of liver fibrosis usually correlates with portal pressure, which is measured as the hepatic venous pressure gradient (HVPG). The fact that portal pressure significantly decreases after treatment may increase cirrhotic patients' long-term survival suggests that measuring HVPG may offer specific information for outcome prediction. The study thus seeks to determine the relationship between the level of the HVPG and endoscopic and clinical parameters in decompensated chronic liver disease (CLD). Thirty patients with CLD were studied and subjected to serum creatinine, total bilirubin, serum sodium, serum albumin, prothrombin time (PT), international normalized ratio (INR), esophagogastroduodenoscopy (upper gastrointestinal (UGI) endoscopy), and transjugular or transfemoral catheterization for HVPG measurement, and Child-Turcotte-Pugh (CTP) score and Model for End-Stage Liver Disease (MELD) score were calculated. The results indicates a strong positive connection between MELD and HVPG, which is statistically significant (r=0.754; p<0.001). Similarly, CTP and HVPG also exhibit a significant positive association (r=0.793; p<0.001) suggesting a link between the severity of liver disease. Additionally, the moderate positive correlation for encephalopathy has a significant value (r=0.584; p=0.001), while the weak positive correlations for serum bilirubin, INR, and HVPG have non-significant values (r=0.244; p=0.194, and r=0.375; p=0.041, respectively). A strong negative connection between serum albumin and HVPG was also found (r=0.546; p=0.005) suggesting a relationship between worsening liver function. In patients with decompensated CLD, the severity of the CLD as measured by the CTP and MELD score corresponds with HVPG, and higher HVPG associated with severe CLD and severe ascites, large varices, and variceal hemorrhage. Higher HVPG in cirrhotic patients also suggests the existence of sequelae, such as varices, severe ascites, and severe hepatic encephalopathy, although HVPG has little bearing on the underlying cause.

Hepatic venous pressure gradient (HVPG) predicts liver failure after transjugular intrahepatic portal shunt: a retrospective cohort study.

Esophagogastric variceal bleeding is a serious complication of decompensated cirrhosis. Transjugular intrahepatic portal shunt (TIPS) is a salvage treatment with clear hemostatic results. However, various complications may occur after TIPS, including postoperative liver failure, and the prognosis is very poor once occurs. Liver failure is a common symptom of severe liver disease with a high mortality rate. This study investigated the incidence of liver failure after TIPS treatment for varicose bleeding. We analyzed the data of patients admitted to the First Affiliated Hospital of Soochow University between January 2013 and December 2018 with portal hypertension with an episode of acute gastroesophageal variceal bleeding. A total of 121 patients were referred to the regional liver unit for TIPS. Hepatic venous pressure gradient (HVPG) and clinical data were collected. Patients with incomplete data were excluded, and 93 patients were ultimately enrolled in the study. Primary outcomes were morbidity and hospital mortality within 4 weeks of surgery. The data were retrospectively and consecutively collected and evaluated by univariate and multivariate analyses to identify risk factors of liver failure. The patients included 58 males (62.37%) and 35 females (37.63%), and the mean age was 58.43±11.85 years. The main cause was hepatitis B virus (HBV), which was found in 50.54% of patient. The overall surgical success rate was 83.87% (78/93). Of 15 treatment-failure patients, 9 (9.68%) died in hospital. Four patients died of liver failure, accounting for 44.44% of postoperative all-cause deaths. Univariate logistic regression analysis showed that only hepatic venous pressure gradient (HVPG) was an independent risk factor for post-TIPS morbidity [relative risk (RR) 1.156; 95% confidence interval (CI): 1.041 to 1.283; P=0.006]. In addition, HVPG was an independent risk factor for hospital mortality within 4 weeks (RR 1.133; 95% CI: 1.021 to 0.539; P=0.016). Post-TIPS liver failure is a serious complication in patients with cirrhosis. Pre-TIPS HVPG level may be used as a predictor of potential short-term postoperative adverse events.

The relationship between portal hypertension and portal hypertensive gastropathy

Background and aim Portal hypertensive gastropathy (PHG) most commonly occurs in the setting of increased portal pressure in patients with cirrhosis. Here, we aimed to understand the correlation between hepatic venous pressure gradient (HVPG) and the presence and severity of PHG in patients with cirrhosis. Methods We examined patients with cirrhosis who underwent HVPG measurement at the Medical University of South Carolina between 2014 and 2020. Extensive demographic, clinical, laboratory, procedural (including precise grading of PHG severity using standard definitions), and outcome data were abstracted at the time of HVPG measurement. Results Three hundred and ten patients with HVPG measurements and cirrhosis were identified. Seventy-three patients having endoscopy within 6 months of HVPG measurement were included (mean age 54 ± 11, 44% female). The most common causes of cirrhosis were alcohol (41%) and non-alcoholic steatohepatitis (32%). The average HVPG was 15 mmHg (±6) and 62 patients had clinically significant portal hypertension (CSPH) (HVPG ≥ 10 mmHg). Of the 73 patients with HVPG measured, 45 (62%) had PHG, including 40 (89%) of whom had CSPH. Out of the 45 patients with PHG, 41 and four had mild or severe PHG, respectively. MELD scores were similar in patients with and without PHG [15 ± 9 (SD) and 17 ± 9, respectively; p = .37]. HVPG was higher in patients with PHG (17 ± 7 mmHg) than those without PHG (13 ± 4 mmHg) (p = .01) but did not differ between mild and severe PHG. Conclusion A weak correlation exists between HVPG level and the presence of PHG.

Decompensation in Advanced Nonalcoholic Fatty Liver Disease May Occur at Lower Hepatic Venous Pressure Gradient Levels Than in Patients With Viral Disease

Portal hypertension is the strongest predictor of hepatic decompensation and death in patients with cirrhosis. However, its discriminatory accuracy in patients with nonalcoholic fatty liver disease (NAFLD) has been challenged because hepatic vein catheterization may not reflect the real portal vein pressure as accurately as in patients with other etiologies. We aimed to evaluate the relationship between hepatic venous pressure gradient (HVPG) and presence of portal hypertension-related decompensation in patients with advanced NAFLD (aNAFLD). Multicenter cross-sectional study included 548 patients with aNAFLD and 444 with advanced RNA-positive hepatitis C (aHCV) who had detailed portal hypertension evaluation (HVPG measurement, gastroscopy, and abdominal imaging). We examined the relationship between etiology, HVPG, and decompensation by logistic regression models. We also compared the proportions of compensated/decompensated patients at different HVPG levels. Both cohorts, aNAFLD and aHVC, had similar baseline age, gender, Child-Pugh score, and Model for End-Stage Liver Disease score. Median HVPG was lower in the aNAFLD cohort (13 vs 15 mmHg) despite similar liver function and higher rates of decompensation in aNAFLD group (32% vs 25%; P= .019) than in the aHCV group. For any of the HVPG cutoff analyzed (&lt;10, 10-12, or 12 mmHg) the prevalence of decompensation was higher in the aNAFLD group than in the aHCV group. Patients with aNAFLD have higher prevalence of portal hypertension-related decompensation at any value of HVPG as compared with aHCV patients. Longitudinal studies aiming to identify HVPG thresholds able to predict decompensation and long-term outcomes in aNAFLD population are strongly needed.

Mac-2 binding protein glycosylation isomer is a potential biomarker to predict portal hypertension and bacterial infection in cirrhotic patients.

ObjectivesMac-2-binding protein glycosylation isomer (M2BPGi) is a novel plasma biomarker for liver fibrosis, but less is known about its role in portal hypertension. We aimed to evaluate the association between M2BPGi and hepatic venous pressure gradient (HVPG) and to investigate its predictive value on prognosis of cirrhotic patients.MethodsForty-eight cirrhotic patients who underwent HVPG measurement in Taipei Veterans General hospital were retrospectively enrolled. The Spearman’s correlation test was used to analyze the correlation between plasma M2BPGi levels and HVPG and other parameters. Cox proportional hazards regression models were used to identify predictors for clinical outcomes.ResultsPlasma M2BPGi levels were higher in cirrhotic patients than healthy subjects and significantly correlated with HVPG levels (rs = 0.45, p = 0.001). On multivariate Cox regression analysis, higher plasma M2BPGi levels [≥ 6 cut-off index (C.O.I)] did not predict mortality within five years for cirrhotic patients and the result was similar in patients without hepatocellular carcinoma. Interestingly, M2BPGi ≥ 6 C.O.I was a potential predictor of bacterial infection within five years [Hazar ratio (HR) = 4.51, p = 0.003]. However, M2BPGi failed to predict occurrence of other cirrhosis-related complications, including variceal bleeding, ascites formation, spontaneous bacterial peritonitis, hepatorenal syndrome and hepatic encephalopathy.ConclusionPlasma M2BPGi levels positively correlated with HVPG and higher serum M2BPGi levels might have a potential role in predicting development of bacterial infection for cirrhotic patients with portal hypertension.

The cut-off value of transient elastography to the value of hepatic venous pressure gradient in alcoholic cirrhosis.

Background/AimsThe hepatic venous pressure gradient (HVPG) reflects portal hypertension, but its measurement is invasive. Transient elastography (TE) is a noninvasive method for evaluating liver stiffness (LS). We investigated the correlation between the value of LS, LS to platelet ratio (LPR), LS-spleen diameter-to-platelet ratio score (LSPS) and HVPG according to the etiology of cirrhosis, especially focused on alcoholic cirrhosis.MethodsBetween January 2008 and March 2017, 556 patients who underwent HVPG and TE were consecutively enrolled. We evaluated LS, LPR, and LSPS according to the etiology of cirrhosis and analyzed their correlations with HVPG.ResultsThe LS value was higher in patients with alcoholic cirrhosis than viral cirrhosis based on the HVPG (43.5 vs. 32.0 kPa, P<0.001). There were no significant differences in the LPR or LSPS between alcoholic and viral cirrhosis groups, and the areas under the curves for the LPR and LSPS in subgroups according to HVPG levels were not superior to that for LS. In alcoholic cirrhosis, the LS cutoff value for predicting an HVPG ≥10 mmHg was 32.2 kPa with positive predictive value (PPV) of 94.5% and 36.6 kPa for HVPG ≥12 mmHg with PPV of 91.0%.ConclusionsThe LS cutoff value should be determined separately for patients with alcoholic and viral cirrhosis. In alcoholic cirrhosis, the LS cutoff values were 32.2 and 36.6 kPa for predicting an HVPG ≥10 and ≥12 mmHg, respectively. However, there were no significant differences in the LPR or LSPS between alcoholic and viral cirrhosis groups.

The Presence of Ascites Affects the Predictive Value of HVPG on Early Rebleeding in Patients with Cirrhosis.

Background and Aims Gastroesophageal variceal bleeding is a serious complication of portal hypertension in cirrhotic patients and could be predicted by hepatic venous pressure gradient (HVPG). However, whether the presence of ascites affects the prognostic value of HVPG for patients with acute variceal bleeding is still unknown. This retrospective study is aimed at investigating the influence of ascites on predictive performance of HVPG for early rebleeding in cirrhotic patients with acute variceal bleeding. Methods In this retrospective study, a total of 148 patients with cirrhosis hospitalized for acute variceal bleeding who underwent HVPG measurement and endoscopic variceal ligation (EVL) for the prevention of rebleeding were included. The receiver operating characteristic curve (ROC) and logistical regression method were employed to analyze the predictive performance of HVPG for early rebleeding. The locally weighted scatterplot smoothing approach was adopted to assess the monotonicity between bleeding risk and HVPG. Results A significantly higher HVPG level was observed in patients with early rebleeding compared to patients without rebleeding in the nonascites cohort. When using HVPG to predict early rebleeding, there was a lower area under curve in the ascites cohort compared to the nonascites cohort. HVPG was recognized as a risk factor for early rebleeding by a logistic regression model only in the nonascites cohort. An overall monotonicity in the trend of change in HVPG and risk for early rebleeding was observed in the nonascites cohort solely. Conclusion The predictive value of HVPG for early rebleeding in patients with cirrhosis that developed acute variceal bleeding is hindered by the presence of ascites.

The predictive value of baseline hepatic venous pressure gradient for variceal rebleeding in cirrhotic patients receiving secondary prevention.

Baseline hepatic venous pressure gradient (HVPG) has been applied for prediction of variceal rebleeding in patients after acute variceal bleeding. However, for patients receiving secondary prevention, there still lacks evidence about the predictive performance of baseline-HVPG for rebleeding. This study aims to investigate the predictive value of baseline-HVPG for variceal rebleeding in cirrhotic patients receiving secondary prevention. This retrospective study included 122 patients with cirrhosis accepting secondary prevention of variceal rebleeding in a university hospital. All the included patients had HVPG measurements before rebleeding and had at least 1-year follow-up after HVPG measurement unless the rebleeding occurred. The rebleeding rate in patients with different HVPG levels and time-dependent predictive performance of baseline-HVPG were analysed. A Cox regression model and P for trend were used to assess the rebleeding risk. Variceal rebleeding occurred in 22 (18.0%) patients during 1-year follow-up. No significant difference was observed in rebleeding rate between patients with HVPG <16 mmHg and HVPG ≥16 mmHg (17.91% vs. 26.41%, P=0.200). A decreasing trend was observed in area under the curve of HVPG for predicting rebleeding by time. The multivariate Cox model showed an overall decreasing trend in hazard ratio of rebleeding (vs. patients with HVPG <12 mmHg) for patients with 12≤ HVPG <16 mmHg, 16≤ HVPG <20 mmHg and HVPG ≥20 mmHg; besides, an increasing P for trend was observed. A single baseline-HVPG measurement was insufficient for predicting rebleeding in patients with cirrhosis who received secondary prevention.

Observation of immediate and mid-term effects of partial spleen embolization in reducing hepatic venous pressure gradient.

Objective:To observe the immediate and mid-term effects of partial spleen embolization (PSE) in reducing hepatic venous pressure gradient (HVPG) in patients with cirrhotic esophagogastric varices.Methods:Patients diagnosed with cirrhosis and esophagogastric varices in our hospital between July 2016 and March 2018 were consecutively selected. Forty-three patients were selected based on the eligibility criteria to undergo PSE. The change in HVPG 5 minutes before and after embolization, was used to determine the immediate effect of PSE on HVPG reduction. HVPG was retested after 6 months to observe the change in the antihypertensive effect along with time.Results:Forty-three patients successfully underwent PSE and HVPG measurements. The HVPG was 17.7 ± 3.9 mmHg and 13.9 ± 3.1 mmHg before and after PSE, respectively, showing a significant decrease (21.5%, P < .05). Among them, 18 cases were retested for HVPG at 6 months after PSE, and the results showed significant differences in the HVPG levels before, immediately and 6 months after PSE. Compared with preoperative PSE, HVPG was decreased by 22.9% and 17.7% (P < 0.05) immediately and at 6 months after operation, respectively. There was no significant change at 6 months after PSE when compared with immediate postoperative PSE. No serious complications were observed in patients during their postoperative hospital stay.Conclusion:PSE immediately reduced the portal pressure, and HVPG remained stable at 6 months after surgery. PSE is considered as a safe and easy to implement method, and is expected to be one of the treatments for reducing the portal pressure.

Spleen and Liver Volumetrics as Surrogate Markers of Hepatic Venous Pressure Gradient in Patients With Noncirrhotic Portal Hypertension.

Noncirrhotic portal hypertension (NCPH) is a rare disease that may lead to serious clinical consequences. Currently, noninvasive tools for the assessment of NCPH are absent. We investigated the utility of spleen and liver volumetrics as a marker of the presence and severity of portal hypertension in this population. A cohort of NCPH patients evaluated between 2003 and 2015 was retrospectively studied. The association of spleen and liver volumes with the hepatic venous pressure gradient (HVPG) level was evaluated using locally weighted scatterplot smoothing curves. A cohort of patients with viral hepatitis‐related liver disease was used as controls. Of the 86 patients with NCPH evaluated during the study period, 75 (mean age, 35 ± 17; 73% males) were included in the final analysis. Patients with portal hypertension had significantly higher spleen and liver to body mass index (BMI) ratios compared to patients with HVPG <5 mm Hg (39.5 ± 27.9 versus 22.8 ± 10.6 cm3/kg/m2, P = 0.003; 91.1 ± 40.1 versus 71.4 ± 16.7 cm3/kg/m2, P = 0.014, for spleen/BMI and liver/BMI, respectively). In contrast to the patients with viral hepatitis, a positive linear correlation was observed in the NCPH cohort between spleen/BMI and liver/BMI (above a cutoff of 25 and 80 cm3/kg/m2, respectively) and HVPG level. Additionally, only in the NCPH cohort was an increase in spleen/BMI range quartile predictive of a higher prevalence of portal hypertension and clinically significant portal hypertension (trend, P = 0.014 and 0.031, respectively). Conclusion: Spleen and liver volumetrics may have utility in the assessment of NCPH as a noninvasive biomarker that can be performed using routine radiologic examinations. Further studies are needed to validate these findings. (Hepatology Communications 2018; 00:000‐000)

Changes of liver hemodynamic and elastography parameters in patients with colorectal liver metastases receiving preoperative chemotherapy: \u201ca note of caution\u201d

BackgroundNew systemic chemotherapy agents have improved prognosis in patients with colorectal liver metastases (CLM), but some of them damage the liver parenchyma and ultimately increase postoperative morbidity and mortality after liver resection. The aims of our study were to determine the degree of hemodynamic and pathological liver injury in CLM patients receiving preoperative chemotherapy and to identify an association between these injuries and postoperative complications after liver resection.MethodsThis is a prospective descriptive study of patients with CLM receiving preoperative chemotherapy before curative liver resection from November 2013 to June 2014. All patients had preoperative elastography and hepatic hemodynamic evaluation. We analyzed clinical preoperative data and postoperative outcomes after grouping the patients by chemotherapy type, development of sinusoidal obstructive syndrome (SOS), and development of major complications.ResultsEleven from the 20 patients included in the study received preoperative oxaliplatin-based chemotherapy (OBC). Nine patients had SOS at pathological analysis and five patients developed major complications. Patients receiving preoperative OBC had higher values of hepatic venous pressure gradient (HVPG) and developed more SOS and major complications. Patients developing SOS had higher values of HVPG and developed more major complications. Patients with major complications had higher values of HVPG, and patients with a HVPG of 5 mmHg or greater had more major complications than those under 5 mmHg (20 vs 80%, p = 0.005).ConclusionsOBC and SOS impair liver hemodynamics in CLM patients. An increase in major complications after liver resection in these patients develops at subclinical HVPG levels.

Correlation of HVPG level with ctp score, MELD Score, ascites, size of varices, and etiology in cirrhotic patients.

Background/Aim:This study intends to determine the correlation of a patient's hepatic venous pressure gradient (HVPG) measurement with six factors: Child–Turcotte–Pugh (CTP) score, model for end-stage liver disease (MELD) score, presence of ascites, size of varices, presence of variceal bleeding, and an etiology of cirrhosis. The study also aims to identify the predictors of higher HVPG measurements that can indirectly affect the prognosis of cirrhotic patients.Patients and Methods:Thirty patients diagnosed with cirrhosis were enrolled prospectively and each patient's HVPG level was measured by the transjugular catheterization of the right or middle hepatic vein. The wedged hepatic venous pressure (WHVP) and free hepatic venous pressure (FHVP) were measured using a 7F balloon catheter. The HVPG level was calculated as the difference between the WHVP and FHVP measurements.Results:The mean HVPG level was higher in alcoholic than in nonalcoholic cirrhosis (19.5 ± 7.3 vs 15.2 ± 4.5 mm Hg, P = 0.13). The mean HVPG was also higher in bleeders compared with nonbleeders (18.5 ± 5.3 vs 10.7 ± 3.1 mmHg, P = 0.001). Patients with varices had a higher mean HVPG level than those without varices (17.4 ± 5.8 vs 11.7 ± 3.9 mmHg, P = 0.04). The difference among the three categories of varices (small, large, and no varices) was statistically significant (P = 0.03). In addition, the mean HVPG level was higher in patients with ascites than in those without ascites (18.7 ± 4.7 vs 11 ± 5.3 mmHg, P = 0.002), and it was significantly higher in patients in CTP class C (21.8 ± 5.5 mmHg) as compared with those in CTP class B (16.9 ± 2.9 mmHg) and CTP class A (10.5 ± 4.1 mmHg; P ≤ 0.001).Conclusion:HVPG levels were significantly higher in patients in CTP class C as compared with those in CTP classes A and B, thereby indicating that an HVPG measurement correlates with severity of liver disease. A high HVPG level signifies more severe liver disease and can predict the major complications of cirrhosis.

Spleen stiffness measurement can predict clinical complications in compensated HCV-related cirrhosis: A prospective study

Hepatic venous pressure gradient (HVPG) measurement represents the best predictor of clinical decompensation (CD) in cirrhotic patients. Recently data show that measurement of spleen stiffness (SS) has an excellent correlation with HVPG levels. Aim of the present prospective study was to assess SS predictive value for CD compared to HVPG, liver stiffness (LS), and other non-invasive tests for portal hypertension in a cohort of patients with HCV-related compensated cirrhosis. From an initial cohort of 124 patients, 92 underwent baseline LS, SS, HVPG measurements and upper gastrointestinal endoscopy at enrolment and then followed-up for 2 years or until the occurrence of the first CD. Univariate and multivariate logistic regression models were used for determining judgement criteria associated parameters. Accuracy of predictive factors was evaluated using c statistic. The final model was internally validated using the bootstrap method. During follow-up, 30 out 92 (32.6%) patients developed CD. At univariate analysis varices at enrolment, all non-invasive parameters, HVPG, and model for end-stage liver disease (MELD) resulted clinical predictors of CD. At multivariate analysis only SS (p=0.0001) and MELD (p=0.014) resulted as predictive factors. A decision algorithm based on the results of a predictive model was proposed to detect patients with low risk of decompensation. This study shows that in compensated cirrhotic patients a SS and MELD predictive model represents an accurate predictor of CD with accuracy at least equivalent to that of HVPG. If confirmed by further studies, SS and MELD could represent valid alternatives to HVPG as prognostic indicator of CD in HCV-related cirrhosis.

Changing Waveform During Respiration on Hepatic Vein Doppler Sonography of Severe Portal Hypertension

The purposes of this study were to assess retrospectively whether the waveform change during respiration on hepatic vein Doppler sonography is a parameter of severe portal hypertension as estimated by the hepatic venous pressure gradient (HVPG) and to compare with a hepatic vein damping index (DI) at expiration. Spectral Doppler sonography of the hepatic vein was performed on 22 consecutive patients who underwent HVPG measurement for portal hypertension with liver cirrhosis. From the maximum and minimum velocities of systolic hepatofugal venous flow on Doppler sonography, 3 parameters were derived: damping index at expiration (DI(exp)), damping index ratio (DI(ratio)), and damping index difference (ΔDI) between inspiration and expiration. Considering an HVPG level of 12 mm Hg or higher as the threshold level for high-grade portal hypertension, we assessed the diagnostic capability of these Doppler sonographic parameters to discriminate using receiver operating characteristic curve analysis. Area under the curve values for the DI(ratio) and ΔDI (0.875 and 0.889, P = .807 and .682, respectively) were slightly higher than the area for the DI(exp) (0.861; respectively). When the DI(exp) was greater than 0.56, the sensitivity and specificity for high-grade portal hypertension were 66.7% and 100.0%, respectively. In the case of the DI(ratio), the sensitivity and specificity were 77.8%, and 100.0% at greater than 0.69. The corresponding sensitivity and specificity at a value of 0.25 or less for the ΔDI were 83.3% and 100.0%. The ratio and difference of the DI of the hepatic vein waveform are helpful parameters in assessing the severity of portal hypertension as well as using the existing DI on its own.

480 WITHDRAWAL OF PROPHYLAXIS AGAINST HBV IN TRANSPLANTED PATIENTS WITH UNDETECTABLE INTRAHEPATIC TOTAL AND CCC-DNA: CLINICAL OUTCOME AFTER TWENTY MONTHS OF FOLLOW-UP

480 WITHDRAWAL OF PROPHYLAXIS AGAINST HBV IN TRANSPLANTED PATIENTS WITH UNDETECTABLE INTRAHEPATIC TOTAL AND CCC-DNA: CLINICAL OUTCOME AFTER TWENTY MONTHS OF FOLLOW-UP

387 PLATELET COUNT/SPLEEN DIAMETER RATIO COMPARED TO HVPG AND TRANSIENT ELASTOGRAPHY TO PREDICT SEVERE PORTAL HYPERTENSION IN PATIENTS WITH LIVER CIRRHOSIS

387 PLATELET COUNT/SPLEEN DIAMETER RATIO COMPARED TO HVPG AND TRANSIENT ELASTOGRAPHY TO PREDICT SEVERE PORTAL HYPERTENSION IN PATIENTS WITH LIVER CIRRHOSIS

QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium

A prolongation of QT interval has been shown in patients with cirrhosis and it is considered as part of the definition of the so-called 'cirrhotic cardiomyopathy'. The aim of the present study was to assess the determinants of QT interval prolongation in cirrhotic patients. Forty-eight male patients with different stages of liver disease were divided into three subgroups according to the Child-Pugh classification. All patients underwent a 24-h ECG Holter recording. The 24-h mean of QT intervals corrected for heart rate (termed QTc) and the slope of the regression line QT/RR were calculated. HRV (heart rate variability), plasma calcium and potassium concentration and HVPG (hepatic venous pressure gradient) were measured. QTc was progressively prolonged from Child A to Child C patients (P=0.001). A significant correlation between QTc and HVPG was found (P=0.003). Patients with alcohol-related cirrhosis presented QTc prolongation more frequently than patients with post-viral cirrhosis (P<0.001). The QT/RR slope was steeper in subjects with alcoholic aetiology as compared with viral aetiology (P=0.02), suggesting that these patients have a further QTc prolongation when heart rate decreases. The plasma calcium concentration was inversely correlated with QTc (P<0.001). The presence of severe portal hypertension was associated with decreased HRV (P<0.001). Cirrhotic patients with a more severe disease, especially of alcoholic aetiology, who have greater HVPG and lower calcium plasma levels, have an altered ventricular repolarization and a reduced vagal activity to the heart, which may predispose to life-threatening arrhythmias.

Correlation of hepatic venous pressure gradient with variceal bleeding, size of esophageal varices, etiology, ascites and degree of liver dysfunction in cirrhosis of liver

An elevated hepatic venous pressure gradient (HVPG) has been associated with risk of variceal bleeding, and outcome and survival after variceal bleeding. In this pilot study, we measured HVPG in 40 patients with liver cirrhosis and studied its relationship with etiology of liver disease, esophageal variceal size, history of variceal bleeding or ascites, biochemical liver tests and Child-Pugh class. There was no procedurerelated complication. The mean (SD) HVPG was similar in patients who had history of variceal bleeding as compared to those who did not (15.4 [2.8] mmHg vs. 13.9 [2.7] mmHg, p=0.1); HVPG had no significant association with etiology of cirrhosis (p=0.4). HVPG levels were significantly higher in patients with larger esophageal varices (grade III/IV vs. I/II: 15.2 [2.7] mmHg vs.13.1 [2.8] mmHg, p=0.04), poorer Child-Pugh class (B or C versus A), and presence of ascites (p=0.04). Thus, HVPG correlated with variceal size, Child-Pugh class, and presence of ascites, but not with variceal bleeding status.

Effect of Sustained Viral Response on Hepatic Venous Pressure Gradient in Hepatitis C–Related Cirrhosis

Interferon-based therapy can improve hepatic histology in chronic hepatitis C (CHC)-related cirrhosis but its effect on portal hypertension is unclear. The aims of this study were to investigate the effect of treatment with peginterferon alfa-2a and ribavirin on hepatic venous pressure gradient (HVPG) in CHC with compensated cirrhosis. Forty-seven patients with compensated biopsy examination-proven cirrhosis were recruited from 2 metropolitan teaching hospitals and were treated for 48 weeks with combination peginterferon alfa-2a 180 microg by subcutaneous injection weekly and ribavirin 800-1200 mg/day orally. A transjugular liver biopsy examination and HVPG measurement were performed at baseline, and 33 patients had a repeat HVPG measurement after 6 months of treatment-free follow-up evaluation. The overall sustained viral response (SVR) was 21%. Posttreatment there was a significant decrease in HVPG level in sustained responders compared with nonresponders (-2.1 +/- 4.8 vs 0.6 +/- 2.8 mm Hg; P = .05). Among patients with portal hypertension, a higher proportion of sustained responders achieved a 20% or greater reduction in HVPG level compared with nonresponders (71% vs 20%; P = .01). There was a significant association between a 20% or greater reduction in HVPG and both histologic response and SVR. Treatment with combination peginterferon plus ribavirin may produce clinically significant reductions in HVPG in patients with CHC-related cirrhosis who achieve an SVR.