Increase In Hepatic Venous Pressure Gradient Research Articles

Spontaneous portosystemic shunt diameter predicts liver function after balloon-occluded retrograde transvenous obliteration.

Background and AimRecently, balloon‐occluded retrograde transvenous obliteration (BRTO), performed for spontaneous portosystemic shunts (SPSS), has been receiving attention as a measure to improve liver function in cirrhotic patients with portal hypertension. However, it is unclear whether SPSS diameter is associated with changes in hepatic venous pressure gradient (HVPG) and liver function after BRTO.MethodsIn 34 cirrhotic patients receiving BRTO for hepatic encephalopathy/gastric varices, the association of SPSS diameter with liver function at baseline and 6 months after BRTO and the accompanying changes in HVPG were investigated.ResultsPatients had Child–Pugh (CP) scores of A/B/C (7/19/8), SPSS diameters of ≤10 mm/11–20 mm/<20 mm (8/21/5), and an average observation period of 3.2 (0.3–8.5) years. SPSS diameter was significantly associated with male sex, alcohol use, and values of albumin, prothrombin time (PT%), and NH3 at baseline. Moreover, the SPSS diameter was significantly correlated with the changes in HVPG observed upon BRTO (r = 0.55, P = 0.005), and a large shunt diameter was significantly associated with a greater increase in HVPG. At 6 months, significant improvements in albumin, PT%, bilirubin, and NH3 were observed overall, but the improvement was marked in those with larger shunt diameters if they had CP A/B.ConclusionSPSS diameter was strongly associated with liver function at baseline and after BRTO and also with changes in HVPG, indicating that SPSS diameter is an important predictor of BRTO outcome.

Change in Portal Pressure and Clinical Outcome in Cirrhotic Patients with Gastric Varices after Plug-Assisted Retrograde Transvenous Obliteration

Background/AimsPlug-assisted retrograde transvenous obliteration (PARTO) is widely used to manage gastric varices with a portosystemic shunt. It is not clear whether portal pressure and the incidence of complications increase after PARTO. The aim of this study was to determine the changes in portal pressure and the associated changes in liver function, ascites, hepatic encephalopathy, and especially esophageal varix (EV) after PARTO.MethodsFrom March 2012 to February 2018, 54 patients who underwent PARTO were analyzed retrospectively. The parameters collected included liver function and episodes of cirrhotic complications before and at 1 and 6 months after PARTO.ResultsThe analysis of 54 patients showed improvement in liver function during the 6-month follow-up period (Model for End-Stage Liver Disease score change from 11.46±4.35 to 10.33±2.96, p=0.021). Among these 54 patients, 25 patients were evaluated for their hepatic venous pressure gradient (HVPG) before and after PARTO (change from 12.52±3.83 to 14.68±5.03 mm Hg; p<0.001). Twenty-five patients with portal pressure measured before and after PARTO were evaluated for risk factors affecting liver function improvement and EV deterioration. No factor associated with portal pressure was affected by liver function improvement. Post-PARTO portal pressure was a risk factor affecting EV deterioration (HVPG-post odds ratio, 1.341; 95% confidence interval, 1.017 to 1.767; p=0.037).ConclusionsThe artificial blockade of the portosystemic shunt evidently leads to an increase in HVPG. Liver function was improved over the 6-month follow-up period. Portal pressure after PARTO was a significant risk factor for EV deterioration. Portal pressure measurement is helpful for predicting the patient’s clinical outcome.

Short‐ and long‐term effects of transarterial chemoembolization on portal hypertension in patients with hepatocellular carcinoma

BackgroundTransarterial chemoembolization (TACE) affects hepatic perfusion, and might have an impact on portal pressure in patients with hepatocellular carcinoma (HCC).ObjectiveThe objective of this article is to report the secondary outcome “hepatic hemodynamics” from the AVATACE trial, a prospective randomized, placebo-controlled trial on the efficacy of conventional TACE in combination with bevacizumab or placebo.MethodsHepatic venous pressure gradient (HVPG) was measured at baseline (prior to first TACE), within nine days (“acute effects”), two months (“intermediate effects”) and six months (“long-term effects”) after the first TACE.ResultsOf 28 patients with early-intermediate stage HCC, n = 20 (71%) had clinically significant portal hypertension (CSPH, HVPG ≥ 10 mmHg) at baseline (median, 12 (interquartile range (IQR): 9–19) mmHg). TACE had neither “acute effects” nor “intermediate effects” on HVPG. However, in 13 patients with available HVPG measurement at month 6, there was a significant increase in HVPG (median, 16 (IQR: 11–19) mmHg) compared with baseline (median, 10 (IQR: 5–12) mmHg; p = 0.007). Portal hypertension-related complications occurred exclusively in patients with CSPH (8 (40%) vs 0).ConclusionsRepeated TACE was associated with a significant long-term increase in HVPG. This should be considered when deciding whether to continue with TACE or switch to systemic treatment, since CSPH drives the development of complications.

The Natural History of Advanced Fibrosis Due to Nonalcoholic Steatohepatitis: Data From the Simtuzumab Trials.

Progression of nonalcoholic steatohepatitis (NASH) is incompletely characterized. We analyzed data on longitudinal changes in liver histology, hepatic venous pressure gradient (HVPG), and serum markers of fibrosis in 475 patients with NASH with bridging fibrosis (F3) or compensated cirrhosis (F4) enrolled in two phase 2b, placebo-controlled trials of simtuzumab. The trials were terminated after 96 weeks because of lack of efficacy, so data from treatment groups were combined. Liver biopsies and HVPG measurements (only for patients with F4 fibrosis) were collected at screening and at weeks 48 and 96. Patients were assessed for Ishak fibrosis stage, hepatic collagen content and alpha-smooth muscle actin (by morphometry), NAFLD Activity Score (NAS), and serum markers of fibrosis. Associations with progression to cirrhosis (in patients with F3 fibrosis) and liver-related clinical events (in patients with F4 fibrosis) were determined. Progression to cirrhosis occurred in 22% (48/217) of F3 patients, and liver-related clinical events occurred in 19% (50/258) of patients with cirrhosis. Factors significantly associated with progression to cirrhosis included higher baseline values of and greater increases in hepatic collagen content, level of alpha-smooth muscle actin, and Enhanced Liver Fibrosis score. Similar factors, plus lack of fibrosis stage improvement (hazard ratio, 9.30; 95% confidence interval, 1.28-67.37), higher HVPG at baseline, and greater increase in HVPG over time, were associated with an increased risk of liver-related clinical events in patients with cirrhosis. Disease progression was not associated with the NAS at baseline or changes in NAS during treatment after adjustment for fibrosis stage. Conclusion: In patients with advanced fibrosis due to NASH, the primary determinant of clinical disease progression is fibrosis and its change over time.

Measurement of Portal Pressure and its Application in the Clinical Setting

AbstractPortal hypertension is a severe, yet common sequela of patients with chronic liver disease and is responsible for many of the complications seen in this population. Measurement of the hepatic venous pressure gradient (HVPG) is the current gold standard technique for identifying and evaluating the severity of portal hypertension. Any increase in HVPG to ≥10 mm Hg is considered clinically significant portal hypertension. Above this threshold, complications of portal hypertension begin to manifest. In addition to assessing portal hypertension, various HVPG thresholds have been shown to have strong prognostic value for risk of complications and therapeutic failure, as well as survival in patients with chronic liver disease. These clinical applications include quantification of disease progression and regression in chronic viral hepatitis, acute alcoholic hepatitis, and hepatocellular carcinoma. Other applications include preoperative evaluation of liver resection and transplantation in patients with cirrhosis and hepatocellular carcinoma, assessment of response to therapy for portal hypertension, and identification of the need for transjugular intrahepatic portosystemic shunt (TIPS) revision.

Subtotal hepatectomy in swine for studying small-for-size syndrome and portal inflow modulation: is it reliable?

BackgroundSmall-for-size syndrome (SFSS) is a feared complication of extended liver resection and partial liver transplantation. Swine models of extended hepatectomy have been developed for studying SFSS and its different treatment options. Although portal inflow modulation (PIM) by splenectomy or splenic artery ligation (SAL) has been proposed in humans to prevent SFSS, such procedures have not yet been evaluated in swine. ObjectivesThe present study was designed to evaluate modifications in splanchnic haemodynamics yielded by extended hepatectomy with and without PIM in swine. MethodsNineteen animals underwent 70% hepatectomy (H70, n = 7), 90% hepatectomy (H90, n = 7) or sham laparotomy (H0, n = 5). Haemodynamic measurements were performed at baseline, after hepatectomy and after PIM by SAL and splenectomy. ResultsPortal vein flow increased after both H70 (273 ml/min/100 g versus 123 ml/min/100 g; P = 0.016) and H90 (543 ml/min/100 g versus 124 ml/min/100 g; P = 0.031), but the hepatic venous pressure gradient (HVPG) increased only after H90 (10.0 mmHg versus 3.7 mmHg; P = 0.016). Hepatic artery flow did not significantly decrease after either H70 or H90. In all three groups, neither splenectomy nor SAL induced any changes in splanchnic haemodynamics. ConclusionsSubtotal hepatectomy of 90% in swine is a reliable model for SFSS inducing a significant increase in HVPG. However, in view of the relevant differences between swine and human splanchnic anatomy, this model is inadequate for studying the effects of PIM by SAL and splenectomy.

To transfuse or not to transfuse in upper gastrointestinal hemorrhage? That is the question

To transfuse or not to transfuse in upper gastrointestinal hemorrhage? That is the question

Hepatic venous pressure gradient: clinical use in chronic liver disease.

Portal hypertension is a severe consequence of chronic liver diseases and is responsible for the main clinical complications of liver cirrhosis. Hepatic venous pressure gradient (HVPG) measurement is the best available method to evaluate the presence and severity of portal hypertension. Clinically significant portal hypertension is defined as an increase in HVPG to >10 mmHg. In this condition, the complications of portal hypertension might begin to appear. HVPG measurement is increasingly used in the clinical fields, and the HVPG is a robust surrogate marker in many clinical applications such as diagnosis, risk stratification, identification of patients with hepatocellular carcinoma who are candidates for liver resection, monitoring of the efficacy of medical treatment, and assessment of progression of portal hypertension. Patients who had a reduction in HVPG of ≥20% or to ≤12 mmHg in response to drug therapy are defined as responders. Responders have a markedly decreased risk of bleeding/rebleeding, ascites, and spontaneous bacterial peritonitis, which results in improved survival. This review provides clinical use of HVPG measurement in the field of liver disease.

Effect of Meal Ingestion on Liver Stiffness in Patients with Cirrhosis and Portal Hypertension

Background and AimsLiver stiffness is increasingly used in the non-invasive evaluation of chronic liver diseases. Liver stiffness correlates with hepatic venous pressure gradient (HVPG) in patients with cirrhosis and holds prognostic value in this population. Hence, accuracy in its measurement is needed. Several factors independent of fibrosis influence liver stiffness, but there is insufficient information on whether meal ingestion modifies liver stiffness in cirrhosis. We investigated the changes in liver stiffness occurring after the ingestion of a liquid standard test meal in this population.MethodsIn 19 patients with cirrhosis and esophageal varices (9 alcoholic, 9 HCV-related, 1 NASH; Child score 6.9±1.8), liver stiffness (transient elastography), portal blood flow (PBF) and hepatic artery blood flow (HABF) (Doppler-Ultrasound) were measured before and 30 minutes after receiving a standard mixed liquid meal. In 10 the HVPG changes were also measured.ResultsPost-prandial hyperemia was accompanied by a marked increase in liver stiffness (+27±33%; p<0.0001). Changes in liver stiffness did not correlate with PBF changes, but directly correlated with HABF changes (r = 0.658; p = 0.002). After the meal, those patients showing a decrease in HABF (n = 13) had a less marked increase of liver stiffness as compared to patients in whom HABF increased (n = 6; +12±21% vs. +62±29%,p<0.0001). As expected, post-prandial hyperemia was associated with an increase in HVPG (n = 10; +26±13%, p = 0.003), but changes in liver stiffness did not correlate with HVPG changes.ConclusionsLiver stiffness increases markedly after a liquid test meal in patients with cirrhosis, suggesting that its measurement should be performed in standardized fasting conditions. The hepatic artery buffer response appears an important factor modulating postprandial changes of liver stiffness. The post-prandial increase in HVPG cannot be predicted by changes in liver stiffness.

High prevalence of normal serum albumin in NASH patients with ascites: A retrospective analysis

Ascites usually occurs in the setting of end-stage liver disease and low serum albumin and is associated with increased mortality. However, some patients develop ascites despite normal serum albumin (NSA), when a higher portal pressure and/or enhanced renal sodium retention would be expected. This study investigated the relationship between the hepatic venous pressure gradient (HVPG) and serum albumin in ascitic patients with different etiologies of cirrhosis and mortality. Records of all patients with non-malignant ascites who underwent HVPG measurement from 2005 to 2009 were reviewed. One hundred and thirty-eight 138 patients met inclusion criteria; 18.8% had NSA. No difference in sodium excretion or diuretic use was noted in patients with and without NSA. NASH patients were more likely to have a NSA (34.2% vs 12.4%; P=0.001) as well as lower HVPG (15 vs 17.9 mmHg; P=0.009) compared to other etiologies. MELD and HVPG predicted overall survival. However, mortality did not differ by disease etiology, though NASH patients had lower CTP (7.6 vs 8.5; P<0.001) and MELD (15.6 vs 18.1; P=0.09) scores, particularly among patients who died. In patients with ascites and NSA, there were no increase in HVPG or urinary sodium retention. NASH patients with ascites had lower HVPG and a higher prevalence of NSA. They also had a higher mortality relative to MELD and CTP scores in other patients. In these patients, mechanisms other than portal and oncotic pressures and sodium retention play a role in ascites development, and increase mortality rate when complicated by low albumin.

Postprandial effects of dark chocolate on portal hypertension in patients with cirrhosis: results of a phase 2, double-blind, randomized controlled trial

In cirrhosis, hepatic endothelial dysfunction as a result of oxidative stress contributes to the postprandial increase in hepatic venous pressure gradient (HVPG). We aimed at testing the hypothesis that dark chocolate, which holds potent antioxidant properties, might attenuate the postprandial increase in HVPG in patients with cirrhosis. In this phase 2, double-blind, controlled study, 22 cirrhotic patients referred for HVPG measurement were included and randomly assigned to receive a liquid meal containing either dark chocolate (active treatment; 85% cocoa, 0.55 g/kg body wt; n = 11) or isocaloric amounts of white chocolate (devoid of cocoa flavonoids; control subjects; n = 11). HVPG, arterial pressure, portal blood flow, serum flavonoids (catechin and epicatechin), and nitric oxide were measured at baseline and 30 min after meal administration. The main outcome measure was the change in HVPG 30 min after the test meal. Postprandial hyperemia was accompanied by a marked increase in HVPG in the white-chocolate group (16.0 ± 4.7-19.7 ± 4.1 mm Hg or +26.4 ± 12.7%; P < 0.0001), whereas the postprandial increase in HVPG was markedly attenuated in the dark-chocolate group (16.9 ± 2.9-18.7 ± 3.5 mm Hg or +11.5 ± 15.9%; P = 0.02 compared with white chocolate). Portal blood flow increased similarly after meals containing dark or white chocolate (median increase: 32% compared with 39%). Plasma flavonoids increased 15-50-fold after dark chocolate consumption. Dark but not white chocolate induced a mild increase in arterial pressure (+8.8 ± 8.8% compared with -0.3 ± 4.9%; P = 0.002). In patients with cirrhosis, dark chocolate blunted the postprandial increase in HVPG by improving flow-mediated hepatic vasorelaxation and ameliorated systemic hypotension. This trial was registered at clinicaltrials.gov as NCT01408966.

Bacterial DNA translocation is associated with systemic circulatory abnormalities and intrahepatic endothelial dysfunction in patients with cirrhosis

Presence of bacterial DNA in noninfected patients with cirrhosis and ascites is associated with a marked inflammatory response including activation of the inducible form of nitric oxide synthase and release of nitric oxide, similar to that observed in patients with spontaneous bacterial peritonitis. Although presence of bacterial DNA is associated with an impaired prognosis, no information is available regarding its hemodynamic consequences. Systemic and hepatic hemodynamics before and after a liquid test meal were assessed in a series of 75 noninfected patients with cirrhosis (55 with ascites). Bacterial DNA was measured by polymerase chain reaction. Bacterial DNA was detected only in patients with ascites. Clinical data and liver function were similar in ascitic patients with presence (n = 21) or absence of bacterial DNA (n = 34). Bacterial-DNA(+) patients had significantly lower mean arterial pressure (P = 0.002) and systemic vascular resistance (P = 0.03) than bacterial-DNA(-) patients. Cardiac output, cardiopulmonary pressures, hepatic venous pressure gradient (HVPG), and hepatic blood flow were similar in both groups. Thirty minutes after the test meal, in response to increased blood flow caused by postprandial hyperemia, there was a significantly greater increase in HVPG and impaired hepatic vasorelaxation in bacterial-DNA(+) as compared with bacterial-DNA(-) patients, which indicates hepatic endothelial dysfunction. Indeed, the increase in HVPG after the test meal significantly correlated with serum bacterial DNA concentration. Presence of bacterial DNA, a marker of bacterial translocation, is associated with aggravation of peripheral vasodilation and with worsening of intrahepatic endothelial dysfunction.

Clinical significance of worsening portal hypertension during long-term medical treatment in patients with cirrhosis who had been classified as early good-responders on haemodynamic criteria

It is established that cirrhotic patients who respond to beta-blockers by lowering their hepatic venous pressure gradient (HVPG) to < or =12 mmHg or by > or =20% of the baseline values are protected from bleeding. However, it is not known whether the effect remains unchanged over the treatment period. A group of 24 patients with cirrhosis and oesophageal varices, treated with beta-blockers+/-nitrates, good-responders on haemodynamic criteria, were followed for up to 76 months with sequential HVPG measurements. Another group of 16 patients was used for validation. HVPG worsened in 10 of the 24 patients during follow-up. Changes in HVPG correlated to concomitant changes in liver function parameters. Variceal bleeding occurred in four of the 10 patients whose HVPG had worsened (bleed; 3-21 months after the measured increase in HVPG) and in none of those with stable HVPG (p=0.02). Patients with increased HVPG also had shorter survival (p=0.05). Worsening of HVPG was an independent predictor of death, additive to Child-Pugh or MELD scores, in a time-dependent Cox's regression analysis. This relationship was confirmed in the validation group. Worsening HVPG during follow-up in patients who had initially been good-responders to medical treatment is related to worsening in hepatic function. The maintenance of a good haemodynamic response to medical treatment of portal hypertension is an excellent predictor of outcome in these patients.

The clinical use of HVPG measurements in chronic liver disease

Portal hypertension is a severe, almost unavoidable complication of chronic liver diseases and is responsible for the main clinical consequences of cirrhosis. Measurement of the hepatic venous pressure gradient (HVPG) is currently the best available method to evaluate the presence and severity of portal hypertension. Clinically significant portal hypertension is defined as an increase in HVPG to >or=10 mmHg; above this threshold, the complications of portal hypertension might begin to appear. Measurement of HVPG is increasingly used in clinical hepatology, and numerous studies have demonstrated that the parameter is a robust surrogate marker for hard clinical end points. The main clinical applications for HVPG include diagnosis, risk stratification, identification of patients with hepatocellular carcinoma who are candidates for liver resection, monitoring of the efficacy of medical treatment, and assessment of progression of portal hypertension. Patients who experience a reduction in HVPG of >or=20% or to <12 mmHg in response to drug therapy are defined as 'responders'. Responders have a markedly decreased risk of bleeding (or rebleeding), ascites, and spontaneous bacterial peritonitis, which results in improved survival.

Clinical trial: the effect of somatostatin vs. octreotide in preventing post‐endoscopic increase in hepatic venous pressure gradient in cirrhotics with bleeding varices

Hepatic venous pressure gradient (HVPG) increases significantly after endoscopic therapy in patients with bleeding oesophageal varices, which may precipitate further haemorrhage. Whether vasoactive drugs can suppress these changes remains unknown. To investigate the efficacy of somatostatin when compared with octreotide in preventing the post-endoscopic increase in HVPG during acute bleeding and whether the changes affect outcome. Thirty-three cirrhotics with bleeding varices were randomized to receive somatostatin (n = 17) or octreotide (n = 16) under double-blind conditions, soon after their admission. HVPG measurements were performed before and immediately after endoscopic treatment. In the somatostatin group, postendotherapy HVPG values did not change significantly when compared with pre-treatment values (18.9 vs. 17.2, P = 0.092). Conversely, in the octreotide group, HVPG increased significantly after endoscopy (18.2 vs. 20.8, P = 0.003). The probability of 6-week survival without treatment failure was significantly higher in the somatostatin group (P = 0.024). Post-endoscopic HVPG value was independently associated with 6-week failure. Somatostatin, but not octreotide, effectively prevents the post-endoscopic increase in HVPG, which may be associated with low probability of treatment failure.

Recent Variceal Bleeding: Doppler US Hepatic Vein Waveform in Assessment of Severity of Portal Hypertension and Vasoactive Drug Response

To prospectively evaluate both the correlation between abnormal Doppler ultrasonography (US) hepatic vein waveforms and the hepatic venous pressure gradient (HVPG) and the response to drug treatment in patients with cirrhosis. Ethics committee approval and informed consent of patients and control subjects were obtained. In 78 patients with cirrhosis (70 men, eight women; mean age, 49.4 years +/- 9.7 [standard deviation]) and a history of variceal bleeding, both the hepatic vein waveform--as measured with Doppler US--and the HVPG were measured, and the relationship between them was analyzed. Hepatic vein Doppler waveforms were classified as triphasic, biphasic, or monophasic. Severe portal hypertension was defined as an HVPG of more than 15 mm Hg. In a subgroup of 21 patients, changes in hepatic vein waveform and HVPG were evaluated after intravenous administration of 2 mg of terlipressin. Statistical analyses were performed with Spearman rank correlation, logistic regression analysis, and cross tabulation. Abnormal hepatic vein waveforms were seen in 72 patients (92%). Forty-four patients (56%) had biphasic waveforms, 28 (36%) had monophasic waveforms, and six (8%) had triphasic waveforms. A positive correlation was found between the extent of abnormalities in hepatic vein waveforms and the increase in HVPG (P < .05). Monophasic waveforms were associated with severe portal hypertension, with a sensitivity of 74% and a specificity of 95%. Twenty patients in the terlipressin subgroup had abnormal baseline waveforms; the baseline waveform improved in 18 patients in association with the HVPG reduction after injection of terlipressin. Doppler US hepatic vein waveform assessment is useful in the noninvasive evaluation of the severity of portal hypertension and the response to vasoactive drugs in patients with portal hypertension and variceal bleeding.

Understanding the splenic contribution to portal flow: The role of splenic artery ligation as inflow modification in living donor liver transplantation

Understanding the splenic contribution to portal flow: The role of splenic artery ligation as inflow modification in living donor liver transplantation

Influence of Hepatic Venous Pressure Gradient on the Prediction of Survival of Patients With Cirrhosis in the MELD Era *

Measurements of portal pressure, usually obtained via the hepatic venous pressure gradient (HVPG) may be a prognostic marker in cirrhosis. The aim of this study was to evaluate the impact of HVPG on survival in patients with cirrhosis in addition to the Model for End-Stage Liver Disease (MELD) score. We also examined whether inclusion of HVPG in a model with MELD variables improves its prognostic ability. Retrospective analyses of all patients who had HVPG measurements between January 1998 and December 2002 were considered. Proportional hazards Cox models were developed. Prognostic calibrative and discriminative ability of the model was evaluated. In this period, 693 patients had a hepatic hemodynamic study, and 393 patients were included. Survival was significantly worse in those patients with greater HVPG value (univariate HR, 1.05; 95% CI, 1.02-1.08; P = .001). HVPG remained as an independent variable in a model adjusted by MELD, ascites, encephalopathy, and age (multivariate HR, 1.03; 95% CI, 1.00-1.06; P = .05) so that each 1-mmHg increase in HVPG had a 3% increase in death risk. In addition, HVPG as well as MELD score variables and age, significantly contributes to the calibrative predictive capacity of the prognostic model; however, discriminative ability improved only slightly (overall C statistic [95% CI]; MELD score variables: 0.71 [0.62-0.80], MELD score variables, age, and HVPG 0.76: [0.69-0.83]). In conclusion, HVPG has an independent effect on survival in addition to the MELD score. Although inclusion of HVPG and age in a survival predicting model would improve the calibrative ability of MELD, its discriminative ability is not significantly improved.

Splanchnic and systemic haemodynamic response to volume changes in patients with cirrhosis and portal hypertension

We investigated the haemodynamic response to volume depletion and subsequent repletion in patients with cirrhosis and portal hypertension. Twelve patients with compensated cirrhosis and portal hypertension were included in the study. The haemodynamic changes occurring after removal of approx. 15% of the blood volume, and subsequently after isovolume repletion with colloid, were assessed. Baseline haemodynamic measurements showed increased cardiac output and a systemic vascular resistance at the lower limit of normal. The hepatic venous pressure gradient (HVPG) was increased, at 18 mmHg. After depletion, arterial pressure, cardiac output and all right-heart-sided pressures decreased, and systemic vascular resistance increased. HVPG decreased to 16.0 mmHg. All the above changes were statistically significant. After blood volume restitution, the haemodynamic values returned to baseline. In particular, an increase in HVPG was shown in four out of the twelve patients (two with ascites and two without), which was small in three of them. However, HVPG remained the same as or lower than the baseline in the other eight patients. Patients with cirrhosis and portal hypertension exhibit an abnormal haemodynamic response to blood volume depletion. After volume repletion, no increase in the portal pressure was noted in this group of patients as a whole, although four out of the twelve patients did show an increase, possibly due to extensive collateral circulation.

Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis

BACKGROUND & AIMS: Increased portal blood flow represents a compensatory mechanism preventing hepatic hypoxia after ethanol consumption. In addition, alcohol increases hepatic vascular resistance. Thus, ethanol consumption, by increasing hepatic vascular resistance and portal flow, may worsen portal hypertension in patients with cirrhosis. The aim of this study was to investigate the effects of ethanol consumption on hepatic hemodynamics in patients with alcohol- induced cirrhosis. METHODS: Measurements of hepatic venous pressure gradient (HVPG), azygos blood flow, hepatic blood flow, heart rate, and arterial pressure were obtained in 16 patients with alcohol-induced cirrhosis and portal hypertension before and after random administration of a noncaloric fruit drink (250 mL, n = 7) or of an identical beverage plus 0.5 g/kg of ethanol (n = 9). RESULTS: Vehicle caused no effects. By contrast, ethanol increased HVPG (P < 0.0001). The increase in HVPG was maximum at 15 minutes and remained significant at 45 minutes (P < 0.05 vs. vehicle). Ethanol increased azygos blood flow (P < 0.05) without changes in hepatic blood flow. Heart rate and arterial pressure slightly increased. CONCLUSIONS: Oral ethanol consumption increases portal pressure and portocollateral blood flow in patients with alcohol-induced cirrhosis. These findings suggest that even moderate alcohol consumption worsens the portal-hypertensive syndrome and, therefore, may increase the risk of variceal bleeding in patients with alcohol-induced cirrhosis. (Gastroenterology 1997 Apr;112(4):1284-9)