Relationship between the hepatic venous pressure gradient and first variceal hemorrhage in patients with cirrhosis: a multicenter retrospective study in Korea.
ABSTRACT Variceal hemorrhage is one of the major complications of cirrhosis and is associated with significant mortality and morbidity. The development of gastroesophageal varices and variceal hemorrhage is the most direct consequence of portal hypertension. Correlations between the hepatic venous pressure gradient (HVPG) and first variceal hemorrhage were examined.
Patients with cirrhosis who underwent HVPG measurement between July 2009 and September 2010 were enrolled (n=535). All patients underwent esophagogastroduodenoscopy to enable the evaluation of gastroesophageal varices.
The HVPG for all patients was 16.46±7.05 mmHg (mean±SD), and was significantly higher among those with first variceal hemorrhage than in those without it. The HVPG was significantly correlated with both Child-Turcotte-Pugh (r=0.488, P<0.001) and Model for End-stage Liver Disease (r=0.478, P<0.001) scores. An HVPG value of 11 mmHg was predictive of first variceal hemorrhage with a sensitivity of 92.4% and a specificity of 27.7%.
The HVPG was higher in patients with first variceal hemorrhage than in those without it.
- SourceAvailable from: PubMed Central[Show abstract] [Hide abstract]
ABSTRACT: Liver stiffness measurement (LSM) has been proposed as a non-invasive method for estimating the severity of fibrosis and the complications of cirrhosis. Measurement of the hepatic venous pressure gradient (HVPG) is the gold standard for assessing the presence of portal hypertension, but its invasiveness limits its clinical application. In this study we evaluated the relationship between LSM and HVPG, and the predictive value of LSM for clinically significant portal hypertension (CSPH) and severe portal hypertension in cirrhosis. LSM was performed with transient elastography in 59 consecutive cirrhotic patients who underwent hemodynamic HVPG investigations. CSPH and severe portal hypertension were defined as HVPG ≥10 and ≥12 mmHg, respectively. Linear regression analysis was performed to evaluate the relationship between LSM and HVPG. Diagnostic values were analyzed based on receiver operating characteristic (ROC) curves. A strong positive correlation between LSM and HVPG was observed in the overall population (r(2)=0.496, P<0.0001). The area under the ROC curve (AUROC) for the prediction of CSPH (HVPG ≥10 mmHg) was 0.851, and the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for an LSM cutoff value of 21.95 kPa were 82.5%, 73.7%, 86.8%, and 66.7%, respectively. The AUROC at prediction of severe portal hypertension (HVPG ≥12 mmHg) was 0.877, and the sensitivity, specificity, PPV, and NPV at LSM cutoff value of 24.25 kPa were 82.9%, 70.8%, 80.6%, and 73.9%, respectively. LSM exhibited a significant correlation with HVPG in patients with cirrhosis. LSM could be a non-invasive method for predicting CSPH and severe portal hypertension in Korean patients with liver cirrhosis.Clinical and molecular hepatology. 12/2013; 19(4):370-5.
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ABSTRACT: Tetrahydrobiopterin (BH4) is an essential cofactor in NO synthesis by endothelial nitric oxide synthase (eNOS) enzymes. It has been previously suggested that reduced intrahepatic BH4 results in a decrease in intrahepatic NO and contributes to increased hepatic vascular resistance and portal pressure in animal models of cirrhosis. The main aim of the present study was to evaluate the relationship between BH4 and portal hypertension (PHT). One hundred ninety-three consecutive patients with chronic liver disease were included in the study. Liver biopsy, measurement of BH4 and hepatic venous pressure gradient (HVPG) were performed. Hepatic fibrosis was classified using the Laennec fibrosis scoring system. BH4 levels were determined in homogenized liver tissues of patients using a high performance liquid chromatography (HPLC) system. Statistical analysis was performed to evaluate the relationship between BH4 and HVPG, grade of hepatic fibrosis, clinical stage of cirrhosis, Child-Pugh class. A positive relationship between HVPG and hepatic fibrosis grade, clinical stage of cirrhosis and Child-Pugh class was observed. However, the BH4 level showed no significant correlation with HVPG or clinical features of cirrhosis. BH4 concentration in liver tissue has little relation to the severity of portal hypertension in patients with chronic liver disease.Journal of Korean medical science 03/2014; 29(3):392-9. · 0.84 Impact Factor
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ABSTRACT: 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.Clinical and molecular hepatology. 03/2014; 20(1):6-14.
Copyright © 2012 by The Korean Association for the Study of the Liver
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/)
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Clinical and Molecular Hepatology 2012;18:391-396
Relationship between the hepatic venous pressure
gradient and first variceal hemorrhage in patients with
cirrhosis: a multicenter retrospective study in Korea
Jin Nyoung Kim1*, Kyoung Min Sohn2*, Moon Young Kim3, Ki Tae Suk2, Soung Won Jeong1, Ho Eun Jung1,
Sae Hwan Lee4, Sang Gyune Kim5, Jae Young Jang1†, Young Seok Kim5, Soon Koo Baik3†, Hong Soo Kim4,
Dong Joon Kim2, and Boo Sung Kim1
1Division of Gastroenterology and Hepatology, Department of Internal Medicine, Soonchunhyang University College of Medicine,
Seoul; 2Division of Gastroenterology and Hepatology, Department of Internal Medicine, Hallym University Chuncheon Sacred Heart
Hospital, Hallym University College of Medicine, Chuncheon; 3Division of Gastroenterology and Hepatology, Department of Internal
Medicine, Wonju Christian Hospital, Yonsei University Wonju College of Medicine, Wonju; 4Division of Gastroenterology and Hepatology,
Department of Internal Medicine, Soonchunhyang University College of Medicine, Bucheon; 5Division of Gastroenterology and
Hepatology, Department of Internal Medicine, Soonchunhyang University College of Medicine, Cheonan, Korea
Background/Aims: Variceal hemorrhage is one of the major complications of cirrhosis and is associated with significant
mortality and morbidity. The development of gastroesophageal varices and variceal hemorrhage is the most direct
consequence of portal hypertension. Correlations between the hepatic venous pressure gradient (HVPG) and first
variceal hemorrhage were examined.
Methods: Patients with cirrhosis who underwent HVPG measurement between July 2009 and September 2010 were
enrolled (n=535). All patients underwent esophagogastroduodenoscopy to enable the evaluation of gastroesophageal
Results: The HVPG for all patients was 16.46±7.05 mmHg (mean±SD), and was significantly higher among those with
first variceal hemorrhage than in those without it. The HVPG was significantly correlated with both Child-Turcotte-Pugh
(r=0.488, P<0.001) and Model for End-stage Liver Disease (r=0.478, P<0.001) scores. An HVPG value of 11 mmHg was
predictive of first variceal hemorrhage with a sensitivity of 92.4% and a specificity of 27.7%.
Conclusions: The HVPG was higher in patients with first variceal hemorrhage than in those without it. (Clin Mol
Keywords: Hepatic venous pressure gradient (HVPG); Variceal hemorrhage
†Co-corresponding author :
Soon Koo Baik
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Wonju Christian Hospital, Yonsei University Wonju College of Medicine,
20 Ilsan-ro, Wonju 220-701, Korea
Tel. +82-33-741-1223, Fax. +82-33-741-1228, E-mail; email@example.com
Jae Young Jang
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Soonchunhyang University Hospital, 22 Daesakwan-gil, Yongsan-gu,
Seoul 140-743, Korea
Tel. +82-2-7099863, Fax. +82-2-7099797, E-mail; firstname.lastname@example.org
CTP, Child-Turcotte-Pugh; HBV, hepatitis B virus; HCV, hepatitis C virus; HVPG, hepatic venous pressure gradient; MELD, Model for End-Stage Liver Disease
*These authors contributed equally to this work.
Received : Jul. 23, 2012 / Revised : Oct. 16, 2012 / Accepted : Oct. 16, 2012
Clin Mol Hepatol
Volume_18 Number_4 December 2012
Portal hypertension in cirrhosis leads to the development of
collateral veins and portosystemic shunts, which in turn increase
cardiac output and splanchnic blood flow, resulting in high portal
venous inflow and persistent portal hypertension. Serious com-
plications can ensue, including gastroesophageal varices, ascites,
renal insufficiency, and hepatic encephalopathy. Variceal bleeding
is the most common and most serious complication. After the first
bleeding episode, variceal bleeding recurs within 1 year in 70% of
patients and the rate of mortality attributable to recurrent bleed-
ing is now approaching 30%.1 Consequently, an assessment of
portal hypertension is very important in caring for patients with
cirrhosis and for predicting their prognosis.
The hepatic venous pressure gradient (HVPG), defined as the
difference between the wedged and free hepatic vein pressures,
is widely used to reflect portal vein pressure. HVPG measurement
is a simple, safe procedure, and the HVPG is thus accepted as the
best predictor of portal hypertension and survival in patients with
cirrhosis. In addition, the HVPG is significantly correlated with the
Child-Turcotte-Pugh (CTP) and Model for End-Stage Liver Disease
(MELD) scores.2-4 Clinically significant portal hypertension is diag-
nosed when the clinical manifestations of the disease appear or
when the portal pressure gradient exceeds a threshold value of
10 mmHg. An HVPG of ≥10 mmHg leads to varices and a value of
≥12 mmHg leads to variceal bleeding;5-7 therefore, the HVPG must
be reduced to <12 mmHg to prevent variceal bleeding.
However, the relationships between the increase in HVPG and
the grade of varices and severity of liver disease are not well es-
tablished.8,9 Consequently, the aim of this study was to determine
the correlations between the HVPG and first variceal hemorrhage
PATIENTS AND METHODS
This study was based on a retrospective cohort in a multicenter
setting. A total of 535 patients with cirrhosis underwent HVPG
measurement at Wonju Christian Hospital Yonsei University Wonju
College of Medicine, Hallym University Chuncheon Sacred Heart
Hospital, and Soonchunhyang University Seoul Hospital. In all
patients, the diagnosis of cirrhosis was made based on clinical
symptoms, and imaging, histologic, and biochemical findings.
Patients with concomitant hepatocellular carcinoma or portal-vein
thrombosis were excluded. Regarding the causes of cirrhosis, con-
firmed hepatitis B surface antigen positivity for at least 6 months
indicated cirrhosis induced by chronic hepatitis B virus (HBV),
hepatitis C virus (HCV) RNA positivity indicated cirrhosis caused by
Figure 1. Hepatic venous pressure measurements made using hepatic vein catheterization. (A) The wedged hepatic venous pressure was
measured upon inserting the catheter further into smaller branches of the hepatic veins, reflecting the intrahepatic portal vein pressure. (B) The
free hepatic venous pressure was measured by inserting the catheter into the hepatic vein via the right jugular vein or the femoral vein.
Jin Nyoung Kim, et al.
Relationship between the hepatic venous pressure gradient and first variceal hemorrhage
chronic hepatitis C, and alcohol-induced cirrhosis was diagnosed
in females/males who consumed on average more than 20/40 g of
alcohol per day over 5-10 years.10
The HVPG, which was measured during clinical care, was esti-
mated from three repeated measurements, and the mean value
was calculated. A catheter was placed percutaneously into the
right hepatic vein through the femoral or jugular veins, and the
pressure in both the wedged position and the free position was
recorded with a 7-F balloon-tipped catheter (Arrow Deutschland,
Erding, Germany). The HVPG was determined by subtracting the
free hepatic venous pressure from the wedged hepatic venous
pressure (Fig. 1).11,12
The endoscopic findings of esophageal varices were classified
according to the General Rules for Recording Endoscopic Findings
of the Japanese Research Society for Portal Hypertension, in which
the form of any varix is graded as F0 (no varicose appearance),
F1 (small: straight, small-caliber varices), F2 (medium: moderately
enlarged, beady varices), or F3 (large: markedly enlarged, nodular
or tumor-shaped varices).13,14
HVPG was measured when liver cirrhosis was diagnosed for
the first time or cirrhotic patient was hospitalized with variceal
hemorrhage. The patients’ medical records were analyzed retro-
spectively, and their MELD and CTP scores were calculated. The
variables used for the two indicators were taken from the results
of examination on or closest to the day of HVPG measurement.
The CTP score was calculated using established criteria. The MELD
score was calculated using a formula developed at the Mayo
Clinic: 3.8×log (bilirubin [mg/dL])+11.2×log (international normal-
ized ratio)+6.4×(etiology score: 0 if cholestatic or alcoholic, 1
Statistical analysis was performed using SPSS software (version
18.0 for Windows, SPSS, Chicago, IL, USA). Quantitative data are
expressed as mean±SD, range, or n (%) values, as appropriate.
The presence of esophageal varices, presence of gastric varices,
variceal hemorrhage, and varix size were compared using the two-
sample t-test and one-way analysis of variance. The correlation
between variables was analyzed using the Pearson correlation
coefficient. The HVPG was compared according to varix size, CTP
score, and MELD score using Student’s t-test. The level of statisti-
cal significance was set at P<0.05 (two-tailed).
This study enrolled 535 patients (440 males, 95 females; mean
Table 1. Clinical characteristics of the patients
Age, years (mean±SD)52.0±9.5
Etiology of cirrhosis
Alcohol 382 (71.4%)
Alcohol+HBV 20 (3.7%)
HCV 9 (1.7%)
Alcohol+HCV 3 (0.6%)
HBV+HCV 1 (0.2%)
Others 15 (2.8%)
F0 142 (26.5%)
F2 200 (37.4%)
F3 59 (11.0%)
GOV1 85 (15.9%)
GOV2 43 (9.0%)
IGV 6 (1.1%)
First bleeding 67 (12.5%)
Rebleeding 54 (10.1%)
A 188 (35.1%)
C 80 (15.0%)
11–20 252 (47.1%)
21–30 32 (6.0%)
HVPG (mean±SD) 16.46±7.05
Data are n (%) values except where stated otherwise.
SD, standard deviation; Others, cryptogenic, autoimmune; CTP, Child-
Turcotte-Pugh; MELD, Model for End-Stage Liver Disease; HVPG, hepatic
venous pressure gradient.
Clin Mol Hepatol
Volume_18 Number_4 December 2012
age 52 years) with cirrhosis. The cause of cirrhosis was alcohol in
382 (71.4%) patients, HBV in 105 (19.6%), alcohol with HBV in 20
(3.7%), HCV in 9 (1.7%), alcohol with HCV in 3 (0.6%), HBV with
HCV in 1 (0.2%), and other causes, including autoimmune hepati-
tis, in 15 (2.8%) patients. The esophageal varices were graded as
F0 in 142 (26.5%) patients, F1 in 134 (25.0%), F2 in 200 (37.4%),
and F3 in 59 (11.0%) patients. Gastric varices were found in 134
(25.0%) patients. The non-hemorrhage group comprised 414 pa-
tients and the variceal hemorrhage group comprised 121 patients.
The CTP classification was A (i.e., a CTP score of 5-6) in 188
(35.1%) patients, B (i.e., a CTP score of 7-9) in 207 (49.9%), and
C (i.e., a CTP score of 10-15) in 80 (15.0%), and the MELD score
was 1-10 in 251 (46.9%) patients, 11-20 in 252 (47.1%), and >20
in 32 (6.0%). The HVPG was 16.46±7.05 mmHg (mean±SD). The
patient’s characteristics are summarized in Table 1.
HVPG according to variceal status
The HVPG was significantly higher in the group with esopha-
geal varices (18.46±6.58 mmHg) than in those without esopha-
geal varices (10.94±5.13 mmHg, P<0.001), and significantly
higher in those with gastric varices (17.99±6.58 mmHg) than in
those without gastric varices (15.98±7.15 mmHg, P=0.006). Of
the 535 patients, 259 (48.4%) had F2 or F3 varices. The HVPG
was significantly higher in the patients with gastric varices than in
patients with small varices (19.23±6.78 vs. 13.87±6.29 mmHg,
P<0.001; Fig. 2). The HVPG differed significantly according to gas-
tric varix type as follows: absence, 15.98±7.14 mmHg; GOV1 and
GOV2, 18.03±6.68 mmHg; and IGV, 15.00±2.83 mmHg (P<0.00;
Table 2, Fig. 2).
HVPG according to CTP and MELD scores
The HVPG was positively correlated with the CTP class (r=0.488,
Table 2. The HVPG according to variceal status
HVPG (mean±SD) P-value*
Esophageal varix size
Gastric varix type
*Statistical significance was calculated using the two-sample t-test and one-
way analysis of variance.
Figure 2. The HVPG relative to varix size and type. (A) The HVPG was significantly higher in patients with large varices (F2, F3; 19.23±6.78 mmHg)
than in those with small varices (F0, F1; 13.87±6.29 mmHg, P<0.001). (B) The HVPG differed significantly according to gastric varix type: absence,
15.98±7.14 mmHg; gastroesophageal varices (GOV)1 and GOV2, 18.03±6.68 mmHg; and isolated gastric varices, 15.00±2.83 mmHg (P=0.014).
Jin Nyoung Kim, et al.
Relationship between the hepatic venous pressure gradient and first variceal hemorrhage
P<0.001) and the MELD score (r=0.478, P<0.001). The HVPG
increased significantly with the CTP class: 12.03±5.58 mmHg for
class A, 18.40±6.27 mmHg for class B, and 21.61±6.95 mmHg
for class C (P<0.001). Similarly, the HVPG differed significantly
with the MELD score, being 12.71±5.86, 19.53±6.46, and
21.77±4.78 mmHg for MELD scores of 1-10, 11-20, and 21-30,
respectively (P<0.001; Table 3).
HVPG, CTP and MELD scores according to
episode of first variceal hemorrhage
The HVPG was significantly higher in the group with first vari-
ceal hemorrhage (18.30±5.75 mmHg) than in those without such
hemorrhage (16.20±7.19 mmHg, P=0.023). However, the CTP and
MELD scores did not differ significantly between the two groups
The HVPG clearly reflects portal pressure in patients with cir-
rhosis. Its relationship with variceal hemorrhage has been well
studied. In particular, it has been found that an HVPG level of
>12 mmHg increases the risk of variceal bleeding, and that the
HVPG is a key predictor of cirrhosis.16 However, the relationships
between the HVPG and first variceal hemorrhage and severity of
liver disease are not well established. Hence, the present study
investigated the correlations between the HVPG and first variceal
Many previous studies have found significant correlations be-
tween the HVPG and variceal hemorrhage. Indeed, the first vari-
ceal hemorrhage is associated with the increased risk of mortality
in the patients with cirrhosis. We found that the HVPG was sig-
nificantly higher in the group with first variceal hemorrhage than
in patients without such hemorrhage, which suggests that this
measure is a good predictor of variceal hemorrhage and confirms
that portal-pressure-lowering drugs are needed to prevent the
first onset of variceal hemorrhage.1,4,17
Gastric varices occur in approximately 25% of patients with
portal hypertension. Although the reported rate of hemorrhage
from gastric varices is lower than that from esophageal varices,
the rupture of gastric varices (and especially fundal varices) tends
to be more severe, requiring more transfusions, and is associated
with a higher mortality rate. We found that the HVPG differed sig-
nificantly between patients with and without gastric varices.
The severity of cirrhosis (CTP score, MELD score) is a risk fac-
tor of variceal hemorrhage. Nevertheless, our study showed that
the CTP and MELD scores did not differ significantly between the
group with first variceal hemorrhage and the group without such
hemorrhage. Although several factors affect variceal hemorrhage,
these suggest that HVPG is more reliable predictive factor of the
first variceal hemorrhage rather than CTP and MELD scores.
Many studies have examined the correlation between the HVPG
and MELD score, some with conflicting results. Lee et al10 mea-
sured the HVPG in 136 patients with decompensated cirrhosis
and found that it was not a significant predictor of mortality. To
determine the predictive nature of the HVPG, prospective studies
with a broad group of patients (e.g., etiology, sex, and geographic
region) are needed. In addition, Huo et al18 and Wang et al19 found
that the MELD score was related to the HVPG and serum sodium
level, and that high MELD and CTP scores, and high HVPG pre-
dicted a negative outcome.
We found significant correlations between the HVPG and both
CTP and MELD scores, which indicates that HVPG monitoring is
clinically beneficial. HVPG of 11 mmHg predicted first variceal
bleeding with a sensitivity of 92.4% and a specificity of 27.7%.
Low specificity of HVPG means that multiple factors such as
thrombocytopenia, coagulation factors, and tense ascites can
Table 3. The HVPG according to CTP classification and MELD score
A (score 5–6)12.03±5.58 mmHg
B (score 7–9) 18.40±6.27 mmHg
C (score 10–15) 21.61±6.95 mmHg
11–20 19.53±6.46 mmHg
*Statistical significance was calculated using one-way analysis of variance.
Table 4. The HVPG, CTP and MELD scores according to first variceal
HVPG 16.20±7.19 mmHg 18.30±5.75 mmHg
CTP score7.48±1.88 mmHg
MELD score 12.14±5.08 mmHg 11.00±4.45 mmHg
Data are mean±SD values.
*Statistical significance was calculated using the two-sample t-test.
Clin Mol Hepatol
Volume_18 Number_4 December 2012
affect variceal hemorrhage. In conclusion, the HVPG was higher
in cirrhotic patients with first variceal hemorrhage than in patients
without such hemorrhage. Hence, the measurement of HVPG
might be beneficial to prevent first variceal hemorrhage in patients
Conflicts of Interest
The authors have no conflicts to disclose.
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