Published online Nov 7, 2026. doi: 10.3748/wjg.121668
Revised: June 23, 2026
Accepted: July 15, 2026
Published online: November 7, 2026
Processing time: 167 Days and 23.7 Hours
The hepatic venous pressure gradient (HVPG) is a widely used metric to assess portal hypertension and predict the risk for variceal bleeding. However, in patients with cirrhosis and large spontaneous portosystemic shunts (SPSS), portal decompression may reduce intrahepatic pressure gradients and lead to an under
To evaluate portal and variceal pressure characteristics in patients with cirrhosis and fundal varices and large SPSS.
This retrospective, single-center study included data from patients with cirrhosis and gastric varices and large SPSS. All patients underwent simultaneous mea
Data from 25 patients were analyzed. The mean GVP was significantly higher than portal vein pressure (PVP) (27.04 ± 7.67 mmHg vs 19.84 ± 7.94 mmHg) and GVP was strongly correlated with PVP. The GVPG was substantially higher than both HVPG and PPG (P < 0.001). Although correlation analyses revealed significant associations among HVPG, PPG, and GVPG, agreement analyses indicated substantial variability, suggesting that they were not interchangeable. Among these parameters, only GVPG differed sig
In patients with cirrhosis and SPSS, conventional HVPG and PPG may underestimate local variceal pressure whereas GVPG may facilitate assessment of bleeding risk, thus meriting prospective multicenter validation.
Core Tip: In patients with large spontaneous portosystemic shunts, the hepatic venous pressure gradient may underestimate the risk of bleeding because of shunt-mediated decompression. The gastric variceal pressure gradient, reflecting local variceal hemodynamics, may provide additional value for risk stratification.
- Citation: Wei W, Xue M, Xu LY. Gastric variceal pressure gradient in patients with large spontaneous shunts: A novel approach to local hemodynamic assessment. World J Gastroenterol 2026; 32(41): 121668
- URL: https://www.wjgnet.com/1007-9327/full/v32/i41/121668.htm
- DOI: https://dx.doi.org/10.3748/wjg.121668
Portal hypertension is a major complication of cirrhosis and its severity dictates the risk for decompensation, which in turn critically influences patient outcomes. As such, accurate assessment of portal pressure is essential for risk stratification and clinical management.
The hepatic venous pressure gradient (HVPG) is the established gold-standard metric for evaluating the severity of portal hypertension[1]. According to current guidelines, an HVPG ≥ 10 mmHg defines clinically significant portal hypertension, a threshold associated with increased risk for varices and decompensation. Measurement of HVPG has broad clinical applications, from risk stratification and therapeutic guidance to the evaluation of novel pharmacological agents and validation of emerging noninvasive diagnostic technologies[2]. However, as an indirect measurement, HVPG reflects hepatic sinusoidal pressure but may not accurately capture regional hemodynamic variations[3], particularly in the presence of large portosystemic shunts (PSS). Endoscopic ultrasound-guided portal pressure gradient (EUS-PPG) measurement has recently emerged as a promising alternative[4,5]. By enabling direct puncture of the portal vein under endosonographic guidance, EUS-PPG offers several advantages over HVPG, including direct pressure acquisition and the potential for concomitant endoscopic intervention(s) during a single session[6]. Nevertheless, similar to HVPG, EUS-PPG measures the pressure within the main portal vein and, may therefore, not fully reflect the localized hemodynamic stress exerted on individual varices.
Gastric varices (GV), particularly those associated with large spontaneous PSS (SPSS) such as gastrorenal shunts (GRV) or splenorenal shunts (SRS), present a unique clinical challenge[7,8]. According to previous reports, large SPSS were defined as having a maximum shunt diameter ≥ 8 mm[9,10]. These shunts can substantially alter portal hemodynamics, resulting in the underestimation of true portal pressure by both HVPG and PPG[11]. Consequently, conventional pressure gradients may inaccurately predict the risk for bleeding in this specific subpopulation. The literature reporting direct measurements of gastric variceal pressure (GVP) remains scarce, and the hemodynamic relationship between main portal vein pressure (PVP) and local variceal pressure is poorly characterized.
As such, this study aimed to evaluate the feasibility and safety of direct GVP measurement and determine whether the GVP gradient (GVPG) defined as directly measured GVP minus inferior vena cava pressure (IVCP) yields superior predictive utility for bleeding risk compared with conventional HVPG and EUS-PPG in this challenging patient popu
This single-center, retrospective, observational study was conducted at The Second Affiliated Hospital of Zhejiang University School of Medicine (Hangzhou, Zhejiang Province, China) between July 2025 and January 2026. Consecutive adults diagnosed with cirrhosis and scheduled for invasive portal pressure assessment were screened for eligibility. All pressure measurements were performed as part of the routine clinical evaluation and therapeutic decision making.
The inclusion criteria were as follows: (1) Age ≥ 18 years; (2) Hospitalization with a confirmed diagnosis of cirrhosis and GV; (3) Presence of a large SPSS with a maximum diameter > 8 mm confirmed by contrast-enhanced CT; and (4) Informed written consent. Cirrhosis was diagnosed based on a combination of clinical, laboratory, radiologic, endoscopic, and/or histologic findings, in accordance with current guideline recommendations. The exclusion criteria were as follows: (1) Significant coagulopathy (international normalized ratio > 1.5); (2) Severe thrombocytopenia (platelet count < 30 × 109/L); (3) Severe systemic comorbidities such as active sepsis, decompensated heart failure, or severe chronic obstructive pulmonary disease; (4) Psychiatric disorders precluding cooperation with the procedure; and (5) Refusal to undergo HVPG or EUS-PPG measurement.
Patients receiving carvedilol routinely discontinued the medication at least 24 hours before pressure measurement in accordance with our institutional protocol. Patients were categorized into 2 groups based on a documented history of variceal hemorrhage before enrollment: Recent (within 4 weeks) and non-recent. Variceal bleeding was defined in accordance with the Baveno VII consensus criteria. The study was approved by the Ethics Committee of The Second Affiliated Hospital of Zhejiang University School of Medicine (approval No. 2025-0822) and all participants provided written informed consent.
All HVPG measurements were performed by interventional radiologists during assessment of portal hypertension. HVPG measurements were performed with patients under local anesthesia using lidocaine via the right internal jugular vein approach and a commercially available transjugular intrahepatic access kit (RUPS-100; Cook Medical, Bloomington, IN, United States). Under digital subtraction angiography guidance and fluoroscopic control, a balloon catheter (Edwards Life Sciences, Irvine, CA, United States) was advanced through the superior vena cava, right atrium, and IVC into the right or middle hepatic veins.
To measure wedged hepatic venous pressure (WHVP), a balloon catheter was advanced into the distal branch of the hepatic vein and inflated to achieve complete occlusion of the hepatic venous outflow. After pressure stabilization, the WHVP was recorded. The balloon was then deflated and the catheter withdrawn to the proximal hepatic vein to obtain the free hepatic venous pressure (FHVP). Each measurement was performed 3 times, the mean value of which was used for analysis. The HVPG was calculated as the difference between WHVP and FHVP.
All procedures were performed by experienced endoscopists with extensive experience in portal hemodynamic assessment following a standardized protocol (Figure 1). Hemodynamic measurements were performed in a single session. Under general anesthesia with endotracheal intubation, patients were placed in the left lateral decubitus position. A pressure transducer system (PT-01; Shenzhen Ante Medical, China) was flushed with heparinized saline (12.5 U/mL) and zeroed at the right atrial level before each measurement. Conventional gastroscopy (GIF-Q260J, Olympus, Tokyo, Japan) was performed to evaluate the varices and red color signs. Endoscopic ultrasonography (EU-ME3; Olympus, Tokyo, Japan) was used to visualize the main portal vein, IVC, and GV.
PVP was measured under EUS guidance using a 22- or 25-gauge needle (Cook Medical, United States) connected to a calibrated pressure transducer. Doppler flow imaging confirmed safe puncture trajectory and correct vessel entry. After waveform stabilization (approximately 30 seconds), the pressure values were recorded. The measurements were repeated 3 times, and the mean value was used for the analysis. The IVCP was measured using the same technique. The EUS-PPG was defined as the difference between PVP and IVCP. GVP was subsequently measured under EUS guidance using the same standardized protocol. The GVPG was calculated as the difference between GVP and IVCP.
Given the limited sample size, analyses focused primarily on group comparisons and association measures, rather than on predictive modeling. Statistical analyses were performed using SPSS version 27.0 (IBM Corporation, Armonk, NY, United States). Continuous variables were assessed for normality using the Shapiro-Wilk test. Normally distributed data are expressed as mean ± SD and were compared using the Student’s t-test. Non-normally distributed data are expressed as median with interquartile range, and were compared using the Mann-Whitney U test. Comparisons between paired non-normally distributed data were performed using the Wilcoxon signed-rank test. Categorical variables are expressed as n (%), and were compared using the χ2 or Fisher’s exact tests, as appropriate.
Correlations between portal pressure measurements were evaluated using Pearson’s or Spearman’s correlation coefficients, according to data distribution. Correlation strength was interpreted based on correlation coefficient and corresponding 95% confidence interval (CI). The agreement between different pressure parameters was further assessed using Bland-Altman analysis, with calculation of the mean difference (bias) and 95% limits of agreement.
Exploratory receiver operating characteristic (ROC) curve analyses were performed to assess the discriminatory ability of each pressure parameter for previous variceal bleeding. The area under the ROC curve (AUC) with corresponding 95%CI are reported descriptively. No formal comparison between AUCs was performed due to limited statistical power. Given the limited sample size, multivariate regression modeling was not performed to avoid overfitting. All statistical tests were two-sided, and P < 0.05 was considered to be significant. A biomedical statistician performed a statistical review of the study.
Data from 25 patients with liver cirrhosis and GV, who underwent invasive portal pressure assessment, were included in this study. The baseline demographic and clinical characteristics of the study cohort are summarized in Table 1.
| Characteristics | Patients enrolled |
| Age, years | 58 ± 14 |
| Male sex | 18 (72) |
| BMI, kg/m2 | 21.57 ± 3.44 |
| Hypertension | 5 (20) |
| Diabetes | 3 (12) |
| Etiology of liver cirrhosis | |
| Viral hepatitis | 18 (72) |
| Alcohol | 1 (4) |
| Other | 6 (24) |
| Laboratory values (median, Q1-Q3) | |
| ALT (U/L) | 26.00 (18.00-39.50) |
| AST (U/L) | 35.00 (29.50-45.00) |
| ALB (g/L) | 35.80 (31.75-38.85) |
| TB (μmol/L) | 19.00 (14.50-24.90) |
| PLT (109/L) | 79.00 (51.50-137.00) |
| PT (second) | 15.00 (14.05-16.20) |
| INR | 1.18 (1.10-1.31) |
| Oesophageal varices | 13 (52) |
| Ascites | 11 (44) |
| Child-Pugh score | |
| A | 18 (72) |
| B | 7 (28) |
| MELD score (median, Q1-Q3) | 9 (7.0-12.0) |
| MELD-Na (median, Q1-Q3) | 9 (8.0-10.5) |
The mean age of the patients was 58 ± 14 years, and the majority were male (72%). The most common etiology of liver cirrhosis was viral hepatitis (72%), followed by other causes (24%) and alcohol consumption (4%). Laboratory parameters reflected the underlying portal hypertension and liver dysfunction, with a median platelet count of 79.00 × 109/L (Q1-Q3: 51.50 × 109/L to 137.00 × 109/L) and a median albumin level of 35.80 g/L (Q1-Q3: 31.75-38.85 g/L). Clinically, con
Detailed characteristics of the GV and their corresponding hemodynamic parameters are reported in Table 2. Among the 25 patients, isolated GV type 1 (IGV1) was the most prevalent type, observed in 14, followed by IGV1 combined with gastro-oesophageal varices (GOV) 1 and GOV2. Large PSS were identified in all patients, with GRV shunts accounting for the majority (76%) and SRS present in the remaining 6. The mean ± SD diameter of the GV was 2.68 ± 0.79 cm, and the mean diameter of the PSS was 1.29 ± 0.31 cm. The mean diameter of the main portal vein was 1.47 ± 0.19 cm.
| Characteristics | Patients enrolled |
| GEVs classification | |
| IGV1 | 14 (56) |
| IGV1 + GOV1 | 6 (24) |
| GOV2 | 5 (20) |
| Portosystemic shunt | |
| Gastro-renal shunt | 19 (76) |
| Spleen-renal shunt | 6 (24) |
| Diameter of gastric varices, cm | 2.68 ± 0.79 |
| Diameter of the portosystemic shunt, cm | 1.29 ± 0.31 |
| Diameter of portal vein, cm | 1.47 ± 0.19 |
| HVPG | |
| HVPG (mmHg) | 6.16 ± 2.56 |
| FHVP (mmHg) | 13.36 ± 5.52 |
| WHVP (mmHg) | 19.80 ± 7.10 |
| EUS-PPG | |
| PPG (mmHg) | 9.04 ± 5.74 |
| IVCP (mmHg) | 10.72 ± 4.73 |
| PVP (mmHg) | 19.84 ± 7.94 |
| GVPG (mmHg) | 16.32 ± 6.18 |
| GVP (mmHg) | 27.04 ± 7.67 |
| Variceal bleeding ≤ 4 weeks | 16 (64) |
The hemodynamic profiles of the cohort are summarized as follows. The conventional HVPG was 6.16 ± 2.56 mmHg, with a WHVP of 19.80 ± 7.10 mmHg. The mean EUS-PPG (calculated as PVP minus IVCP) was 9.04 ± 5.74 mmHg. The directly measured GVP was 27.04 ± 7.67 mmHg; consequently, the calculated GVPG was 16.32 ± 6.18 mmHg, which was substantially higher than both the HVPG and the PPG in this patient cohort. As shown in Figure 2A, the GVPG con
The correlations and agreements among the pressure parameters were further evaluated. A strong positive correlation was observed between directly measured PVP and GVP, with a Spearman correlation coefficient of 0.856 (P < 0.001) (Figure 2B). However, Bland-Altman analysis revealed a substantial systematic bias of 7.20 mmHg (95%CI: 5.77-8.63), indicating that GVP was consistently higher than PVP across the entire pressure range (Figure 2C).
PPG exhibited a strong positive correlation with HVPG (Spearman’s r = 0.721, P < 0.001) (Figure 2D). GVPG was also strongly correlated with PPG (Spearman’s r = 0.796, P < 0.001) (Figure 2E). In addition, a moderate but statistically significant correlation was observed between GVPG and HVPG (Spearman r = 0.537, P = 0.006) (Figure 2F). Bland-Altman analysis demonstrated a mean bias of -2.88 mmHg (95%CI: -4.68 to -1.08), indicating that PPG values were generally higher than HVPG values (Figure 2G). Bland-Altman analysis revealed a mean bias of -7.28 mmHg (95%CI: -8.70 to -5.86) between PPG and GVPG (Figure 2H). The Bland-Altman analysis comparing HVPG and GVPG demonstrated the largest mean bias among all comparisons [-10.16 mmHg (95%CI: -12.32 to -8.00)], indicating that GVPG values were substantially higher than HVPG values (Figure 2I). Overall, these findings suggest that conventional pressure gradients may substantially underestimate the true pressure burden on GV.
To identify factors associated with GV bleeding, the demographic, clinical, and hemodynamic parameters between patients with (n = 15) and without (n = 10) a history of variceal bleeding within 4 weeks before enrollment were compared (Table 3). The 2 groups were well balanced with regard to age, sex, body mass index, etiology of liver cirrhosis, and liver function, as assessed according to Child-Pugh class and MELD score. The use of non-selective beta-blockers was comparable between the bleeding and non-bleeding groups (60.0% vs 50.0%, P = 0.244). Regarding the anatomical characteristics of GV, the distribution of GEV types exhibited no significant difference between the groups (P = 0.206), although IGV1 was more common in the non-bleeding group (80.00% vs 40.00%), whereas the combined types (IGV1 + GOV1 and GOV2) were more prevalent in the bleeding group. The PSS type was similar between the groups (P = 0.653). Notably, the diameter of the PSS was significantly larger in patients with recent bleeding compared to those without (1.39 ± 0.31 cm vs 1.13 ± 0.23 cm; P = 0.034). The diameter of GV showed a trend toward being larger in the bleeding group (2.87 ± 0.80 cm vs 2.38 ± 0.71 cm; P = 0.137), while portal vein diameter demonstrated a trend toward being smaller (14.16 ± 1.91 cm vs 15.42 ± 1.71 cm; P = 0.080).
| Characteristics | No recent bleeding (n = 10) | Recent bleeding (n = 15) | P value |
| Age, years | 61.40 ± 12.50 | 57.33 ± 15.18 | 0.470 |
| Male sex | 7 (70.00) | 11 (73.33) | 0.856 |
| BMI, kg/m2 | 20.95 ± 2.20 | 21.99 ± 4.10 | 0.560 |
| Etiology of liver cirrhosis | 0.090 | ||
| Viral hepatitis | 4 (40.00) | 13 (86.67) | |
| Alcohol | 1 (10.00) | 0 (0) | |
| Other | 5 (50.00) | 2 (13.33) | |
| Child-Pugh score | 0.659 | ||
| A | 8 (80.00) | 10 (66.67) | |
| B | 2 (20.00) | 5 (33.33) | |
| MELD score (median, Q1-Q3) | 8 (7.0-13.0) | 10 (9.0-12.0) | 0.382 |
| MELD-Na (median, Q1-Q3) | 8 (7.0-10.5) | 9 (9.0-11.0) | 0.160 |
| Non-selective beta-blockers | 5 (50.00) | 9 (60.00) | 0.244 |
| GEVs classification | 0.206 | ||
| IGV1 | 8 (80.00) | 6 (40.00) | |
| IGV1 + GOV1 | 1 (10.00) | 5 (33.33) | |
| GOV2 | 1 (10.00) | 4 (26.67) | |
| Portosystemic shunt | 0.653 | ||
| Gastro-renal shunt | 7 (70.00) | 12 (80.00) | |
| Splenorenal shunt | 3 (30.00) | 3 (20.00) | |
| Diameter of gastric varices, cm | 2.38 ± 0.71 | 2.87 ± 0.80 | 0.137 |
| Diameter of the portosystemic shunt, cm | 1.13 ± 0.23 | 1.39 ± 0.31 | 0.034a |
| Diameter of portal vein, cm | 15.42 ± 1.71 | 14.16 ± 1.91 | 0.080 |
| PVP, mmHg | 19.10 ± 9.70 | 20.33 ± 6.86 | 0.420 |
| IVCP, mmHg | 12.20 ± 5.55 | 9.73 ± 4.00 | 0.317 |
| GVP, mmHg | 25.40 ± 9.40 | 28.13 ± 6.38 | 0.156 |
| HVPG, mmHg | 5.00 ± 2.45 | 6.93 ± 2.40 | 0.054 |
| PPG, mmHg | 6.70 ± 5.18 | 10.60 ± 5.73 | 0.075 |
| GVPG, mmHg | 13.20 ± 5.13 | 18.40 ± 6.07 | 0.030a |
Among the various pressure measurements and gradients, GVPG was the only parameter that exhibited a statistically significant difference between groups. Patients with recent bleeding had significantly higher GVPG compared to those without bleeding (18.40 ± 6.07 mmHg vs 13.20 ± 5.13 mmHg; P = 0.030) (Figure 2J). Other pressure parameters, including GVP, HVPG, and PPG, demonstrated numerical trends, but did not reach statistical significance. Therefore, GVPG may serve as a more sensitive indicator of bleeding risk than conventional pressure gradients in this patient population.
Exploratory ROC curve analysis was performed to assess the ability of different portal pressure parameters to discriminate patients with recent variceal bleeding from those without. As shown in Figure 2K and L, the AUC for HVPG was 0.730, 0.713 for PPG, and 0.760 for GVPG. Among these parameters, GVPG demonstrated the highest AUC. When PVP and GVP were analyzed individually, the AUCs were 0.597 and 0.670, respectively, both of which were lower than those observed for GVPG. Overall, these findings suggest a moderate discriminatory ability of gradient-based mea
All pressure measurements were performed as part of routine clinical evaluation of portal hypertension. There were no major procedure-related adverse events, including bleeding, perforation, infection, or hemodynamic instability. All patients tolerated the procedure without the need for unplanned interventions or prolonged hospitalization. These fin
This retrospective study systematically evaluated portal and variceal pressures in patients with fundal varices and SPSS. The variceal pressure significantly exceeded the main PVP, highlighting the hemodynamic heterogeneity introduced by spontaneous shunting. Importantly, we propose a novel gradient-based parameter, the GVPG. While absolute pressure alone did not reliably discriminate recent bleeding, GVPG demonstrated a moderate discriminatory ability, suggesting that pressure gradients may better reflect the local hemodynamic environment associated with variceal rupture.
The predominance of hepatitis B-related cirrhosis in our cohort aligns with the epidemiological profile of China and the Asia-Pacific region[12], enhancing the regional clinical relevance of our findings. Although all patients had fundal varices requiring intervention, most retained preserved hepatic function (Child-Pugh A), minimizing confounding from end-stage liver failure and supporting the procedural feasibility of invasive measurements[13].
Notably, all patients presented with large SPSS and substantial mean fundal variceal diameters, representing a clinically challenging subgroup. Consistent with previous studies, the HVPG and EUS-PPG were positively correlated, reflecting their shared representation of global portal pressure[14]. Although GVP was strongly correlated with PVP, Bland-Altman analysis revealed a systematic bias, indicating that these measurements reflect distinct hemodynamic compartments. HVPG has long been the reference standard for assessing portal hypertension and stratifying variceal bleeding risk, with a widely accepted threshold of 12 mmHg considered to be critical for rupture. However, our findings suggest that this framework may not be applicable to patients with prominent shunt pathways and fundal varices. To the best of our knowledge, no previous study has specifically evaluated GVPG. Therefore, we introduced this gradient-based parameter, hypothesizing that, in patients with large shunts, the local pressure gradient may better capture the mechanical forces driving variceal rupture than the absolute pressure value. In our exploratory cohort, GVPG was markedly higher than concurrently measured HVPG and PPG values. These differences support the clinical observation that intrahepatic pressure gradients can be substantially attenuated by shunt-mediated “steal” phenomena, whereas directly measured variceal pressure remained elevated. This may, in part, explain why patients with an apparently low HVPG still experience a high incidence of recent bleeding.
Beyond the hemodynamic findings, the feasibility and safety of EUS-guided pressure assessment merit consideration. In our cohort, measurements were performed during routine endoscopy with the patients under general anesthesia by experienced endoscopists and no major procedure-related adverse events were observed. This safety profile is supported by 3 key considerations. First, our institution has extensive experience, with > 130 successful procedures before this study, demonstrating technical reliability. Second, the existing literature consistently reports favorable safety outcomes, providing external validation[15-17]. Third, a pragmatic risk-adaptive strategy was implemented. In patients undergoing clinically indicated therapy, the pressure was measured immediately before sclerotherapy or ligation using a 22-gauge needle. For surveillance-only cases, a 25-gauge needle, the smallest caliber available, was selected to minimize trauma while preserving measurement stability. No severe puncture-related bleeding or need for rescue intervention was recorded, and both needle sizes were well tolerated[18-20].
However, a standard platelet count threshold for EUS-PPG in patients with cirrhosis has not yet been established. Although earlier practices used a precautionary cut-off ≥ 50 × 109/L for high-risk procedures[21], recent guidelines support a more nuanced approach[22], with individualized assessment, even at 20 × 109/L to 50 × 109/L, when local hemostasis is achievable[23]. Patients with platelet counts < 20 × 109/L generally warrant preoperative platelet-boosting therapy[24]. In our cohort, we pragmatically adopted an inclusion criterion of platelet count > 30 × 109/L, with six patients in the 30 × 109/L to 50 × 109/L range. Despite this lower threshold, no severe puncture-related bleeding occurred, and minor oozing was self-limiting. This experience suggests that with tailored planning and risk stratification, pressure measurement may be safely performed in selected patients with thrombocytopenia under careful endoscopic observation and multidisciplinary management. However, this approach should be individualized for broader hemostatic assessment.
From a clinical perspective, our findings have important implications for risk stratification in patients with large SPSS. In this subgroup, HVPG and main portal pressure measurements may underestimate bleeding risk because of shunt-mediated decompression of the portal trunk. In contrast, the GVPG incorporates both local variceal pressure and systemic outflow conditions, potentially providing a more physiologically relevant marker of rupture risk. Although exploratory, our findings suggest that the direct assessment of GVPG may improve the identification of high-risk patients with fundal varices and prominent shunts. Specifically, patients with an elevated GVPG despite a low HVPG may benefit from earlier interventions targeting the variceal complex or shunt pathway, such as endoscopic therapy or shunt embolization, rather than management strategies based solely on conventional HVPG thresholds. Therefore, local gradient-based hemo
The present study had several limitations, the first of which were its retrospective, single-center design and relatively small sample size, limited statistical power, which potentially introduced selection bias. Second, given the limited number of patients and bleeding events, this study was not designed to identify independent factors associated with gastric variceal bleeding. Therefore, the observed association between GVPG and recent bleeding should be considered exploratory and hypothesis-generating. Furthermore, the exploratory nature of the study precludes definitive conclusions regarding the predictive performance of GVPG, and the lack of longitudinal follow-up limits assessment of its prognostic value for future bleeding events. Third, although carvedilol was routinely withheld for at least 24 hours before pressure measurement in accordance with our institutional protocol, and only one patient underwent pressure assessment during somatostatin infusion, the retrospective design precluded complete control of medications that may influence portal hemodynamics. Moreover, although the proportion of carvedilol use was comparable between patients with and without recent bleeding, the potential residual effects of non-selective beta-blockers and other vasoactive agents cannot be entirely excluded. Therefore, residual confounding related to medication use remains possible. Fourth, formal comparisons among the pressure parameters were constrained by insufficient statistical power. Finally, all pressure measurements were performed at a specialized center with expertise in EUS-guided vascular access, and the reproducibility and safety in other settings require further validation. Future multicenter prospective studies with larger cohorts, standardized medication protocols, and longitudinal follow-up are warranted.
Conventional portal pressure measurements may underestimate local variceal hemodynamic stress in patients with fundal varices and large SPSS. Direct assessment of GVPG offers a physiologically grounded approach for characterizing bleeding risk in this anatomically complex subgroup. Although exploratory and limited by the sample size, our findings suggest that gradient-based local pressure evaluation may complement traditional HVPG assessments and inform individualized therapeutic strategies. However, larger prospective studies are required to confirm these findings.
We acknowledge all the patients and research staff who participated in this study.
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