Published online May 27, 2026. doi: 10.4240/wjgs.v18.i5.118030
Revised: January 16, 2026
Accepted: February 12, 2026
Published online: May 27, 2026
Processing time: 156 Days and 23.8 Hours
Clinically significant portal hypertension (CSPH) drives major complications in cirrhosis. While hepatic venous pressure gradient is the gold standard for CSPH diagnosis, its invasiveness limits routine use. Liver stiffness measurement (LSM) and spleen stiffness measurement (SSM) offer non-invasive alternatives, but their utility in tracking transjugular intrahepatic portosystemic shunt (TIPS)-induced hemodynamic changes remains unclear.
To assess the correlation of LSM/SSM with baseline portocaval pressure gradient (PPG) and ΔPPG, and to evalutate their predictive value for hemodynamic success (post-PPG ≤ 10 mmHg).
We retrospectively analyzed 39 patients underwent TIPS. LSM and SSM were measured via vibration-controlled transient elastography pre- and post-TIPS. PPG was recorded invasively during the procedure. Correlations between stiffness parameters and PPG were assessed using Spearman’s test; diagnostic perfor
PPG dropped from 17.6 ± 4.1 mmHg to 7.0 ± 2.3 mmHg (P < 0.001). SSM decreased significantly (61.7 ± 17.1 kPa to 26.9 ± 11.6 kPa; P < 0.001) and correlated with baseline PPG (r = 0.41, P < 0.001) and ΔPPG (r = -0.57, P < 0.001). LSM showed no significant correlation with PPG or ΔPPG. None of the stiffness metrics reliably predicted successful TIPS response (all area under the curve < 0.7).
SSM dynamically reflects TIPS-induced portal pressure changes, outperforming LSM as a non-invasive marker. Despite limited predictive value here (small cohort, etiological heterogeneity), it remains valuable for TIPS mo
Core Tip: This study demonstrates that spleen stiffness measurement (SSM), assessed by vibration-controlled transient elastography, strongly correlates with both baseline portal pressure and its reduction after transjugular intrahepatic portosystemic shunt (TIPS), outperforming liver stiffness measurement. Although neither parameter reliably predicts successful hemodynamic response to TIPS, SSM emerges as a robust non-invasive tool for monitoring portal pressure changes over time, particularly valuable when repeated invasive measurements are impractical.
- Citation: Zhou RQ, Yang PJ, Liu LG, Zhang JB, Ye ZD, Tan HD. Spleen stiffness accurately tracks early and sustained portal pressure changes after transjugular intrahepatic portosystemic shunt. World J Gastrointest Surg 2026; 18(5): 118030
- URL: https://www.wjgnet.com/1948-9366/full/v18/i5/118030.htm
- DOI: https://dx.doi.org/10.4240/wjgs.v18.i5.118030
Clinically significant portal hypertension (CSPH), defined as a hepatic venous pressure gradient (HVPG) ≥ 10 mmHg, is a pivotal turning point in the natural history of compensated advanced chronic liver disease (cACLD) and cirrhosis. It acts as the core driver of severe liver-related complications, including esophageal variceal bleeding, refractory ascites, and hepatic encephalopathy, all of which drastically worsen patient prognosis[1,2]. For instance, patients with cACLD and CSPH face a substantially higher risk of liver decompensation; notably, the median survival time plummets from 12 years in the compensated stage to merely 2 years once decompensation occurs[2,3]. The gold standard for diagnosing CSPH remains invasive HVPG measurement, which quantifies the pressure difference between wedged and free hepatic venous pressures to directly reflect portal pressure[4-6]. However, HVPG is hampered by inherent limitations: It requires specialized expertise and equipment, carries risks of bleeding or infection, and is not feasible for routine monitoring or widespread use in non-tertiary centers[5,7,8]. This clinical unmet need has fueled the development of non-invasive tools for CSPH assessment, with liver stiffness measurement (LSM) and spleen stiffness measurement (SSM) emerging as leading candidates.
LSM, primarily evaluated via vibration-controlled transient elastography (VCTE), has been extensively validated for assessing liver fibrosis and indirectly predicting portal hypertension (PH)[2,5]. The Baveno VII guidelines proposed the “rule of 5” to stratify CSPH risk in cACLD: LSM < 15 kPa combined with a platelet count ≥ 150 × 109/L to rule out CSPH, and LSM ≥ 25 kPa to rule in CSPH[9,10]. SSM, a relatively novel non-invasive modality, has gained recognition for its superior ability to mirror portal hemodynamics. Unlike LSM, SSM is not affected by hepatic inflammation or cholestasis, as it primarily reflects splenic congestion and hyperdynamic splanchnic circulation, which are the key pathophysiological features of CSPH[2,6].
While prior studies have explored the role of LSM and SSM in diagnosing CSPH, their utility in tracking transjugular intrahepatic portosystemic shunt (TIPS)-induced changes in portal pressure remains incompletely understood. Emerging evidence suggests that SSM may dynamically reflect portal pressure fluctuations. Existing studies have shown that in patients undergoing TIPS, SSM evaluated via acoustic radiation force impulse (ARFI) imaging or shear wave elastography is capable of reflecting portal pressure changes before and after TIPS, predicting the extent of HVPG reduction after TIPS, assessing preoperative portal pressure severity in patients with non-cirrhotic PH, as well as predicting survival and monitoring shunt dysfunction after TIPS[11-14].
However, the relationship between LSM/SSM before TIPS and baseline portocaval pressure gradient (PPG), as well as the correlation between changes in LSM/SSM (ΔLSM, ΔSSM) and changes in PPG (ΔPPG) before and after TIPS, has not been systematically investigated. Such data are crucial to validate LSM and SSM as surrogate markers for TIPS efficacy, potentially replacing or complementing invasive PPG measurements.
In this study, we aim to address this knowledge gap by retrospectively analyzing a cohort of patients undergoing TIPS placement. Specifically, we aimed to: (1) Assess the correlation between LSM/SSM before TIPS placement (measured via VCTE with a 50-Hz liver probe and 100-Hz spleen-dedicated probe, respectively) and baseline PPG; (2) Evaluate the relationship between changes in LSM/SSM and changes in PPG before and after TIPS; and (3) Determine the diagnostic performance of LSM and SSM in identifying a successful hemodynamic response to TIPS. We seek to establish whether LSM and SSM can serve as reliable non-invasive tools for evaluating TIPS efficacy, ultimately improving the long-term management of patients with CSPH across different liver disease etiologies.
The study protocol was approved by the Institutional Review Board of China-Japan Friendship Hospital (No. 2024-KY-090). The informed consent for the study was obtained from all the patients. Written informed consent was obtained from all participants in accordance with the Declaration of Helsinki (2008).
From January 2024 to August 2025, 68 consecutive patients with PH who underwent TIPS placement, TIPS revision or post-TIPS angiography at our hospital were retrospectively reviewed. All patients developed PH which was verified by clinical data and assisted by laboratory parameters.
Inclusion criteria of TIPS placement were: (1) Aged ranged from 20 to 70 years; (2) Clinically confirmed PH with esophageal/gastric variceal bleeding refractory to medical and endoscopic therapy, refractory ascites, hydrothorax, or hepatorenal syndrome; (3) Preoperative enhanced computed tomography confirming that the anatomy of the portal vein and inferior vena cava is suitable for TIPS; and (4) Intraoperative portal vein pressure measurement confirming a PPG > 12 mmHg. Exclusion criteria of TIPS were: (1) Patients with portal vein thrombosis, cavernous transformation, and other situations that are not suitable for TIPS; (2) Child-Pugh score of greater than 13; (3) Chronic heart, lung or renal dysfunction; and (4) Patients with overt hepatic encephalopathy.
Laboratory parameters were collected within 3 days before and after TIPS placement, including hemoglobin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, γ-glutamyl transferase, serum albumin, serum total bilirubin, serum creatinine, platelets, international normalised ratio (INR), prothrombin time (PT) and white blood cells (WBC). Ascites was classified based on abdominal computerized tomography or ultrasound findings.
LSM and SSM were performed on the same day with patients positioned supine, both arms in maximum abduction, and following a fasting period of at least 4 hours. Measurements were conducted using the FibroScan® Pro (Echosens, France) device by a single experienced operator. LSM was performed with either M or XL probes, depending on the thickness of subcutaneous fat, whereas SSM was exclusively performed using a 100-Hz module. Two separate sets with a minimum of 10 measurements each were obtained for SSM and LSM, and the average value was recorded. Quality criteria for SSM were analogous to those applied for LSM [60% success rate and interquartile range (IQR) < 30% of median]. Spleen marking was performed with an ultrasound probe prior to SSM.
TIPS was performed with the patient in the supine position. Femoral vein and femoral artery access were established. From femoral vein access: Right atrial and inferior vena cava pressures were measured; hepatic vein angiography was performed to confirm hepatic vein location and patency. From femoral artery access: The superior mesenteric artery was selected for indirect portography. Jugular vein puncture was performed, and a RUPS-100 suite (Cook Medical, Bloomington, IN, United States) was inserted into the hepatic vein. The portal vein was punctured at an appropriate angle from the hepatic vein. After successful portal vein puncture, portal vein pressure was measured to calculate PPG, and direct portography was performed to evaluate portal vein anatomy and collateral circulation. If gastroesophageal collateral vessels had a diameter > 8 mm, embolization was performed with elastic coils (Interlock, Boston Scientific, Marlborough, MA, United States). The puncture tunnel was dilated, and a Viatorr stent (W.L. Gore & Associates, Newark, DE, United States) was implanted. Post-implantation portal vein pressure was measured to recalculate PPG, and portography was repeated to confirm stent patency.
After TIPS placement, routine monitoring (electrocardiogram, blood pressure, blood oxygen saturation) was performed. Diuretics were used to reduce cardiac preload; lactulose, ornithine, and aspartate were administered for hepatic encephalopathy prophylaxis.
Statistical analyses were performed using SPSS 24.0 (SPSS Inc., Chicago, IL, United States) and R statistical software (version 4.3.2; R Foundation for Statistical Computing, Vienna, Austria), with a two-tailed P value < 0.05 considered statistically significant. Quantitative variables were expressed as mean ± SD if normally distributed (intergroup differences analyzed via t-test) or median (25%-75% IQR) if non-normally distributed (intergroup differences analyzed via rank-sum test); for paired measurements before and after intervention, the paired Wilcoxon signed-rank test was used to evaluate statistical significance of changes. Spearman’s rank correlation coefficient was applied to analyze relationships between non-normally distributed data. Receiver operating characteristic (ROC) curve analysis was used to assess the diagnostic performance of relevant indicators for predicting this outcome, with area under the curve [AUC, with 95% confidence interval (CI)]; dotplots and box-and-whisker plots were used to visualize variable differences and distributions across outcome groups, respectively.
A total of 68 consecutive patients with PH who underwent TIPS placement, TIPS revision, or post-TIPS angiography (from January 2024 to August 2025) were initially screened. As shown in Figure 1. 27 patients were excluded: 18 underwent post-TIPS angiography only, 6 underwent TIPS revision, and 3 had TIPS placement failure. Additionally, 2 patients were excluded due to unsuccessful VCTE (LSM/SSM) measurements caused by severe ascites. Finally, 39 patients who successfully underwent TIPS and completed pre- and post-TIPS VCTE were included in the final analysis.
Baseline demographic, clinical, and etiological features of the 39 patients are summarized in Table 1. The median age was 60.2 years (IQR: 56.0-66.0 years), with 22 (56.4%) male patients. The median body mass index was 24.1 kg/m² (IQR: 21.1-27.3 kg/m²).
| Patients characteristics | Value |
| Age (years) | 60.2 (56.0-66.0) |
| Male gender | 22 (56.4) |
| Body mass index (kg/m2) | 24.1 (21.1-27.3) |
| Etiology of portal hypertension | |
| HBV/HCV | 9 (23.1) |
| PSVD | 9 (23.1) |
| Cryptogenic | 8 (20.5) |
| PBC | 6 (15.4) |
| Alcohol | 6 (15.4) |
| NASH | 1 (2.6) |
| Child-Pugh grade | |
| A, B, C | 20 (51.3), 17 (43.6), 2 (5.1) |
| MELD score | 8.6 (4.6-10.9) |
| Indication for TIPS placement | |
| Variceal bleeding | 33 (84.6) |
| Refractory ascites | 6 (15.4) |
Etiology of PH: Hepatitis B virus/hepatitis C virus infection (9 patients, 23.1%), porto-sinusoidal vascular disorder (PSVD) (9 patients, 23.1%), cryptogenic liver disease (8 patients, 20.5%), primary biliary cholangitis (6 patients, 15.4%), alcoholic liver disease (6 patients, 15.4%), and non-alcoholic steatohepatitis (NASH) (1 patient, 2.6%). Liver function and TIPS indication: 20 (51.3%) patients were Child-Pugh grade A, 17 (43.6%) grade B, and 2 (5.1%) grade C. The median model of end-stage liver disease score was 8.6 (IQR: 4.6-10.9). The primary indication for TIPS was variceal bleeding (33 patients, 84.6%), followed by refractory ascites (6 patients, 15.4%). Notably, 51.3% of patients were Child-Pugh A (n = 20), which is higher than typical TIPS cohorts. This reflects our center’s practice of prioritizing TIPS for acute variceal bleeding (84.6% of indications) over refractory ascites, as Child-A patients are less likely to develop ascites-related complications.
Changes in laboratory parameters, PPG, LSM, and SSM before and after TIPS are summarized in Table 2 and visualized in Figures 2 and 3.
| Characteristics | Before TIPS (n = 39) | After TIPS (n = 39) | P value |
| ALT (U/L) | 33.97 ± 34.05 | 67.79 ± 79.35 | < 0.001 |
| AST (U/L) | 45.41 ± 55.65 | 97.77 ± 117.26 | < 0.001 |
| ALP (U/L) | 113.13 ± 130.62 | 119.23 ± 202.33 | 0.261 |
| γ-GT (U/L) | 78.18 ± 116.36 | 73.10 ± 107.24 | 0.085 |
| Serum albumin (g/L) | 34.04 ± 5.10 | 33.08 ± 5.61 | 0.207 |
| Serum total bilirubin (μmol/L) | 26.31 ± 15.94 | 33.72 ± 21.84 | 0.005 |
| Serum creatinine (μmol/L) | 74.48 ± 30.78 | 75.03 ± 32.77 | 0.867 |
| Platelets (109/L) | 90.28 ± 68.96 | 33.97 ± 34.05 | 0.460 |
| INR | 1.27 ± 0.15 | 1.38 ± 0.24 | < 0.001 |
| PT | 15.22 ± 1.60 | 16.93 ± 2.27 | < 0.001 |
| WBC (109/L) | 4.44 ± 3.54 | 6.34 ± 4.25 | 0.001 |
| Hemoglobin (g/L) | 87.72 ± 26.66 | 86.18 ± 29.12 | 0.464 |
Significant changes were observed in several liver function and coagulation indices post-TIPS: ALT increased from 33.97 ± 34.05 U/L to 67.79 ± 79.35 U/L (P < 0.001), and AST increased from 45.41 ± 55.65 U/L to 97.77 ± 117.26 U/L (P < 0.001). Serum total bilirubin increased from 26.31 ± 15.94 μmol/L to 33.72 ± 21.84 μmol/L (P = 0.005). INR increased from 1.27 ± 0.15 to 1.38 ± 0.24 (P < 0.001), and PT prolonged from 15.22 ± 1.60 seconds to 16.93 ± 2.27 seconds (P < 0.001). WBC count increased from 4.44 ± 3.54 × 109/L to 6.34 ± 4.25 × 109/L (P = 0.001). No significant changes were observed in other laboratory parameters.
A dramatic and statistically significant reduction in mean PPG was observed (from 17.6 ± 4.1 mmHg before TIPS to 7.0 ± 2.3 mmHg after TIPS, P < 0.001), which met the therapeutic goal of PPG ≤ 10 mmHg and was visually validated in Figure 2A. Notable differences in LSM’s statistical significance emerged between analytical approaches, while SSM showed consistently significant reductions: In overall analysis, LSM numerically decreased from 27.6 ± 15.7 kPa to 24.4 ± 14.1 kPa (non-significant, Figure 2B), whereas SSM dropped substantially from 61.7 ± 17.1 kPa to 26.9 ± 11.6 kPa (P < 0.001, Figure 2C), consistent with improved portal hemodynamics; in paired analysis accounting for intra-patient variability, all three parameters (PPG, LSM, SSM) exhibited significant reductions (all P < 0.001, Figure 3), with Figure 3B confirming LSM’s significant decline, resolving its non-significant trend in overall analysis and highlighting the value of paired analysis’ value in minimizing inter-individual variability. Collectively, these data indicate SSM is a more robust marker of portal pressure changes in the overall cohort, while paired analysis reveals LSM also reflects TIPS-induced hepatic hemodynamic improvements, albeit with greater sensitivity to analytical approach.
Spearman’s correlation analysis was performed to explore the relationship between pre-LSM/pre-SSM and pre-PPG, given the non-normal distribution of these hemodynamic and stiffness parameters. As shown in Figure 4A, pre-SSM exhibited a moderate positive correlation with pre-PPG (r = 0.41, P < 0.001), indicating that higher baseline spleen stiffness was associated with more severe pre-TIPS PH.
To determine whether changes in stiffness measurements could reflect TIPS-induced portal pressure reduction, we analyzed the correlation between ΔSSM and ΔPPG. As illustrated in Figure 4B, ΔSSM was strongly negative correlated with ΔPPG (r = -0.57, P < 0.001): A greater reduction in spleen stiffness post-TIPS corresponded to a larger decrease in portal pressure, consistent with improved splenic congestion and normalized splanchnic hemodynamics. Pre-LSM showed no significant correlation with pre-PPG and ΔLSM also had no significant correlation with ΔPPG (data not shown).
A ROC curve analysis was conducted to assess whether pre-LSM/SSM, post-LSM/SSM, or ΔLSM/ΔSSM could predict a successful hemodynamic response to TIPS (defined as post-PPG ≤ 10 mmHg). Notably, none of the tested stiffness-based indicators achieved clinically meaningful predictive ability for good TIPS hemodynamic response. All AUC values were failing to meet the widely accepted standard of AUC ≥ 0.7 for modest clinical utility (Figure 5). Even the highest-performing indicator (pre-SSM) showed only minimal discriminative value, with its results further limited by wide 95%CI, reflecting instability likely due to small sample size and heterogeneous PH etiologies. Post-TIPS stiffness measurements and changes in stiffness (ΔLSM/ΔSSM) performed similarly poorly, with no indicator demonstrating a balance of sensitivity and specificity that would support clinical application. The dLSM Model (thick purple line) curve plots the net benefit across the range of Pt. The dLSM Model provides a greater net benefit than the Treat All (light blue line) and Treat None (thin purple line) strategies over the range of Pt ≈ 0.0 to 0.75 (Figure 6). This indicates that within this broad clinical risk tolerance range, using the dLSM index to guide intervention is clinically superior to treating all patients or treating no patients, as it effectively reduces unnecessary interventions while maintaining favorable true positive rates.
TIPS remains a cornerstone interventional therapy for refractory complications of CSPH, such as acute variceal bleeding unresponsive to medical therapy or refractory ascites, by establishing a direct shunt between the portal and hepatic venous systems to reduce PPG. The primary objective of TIPS is to normalize portal hemodynamics: A reduction in PPG to < 12 mmHg or a ≥ 25% decrease from baseline is deemed a successful hemodynamic response, which correlates with lower rates of recurrent variceal bleeding and ascites[11,13]. However, both PPG and HVPG (the gold standard for CSPH diagnosis, defined as HVPG ≥ 10 mmHg) require invasive catheterization, limiting serial post-procedural monitoring due to risks of bleeding, infection, and radiation exposure[7,15]. This unmet need has driven the development of non-invasive surrogates, with LSM and SSM via VCTE emerging as the most promising candidates.
LSM has been extensively validated for assessing liver fibrosis and indirectly predicting PH[2,5,9]. The Baveno VII guidelines proposed the “rule of 5” to stratify CSPH risk in cACLD: LSM < 15 kPa combined with a platelet count ≥ 150 × 109/L to rule out CSPH, and LSM ≥ 25 kPa to rule in CSPH[9,10]. Nevertheless, LSM has critical drawbacks that limit its utility for assessing portal hemodynamics-especially in the context of TIPS.
First, LSM predominantly reflects hepatic fibrosis rather than direct portal pressure changes. As PH progresses, hyperdynamic splanchnic circulation (rather than intrahepatic resistance alone) becomes the dominant driver of elevated portal pressure, a factor LSM cannot capture[7]. This is evident in our study, where pre-TIPS LSM showed no significant correlation with pre-PPG. Second, LSM accuracy is easily confounded by non-fibrotic factors such as liver inflammation, cholestasis, or obesity-factors that do not directly correlate with portal pressure[2,16]. For example, in patients with ALT levels exceeding 2 × the upper limit of normal, LSM values may be artificially elevated independent of fibrosis, leading to overestimation of CSPH[16]. This confounding effect is particularly relevant in TIPS patients, as post-procedural transient hepatic injury (evident in our study as elevated ALT/AST, P < 0.001) can further distort LSM readings, masking true changes in portal pressure. Third, LSM’s performance for CSPH diagnosis is suboptimal in diverse patient populations. A prospective study of 185 cACLD patients found that LSM ≥ 25 kPa (the Baveno VII “rule-in” threshold) had a positive predictive value (PPV) of only 82.4% overall, with PPV dropping below 90% in patients with ongoing liver disease[5]. Even in the Baveno VII “grey zone” (LSM 15-25 kPa), which includes up to 50% of cACLD patients, LSM cannot reliably distinguish between those with and without CSPH, necessitating additional testing[10]. These limitations highlight why LSM failed to correlate with ΔPPG post-TIPS in our study and underscore the need for a non-invasive tool that more accurately captures the hemodynamic alterations underlying CSPH.
SSM, a relatively novel non-invasive modality, has gained recognition for its superior ability to mirror portal hemodynamics. Unlike LSM, SSM is not affected by hepatic inflammation or cholestasis, as it primarily reflects splenic congestion and hyperdynamic splanchnic circulation, which are the key pathophysiological features of CSPH[6]. A wealth of evidence from the specified cohorts supports SSM’s diagnostic and prognostic value for CSPH. In a prospective study of 242 cACLD patients, SSM exhibited excellent predictive capacity for liver decompensation (a surrogate for CSPH-related complications) with an area under the ROC curve (AUROC) of 0.823, outperforming LSM (AUROC = 0.715); a cutoff of 50.0 kPa identified patients at significantly higher decompensation risk[2]. A multicenter study further validated that SSM > 50 kPa (measured via VCTE with a 100-Hz spleen-dedicated probe) achieved a PPV of 98.0% and a specificity of 98.8% for ruling in CSPH, with consistent performance across subgroups of patients with or without etiology suppression[5]. For patients with metabolic-associated steatotic liver disease, SSM correlated strongly with HVPG (r = 0.74, P < 0.0001), even in those with steatosis-induced LSM confounding[8].
The incremental value of SSM is further highlighted by composite models. The Non-Invasive CSPH Estimated Risk model (incorporating SSM, LSM, platelet count, and body mass index) demonstrated a significantly higher AUROC (0.906) for CSPH diagnosis compared to the ANTICIPATE ± NASH model (0.863) in a European cohort of 407 cACLD patients[10]. In patients with high HVPG (16.8 ± 5.8 mmHg, mean ± SD), SSM measured by two-dimensional magnetic resonance elastography showed a strong correlation with HVPG (r = 0.638; P < 0.001), far surpassing the weak correlation observed for liver stiffness (r = 0.292; P = 0.04)[6].
These properties translate to SSM’s utility in evaluating TIPS efficacy. Our study found a strong correlation between ΔSSM and ΔPPG (r = 0.57, P = 1.4 × 10-4), indicating that greater SSM reductions after TIPS corresponded to larger PPG decreases. This aligns with preliminary ARFI elastography data showing that post-TIPS SSM reduction correlates with portal vein pressure improvement and a study using shear wave elastography, where pre-TIPS SSM predicted the magnitude of HVPG reduction after TIPS[11,13]. Notably, SSM decreased substantially from 61.7 ± 17.1 kPa to 26.9 ± 11.6 kPa post-TIPS (P < 0.001) in both overall and paired analyses, whereas LSM required paired analysis to detect a significant reduction. This confirms SSM’s robustness to inter-individual confounding.
We found that pre-SSM exhibited a moderate positive correlation with pre- PPG (r = 0.41, P = 9.6 × 10-3) is consistent with SSM’s role as a surrogate for baseline portal pressure. This correlation, though not perfect, likely reflects the heterogeneity of our cohort (including 23.1% non-cirrhotic PH, e.g., PSVD), where SSM’s performance is known to be lower[10]. For example, in Budd-Chiari syndrome (a non-cirrhotic PH cause), SSM’s correlation with HVPG is weaker than in cirrhotic PH, suggesting divergent stiffness-pressure mechanisms[14]. In contrast, pre-LSM showed no correlation with PPG, reinforcing its limitation as a portal pressure surrogate-especially in advanced liver disease where fibrosis is less tightly linked to portal hemodynamics[7].
Furthermore, the strong ΔSSM-ΔPPG correlation confirms SSM’s ability to capture dynamic hemodynamic im
This study has several limitations. First, the additional cost of the spleen-dedicated 100-Hz VCTE probe may limit its widespread adoption. Second, the study population exhibited heterogeneous etiology (23.1% non-cirrhotic PH, e.g., PSVD), which may affect SSM’s diagnostic accuracy. Third, the lack of long-term follow-up data (e.g., shunt patency, late TIPS dysfunction) prevents evaluation of SSM/LSM’s temporal stability and prognostic utility. Notably, the early post-TIPS period (within 7 days) is associated with acute hepatocellular injury and inflammation (documented by AST/ALT elevation in this study), which may transiently elevate LSM and obscure true hemodynamic changes. Future studies with longitudinal LSM/SSM measurements are warranted.
In conclusion, this retrospective study demonstrates that SSM dynamically reflects early TIPS-induced portal pressure reduction and outperforms LSM as a non-invasive hemodynamic marker. However, due to the lack of long-term data, its utility for monitoring delayed hemodynamic adaptation or late TIPS dysfunction remains unproven.
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