Advances in precise assessment of portal pressure in porto-sinusoidal vascular disease
image: Precise portal pressure assessment is increasingly driving precision management in PSVD. The diagnostic paradigm has shifted from exclusion-based criteria to the PSVD concept centered on specific vascular lesions, while assessment has evolved from reliance on invasive HVPG to a stratified strategy led by multimodal non-invasive tools and supported by minimally invasive methods. Ultrasound elastography identifies the characteristic liver–spleen stiffness dissociation pattern, and CT/MRI radiomics further enable non-invasive quantitative pressure modeling. Future research will move toward non-invasiveness, digitalization, and intelligent systems. Standardization of EUS-PPG and emerging tools such as sublingual vein imaging may improve direct or surrogate pressure assessment. Meanwhile, AI integrating clinical, imaging, and multi-omics data may enable precise subtyping and dynamic prognostic prediction of complications. Ultimately, combining optimized pressure assessment with data-driven precision stratification will enable more individualized interventions and improve survival in PSVD patients. Collectively, these advances may facilitate the transition from conventional portal hypertension assessment toward precision-guided management in PSVD.
Credit: Qingchun Fu, Muyun Liu
PSVD accounts for 15–34% of portal hypertension cases in developing countries versus 3–6% in Western countries. Pathophysiology centres on hyperdynamic circulation and increased intrahepatic vascular resistance, with two subtypes: increased splenic venous flow and occlusion of small intrahepatic portal vein branches (obliterative portal venopathy), supporting the "double‑hit" hypothesis. Precipitating factors (43–58%) include immune disorders, haematologic diseases, thrombophilia, HIV, recurrent infections, congenital defects, and drug exposure.
Advances in Portal Pressure Assessment
Diagnosis requires adequate liver histopathology (core biopsy ≥20 mm) confirming absence of cirrhosis and presence of characteristic vascular lesions.
Invasive methods: Hepatic vein angiography shows intrahepatic venovenous communications in >50% of patients, impairing WHVP measurement. HVPG is often normal or mildly elevated (<10 mmHg). In 53 PSVD patients, mean HVPG was only 8.9 mmHg; HVPG correlated poorly with platelet count and failed to predict major outcomes. HVPG thus underestimates severity and has limited prognostic value.
EUS‑guided direct PPG: Directly measures the portal‑systemic pressure gradient. Preliminary data showed carvedilol reduced mean EUS‑PPG from 17.1 to 15.1 mmHg, whereas only 44.4% achieved the traditional HVPG response threshold, confirming HVPG underestimates decompression in PSVD.
Non‑Invasive Assessment
Ultrasonic elastography: LSM is usually normal/mildly elevated, whereas SSM is significantly elevated due to splenic congestion. This dissociation distinguishes PSVD from cirrhosis. SSM ≤40 kPa with bilirubin <1 mg/dL safely excludes high‑risk varices. Limitations include obesity and acute inflammation.
CT: Shows heterogeneous liver enhancement and segment IV/I enlargement. CT radiomics (liver surface nodularity, AUC 0.88; virtual PPG, r = 0.92) enables non‑invasive pressure assessment and variceal risk prediction.
MRI: Hepatobiliary‑phase MRI shows homogeneous high signal intensity (vs. heterogeneous low signal in cirrhosis). MR elastography shows increased spleen stiffness with normal/mildly elevated liver stiffness. MRI radiomics, splenic ECV, 4D‑flow MRI, and virtual HVPG models show promise.
Digital and intelligent assessment: CT/MRI radiomics predict portal hypertension severity and outcomes. AI may improve PSVD vs. cirrhosis differentiation. Current evidence is limited by small samples, retrospective designs, and lack of standardisation.
Laboratory biomarkers: Platelet count reflects hypersplenism but has limited accuracy alone. Von Willebrand factor antigen reflects endothelial injury and correlates with HVPG; combined as the VITRO score, it improves risk stratification. Because PSVD involves endothelial injury rather than cirrhotic fibrosis, cirrhosis‑derived biomarkers are insufficient.
Therapeutic Interventions
Non‑selective β‑blockers remain first‑line. Carvedilol reduces EUS‑PPG, but only 44.4% achieve traditional HVPG response thresholds, suggesting HVPG underestimates decompression. NSBBs plus endoscopic ligation appear effective. TIPS is an option in selected patients but is technically challenging. Portal vein thrombosis (5‑year incidence ~16%) forms a vicious cycle with portal hypertension; anticoagulation may improve recanalisation.
Prognosis
PSVD generally has a better prognosis than decompensated cirrhosis, with 1‑, 5‑, and 10‑year transplant‑free survival of 97%, 83%, and 72%. Prognostic assessment centres on portal pressure, portal vein thrombosis, biochemical markers, and comorbidities. Advanced age, severe comorbidities, ascites, hyperbilirubinaemia, renal dysfunction, and hypoalbuminaemia predict poor outcome.
Limitations
HVPG underestimates severity and lacks PSVD‑specific thresholds. EUS‑PPG is invasive and lacks standardised cutoffs. Elastography is influenced by fibrosis and splenic congestion. Radiomics and AI models are limited by retrospective designs, small samples, and insufficient external validation.
Future Directions
Future research should establish standardised, disease‑specific assessment strategies. Integration of multimodal approaches—direct pressure measurement, advanced imaging, elastography, molecular biomarkers, and AI—may enable accurate haemodynamic evaluation, dynamic monitoring, and individualised management. Large prospective multicentre studies are needed.
Conclusions
Precise portal pressure assessment is driving precision management in PSVD. The diagnostic paradigm has shifted from exclusion‑based criteria to the PSVD concept centred on specific vascular lesions, and assessment has evolved from invasive HVPG to a stratified strategy led by multimodal non‑invasive tools. Future research will move toward non‑invasiveness, digitalisation, and intelligent systems. AI integrating clinical, imaging, and multi‑omics data may enable precise subtyping and dynamic prognostic prediction, improving survival in PSVD patients.
Full text
https://www.xiahepublishing.com/2310-8819/JCTH-2026-00334
The study was recently published in the Journal of Clinical and Translational Hepatology.
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