Abstract
BACKGROUND: The optimal hemodynamic threshold for portal pressure gradient (PPG) following transjugular intrahepatic portosystemic shunt (TIPS) for ascites remains uncertain. OBJECTIVE: This study aimed to elucidate the relationship between post-TIPS PPG and clinical outcomes in patients undergoing small-diameter (8-mm) TIPS for ascites. DESIGN: Single-center retrospective study. METHODS: From June 2015 to June 2023, consecutive patients receiving small-diameter (8-mm) TIPS for refractory or recurrent ascites were considered for inclusion retrospectively. The impact of PPG on clinical outcomes-including ascites response, overt hepatic encephalopathy (OHE), further decompensation, and mortality-was evaluated using Fine and Gray competing risk regression models, both unadjusted and adjusted for potential confounders. RESULTS: A total of 143 patients were included in the analysis, of whom 65.7% had refractory ascites, with a median Child-Pugh score of 9. Receiver operating characteristic (ROC) curve analysis identified post-TIPS PPG as a reliable predictor of ascites response (cutoff: 10.5 mmHg, area under curves (AUC): 0.733, p < 0.001) and OHE (cutoff: 7.5 mmHg, AUC: 0.716, p < 0.001). Univariate and multivariate Fine and Gray competing risk regression analyses further revealed that patients with PPG between 8 and 10 mmHg had favorable outcomes, including a lower incidence of ascites (>10 vs 8-10 mmHg: hazard ratio (HR) = 5.74, 95% confidence interval (CI) 2.11-15.58, p < 0.001), a reduced risk of OHE (<8 vs 8-10 mmHg: HR = 2.87, 95% CI 1.29-6.35, p = 0.010), and a decreased risk of further decompensation (>10 vs 8-10 mmHg: HR = 2.78, 95% CI 1.43-5.41, p = 0.003; <8 vs 8-10 mmHg: HR = 2.42, 95% CI 1.20-4.90, p = 0.014) after TIPS placement. CONCLUSION: This study revealed that post-TIPS PPG was associated with clinical outcomes in patients with refractory or recurrent ascites undergoing small-diameter TIPS. A post-TIPS PPG of 8-10 mmHg seems to be the optimal range, effectively controlling ascites without significantly increasing the risk of shunt-related hepatic encephalopathy, while also reducing the risk of further decompensation.