Pan-Immune-Inflammation Value: Related to Perforation Diameter and Pulmonary Artery Pressure in Ventricular Septal...

This study investigated the relationship between the pan-immune-inflammation value (PIV) and the perforation diameter in patients with ventricular septal rupture (VSR), as well as the changes in pulmonary artery systolic pressure (ΔPASP) after transcatheter closure.

The clinical data from 133 VSR patients who underwent transcatheter closure were analyzed. Patients were divided into high and low PIV groups based on a median cutoff value of 6. Boruta was used for exploratory variable screening; prespecified covariate sets were used for adjusted models. A generalized additive model (GAM) was used to explore the potential nonlinear relationships. Where a nonlinear association was suggested by the GAM, a piecewise linear regression model was subsequently fitted to precisely quantify the threshold effects and the differential associations of PIV/100 with ΔPASP and perforation diameter on either side of the identified inflection point.

One hundred thirty-three patients with VSR (mean age 67 years, 50.6% female) were enrolled. Linear regression showed no statistically significant association between PIV/100 and ΔPASP. GAM suggested a possible nonlinear pattern between PIV/100 and ΔPASP (and perforation diameter). In piecewise models, an inverse association was observed above the break point, but this pattern was attenuated after multivariable adjustment and in sensitivity analyses. In discrimination analyses, adding PIV/100 to the baseline model yielded a modest numerical increase in AUC, but the incremental gain was not statistically significant.

PIV may serve as an adjunct inflammatory marker in VSR patients undergoing transcatheter closure; however, the break point findings are exploratory and the incremental predictive value warrants validation in larger, independent cohorts with better adjudication of infection/systemic inflammation.