Citations

Abstract Background: Early postoperative mortality remains a major clinical challenge in left ventricular assist device implantation. Accurate preoperative identification of high-risk patients could optimize candidate selection and improve perioperative management. Methods: From February 2021 to March 2025, 60 patients who underwent LVAD implantation at Zhongshan Hospital, Fudan University were included in the present study. Early mortality was defined as death within 2 months postoperatively, a threshold derived from survival analysis showing a distinct early hazard phase. Preoperative demographic, echocardiographic, hemodynamic, and laboratory variables were evaluated. Predictor selection used least absolute shrinkage and selection operator (LASSO) logistic regression with 10-fold cross-validation, followed by multivariable Firth logistic regression. Internal validation employed bootstrap resampling (1,000 iterations). Results: The mean age was 55 ± 10 years, and 50 (83%) patients had dilated cardiomyopathy. Kaplan–Meier analysis indicated an early hazard phase, with all deaths occurring by ~ 1.7 months after implantation. LASSO selected age, MELD-XI, passive cardiac index (PasCI), and mixed venous oxygen saturation (SvO₂) for multivariable modeling. In the final Firth model, lower SvO₂ (odds ratio [OR] 0.92; 95% CI 0.83–1.00; p = 0.048) and older age (OR 1.13; 95% CI 1.00–1.35; p = 0.059) were associated with higher early mortality. Internal validation yielded an optimism-adjusted AUC of 0.84. Conclusions: In this exploratory study, lower preoperative SvO₂ and older age were the principal predictors of early mortality after LVAD implantation. Our internally validated risk assessment model supports preoperative risk prediction and stratification; however, confirmation in larger, multicenter cohorts is warranted before broader adoption. (246/250)

AbstractBackgroundRejection of Gal‐free (GTKO) donor pig cardiac xenografts is strongly associated with vascular non‐Gal antibody binding, endothelial cell (EC) injury, and activation and microvascular thrombosis. We adopted a pig‐to‐SCID/beige small animal transplant model to compare the pathogenicity of baboon and human anti‐pig antibody.MethodsWild‐type (GT+) or GTKO porcine coronary arteries (PCAs) were transplanted into the infrarenal aorta of SCID/beige mice. Three days after transplant, recipients were infused with anti‐pig antibody (anti‐SLA class I, an isotype control, naive or sensitized baboon serum, or naive human serum). PCAs were recovered 24 h after antibody infusion and examined using histology, immunohistochemistry, and in situ hybridization.ResultsDose‐dependent intragraft thrombosis occurred after infusion of anti‐SLA I antibody (but not isotype control) in GT+ and GTKO PCA recipients. Naive baboon serum induced thrombosis in GT+ grafts. Thrombosis was significantly reduced by pre‐treating naive baboon serum with Gal polymer and not observed when this serum was infused to GTKO PCA recipients. Naive human serum caused dose‐dependent intragraft thrombosis of GTKO PCAs. In all cases, thrombosis involved graft‐specific vascular antibody and complement deposition, macrophage adherence, EC delamination, and subendothelial thrombus formation.ConclusionsThis study provides the first direct in vivo comparison of the pathogenicity of naive human and baboon serum. The results suggest that human preformed non‐Gal antibody may have increased pathogenicity compared to baboon. This model, which showed a rejected graft histopathology similar to antibody‐mediated rejection in cardiac xenotransplantation, may be useful to assess the pathogenicity of individual protein or carbohydrate specific non‐Gal reactive antibodies.