Bioresorbable scaffolds (BRS; also referred to as bioresorbable vascular scaffolds, BVS) represent a promising approach in interventional cardiology, offering theoretical advantages such as temporary mechanical support followed by complete resorption. However, clinical experience has revealed challenges, including late-stage scaffold thrombosis and heterogeneous scaffold discontinuity during degradation, prompting investigation into host immune responses. Neutrophil extracellular traps (NETs), which are network-like structures composed of decondensed chromatin decorated with antimicrobial proteins, have emerged as critical mediators of vascular inflammation and thrombosis. This review explores the intersection between NET biology and BRS performance, investigating how NETosis affects biocompatibility, degradation kinetics, and device-related complications. We discuss the molecular mechanisms that trigger neutrophil activation and NET formation in scaffold materials, the effect of NET components on polymeric and metallic scaffold degradation, and emerging biomarkers to monitor NET-mediated complications. We also evaluate therapeutic strategies targeting NET pathways, including DNase-based therapies, peptidylarginine deiminase 4 (PAD4) inhibitors, and anti-inflammatory coatings that can optimize next-generation BRS outcomes. Understanding the immunological environment surrounding bioresorbable vascular devices is crucial for developing scaffolds that deliver predictable degradation while minimizing adverse inflammatory responses.
Dinc et al. (Fri,) studied this question.