Inflammation After Transcatheter Aortic Valve Implantation: Mechanisms, Risk Stratification, and Therapeutic Implications

Transcatheter aortic valve implantation (TAVI) elicits a sterile inflammatory response that is almost universal, yet highly heterogeneous in both magnitude and clinical impact. Initiated by endothelial injury, ischemia–reperfusion, and residual bioprosthetic immunogenicity, peri-procedural inflammation converges on activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and downstream interleukin-1β (IL-1β) and IL-6 signaling, leading to increased C-reactive protein levels. This response is further modulated by patient susceptibility, procedural complexity, and device-specific characteristics. While a controlled response promotes tissue repair and healing, exaggerated activation, which manifests as systemic inflammatory response syndrome in up to two-thirds of patients, has been consistently associated with higher mortality, conduction disturbances, new-onset atrial fibrillation, acute kidney injury (AKI), and subclinical leaflet thrombosis. Emerging evidence also implicates gut microbiome-derived metabolites and xenoantigen-driven adaptive immunity as additional contributors to the overall inflammatory burden. Serial biomarker assessment, including C-reactive protein trajectories, neutrophil-to-lymphocyte ratio, cancer antigen 125 (CA-125), and novel composite indices such as the neutrophil percentage-to-albumin ratio, combined with multimodality imaging, allows increasingly refined risk stratification. However, no anti-inflammatory therapy is currently established for routine use after TAVI. Colchicine has shown proof-of-concept signals, sodium–glucose cotransporter 2 inhibitors have demonstrated clinical benefit with pleiotropic anti-inflammatory properties, and lessons from IL-1 and IL-6 inhibition trials in ischemic heart disease provide a translational roadmap. This narrative review synthesizes the epidemiology, mechanisms, clinical consequences, and assessment of peri-TAVI inflammation. Moreover, this review proposes a pragmatic inflammatory subphenotyping framework that integrates baseline risk, procedural exposure, and biomarker kinetics. Such a framework may help bridge the gap between observational associations and precision-based therapeutic strategies, shifting peri-TAVI inflammation from a prognostic marker to a modifiable determinant of outcome.