The Inflammatory Response to Transcatheter Aortic Valve Replacement

Inflammation is common in response to transcatheter aortic valve replacement (TAVR), resulting from endothelial damage, procedure-related hypoperfusion, and immunogenicity against the bioprosthesis. The systemic inflammatory response after TAVR comprises a spectrum ranging from asymptomatic biomarker elevation to dramatic clinical manifestations. Although local inflammation post-TAVR is part of physiological healing, a hyperinflammatory response increases the risk for conduction disturbances, new-onset atrial fibrillation, acute kidney injury, prolonged hospitalization, mortality, and subclinical leaflet thrombosis. Unfavorable monocyte and T helper cell signatures can predispose to worse outcomes in connection with hyperinflammation. Strategies are needed to control key drivers of hyperinflammation after TAVR (eg, avoiding prolonged hypotension during transcatheter aortic valve deployment, periprocedural colchicine or glucocorticoids, targeted monoclonal antibodies, a healthy gut microbiome) and to identify patients in whom modulation of inflammatory pathways may optimize outcomes. This review provides a detailed description of the epidemiology, pathophysiology, and consequences of the inflammatory response to TAVR and discusses emerging treatment pathways.