The impact of leaflet thrombosis on transcatheter aortic valve degeneration: a narrative review

Transcatheter aortic valve implantation (TAVI) has expanded into younger and lower-risk patients, making long-term valve durability increasingly important. Leaflet thrombosis, most commonly identified on computed tomography as hypoattenuated leaflet thickening (HALT), is common after TAVI. Whether leaflet thrombosis contributes to structural valve deterioration (SVD) remains incompletely understood. To summarize the current evidence on the relationship between leaflet thrombosis and SVD after TAVI, with a focus on clinical outcomes, imaging findings, antithrombotic therapy, and pathophysiological mechanisms. This narrative review synthesizes available clinical, imaging, mechanistic, histopathological and antithrombotic literature addressing leaflet thrombosis and valve durability after TAVI. CT studies show that leaflet thrombosis occurs in 13-32% of patients within the first post-procedural year. Although some lesions resolve spontaneously, longitudinal imaging studies demonstrate persistence in a substantial proportion of patients, supporting the presence of an underlying valve-related substrate. HALT has not consistently been associated with adverse valve hemodynamics during the first year after implantation. Long-term TAVI durability studies report low rates of severe SVD (0.8-1.5% up to 10 years), although outcomes vary according to valve generation and study population. The 10-year NOTION and PARTNER 2A data provide important long-term durability information, but neither study included systematic longitudinal CT assessment of leaflet thrombosis. Observational studies linking early HALT to subsequent hemodynamic valve deterioration have yielded conflicting results. Indirect evidence from anticoagulation studies and histopathological investigations supports biological plausibility for a relationship between leaflet thrombosis and progressive leaflet injury, but does not establish causality. Leaflet thrombosis is a frequent imaging finding after TAVI and may persist over time, but its contribution to long-term SVD remains uncertain. Current evidence supports a potential biological relationship between leaflet thrombosis and valve degeneration but does not demonstrate that HALT is a causal precursor of clinically relevant SVD. Prospective studies combining serial CT imaging with long-term, standardized assessment of structural valve outcomes are required to resolve this question.