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Background: Lipoprotein(a) [Lp(a)] has emerged as a key mediator of calcific aortic valve disease and is strongly linked to the development and progression of aortic stenosis (AS). Whether elevated Lp(a) influences disease severity, long-term prognosis, or both in patients undergoing transcatheter aortic valve implantation (TAVI) remains uncertain. Methods: This multicenter study included 213 patients with severe symptomatic AS undergoing TAVI between 2016 and 2018. Pre-procedural Lp(a) concentrations were measured using a standardized immunoturbidimetric assay. Associations with long-term all-cause mortality were evaluated using Kaplan-Meier analyses and Cox proportional hazards models. The relationship between Lp(a) and AS severity was assessed using correlation analyses, multivariable linear regression models, and restricted cubic spline analyses. Anatomical and hemodynamic measures included aortic valve calcium score (AVCS), peak aortic jet velocity (AV Vmax), and transvalvular pressure gradients. Results: During a median follow-up of 7.58 years (IQR 4.33-8.66 years), Lp(a) was not associated with all-cause mortality, irrespective of whether it was analyzed as a continuous variable, according to established clinical thresholds, or across quartiles. In contrast, higher Lp(a) concentrations were associated with greater valvular calcification and more severe hemodynamic obstruction. These associations remained significant after adjustment for age, sex, diabetes mellitus, and renal function. Restricted cubic spline analyses suggested predominantly linear associations without evidence of significant non-linearity. Conclusions: Elevated Lp(a) concentrations were associated with greater anatomical and hemodynamic severity of AS but not with long-term mortality after TAVI. These findings suggest that elevated Lp(a) is associated with greater anatomical and hemodynamic severity of calcific aortic valve disease but was not linked to long-term mortality after TAVI.