Key result
Elevated pre-procedural Lp(a) is associated with more severe AS but not post-TAVI mortality.
Why the study?
Whether elevated Lp(a) influences disease severity, long-term prognosis, or both in patients undergoing TAVI remains uncertain.
Does elevated Lipoprotein(a) influence long-term all-cause mortality or disease severity in patients with severe symptomatic aortic stenosis undergoing TAVI?
Cohort (n=213)
Yes
Does elevated Lipoprotein(a) influence long-term all-cause mortality or disease severity in patients with severe symptomatic aortic stenosis undergoing TAVI?
Hazard Ratio: 1 (95% CI 0.996–1.004)
p-value: p=0.931
Elevated Lp(a) is associated with more severe anatomical and hemodynamic aortic stenosis but does not impact long-term survival after TAVI.
Elevated pre-TAVI Lp(a) was associated with greater AS severity but not mortality; leaves open its role in progression and as a therapeutic target.
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.
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Clodi et al. (2026) conducted a cohort in Severe symptomatic aortic stenosis (n=213). Elevated Lipoprotein(a) concentrations vs. Lower Lipoprotein(a) concentrations was evaluated on Long-term all-cause mortality (HR 1.000, 95% CI 0.996-1.004, p=0.931). Elevated pre-procedural Lipoprotein(a) concentrations were associated with greater anatomical and hemodynamic severity of aortic stenosis but not with long-term all-cause mortality after TAVI (HR 1.000).
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