From Valve Disease to Valve Replacement: Lipoprotein(a) Is Associated with Aortic Stenosis Severity but Not Prognosis After TAVI

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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Journal
Medical Sciences
Published
2026-08-14
DOI
https://doi.org/10.3390/medsci14040484
Primary Topic
Lipoproteins and Cardiovascular Health
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article
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article

From Valve Disease to Valve Replacement: Lipoprotein(a) Is Associated with Aortic Stenosis Severity but Not Prognosis After TAVI

Bernhard Scharinger, Iris Kremser, Vera Paar, Elke Boxhammer et al.
Medical Sciences
Lipoproteins and Cardiovascular Health
article

From Valve Disease to Valve Replacement: Lipoprotein(a) Is Associated with Aortic Stenosis Severity but Not Prognosis After TAVI

Bernhard Scharinger, Iris Kremser, Vera Paar, Elke Boxhammer, Clemens Steinwender, Klaus Hergan, Christian Reiter, Janne Cadamuro, Maximilian Gressl, Moritz Brandt, Jürgen Kammler, Nikolaos Schörghofer, Christoph Knapitsch, Gretha Hecke, Nikolaus Clodi, Uta C. Hoppe, Hermann Blessberger, Michael Lichtenauer, Martin Clodi
article en

Abstract

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.

Medical SciencesVol. 14(4)
Johannes Kepler University of Linz (AT), Paracelsus Medical University (AT), Ordensklinikum Linz Barmherzige Schwestern (AT), Kepler Universitätsklinikum (AT), Krankenhaus Barmherzige Brüder (DE), Hospital of the Brothers of St. John of God (AT)
Good health and well-being
Openalex Percentile: Top 7%
Lipoproteins and Cardiovascular Health
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