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

Lp(a) was not associated with all-cause mortality after TAVI regardless of how it was analyzed.

• 213 patients with severe symptomatic AS undergoing TAVI between 2016 and 2018 were included in this multicenter study.
• Median follow-up was 7.58 years (IQR 4.33–8.66 years).
• No association with all-cause mortality was found whether Lp(a) was analyzed as a continuous variable, according to established clinical thresholds, or across quartiles.
• Associations were evaluated using Kaplan-Meier analyses and Cox proportional hazards models.

Higher Lp(a) concentrations were associated with greater valvular calcification as measured by aortic valve calcium score (AVCS).

• The association between Lp(a) and AVCS remained significant after adjustment for age, sex, diabetes mellitus, and renal function.
• Restricted cubic spline analyses suggested a predominantly linear association without evidence of significant non-linearity.
• Pre-procedural Lp(a) concentrations were measured using a standardized immunoturbidimetric assay.
• Multivariable linear regression models were used to assess the relationship between Lp(a) and AS severity measures.

Higher Lp(a) concentrations were associated with more severe hemodynamic obstruction of the aortic valve.

• Hemodynamic measures included peak aortic jet velocity (AV Vmax) and transvalvular pressure gradients.
• These associations remained significant after adjustment for age, sex, diabetes mellitus, and renal function.
• Restricted cubic spline analyses indicated predominantly linear associations for hemodynamic parameters without significant non-linearity.
• Correlation analyses and multivariable linear regression models were used to assess these relationships.

Lp(a) is identified as a key mediator of calcific aortic valve disease and is strongly linked to the development and progression of aortic stenosis.

• This association is established in the background literature motivating the study.
• The study specifically focused on patients with severe symptomatic AS to examine whether elevated Lp(a) influences disease severity, long-term prognosis, or both.
• The study population of 213 patients all had severe symptomatic AS requiring TAVI, representing an advanced disease stage.

The study design was multicenter and included standardized pre-procedural Lp(a) measurement with long-term follow-up exceeding seven years on average.

• 213 patients were enrolled across multiple centers between 2016 and 2018.
• Lp(a) was measured using a standardized immunoturbidimetric assay prior to the TAVI procedure.
• Median follow-up was 7.58 years with an IQR of 4.33–8.66 years.
• Both anatomical (AVCS) and hemodynamic (AV Vmax, transvalvular pressure gradients) measures of AS severity were assessed.

The findings suggest that Lp(a)'s role in aortic stenosis may be primarily in disease initiation and progression rather than in post-TAVI outcomes.

• Elevated Lp(a) was associated with greater anatomical and hemodynamic severity of calcific aortic valve disease.
• Elevated Lp(a) was not linked to long-term mortality after TAVI.
• The authors conclude that 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.