Aortic stenosis
Elevated Lp(a) predicts both higher mortality and faster bioprosthetic valve degeneration after TAVR in 601 patients (J Clin Lipidol 2025)
Original title: Association between lipoprotein(a) and long-term prognosis in patients receiving transcatheter aortic valve replacement
In 601 patients with severe aortic stenosis who underwent transcatheter aortic valve replacement (TAVR) (mean age 75.5 years, 58.7% male), 137 patients (22.7%) died over a median 3.9-year follow-up. After multivariable adjustment, elevated baseline Lp(a) (30 mg/dL or above) independently predicted all-cause mortality (hazard ratio 1.81, 95% CI 1.27-2.57, P = .001), cardiovascular mortality (hazard ratio 2.02, 95% CI 1.12-3.66, P = .020), and possible structural valve degeneration on Doppler echocardiography (subdistribution hazard ratio 3.40, 95% CI 1.32-8.79, P = .012). The findings held using a 50 mg/dL threshold as well. This is among the first studies to link elevated Lp(a) not only to mortality but specifically to accelerated bioprosthetic valve degeneration after TAVR, suggesting Lp(a) may warrant consideration in long-term post-TAVR risk assessment.
Original abstract
Background: Lipoprotein(a) (Lp[a]) has been identified as a significant risk factor for aortic stenosis (AS). However, its impact on outcomes post-transcatheter aortic valve replacement (TAVR) remains unknown.
Objective: To investigate the association between Lp(a) levels and long-term outcomes as well as its impact on the bioprosthetic valve degeneration in patients post-TAVR.
Methods: Patients with severe AS who underwent TAVR were consecutively recruited. Lp(a) was measured before TAVR procedure. The subjects were divided according to levels of Lp(a). The outcomes were all-cause mortality and possible structural valve degeneration (SVD) measured by Doppler echocardiography. Cox regression models and competing risk models were used to explore the association between Lp(a) levels and outcomes.
Results: Of the 601 included patients (mean age: 75.5 ± 7.2, male: 58.7%), 137 patients (22.7%) experienced mortality after a median follow-up of 3.9 years. After multivariable adjustment, elevated Lp(a) (defined as ≥30 mg/dL) was identified as an independent predictor of all-cause mortality (hazard ratio [HR]: 1.81, 95% CI: 1.27-2.57, P = .001) and cardiovascular mortality (HR: 2.02, 95% CI: 1.12-3.66, P = .020). Elevated Lp(a) was also associated with increased risk of possible SVD (subdistribution HR: 3.40, 95% CI: 1.32-8.79, P = .012). Using a threshold value of 50 mg/dL for elevated Lp(a) still supported the main findings.
Conclusion: Elevated baseline Lp(a) levels are associated with poor clinical outcomes and possible SVD in patients with severe AS undergoing TAVR. Further research is warranted to confirm these findings.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.