Serum Lipoprotein(a) and Bioprosthetic Aortic Valve Degeneration

Aims: Bioprosthetic aortic valve degeneration demonstrates pathological similarities to aortic stenosis. Lipoprotein(a) [Lp(a)] is a well-recognised risk factor for incident aortic stenosis and disease progression. The aim of this study was to investigate whether serum Lp(a) concentrations are associated with bioprosthetic aortic valve degeneration.
Methods and results: In a post hoc analysis of a prospective multimodality imaging study (NCT02304276), serum Lp(a) concentrations, echocardiography, contrast-enhanced computed tomography (CT) angiography and 18F-sodium fluoride (18F-NaF) positron emission tomography (PET) were assessed in patients with bioprosthetic aortic valves. Patients were also followed up for 2 years with serial echocardiography. Serum Lp(a) concentrations (median 19.9 [8.4 to 76.4] mg/dL) were available in 97 participants (mean age 75±7 years, 54% men). There were no baseline differences across the tertiles of serum Lp(a) concentrations for disease severity assessed by echocardiography (median peak aortic valve velocity: highest tertile 2.5 [2.3 to 2.9] m/s versus lower tertiles 2.7 [2.4 to 3.0] m/s, p=0.204), or valve degeneration on CT angiography (highest tertile n=8 versus lower tertiles n=12, p=0.552) and 18F-NaF PET (median tissue-to-background ratio: highest tertile 1.13 [1.05 to 1.41] versus lower tertiles 1.17 [1.06 to 1.53], p=0.889). After 2 years of follow up, there were no differences in annualized change in bioprosthetic hemodynamic progression (change in peak aortic valve velocity: highest tertile (0.0 [-0.1 to 0.2] m/s/year versus lower tertiles 0.1 [0.0 to 0.2] m/s/year, p=0.528) or the development of structural valve degeneration.
Conclusion: Serum lipoprotein(a) concentrations do not appear to be a major determinant or mediator of bioprosthetic aortic valve degeneration.