Key result
Patients with metabolic syndrome required bioprosthetic heart valve reoperation significantly sooner than those without metabolic syndrome (median 8.0 vs 10.0 years, p=0.005).
Why the study?
Bioprosthetic heart valves suffer from limited durability due to structural valve degeneration, and metabolic syndrome is a risk factor and highly prevalent phenotype in valvular heart disease.
Does polyoxazoline modification of bioprosthetic heart valves mitigate structural valve degeneration in the setting of metabolic syndrome?
Cohort (n=251)
Yes
Does polyoxazoline modification of bioprosthetic heart valves mitigate structural valve degeneration in the setting of metabolic syndrome?
Absolute Event Rate: 8% vs 10%
p-value: p=0.005
Metabolic syndrome accelerates bioprosthetic heart valve structural degeneration, which can be mitigated by polyoxazoline modification of the valve leaflets to reduce protein infiltration and calcification.
Metabolic syndrome may accelerate bioprosthetic valve degeneration; animal data leave open polyoxazoline mitigation and clinical translation.
Bioprosthetic heart valves (BHV), made from glutaraldehyde-fixed xenografts, are widely used for surgical and transcatheter valve interventions but suffer from limited durability due to structural valve degeneration (SVD). We focused on metabolic syndrome (MetS), a risk factor for SVD and a highly prevalent phenotype in patients affected by valvular heart disease with a well-recognized cluster of comorbidities. Multicenter patient data (N = 251) revealed that patients with MetS were at significantly higher risk of accelerated SVD and required BHV replacement sooner. Using a next-generation proteomics approach, we identified significantly differential proteomes from leaflets of explanted BHV from MetS and non-MetS patients (N = 24). Given the significance of protein infiltration in MetS-induced SVD, we then demonstrated the protective effects of polyoxazoline modification of BHV leaflets to mitigate MetS-induced BHV biomaterial degeneration (calcification, tissue cross-linking, and microstructural changes) in an ex vivo serum model and an in vivo with MetS rat subcutaneous implants.
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Abramov et al. (2022) conducted a cohort in Bioprosthetic heart valve structural valve degeneration (n=251). Metabolic syndrome vs. No metabolic syndrome was evaluated on Duration of implant (years) (p=0.005). Patients with metabolic syndrome required bioprosthetic heart valve reoperation significantly sooner than those without metabolic syndrome (median 8.0 vs 10.0 years, p=0.005).
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