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Association between plasma lipoprotein levels and bioprosthetic valve structural degeneration
  1. Mohamed Jalloul Nsaibia1,
  2. Ablajan Mahmut1,
  3. Haifa Mahjoub2,
  4. Abdellaziz Dahou2,
  5. Rihab Bouchareb1,
  6. Marie-Chloé Boulanger1,
  7. Jean-Pierre Després3,
  8. Yohan Bossé4,
  9. Benoît J Arsenault2,
  10. Eric Larose2,
  11. Philippe Pibarot2,
  12. Patrick Mathieu1
  1. 1Laboratory of Cardiovascular Pathobiology, Department of Surgery, Quebec Heart and Lung Institute/Research Center, Laval University, Quebec, Quebec, Canada
  2. 2Department of Medicine, Laval University, Québec, Quebec, Canada
  3. 3Department of Kinesiology, Laval University, Québec, Quebec, Canada
  4. 4Department of Molecular Medicine, Laval University, Québec, Quebec, Canada
  1. Correspondence to Dr Patrick Mathieu, Institut de Cardiologie et de Pneumologie de Québec/Quebec Heart and Lung Institute, 2725 Chemin Ste-Foy, Québec, QC G1V-4G5, Canada; patrick.mathieu{at}chg.ulaval.ca

Abstract

Introduction Structural valve degeneration (SVD) leads to the failure of aortic valve bioprostheses. It is suspected that lipid-derived factors could play a role in SVD. We hypothesised that oxidised low-density lipoprotein (OxLDL), OxLDL/LDL, OxLDL/high-density lipoprotein (OxLDL/HDL) and proprotein convertase subtilisin/kexin 9 (PCSK9) may be associated with SVD.

Methods We included 199 patients who underwent an aortic valve replacement with a bioprosthesis and had an echocardiography follow-up to evaluate the function of the prosthesis. SVD was defined as an increase in mean transprosthetic gradient (≥10 mm Hg) or a worsening of transprosthetic regurgitation (≥1/3) during the follow-up.

Results After a mean follow-up of 8±3.5 years, 41(21%) patients developed SVD. The univariate predictors of SVD were LDL (p=0.03), apolipoprotein B (p=0.01), OxLDL (p=0.02), OxLDL/HDL (p=0.009) and LDL associated with small, dense particles (LDL-C<255Å) (p=0.02). In a model adjusted for covariates, only OxLDL/HDL (OR 1.49, 95%CI 1.08 to 2.07 per 10 units, p=0.01) remained associated with SVD. There was a significant interaction between OxLDL/HDL and PCSK9 on SVD (p=0.05). After adjustment, compared with patients with low OxLDL/HDL (median, <25.4) and low PCSK9 (median, <298 ng/mL) (referent), patients with both an elevated OxLDL/HDL ratio and PCSK9 had a higher risk of SVD (OR 2.93, 95% CI 1.02 to 9.29, p=0.04).

Conclusions OxLDL/HDL ratio is independently associated with SVD.

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