Objectives: This study sought to identify the clinical and metabolic determinants of bioprosthetic valve degeneration.
Background: Structural valve degeneration (SVD) is the major cause of bioprosthetic valve failure. Recent retrospective studies have reported an association between atherosclerotic risk factors and development of SVD.
Methods: A total of 203 consecutive patients with aortic bioprosthetic valves were recruited. Doppler echocardiography and multidetector computed tomography (CT) examinations were performed for assessment of bioprosthesis calcification and abdominal adiposity. A cardiometabolic risk profile was also obtained. SVD was defined as an increase in mean transprosthetic gradient of ≥ 10 mm Hg and/or a worsening of transprosthetic regurgitation ≥ 1/3 class between 1-year post-operative echo and last follow-up echo (mean follow-up time was 8 ± 3 years).
Results: Forty-two patients (20%) were identified as developing SVD. Patients with SVD had significantly higher plasma total-cholesterol (4.6 ± 1.1 mmol/l vs. 4.1 ± 0.9 mmol/l, p = 0.05), low-density lipoprotein-cholesterol (2.5 ± 1.0 mmol/l vs. 2.2 ± 0.7 mmol/l, p = 0.02), and apolipoprotein B (ApoB) levels (0.71 ± 0.22 g/l vs. 0.64 ± 0.17 g/l, p = 0.02) and higher ApoB/ApoA-I ratios (0.48 ± 0.17 vs. 0.41 ± 0.11, p = 0.004) than those with no SVD. Multivariate analysis revealed that increased ApoB/ApoA-I ratio (odds ratio [OR]: 1.41, 95% confidence interval [CI]: 1.10 to 1.82 per 0.1 increment; p = 0.007) and the use of bisphosphonates (OR: 3.57, 95% CI: 1.14 to 10.80 p = 0.02) were the strongest independent predictors of SVD.
Conclusions: This is the first study to report a strong association between increased ApoB/ApoA-I ratio and the risk of developing SVD among patients with aortic bioprosthetic valves. Further studies are needed to determine if an elevated ApoB/ApoA-I ratio, which reflects the balance of proatherogenic and antiatherogenic lipoproteins, is a risk marker or a risk factor for SVD.
Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.