ApoB/ApoA-I ratio is associated with increased risk of bioprosthetic valve degeneration.

Abstract

This study sought to identify the clinical and metabolic determinants of bioprosthetic valve degeneration. 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. 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). 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. 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.