Metabolic syndrome induces neovascularization in calcific aortic stenosis

Introduction Aortic stenosis (AS) is an inflammatory disease in which neovascularization process develops. We hypothesized that the metabolic syndrome (MS) would influence the neovascularization process in AS valves. Methods In 40 patients a quantitative analysis of blood vessels in AS valves along with the blood lipid profile were determined to establish relationships between the clinical atherosclerotic risk factors including the MS. Results Age, gender, hypercholesterolemia, smoking, diabetes, as well as treatment with statins or ACE inhibitors had no significant effect on the extent of neovascularization. Factors associated with the neovascularization process were obesity (1.6±0.5 blood vessels/400x field vs 0.7±0.3 blood vessels/400x field; p=0.14), hypertension (1.5±0.5 blood vessels/400x field vs 0.6±0.4 blood vessels/400x field; p=0.13) and MS (2.3±0.6 blood vessels/400x field vs 0.4±0.3 blood vessels/400x field; p=0.0002). In multivariate analysis, the MS was the only independent predictor of valve neovascularization. HDL‐cholesterol level was inversely correlated with neovascularization (r=‐0.49; p=0.009). We documented in 53% of MS patients, rich cellular islands in which blood vessels were abundant. Cellular islands were densely infiltrated by endothelial progenitor cells (EPC) (CD45+ CD133+) which correlated with the number of blood vessels(r=0.65; p=0.0006). Conclusion AS is a disease characterized by the formation of new blood vessels which is independently determined by the MS. The level of HDL and the number of EPC are among the mechanisms influencing the neovasacularization process in AS.