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Endothelial function and inflammation

[Speaker] Yukihito Higashi:1
1:Hiroshima University, Japan

Inflammation also as well as oxidative stress independently or concomitantly lead to atherosclerosis through progression of endothelial dysfunction, resulting in cardiovascular complications. In a clinical setting, subjects with helicobacter pylori (HP), Kawasaki disease and periodontitis and patients with Buerger's disease (TAO) and atherosclerotic peripheral arterial disease (ASO) are ideal models for determining how endothelium-dependent vasodilation is affected by inflammation. Flow-mediated vasodilation (FMD) as an index of endothelial function was significantly lower and the levels of hs-CRP was significantly higher in subjects with seropositive antibodies to HP than in subjects with seronegative antibodies to HP. FMD was significantly lower in Kawasaki disease without classical cardiovascular risk factors than in controls. FMD in children with aneurysm was significantly impaired compared to that in those without. Vascular response to acetylcholine was significantly less in patients with periodontitis than in healthy control subjects. After endothelial nitric oxide synthase (eNOS) inhibitor L-NMMA infusion, there was no significant difference between vascular response to acetylcholine in the two groups. Vascular response to acetylcholine was increased significantly by treatment, whereas there was no significant difference between vascular response to acetylcholine in the untreated group before and after treatment. L-NMMA completely abolished the periodontal therapy-induced augmentation of vascular response to acetylcholine. Serum concentrations of IL-6 and hs-CRP were significantly higher in patients with periodontitis than in healthy subjects. Treatment of periodontitis significantly decreased serum concentrations of IL-6 and hs-CRP. There was no significant difference in FMD between the TAO group and ASO group. The number of circulating progenitor cells (CPCs) and migration of circulating CPCs were similar in the TAO group and control group, whereas the number of circulating CPCs were significantly lower in the ASO group than in other groups. There was a significant correlation between CRP and FMD and migration of CPCs. Both inflammation and endothelial dysfunction independently or concomitantly lead to atherosclerosis, resulting in cardiovascular complications. From a clinical perspective, it is important to select an appropriate intervention that is effective in improving endothelial dysfunction. Therapy for inflammation should improve endothelial function through an increase in NO bioavailability.
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