Abstract 955: Vascular Function and Endothelial Progenitor Cells in Thromboangiitis Obliterans (Buerger’s Disease)

• Published in: Circulation Vol. 118; no. suppl_18
• Main Authors: Nishioka, Kenji, Higashi, Yukihito, Umemura, Takashi, Jituiki, Daisuke, Goto, Chikara, Nakamura, Syuji, Hidaka, Takayuki, Fujii, Yuichi, Soga, Jyunko, Hata, Takaki, Idei, Naomi, Fujimura, Noritaka, Teragawa, Hiroki, Kihara, Yasuki
• Format: Journal Article
• Language: English; Japanese
• Published: Ovid Technologies (Wolters Kluwer Health) 28.10.2008
• DOI: 10.1161/circ.118.suppl_18.s_635-c
• ISSN: 0009-7322

Abstract only Background: Buerger’s disease is associated with endothelial dysfunction. Several lines of evidence have shown that the circulating number and function of endothelial progenitor cells (EPCs) are surrogate biologic markers for cardiovascular diseases. Methods and Results: The purpose of this study was to evaluate the role of EPCs in endothelial function in Buerger’s disease. We measured flow-mediated vasodilation (FMD), nitroglycerine (NTG)-induced vasodilation, circulating levels of EPCs, cell migration response to vascular endothelial growth factor (VEGF), and serum levels of VEGF in 25 patients with Buerger’s disease and 25 age- and sex-matched healthy subjects, and 25 patients with atherosclerosis obliterans (ASO). Vascular reactivity of brachial artery was measured by using high-resolution ultrasound. Circulating EPCs were quantified by flow cytometry. Cell migration assay was performed by the Boyden chamber technique. FMD was lower in both the Buerger’s group and the ASO group than in the control group (Buerger; 6.6±3.1%, ASO; 5.5±5.4%, vs. control; 10.6±3.3%, p<0.01, respectively). There was no significant difference in FMD between the Buerger’s group and ASO group. The number of circulating EPCs was similar in the Buerger’s group and control group, whereas the number of circulating EPCs was lower in the ASO group than in other groups (Buerger; 966±543/mL; control; 980±424/mL, vs. ASO; 466±339/mL, p<0.01, respectively). Cell migration to VEGF was similar in the Buerger’s group and control group, whereas cell migration was lower in the ASO group than in other groups (Buerger; 12.8±4.1/hpf; control; 13.2±3.5/hpf, vs. ASO; 4.2±1.1/hpf, p<0.01, respectively). Serum VEGF levels was higher in the Buerger’s and ASO groups than in the control group, whereas serum VEGF levels was similar in the Buerger’s group and ASO group. Conclusions: These findings suggest that FMD was impaired in patient with Burger’s disease as well as patients with ASO compared with normal control subjects and that the number and function of EPCs were not decreased in patients with Burger’s disease. EPCs may be mobilized to restore endothelial function in Buerger’s disease. In patients with ASO, both the mobilizations of EPCs and endothelial function were impaired.