The observed efficacy of cilostazol is not fully explained. Most investigators hypothesized that cilostazol exhibits its pharmacologic effects via antiplatelet, vasodilatory, and antithrombotic activities. Other postulated mechanisms of cilostazol action include a) anti-proliferative function by preventing restenosis after PCI, b) improved lipid profiles and c) prevent atherosclerosis via inhibition of the expression of the adhesion molecule. Some of these hypotheses may be valid, but clearly more confirmatory studies are needed. Although cilostazol has all the above properties, its effect on the expression of VEGF and oxidative stress biomarkers is not known For that purpose, we plan to study the changes in lipoprotein levels, proangiogenetic factors, inflammation, oxidative stress and endothelial activation following 12 weeks of cilostazol in a group of 40 HD patients. We feel that the present study may help to shed some lights and broaden our understanding of the pathophysiological mechanisms underlying the beneficial effects of cilostazol and give further insights on the role of antiplatelet drugs in PAD both by improving clinical symptoms and plausibly by reducing cardiovascular events