Background:
Cilostazol is an antiplatelet agent, which is known also to have protective effects on endothelial cell. We studied effects of cilostazol on markers of inflammation and endothelial cell damage in patients with severe carotid disease, who underwent carotid endoarterectomy (CEA).
Methods:
We measured high sensitivity CRP (hsCRP), soluble vascular cellular adhesion molecule (VCAM)-1, soluble E-selectin, soluble intercellular adhesion molecule-1 and von Willebrand Factor antigen (vWF) in 45 patients who underwent CEA (38 males and 7 females, mean age was 69 years). Venous blood was taken from each patient before (Pre) and 3 days (Day3), 10 days (Day10), 4 weeks and 1 year (Post) after CEA. Each marker was compared between patients who were treated with aspirin alone (aspirin group, 18 cases) and those treated with cilostazol alone or cilostazol plus aspirin (cilostazol group, 17 cases).
Results:
The levels of hsCRP, VCAM-1, E-selectin and vWF at Day3 and the levels of hsCRP and VCAM-1 on Day10 were significantly higher than those at PreCEA. The alterations of those markers were not significantly different between the aspirin and cilotazol groups. The levels of hsCRP in the cilostazol group were significantly lower than those in aspirin group at both PreCEA and PostCEA. The levels of VCAM-1 at PreCEA in the cilostazol group were significantly lower than those in the aspirin group.
Conclusions:
The results suggested that cilostazol inhibits inflammation and endothelial cell damage in patients with severe carotid disease, although its protective effects did not reduce the endothelial cell damage induced by CEA when compared with aspirin.
Effects of high glucose on human umbilical vein endothelial cell permeability and myosin light chain phosphorylation
