Cilostazol does not improve peripheral arterial disease-linked oxidative stress

Cilostazol is a drug widely used to treat peripheral arterial disease (PAD) in patients with advanced atherosclerosis. It is an inhibitor of platelet aggregation and causes arterial vasodilatation. It has been speculated that cilostazol might act to improve oxidative stress in these patients.

We analyzed 25 patients with demonstrated lower limb peripheral arterial disease to determine whether lipid peroxidation (LPO) or total antioxidant capacity (TAC) were modified after 6 months of cilostazol treatment (postintervention phase) with respect to the basal phase.

Analysis of plasma samples determined that LPO levels decreased significantly over the postintervention phase (26±15 vs. 11±7 pM, P=0.0003). However, when TAC levels were analyzed, no significant differences were observed (0.80±0.21 vs. 0.85±0.17 mM, P=0.42). Under basal conditions, LPO showed a positive correlation to treatment as judged by the ankle-brachial index (r=0.800, P=0.002) as well as uric acid (r=0.508, P=0.03) and CRP (r=0.481, P=0.05) levels. In contrast, TAC negatively correlated with triglycerides (r=-0.879, P<0.0001) and microalbuminuria (r=-0.868, P<0.0001). In the postintervention phase, TAC negatively correlated with HbA1c (r=-0.570, P=0.02) and triglycerides (r=-0.864, P<0.0001).

Our data indicate that cilostazol treatment does not improve oxidative stress in PAD patients after 6 months of treatment. However, lipid peroxidation and total antioxidant capacity were affected by cilostrazol treatment, which could be related to altered reactive oxygen species production. Further research may be needed to determine the critical dose of cilostazol to clarify the protective role of this drug in PAD.