title: Endothelial dysfunction in the smokers can be improved with oral cilostazol treatment.
abstract: BACKGROUND
  Smoking is one of well known environmental factors causing endothelial dysfunction and plays important role in the atherosclerosis. We investigated the effect of cilostazol could improve the endothelial dysfunction in smokers with the measurement of flow-mediated dilatation (FMD).
  
  
  METHODS
  We enrolled 10 normal healthy male persons and 20 male smokers without any known cardiovascular diseases. After measurement of baseline FMD, the participants were medicated with oral cilostazol 100 mg bid for two weeks. We checked the follow up FMD after two weeks and compared these values between two groups.
  
  
  RESULTS
  There was no statistical difference of baseline characteristics including age, body mass index, serum cholesterol profiles, serum glucose and high sensitive C-reactive protein between two groups. However, the control group showed significantly higher baseline endothelium-dependent dilatation (EDD) after reactive hyperemia (12.0 ± 4.5% in the control group vs. 8.0 ± 2.1% in the smoker group, p = 0.001). However, endothelium-independent dilatation (EID) after sublingual administration of nitroglycerin was similar between the two groups (13.6 ± 4.5% in the control group vs. 11.9 ± 4.9% in the smoker group, p = 0.681). Two of the smoker group were dropped out due to severe headache. After two weeks of cilostazol therapy, follow-up EDD were significantly increased in two groups (12.0 ± 4.5% to 16.1 ± 3.7%, p = 0.034 in the control group and 8.0 ± 2.1% to 12.2 ± 5.1%, p = 0.003 in the smoker group, respectively). However, follow up EID value was not significantly increased compared with baseline value in both groups (13.6 ± 4.5% to 16.1 ± 3.7%, p = 0.182 in the control group and 11.9 ± 4.9% to 13.7 ± 4.3%, p = 0.430 in the smoker group, respectively).
  
  
  CONCLUSIONS
  Oral cilostazol treatment significantly increased the vasodilatory response to reactive hyperemia in two groups. It can be used to improve endothelial function in the patients with endothelial dysfunction caused by cigarette smoking.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, School of Medicine, Chungnam National University, Chungnam National University Hospital, Daejeon Cardiocerebrovascular Center, Daejeon, Korea.
authors.forename: Kyu Seop
authors.initials: KS
authors.lastname: Kim
authors.forename: Hyung Seo
authors.initials: HS
authors.lastname: Park
authors.forename: Il Soon
authors.initials: IS
authors.lastname: Jung
authors.forename: Jae-Hyeong
authors.initials: JH
authors.lastname: Park
authors.forename: Kye Taek
authors.initials: KT
authors.lastname: Ahn
authors.forename: Seon-Ah
authors.initials: SA
authors.lastname: Jin
authors.forename: Yong Kyu
authors.initials: YK
authors.lastname: Park
authors.forename: Jun Hyung
authors.initials: JH
authors.lastname: Kim
authors.forename: Jae-Hwan
authors.initials: JH
authors.lastname: Lee
authors.forename: Si Wan
authors.initials: SW
authors.lastname: Choi
authors.forename: Jin-Ok
authors.initials: JO
authors.lastname: Jeong
authors.forename: In-Whan
authors.initials: IW
authors.lastname: Seong