J Cardiovasc Ultrasound.  2011 Mar;19(1):21-25. 10.4250/jcu.2011.19.1.21.

Endothelial Dysfunction in the Smokers Can Be Improved with Oral Cilostazol Treatment

Affiliations
  • 1Division of Cardiology, Department of Internal Medicine, School of Medicine, Chungnam National University, Chungnam National University Hospital, Daejeon Cardiocerebrovascular Center, Daejeon, Korea. jaehpark@cnuh.co.kr

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).
CONCLUSION
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.

Keyword

Endothelial dysfunction; Smoking; Cilostazol

MeSH Terms

Administration, Sublingual
Atherosclerosis
Body Mass Index
C-Reactive Protein
Cardiovascular Diseases
Cholesterol
Dilatation
Follow-Up Studies
Glucose
Headache
Humans
Hyperemia
Male
Nitroglycerin
Smoke
Smoking
Tetrazoles
C-Reactive Protein
Cholesterol
Glucose
Nitroglycerin
Smoke
Tetrazoles

Figure

  • Fig. 1 Comparison of endothelium-dependent dilatation (EDD) (A) and endothelium-independent dilatation (EID) (B) in the control and smoker group. Data are expressed as the mean ± standard deviation.

  • Fig. 2 Effect of cilostazol treatment on endothelium-dependent dilatation (EDD) in the control group (A) and smoker group (B). A significant effect of cilostazol treatment on EDD is observed.

  • Fig. 3 Effect of cilostazol treatment on endothelium-independent dilatation (EID) in the control group (A) and smoker group (B). There is no significant difference between baseline and post-treatment values. Also, there is no statistical significance between post EID values of two groups.


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