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Oral sarpogrelate can improve endothelial dysfunction as effectively as oral cilostazol, with fewer headaches, in active young male smokers

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Abstract

Sarpogrelate and cilostazol are two commonly used adjunctive antiplatelet agents that also can be used to improve endothelial dysfunction. We compared the effects of sarpogrelate and cilostazol on endothelial dysfunction in active male smokers with flow-mediated dilatation (FMD). We enrolled and compared baseline and follow-up FMD in 20 young male smokers without any known cardiovascular diseases. Two participants who were initially medicated with cilostazol dropped out because of severe headache after taking medication. However, they continued the other experiment with sarpogrelate medication. Baseline endothelium-dependent dilatation (EDD) after reactive hyperemia was 7.5 % ± 1.9 % and endothelium-independent dilatation (EID) after sublingual administration of nitroglycerin was 13.3 % ± 3.4 %. After a 2-week treatment of cilostazol, follow-up EDD significantly increased (7.7 % ± 1.9 to 8.8 ± 2.0 %, P = 0.016), but follow-up EID changed insignificantly (13.2 % ± 3.5 to 12.5 % ± 3.9 %, P = 0.350). With the sarpogrelate treatment, follow-up EDD was significantly increased (7.4 % ± 1.9 % to 8.8 % ± 1.9 %, P = 0.021), but follow-up EID was similar (13.5 % ± 3.5 to 14.0 % ± 3.2 %, P = 0.427). There was no clinical significance between the two groups on follow-up EDD and EID (P = 0.984 and 0.212, respectively). However, the mean score of intensity of headache was significantly higher in the cilostazol group than in the sarpogrelate group (3.8 % ± 2.5 % vs 1.4 % ± 2.2 %, P = 0.005). EDD showed a similar significant increase with 2-week treatment of cilostazol and sarpogrelate. However, intensity of headaches was significantly higher in the cilostazol group.

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Correspondence to Jae-Hyeong Park.

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Jeong, I.S., Park, JH., **, S.A. et al. Oral sarpogrelate can improve endothelial dysfunction as effectively as oral cilostazol, with fewer headaches, in active young male smokers. Heart Vessels 28, 578–582 (2013). https://doi.org/10.1007/s00380-012-0282-1

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