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Thromb Haemost 1998; 79(01): 54-58
DOI: 10.1055/s-0037-1614219
Review Article
Schattauer GmbH

Clinical Significance of Neutrophil Adhesion Molecules Expression after Coronary Angioplasty on the Development of Restenosis

Teruo Inoue
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Yoshihiko Sakai
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Tsuneo Fujito
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Kazuhiro Hoshi
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Terumi Hayashi
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Kan Takayanagi
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
,
Shigenori Morooka
From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan
› Author AffiliationsThis study was supported in part by a grant from Kyowa Hakko Kogyo Co., Ltd., Tokyo, Japan.
Further Information

Publication History

Received 01 April 1997

Accepted after resubmission 04 September 1997

Publication Date:
08 December 2017 (online)

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Summary

To investigate the neutrophil activation process following percutaneous transluminal coronary angioplasty (PTCA), we examined the expressions of Mac-1 (CD11b/CD18), L-selectin (CD62L), and sialyl-LewisX (SLX) on the surface of neutrophils after the PTCA procedure, by flow cytometric analysis. Twenty-nine patients with single vessel coronary artery disease of the left anterior descending artery who underwent elective PTCA were enrolled. In the 17 patients without restenosis at the follow-up angiography, the mean channel fluorescence intensity (MFI) for CD18, CD62L and SLX did not change after PTCA. Only the CD11b level was increased at 48 h after the PTCA. In the remaining 12 patients who developed restenosis, the MFI values for CD18 and CD11b were increased at 24 h and 48 h after the PTCA. The MFI value for CD62L was decreased and that for SLX was increased at 48 h after the PTCA. These changes were more prominent in the coronary sinus blood samples than in those of the peripheral blood samples.

Our data indicate the down-regulation of L-selectin, probably by shedding, as well as the up-regulations of Mac-1 and sialyl-LewisX, especially in patients with restenosis. It is suggested that neutrophil activation by an interaction between the selectin family and carbohydrate ligands after PTCA may play a role in the development of restenosis, as does the integrin family.

 

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