Clinical significance of neutrophil adhesion molecules expression after coronary angioplasty on the development of restenosis

• Published in: Thrombosis and haemostasis Vol. 79; no. 1; p. 54
• Main Authors: Inoue, T, Sakai, Y, Fujito, T, Hoshi, K, Hayashi, T, Takayanagi, K, Morooka, S
• Format: Journal Article
• Language: English
• Published: Germany 01.01.1998
• Subjects: Angioplasty, Balloon, Coronary; Antigens, Surface - blood; Cell Adhesion Molecules - analysis; Coronary Disease - blood; Female; Humans; L-Selectin - blood; Lewis Blood-Group System - immunology; Macrophage-1 Antigen - blood; Male; Middle Aged; Neutrophil Activation; Oligosaccharides - blood; Recurrence
• ISSN: 0340-6245
• DOI: 10.1055/s-0037-1614219

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.