Association of Neutrophil Adhesion Molecules Expression and Change of sICAM-1 Concentration after Coronary Artery Stenting with Later Restenosis.
10.4070/kcj.2001.31.1.45
- Author:
Jin Su HWANG
;
Jei Keon CHAE
;
Bang Ju LA
;
Byung Hyun RHEE
;
Won Ho KIM
;
Jae Ki KO
- Publication Type:Original Article
- MeSH:
Angina, Stable;
Angina, Unstable;
Angiography;
Antibodies, Monoclonal;
Arteries;
Constriction, Pathologic;
Coronary Vessels*;
Enzyme-Linked Immunosorbent Assay;
Flow Cytometry;
Follow-Up Studies;
Humans;
Hyperplasia;
Myocardial Infarction;
Neutrophils*;
Stents*;
Veins
- From:Korean Circulation Journal
2001;31(1):45-53
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Neointimal hyperplasia, as the most important mechanism of restenosis after intracoronary artery stenting, its severity is closely correlated with the degree of local inflammatory reaction initiated by vasular injury during stenting procedure. So, we proceeded this study to determine whether inflammatory markers such as CD11b/CD18 (Mac-1) adehsion molecules of neutrophils, sICAM-1 (soluble intercellular adhesion molecule-1), ESR, and CRP increase or not in the peripheral circulation after coronary artery stenting, and whether there is any association between these findings and the degree of later restenosis. METHOD: 32 patients (chronic stable angina 4, unstable angina 17, acute myocardial infarction 11) underwent single vessel coronary artery stenting were enrolled in our study. Blood samples were obtained from peripheral vein just before coronary artery stenting and 48 hours thereafter. The degrees of CD11b/CD18 expression on the surface of neutrophils were analyzed by flow cytometry with monoclonal antibodies, and sICAM-1 by ELISA method. At each times, ESR and CRP were also measured. Follow-up coronary artery angiography was performed with QCA analysis at least 6 months later. We compared the each 48 hours values with the baseline (just before procedure) values. Percentage increments (as a ratio 48 hours values to baseline) of CD11b/CD18 expression, sICAM-1, ESR, and CRP levels were also compared with the results of follow-up QCA analysis. RESULTS: Restenosis (diameter stenosis > or = 50%) occurred in 6 patients (19%) at follow up angiography. 48 hours values of CD11b/CD18 expression, sICAM-1, ESR, and CRP were significantly elevated from the baseline values (each p values, CD11b : < 0.0001, CD18 : 0.01, sICAM-1 : < 0.0001, ESR : 0.005, and CRP : 0.001). The percentage increments of CD11b/CD18 expression were more elevated in restenosis group than nonrestenosis group (CD11b : 341+/-215%/74+/-95%, CD18 : 84+/-60%/17+/-37%, each p < 0.001, 0.001). There was some positive correlation between the percentage increments in the expression of CD11b and the late loss index at the follow up angiography (r=.43, p<0.05). CONCLUSIONS: Through this study, we found that the activation of neutrophils was occurred, and that sICAM-1 level was increased after coronary artery stenting in the peripheral blood. There was some correlations between the degree of CD11b expression on the surface of neutrophils and the severity of late lumen loss of inserted stents. The measurements of increased neutrophil adhesion molecules of CD11b/CD18 levels at 48hrs after coronary stenting may have a value as the predictor of subsequent late restenosis.
