Comparison of activation process of platelets and neutrophils after coronary stent implantation versus balloon angioplasty for stable angina pectoris.
The pathophysiologic features of stent-induced cellular responses of platelets and leukocytes have not been established. This study was designed to clinically investigate the activation of platelets and neutrophils after coronary stenting and to identify its effects on the long-term results of coronary stents. Forty-eight consecutive patients with left anterior descending coronary artery disease indicating coronary intervention were randomly assigned to either a balloon angioplasty group or a coronary stent group. Flow cytometric analysis demonstrated that the transcardiac gradient (the value of coronary sinus blood minus the value of peripheral blood) of platelet surface expression of CD62P (p < 0.001) and CD63 (p < 0.01) increased immediately after coronary stenting, but increased less significantly immediately after balloon angioplasty (CD62P, p < 0.01; CD63, p < 0.05). These increases were persistently observed after coronary stenting but transiently after balloon angioplasty alone during a 48-hour observation period after the procedures. The gradient for neutrophil surface expression of CD11b increased, and that of CD62 L decreased 48 hours after coronary stenting (CD11b, p < 0.001; CD62 L, p < 0.05), but these changes showed less significance 48 hours after balloon angioplasty alone (CD11b, p < 0.05; CD62 L, p = NS). The gradients 48 hours after the procedures for both CD62P (r = 0.39, p < 0.05) and CD11b (r = 0.44, p < 0.01) were independently correlated with the late loss in the stent group, whereas the correlation was seen only for CD11b (r = 0.38, p < 0.05) in the balloon angioplasty group. Both platelet and neutrophil activation was greater after coronary stenting than after balloon angioplasty. Cellular interactions between platelets and neutrophils may be related to the progression of neointimal proliferation leading to restenosis after coronary stent implantation.
Inoue
T
T
Department of Cardiology, Koshigaya Hospital and Institute for Medical Science, Dokkyo University School of Medicine, Koshigaya City, Saitama, Japan.
Sohma
R
R
Miyazaki
T
T
Iwasaki
Y
Y
Yaguchi
I
I
Morooka
S
S
D000787:Angina Pectoris / Q000097:blood / Q000000981:diagnostic imaging / Q000276:immunology* / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects* / Q000295:instrumentation*; D015703:Antigens, CD / Q000032:analysis; D001792:Blood Platelets / Q000737:chemistry; D017023:Coronary Angiography; D018450:Disease Progression; D005260:Female; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006801:Humans; D007958:Leukocyte Count; D016177:Macrophage-1 Antigen / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018375:Neutrophil Activation; D009504:Neutrophils / Q000737:chemistry; D019007:P-Selectin / Q000032:analysis; D010865:Pilot Projects; D015539:Platelet Activation; D010976:Platelet Count; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D012008:Recurrence; D015607:Stents / Q000009:adverse effects*; D060149:Tetraspanin 30; D013997:Time Factors
D015703:Antigens, CD; C554586:CD63 protein, human; D016177:Macrophage-1 Antigen; D019007:P-Selectin; D010980:Platelet Membrane Glycoproteins; D060149:Tetraspanin 30