Comparison of activation process of platelets and neutrophils after coronary stent implantation versus balloon angioplasty for stable angina pectoris

https://doi.org/10.1016/S0002-9149(00)01159-0Get rights and content

Abstract

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.

Section snippets

Patients

The subjects were 48 consecutive patients with isolated atherosclerotic coronary artery disease of the proximal left anterior descending artery who underwent initial elective coronary angioplasty. All of the patients exhibited clinically stable class I or II effort angina without previous myocardial infarction, according to the Canadian Cardiovascular Society. The target lesions were all type A or type B lesions as described by the American College of Cardiology/American Heart Association Task

Results of coronary intervention

In the balloon angioplasty group, 2 patients underwent stent implantation in bailout situations. Thus, 22 patients in the balloon angioplasty group were eligible for data analysis. In 3 patients in the stent group, the Palmatz-Schatz stent could not be advanced to the lesion, so other stents were implanted. Thus, a total of 21 patients in the stent group were eligible for data analysis. None of these 21 patients experienced acute or subacute stent thrombosis.

Baseline characteristics, procedural variables, and quantitative coronary angiographic results

The clinical background was similar

Platelet activation after coronary stenting

Flow cytometric analysis of platelet activation markers such as P-selectin (CD62P) and CD63 expressed on the platelet membrane surface has facilitated the direct detection of platelets activated in vivo.17 P-selectin is an adhesion molecule included in the selectin family, which potentially binds to leukocyte carbohydrate ligands and mediates adhesion of activated platelets to neutrophils and monocytes.18, 19, 20 P-selectin is a component of the α-granule of resting platelets that is only

Acknowledgements

We thank Richard A. Schatz, MD, Scripps Clinic, La Jolla, California, for his critical review of this manuscript and Gregory J. del Zoppo, MD, Scripps Research Institute, La Jolla, California, for helpful suggestions.

References (30)

  • J.R Wilentz et al.

    Platelet accumulation in experimental angioplastytime course and relation to vascular injury

    Circulation

    (1987)
  • W Terres et al.

    Residual platelet function under acetylsalicylic acid and the risk of restenosis after coronary angioplasty

    J Cardiovasc Pharmacol

    (1992)
  • T Inoue et al.

    Early detection of platelet activation after coronary angioplasty

    Coron Artery Dis

    (1996)
  • S De Servi et al.

    Granulocyte activation after coronary angioplasty in human

    Circulation

    (1990)
  • F.J Newmann et al.

    Neutrophil and platelet activation at balloon-injured coronary artery plaque in patients undergoing angioplasty

    J Am Coll Cardiol

    (1996)
  • Cited by (117)

    • Myeloid-related protein-8/14 in acute coronary syndrome

      2017, International Journal of Cardiology
    • Graded metal carbon protein binding films prepared by hybrid cathodic arc - Glow discharge plasma assisted chemical vapor deposition

      2015, Surface and Coatings Technology
      Citation Excerpt :

      During heart transplantation using cardiopulmonary bypass heart-lung machines, patients exhibit an inflammatory response which is characterized by increased expression of at least ten leukocyte cluster-of-differentiation (CD) antigens [7]. Coronary artery disease is primarily caused by the inflammation of coronary vessel walls [8] and a study on coronary stents provided strong evidence that increased inflammation can arise from the use of bare stents [9]. To minimize these inflammatory responses, attempts have been made to cover surfaces which are exposed to blood with protein molecules such as albumin derived from human blood plasma.

    View all citing articles on Scopus

    This study was supported by grants from Kyowa Hakko Kogyo Co., Ltd., Tokyo, Japan, and the Vehicle Racing Commemorative Foundation, Tokyo, Japan. Manuscript received February 2, 2000; revised manuscript received and accepted May 31, 2000.

    View full text