Author + information
- Received March 21, 1995
- Revision received October 25, 1995
- Accepted November 10, 1995
- Published online March 15, 1996.
- Franz-Josef Neumann, MD∗,
- Ilka Ott, MD,
- Meinrad Gawaz, MD,
- Georg Punchner and
- Albert Schömig, MD
- ↵∗Address for correspondence: Dr. Franz-Josef Neumann, I. Medizinische Klinik der Technischen Universität München, Klinikum rechts der Isar, Ismaninger Strasse 22, 81675 Munich, Germany.
Objectives. This study sought to investigate changes in the expression of activation-dependent adhesion receptors on neutrophils and platelets after exposure to the balloon-injured coronary artery plaque.
Background. Activation of blood cells at the balloon-injured coronary artery plaque may contribute to abrupt vessel closure and late restenosis after percutaneous transluminal coronary angioplasty.
Methods. In 30 patients undergoing elective coronary angioplasty, blood specimens were obtained through the balloon catheter proximal to the plaque before dilation and distal to the plaque after dilation. Simultaneous blood samples obtained through the guiding catheter served as control samples. Total surface expression of the inducible fibrinogen receptor (CD41) and surface expression of the activated fibrinogen receptor (LIBS1) on platelets as well as Mac-1 (CD11b) and L-selectin (CD62L) surface expression on neutrophils were assessed by flow cytometry.
Results. After exposure to the dilated coronary artery plaque, surface expression of LIBS1 on platelets increased by 40.5 ± 11.0 mean (±SE) fluorescence (p = 0.001) and that of CD11b on neutrophils increased by 20.1 ± 4.4 mean fluorescence (p = 0.018). Concomitantly, anti-CD62L binding on neutrophils decreased by 6.6 ± 2.4 mean fluorescence (p = 0.022). In contrast, surface expression of the adhesion receptors did not change significantly between the coronary ostium and the prestenotic coronary segment.
Conclusions. The results of this study demonstrate neutrophil and platelet activation at the balloon-injured coronary artery plaque. This cellular activation may serve as a target for pharmacologic interventions to improve the outcome of coronary angioplasty.
☆ This study was funded by the Deutsche Forschungsgemeinschaft (Ne 540/1-1 and Ga 381/2-1), Bonn-Bad Godesberg, Germany.
- Received March 21, 1995.
- Revision received October 25, 1995.
- Accepted November 10, 1995.