INCREASED NEUTROPHIL-PLATELET ADHESION IN PATIENTS WITH UNSTABLE ANGINA

Background Neutrophil-platelet adhesion may occur as a consequence of platelet activation. The role of this heterotypic adhesion in ischemic disorders is poorly understood thus far. Methods and Results Systemic venous blood samples were taken from 25 patients with stable angina p ectoris and 25 patients with unstable angina pectoris. Neutrophil acti vation and neutrophil-platelet adhesion were evaluated by two-color fl ow cytometry. Patients with unstable angina showed a significant incre ase in neutrophil-platelet adhesion compared with patients with stable angina (mean+/-SEM, 132.1+/-20.5 versus 29.8+/-4.7 anti-glycoprotein IIb/IIIa mean fluorescence intensity, P=.0001). Systemic neutrophil ac tivation was found in patients with unstable angina compared with thos e with stable angina assessed by cell surface CD11b expression and she dding of L-selectin (115.6+/-10.3 versus 74.0+/-6.3 anti-CD11b mean fl uorescence intensity, P=.002; 49.8+/-6.0 versus 72.1+/-4.0 anti-L-sele ctin mean fluorescence intensity, P=.006). Markers of neutrophil activ ation were related to the extent of neutrophil-platelet adhesion (CD11 b: r=.5, P=.0005; L-selectin: r=.42, P=.012). In vitro studies reveale d that binding of purified platelet membranes to control neutrophils c aused a dose-dependent increase in CD11b surface expression, a decreas e in surface L-selectin, and the release of superoxide anions. Conclus ions Thus, this study demonstrates that increased neutrophil-platelet adhesion may contribute to neutrophil activation in unstable angina.