Increased neutrophil-platelet adhesion in patients with unstable angina

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.

Systemic venous blood samples were taken from 25 patients with stable angina pectoris and 25 patients with unstable angina pectoris. Neutrophil activation and neutrophil-platelet adhesion were evaluated by two-color flow cytometry. Patients with unstable angina showed a significant increase 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 activation was found in patients with unstable angina compared with those with stable angina assessed by cell surface CD11b expression and shedding of L-selectin (115.6 +/- 10.3 versus 74.0 +/- 6.3 anti-CD11b mean fluorescence intensity, P = .002; 49.8 +/- 6.0 versus 72.1 +/- 4.0 anti-L-selectin mean fluorescence intensity, P = .006). Markers of neutrophil activation were related to the extent of neutrophil-platelet adhesion (CD11b: r = .5, P = .0005; L-selectin: r = .42, P = .012). In vitro studies revealed that binding of purified platelet membranes to control neutrophils caused a dose-dependent increase in CD11b surface expression, a decrease in surface L-selectin, and the release of superoxide anions.

Thus, this study demonstrates that increased neutrophil-platelet adhesion may contribute to neutrophil activation in unstable angina.