Is neutrophil-platelet adhesion and activation increased in patients with unstable angina compared to those with stable angina?
Increased neutrophil-platelet adhesion is observed in unstable angina and may contribute to systemic neutrophil activation, highlighting a potential pathophysiological mechanism in acute coronary syndromes.
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 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. CONCLUSIONS: Thus, this study demonstrates that increased neutrophil-platelet adhesion may contribute to neutrophil activation in unstable angina.
Ott et al. (1996) studied this question.