S. Deservi et al., CLINICAL AND ANGIOGRAPHIC CORRELATES OF LEUKOCYTE ACTIVATION IN UNSTABLE ANGINA, Journal of the American College of Cardiology, 26(5), 1995, pp. 1146-1150
Objectives. This study sought to evaluate the relation, if any, betwee
n clinical and angiographic findings in patients with unstable angina
and monocyte and neutrophil CD11b/CD18 receptor density. The expressio
n of HLA-DR molecules on T lymphoctes, an index of activation of these
cells, was also investigated. Background. Although activation of neut
rophils and monocytes has recently been shown in unstable angina, no s
tudies have correlated activation indexes with clinical and angiograph
ic features of patients with this clinical condition. Methods. Sixty p
atients underwent diagnostic coronary arteriography and simultaneous b
lood sampling from the aorta and coronary sinus before injection of co
ntrast medium. Cell surface receptors were detected by direct immunofl
uorescence evaluated by how cytometry using monoclonal antibodies tagg
ed,vith fluorescent markers. Results. In 38 patients with unstable ang
ina, neutrophils and monocytes showed a significantly higher expressio
n of CD11b/CD18 adhesion receptors in coronary sinus than aortic blood
(p < 0.0001 and p > 0.001, respectively). When these patients were an
alyzed according to clinical characteristics or angiographic findings,
no difference in CD11b/CD18 receptor expression in coronary sinus blo
od was found between the various subgroups, except for patients with a
t least one episode of chest pain at rest within 48 h of coronary arte
riography and a higher neutrophil adhesion molecule density than patie
nts who remained asymptomatic (p = 0.04), Lymphocytes in patients with
stable and unstable angina showed a similar percent expression of CD2
/CD19 and CD3/HLA-DR antigens, with no difference betffeen aortic and
coronary sinus blood. Conclusions. These results in a larger cohort co
nfirm previous data that neutrophil and monocyte CD11b/CD18 adhesion m
olecules show a higher expression in the coronary sinus blood of patie
nts with unstable angina. Among clinical and angiographic findings in
patients with unstable angina, only the occurrence of chest pain withi
n 38 h of coronary angiography was related to significantly higher val
ues of neutrophil fluorescence intensity, suggesting that the degree o
f neutrophil activation is related to the proximity of rest angina epi
sodes to blood sampling. Finally, our data do not support the concept
of systemic or transcardiac lymphocyte activation in unstable angina.