Circulation, Vol 90, 1662-1668, Copyright © 1994 by American Heart Association
B Jude, B Agraou, EP McFadden, S Susen, C Bauters, P Lepelley, C Vanhaesbroucke, P Devos, A Cosson and P Asseman
BACKGROUND: Platelet activation plays a pivotal role in the pathogenesis of
acute coronary disease. Monocytes are involved in the progression of
atherosclerosis and are potent activators of blood coagulation through
their ability to synthesize tissue factor (TF). The aim of this study was
to compare markers of monocyte and coagulation activation in the systemic
blood of patients with unstable angina, acute myocardial infarction, or
stable angina. METHODS AND RESULTS: We studied 26 patients with unstable
angina (10 +/- 5 hours after the onset of the last episode of pain), 18
patients with acute myocardial infarction (5 +/- 4 hours after the onset of
pain), and 34 patients with stable angina. We measured levels of TF
expression in peripheral blood mononuclear cells (isolated by gradient
centrifugation and incubated for 16 hours, with or without endotoxin
stimulation), levels of plasma prothrombin fragment 1 + 2 (F1 + 2), and
levels of fibrinogen in peripheral blood. In patients with unstable angina,
both stimulated and unstimulated cells exhibited higher levels of TF
expression than in patients with stable angina (P = .0001). In patients
with acute myocardial infarction, monocyte TF activity did not differ from
that in patients with stable angina. Mean levels of F1 + 2 and of
fibrinogen did not differ significantly between groups. Only in the
unstable angina group, a modest correlation was found between fibrinogen (r
= .72, P = .005) and F1 + 2 levels (r = .54, P = .001) levels and the
degree of monocyte TF expression. In patients with unstable angina,
monocyte TF expression (both stimulated and unstimulated, assessed by
biological activity and by antigen techniques) and fibrinogen levels were
correlated with the time elapsed from the beginning of the most recent
episode of pain (.61 < r < .72, .02 < P < .0001). By contrast,
there was no correlation between these variables and the time from onset of
pain in patients with acute myocardial infarction. CONCLUSIONS: A
time-dependent activation of systemic monocytes and a time-dependent
increase in fibrinogen levels occurs in unstable angina but not in
myocardial infarction. These findings provide further evidence that a
specific inflammatory process occurs in unstable angina. Further studies
are required to determine whether monocyte activation is a cause or a
consequence of plaque instability in patients with unstable angina and to
clarify the interrelations between platelet and monocyte activation in
these circumstances.
ARTICLES
Evidence for time-dependent activation of monocytes in the systemic circulation in unstable angina but not in acute myocardial infarction or in stable angina
Laboratoire d'Hematologie, Hopital Cardiologique, Lille, France.
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