Circulation, Vol 86, 790-797, Copyright © 1992 by American Heart Association
GG Serneri, R Abbate, AM Gori, M Attanasio, F Martini, B Giusti, P Dabizzi, L Poggesi, PA Modesti and F Trotta
BACKGROUND. Blood clotting activation is an important component of the
inflammatory response; the outbursts of unstable angina are usually
associated with increased thrombin formation and coronary mural thrombosis.
METHODS AND RESULTS. To investigate 1) whether monocyte activation is
responsible for the enhanced thrombin formation during bursts of unstable
angina and 2) what mechanism(s) might be responsible for monocyte
activation, we studied patients with unstable angina (n = 31), stable
effort angina (n = 23), left endoventricular thrombosis (n = 8), and
control subjects (n = 44), measuring plasma fibrinopeptide A (FPA) levels
and the capacity of monocytes to express procoagulant activity (PCA) and of
lymphocytes to modulate this expression. Patients with unstable angina and
patients with endoventricular thrombosis had significantly (p less than
0.0001) higher FPA plasma levels than patients with effort angina and
control subjects. However, only monocytes from unstable angina patients
expressed significantly increased PCA characterized as tissue factor-like
activity (units/10(5) monocytes, median and range; 120, 1.1-463.2 versus
10.8, 0.8-39.1 in control subjects; p less than 0.0001 versus the other
groups). When 14 patients with unstable angina were restudied 8-12 weeks
later, they showed neither elevated plasma FPA levels nor monocyte PCA. In
unstable angina patients, there was a correlation between FPA and PCA (r =
0.56, p less than 0.001). For expression of PCA by monocytes, both an
incubation of at least 2 hours with lymphocytes and direct monocyte-
lymphocyte contact were needed. In reconstitution and cross-mixing
experiments, only lymphocytes from patients with active unstable angina
induced the expression of PCA by monocytes from both control and patient
groups. CONCLUSIONS. The results demonstrate that the increased thrombin
formation in unstable angina patients is due to the expression of tissue
factor-like activity by activated monocytes. The monocyte activation
appears to be a part of a lymphocytic cell-instructed response
intermittently triggered by unknown factors.
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Transient intermittent lymphocyte activation is responsible for the instability of angina
Clinica Medica I, University of Florence, Italy.
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