Copyright © 1997 by the European Society of Cardiology.
© 1997 The European Society of Cardiology
Reduction of monocyte-platelet interaction and monocyte activation in patients receiving antiplatelet therapy after coronary stent implantation
Medizinische Klinik, Technische Universität München München, Germany
Received 22 May 1997; accepted 30 May 1997.
Correspondence: Dr Andreas May, Haemostasis Research Unit, Max-Planck-Institute, Kerckhoff-Klinik, Sprudelhof 11, 61231 Bad Nauheim, Germany
Abstract
BACKGROUND: Monocyte activation induces different procoagulant and proadhesive inflammatory responses and thus may play a role in thrombotic complications after coronary interventions. Monocyte-platelet interaction may trigger these effects inducing monocyte activation.
AIMS: To characterize the effect of antiplatelet vs anticoagulation therapy on monocyte-platelet interaction and monocyte function after intracoronary stenting.
METHODS AND RESULTS: Immediately before, and during the first 12 days after successful coronary stenting, monocyteplatelet conjugates and monocyte function were assessed by flow cytometric detection of GPIIb/IIIa (CD41) on monocytes and by monocyte surface exposure of Mac-1 (CD11b/ CD18) and L-selectin (CD62L). Twenty patients receiving combined antiplatelet therapy (ticlopidine, aspirin) were compared to 20 patients with standard anticoagulation (phenprocoumon, overlapping heparin, aspirin). Before stenting, monocyte-platelet conjugates and Mac-1 surface expression in both groups were significantly increased, while L-selectin was significantly diminished. Anticoagulation did not change these variables significantly during the subsequent 12 days. In contrast, antiplatelet therapy reduced platelet-monocyte conjugates by 46±9·3% (mean±SEM, P=0·0019) within 4 days, which was associated with a decrease in Mac-1 expression (28±6·7%, P=0·0013) and an increase in L-selectin (56±15·0%, P=0·0061).
CONCLUSION: After intracoronary stenting, combined antiplatelet therapy, but not anticoagulation, causes reduction of monocyte-platelet interaction, which is associated with monocyte deactivation. This may contribute to a decreased risk for thrombotic events.
Key Words: Stent • monocytes • ticlopidine • anticoagulation
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