Clinical Studies
Increased Platelet Reactivity and Circulating Monocyte-Platelet Aggregates in Patients With Stable Coronary Artery Disease

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Abstract

Objectives. We sought to examine whether patients with stable coronary artery disease (CAD) have increased platelet reactivity and an enhanced propensity to form monocyte-platelet aggregates.

Background. Platelet-dependent thrombosis and leukocyte infiltration into the vessel wall are characteristic cellular events seen in atherosclerosis.

Methods. Anticoagulated peripheral venous blood from 19 patients with stable CAD and 19 normal control subjects was incubated with or without various platelet agonists and analyzed by whole blood flow cytometry.

Results. Circulating degranulated platelets were increased in patients with CAD compared with control subjects (mean [±SEM] percent P-selectin–positive platelets: 2.1 ± 0.2 vs. 1.5 ± 0.2, p < 0.01) and were more reactive to stimulation with 1 μmol/liter of adenosine diphosphate (ADP) (28.7 ± 3.9 vs. 16.1 ± 2.2, p < 0.01), 1 μmol/liter of ADP/epinephrine (51.4 ± 4.6 vs. 37.5 ± 3.8, p < 0.05) or 5 μmol/liter of thrombin receptor agonist peptide (TRAP) (65.7 ± 6.8 vs. 20.2 ± 5.1, p < 0.01). Patients with stable CAD also had increased circulating monocyte-platelet aggregates compared with control subjects (percent platelet-positive monocytes: 15.3 ± 3.0 vs. 6.3 ± 0.9, p < 0.01). Furthermore, patients with stable CAD formed more monocyte-platelet aggregates than did control subjects when their whole blood was stimulated with 1 μmol/liter of ADP (50.4 ± 4.5 vs. 28.1 ± 5.3, p < 0.01), 1 μmol/liter of ADP/epinephrine (60.7 ± 4.3 vs. 48.0 ± 4.8, p < 0.05) or 5 μmol/liter of TRAP (67.6 ± 5.7 vs. 34.3 ± 7.0, p < 0.01).

Conclusions. Patients with stable CAD have circulating activated platelets, circulating monocyte-platelet aggregates, increased platelet reactivity and an increased propensity to form monocyte-platelet aggregates.

Abbreviations

ADP
adenosine diphosphate
CAD
coronary artery disease
FITC
fluorescein isothiocyanate
GP
glycoprotein
Ig
immunoglobulin
RANTES
regulated on activation normal T cell expressed presumed secreted
TRAP
thrombin receptor activating peptide

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This work was supported by Grants GM35141-10 and GM24891-18 from the National Institutes of Health, Bethesda, Maryland and the U.S. Navy (Office of Naval Research Contract N00014-94-C-0149), with the funds provided by the Naval Medical Research and Development Command. The opinions or assertions contained herein are those of the authors and should not be construed as official or reflecting the views of the Navy Department or Naval Service at large.