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.