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.
Platelet-dependent thrombosis and leukocyte infiltration into the vessel wall are
characteristic cellular events seen in atherosclerosis.
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.
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 micromol/liter
of adenosine diphosphate (ADP) (28.7 +/- 3.9 vs. 16.1 +/- 2.2, p < 0.01), 1 micromol/liter
of ADP/epinephrine (51.4 +/- 4.6 vs. 37.5 +/- 3.8, p < 0.05) or 5 micromol/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
micromol/liter of ADP (50.4 +/- 4.5 vs. 28.1 +/- 5.3, p < 0.01), 1 micromol/liter
of ADP/epinephrine (60.7 +/- 4.3 vs. 48.0 +/- 4.8, p < 0.05) or 5 micromol/liter of
TRAP (67.6 +/- 5.7 vs. 34.3 +/- 7.0, p < 0.01).
Patients with stable CAD have circulating activated platelets, circulating monocyte-platelet
aggregates, increased platelet reactivity and an increased propensity to form monocyte-platelet
aggregates.