INCREASED PLATELET REACTIVITY AND CIRCULATING MONOCYTE-PLATELET AGGREGATES IN PATIENTS WITH STABLE CORONARY-ARTERY DISEASE

Objectives. We sought to examine whether patients with stable coronary artery disease (CAD) have increased platelet reactivity and an enhanc ed propensity to form monocyte-platelet aggregates. Background. Platel et-dependent thrombosis and leukocyte infiltration into the vessel wal l are characteristic cellular events seen in atherosclerosis. Methods. Anticoagulated peripheral venous blood from 19 patients with stable C AD and 19 normal control subjects was incubated with or without variou s platelet agonists and analyzed by whole blood Bow cytometry, Results . Circulating degranulated platelets were increased in patients with C AD compared with control subjects (mean [+/-SEM] percent P-selectin-po sitive platelets: 2.1 +/- 0.2 vs, 1.5 +/- 0.2, p < 0.01) and were more reactive to stimulation with 1 mu mol/liter of adenosine diphosphate (ADP) (28.7 +/- 3.9 vs. 16.1 +/- 2.2, p < 0.01), 1 mu mol/liter of ADP /epinephrine (51.4 +/- 4.6 vs, 37.5 +/- 3.8, p < 0.05) or 5 mu mol/lit er 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 circul ating monocyte-platelet aggregates compared with control subjects (per cent platelet positive monocytes: 15.3 +/- 3.0 Vs, 6.3 +/- 0.9, p < 0. 01), Furthermore, patients with stable CAD formed more monocyte-platel et aggregates than did control subjects when their whole blood was sti mulated with 1 mu mol/liter of ADP (50.4 +/- 4.5 vs. 28.1 +/- 5.3, p < 0.01), 1 mu mol/liter of ADP/epinephrine (60.7 +/- 4.3 vs. 48.0 +/- 4 .8, p < 0.05) or 5 mu mol/liter of TRAP (67.6 +/- 5.7 vs, 34.3 +/- 7.0 , p < 0.01), Conclusions. Patients with stable CAD have circulating ac tivated platelets, circulating monocyte platelet aggregates, increased platelet reactivity and an increased propensity to form monocyte-plat elet aggregates. (C) 1998 by the American College of Cardiology.