ORIGINAL ARTICLESEnhanced platelet/endothelial activation in depressed patients with acute coronary syndromes: evidence from recent clinical trialsSerebruany, Victor La; Glassman, Alexander Hb; Malinin, Alex Ia; Sane, David Cc; Finkel, Mitchell Sd; Krishnan, Ranga Re; Atar, Danf; Lekht, Vladimira; O'Connor, Christopher MeAuthor Information aSinai Center for Thrombosis Research, Johns Hopkins University, Baltimore, Maryland, bColumbia University, New York, New York, cWake Forest University, Winston-Salem, North Carolina, dWest Virginia University, Morgantown, West Virginia, eDuke University Medical Center, Durham, North Carolina, USA and fAker University, Oslo, Norway. Correspondence and requests for reprints to Dr Victor L. Serebruany, Center for Thrombosis Research, Sinai Hospital of Baltimore, 2401 West Belvedere Avenue, Schapiro Research Building — R 202, Baltimore, MD 21215, USA. Tel: +1 410 601 5266; fax: +1 410 601 9061; e-mail: Heartdrug@aol.com Received 27 November 2002 Revised 7 March 2003 Accepted 18 March 2003 Blood Coagulation & Fibrinolysis: September 2003 - Volume 14 - Issue 6 - p 563-567 Buy Abstract Platelets play a key role in the progression of acute coronary syndromes (ACS). Clinical depression alone is also associated with enhanced platelet activation. The purpose of this study was to compare concentrations of established biomarkers of enhanced platelet/endothelial activation in clinically depressed versus non-depressed patients enrolled in recent clinical trials for ACS. Two hundred and eighty-one baseline plasma samples from patients with acute myocardial infarction (ASSENT-2; n = 41), with ACS (PRONTO; n = 126) and with clinical depression plus previous acute coronary syndrome within 6 months (SADHART; n = 64), and from normal healthy controls (n = 50) were analyzed. Blood was drawn before applying any therapeutic strategies including interventions, thrombolytics, infusions, and selective serotonin re-uptake inhibitors. Platelet factor 4, β-thromboglobulin, platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane, prostacyclin, vascular cell adhesion molecule-1, and E-selectin were measured by enzyme-linked immunosorbent assay by a single core laboratory. Patients with ACS exhibited a higher degree of platelet activation than controls independently of the presence of depression. Plasma levels of P-selectin, thromboxane, prostacyclin, and vascular cell adhesion molecule-1 were the highest in the acute myocardial infarction group when compared with ACS despite the presence or absence of clinical depression. Surprisingly, patients with ACS and depression exhibited the highest levels of platelet factor 4, β-thromboglobulin, and platelet/endothelial cell adhesion molecule-1 when compared with myocardial infarction or angina patients without clinical depression. E-selectin plasma level was constantly elevated compared with controls but did not differ among the groups dependent on the incidence of depression. The depressed plus ACS group had higher plasma levels of all biomarkers compared with the non-depressed patients. Retrospective analysis of the data from several clinical trials reveals that clinical depression is associated with enhanced activation of platelet/endothelial biomarkers even above the level expected in ACS. These findings may contribute to the unfavorable outcome associated with clinical depression in patients with ACS. © 2003 Lippincott Williams & Wilkins, Inc.