Mental Stress-Induced Platelet Activation Among Patients With Coronary Artery Disease.

Author: Reid GJ, Seidelin PH, Kop WJ, Irvine MJ, Strauss BH, Nolan RP, Lau HK, Yeo EL.
Affiliation:
Department of Psychology (G.J.R.), University of Western Ontario, London, Ontario, Canada; Department of Family Medicine (G.J.R.), University of Western Ontario, London, Ontario, Canada; Public Health Science (G.J.R.), University of Toronto, Toronto, Ontario, Canada; Medicine (G.J.R., P.H.S., B.H.S., H.K.L., E.L.Y.), University of Toronto, Toronto, Ontario, Canada; University Health Network (G.J.R., P.H.S., M.J.I., R.P.N., E.L.Y.), Toronto, Ontario, Canada; Division of Cardiology (W.J.K.), University of Maryland Medical Center, Baltimore, Maryland; Department of Psychology (M.J.I.), York University, Toronto, Ontario, Canada; Schulich Heart Center (B.H.S.), Sunnybrook Health Sciences Center, Toronto, Ontario, Canada; Institute of Medical Sciences and the Department of Psychiatry (R.P.N.), University of Toronto, Toronto, Ontario, Canada; Division of Hematology and Oncology (H.K.L.), St. Michael\'s Hospital, Toronto, Ontario, Canada.
Conference/Journal: Psychosom Med.
Date published: 2009 Feb 27
Other: Word Count: 189


Objective: To study patients with coronary artery disease (CAD) scheduled for coronary angioplasty and to examine platelet activation in response to mental stress as a potential mechanism involved in the association between psychosocial factors and cardiac outcomes. Psychosocial factors have been identified as risk factors for CAD and adverse cardiac outcomes, although the underlying mechanisms are poorly understood. Methods: Markers of platelet activation and platelet reactivity in response to experimentally induced mental stress (mental arithmetic and anger recall) were examined, using flow cytometry analysis and beta-thromboglobulin (BTG) assays among 249 CAD patients (age = 60.3 +/- 9.0 years, 15% women) who were scheduled to undergo elective percutaneous coronary intervention. Results: Mental stress-induced increases in platelet activation (CD41 (GP IIb/IIIa), p = .002; percent of mononuclear cells positive for CD41, p = .01; CD62P (P-selectin) expression, p = .005; and percent platelets positive for CD62P, p < .001). The degree of platelet reactivity was not related to demographic, clinical, or psychological variables, or cardiovascular hemodynamic changes. Conclusions: Experimentally induced mental stress induced platelet activation in patients with CAD. This mechanism may partially explain the link between psychosocial variables and the development of adverse cardiac outcomes in patients with CAD.

BACK