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

From the 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.

Address correspondence and reprint requests to Graham J. Reid, University of Western Ontario, Westminster Hall, Room 319E, London ON N6A 3K7. E-mail: greid{at}uwo.ca

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 β-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.

Key Words: platelet activation • mental stress • psychological stress • reactivity

Abbreviations: ACE = angiotensin-converting enzyme; ASA = acetylsalicylic acid; CAD = coronary artery disease; BDI = Beck Depression Inventory; BP = blood pressure; bpm = beats per minute; BTG = β-thromboglobulin; DBP = diastolic blood pressure; FDR = false discovery rate; GP = glycoprotein; HR = heart rate; MLD = minimum lumen diameter; MI = myocardial infarction; MNC = mononuclear cells; NE = norepinephrine; PCI = percutaneous coronary interventions; SBP = systolic blood pressure; STAEI = State-Trait Anger Expression Inventor.