Platelet Activation by Emotional Stress in Patients With Coronary Artery Disease

Grignani, Guido MD
Soffiantino, Francesco MD
Zucchella, Marisa MD
Pacchiarini, Lucia MD
Tacconi, Fiorenzo MD
Bonomi, Elisabetta MD
Pastoris, Aronne CD
Sbaffi, Andrea MD
Fratino, Pietro MD
Tavazzi, Luigi MD, FESC, FACC

From the Department of Internal Medicine (G.G., M.Z., L.P., F.T., E.B., P.F.), Section of Medical Pathology, University of Pavia, the Division of Cardiology (F.S., L.T.), “Clinica del Lavoro” Foundation, Medical Center of Rehabilitation, Institute of Care and Research, Veruno (Novara), and the Clinical Analysis Laboratory (A.P., A.S.), USSL 54, “S.S. Trinita” Hospital, Borgomanero (Novara), Italy.

Address for correspondence: Dr. Guido Grignani, Department of Internal Medicine, Section of Medical Pathology, University of Pavia, 27100 Pavia, Italy.

Circulation 83(4):p II-136, April 1991.

We studied the effects of experimentally induced emotional stress (mental arithmetic) on different hemodynamic parameters, catecholamine levels, and serum and platelet function tests in 25 postinfarction patients and in 10 apparently healthy, age-matched control subjects. Mental stress (10 minutes) induced significant increments in heart rate, systolic blood pressure, diastolic blood pressure, double product, and cardiac output, indicating a sympathoadrenal stimulation that was confirmed by a significant increase in serum epinephrine and norepinephrine levels. All of the effects disappeared at minute 10 of recovery. Concomitantly, the test produced a significant increase in platelet aggregation (induced by 3, uM ADP or 1, ug/ml collagen), the formation of circulating platelet aggregates, and an increase in thromboxane B2 levels in plasma and serum. These effects were also rapidly reversible. Similar activation of hemodynamic parameters and a similar but less evident increase in platelet function by emotional stress were observed in control subjects. A possible artifact due to factitious platelet activation by catheter sampling was excluded with experiments in which a 40-minute rest was introduced after the baseline period and before mental stress; platelet activation did not occur during baseline or rest periods, only after emotional stress. Furthermore, the antiplatelet drug dipyridamole reduced the stress-induced formation of platelet aggregates in postinfarction patients. These results demonstrate the existence of a direct link between emotional stress and platelet function and offer an explanation of one of the mechanisms through which mental stress may be involved in the development of coronary artery disease.