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ORIGINAL ARTICLES |
From the Department of Clinical Psychology and Psychotherapy (P.H.W., U.E.), University of Zurich, Switzerland; Department of Medicine (L.S.R.), Cardiology Branch, University of California, San Diego, California; and the Department of General Internal Medicine (R.v.K.), Bern University Hospital, Inselspital, and University of Bern, Bern, Switzerland.
Address correspondence and reprint requests to Petra H. Wirtz, Department of Clinical Psychology and Psychotherapy, University of Zurich, Binzmühlestrasse 14, Box 26, CH-8050 Zurich, Switzerland. E-mail: p.wirtz{at}psychologie.uzh.ch
Objective: To investigate the relationship between social support and coagulation parameter reactivity to mental stress in men and to determine if norepinephrine is involved. Lower social support is associated with higher basal coagulation activity and greater norepinephrine stress reactivity, which in turn, is linked with hypercoagulability. However, it is not known if low social support interacts with stress to further increase coagulation reactivity or if norepinephrine affects this association. These findings may be important for determining if low social support influences thrombosis and possible acute coronary events in response to acute stress. We investigated the relationship between social support and coagulation parameter reactivity to mental stress in men and determined if norepinephrine is involved.
Methods: We measured perceived social support in 63 medication-free nonsmoking men (age (mean ± standard error of the mean) = 36.7 ± 1.7 years) who underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma D-dimer, fibrinogen, clotting Factor VII activity (FVII:C), and plasma norepinephrine at rest as well as immediately after stress and 20 minutes after stress.
Results: Independent of body mass index, mean arterial pressure, and age, lower social support was associated with higher D-dimer and fibrinogen levels at baseline (p < .012) and with greater increases in fibrinogen (β = –0.36, p = .001; 
R2 = .12), and D-dimer (β = –0.21, p = .017; R2 = .04), but not in FVII:C (p = .83) from baseline to 20 minutes after stress. General linear models revealed significant main effects of social support and stress on fibrinogen, D-dimer, and norepinephrine (p < .035). Controlling for norepinephrine did not change the significance of the reported associations between social support and the coagulation measures D-dimer and fibrinogen.
Conclusions: Our results suggest that lower social support is associated with greater coagulation activity before and after acute stress, which was unrelated to norepinephrine reactivity.
Key Words: social support • coagulation • clotting factor VII:C • D-dimer • fibrinogen • psychological stress
Abbreviations: CVD = cardiovascular disease; ACS = acute coronary syndromes; BMI = body mass index; MAP = mean arterial pressure; BP = blood pressure; SD = standard deviation; AUC = area under the curve; TSST = Trier Social Stress Test; FVII:C = clotting Factor VII activity; FVIII:C = clotting Factor VIII activity.
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