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Effects of Psychological Stress and Psychiatric Disorders on Blood Coagulation and Fibrinolysis

A Biobehavioral Pathway to Coronary Artery Disease?

From the Departments of Psychiatry (P.J.M., J.E.D.) and Medicine (C.F.), University of California, San Diego, California and the Division of Psychosocial Medicine (R.v.K.), University Hospital, Zurich, Switzerland.

View larger version (27K): [in a new window]   Fig. 1. The scheme depicts coagulation pathways in the solid lines (—) and fibrinolysis pathways in the dashed lines (– – –). Anticoagulant steps are drawn in dash-dotted lines (-·-·-). Roman numerals indicate coagulation factors. Prethrombotic markers of a hypercoagulable state are depicted in boxes. a2-AP = 2-antiplasmin, AT III = antithrombin III, DD = fibrin D-dimer, F1+2 = prothrombin fragments 1+2, FDP = fibrinogen/fibrin degradation products, FPA = fibrinopeptide A, PAP = plasmin-2-antiplasmin complex, t-PA = tissue plasminogen activator, PAI-1 = type 1 plasminogen activator inhibitor, and vWF = von Willebrand factor. The sign "" indicates inhibition steps of thrombin, plasmin, and t-PA. See text for description and explanation of circled numbers.

View larger version (28K): [in a new window]   Fig. 2. A, weekly incidents of newly referred patients with myocardial infarction before and after the earthquake. The admission rate was about 3.5-fold increased during the 4 weeks immediately after the disaster, compared with the mean incidence for each week of the previous 3 years. B, D-dimer levels were significantly increased 1 to 2 weeks after the earthquake, indicating activation of the coagulation cascade in response to the disaster. (Redrawn from Matsuo et al. [72] with permission.)