[Changes in blood coagulation in stress and depression--from evolution to gene regulation].
Mental stress and depression are characterized by a hypercoagulable state, which might mediate the increased coronary risk in individuals who feel stressed or depressed. Changes in blood coagulation and fibrinolysis with stress and depression are largely mediated by the sympathetic nervous system via catecholamine and adrenergic receptor activity. Stress might also affect coagulation activity via an influence on the regulation of genes coding for coagulation and fibrinolysis molecules. There is some evidence that non-selective beta-blocking agents decrease hypercoagulability elicited by acute stress. The selective serotonin reuptake inhibitors appear to normalize increased platelet activity in depression. Prospective studies need to show whether there is an association between coagulation abnormalities in stress and depression with hard cardiovascular end-points and whether such an association is favorably affected by therapeutic interventions (e.g., medication, psychotherapy, stress management).
von Känel
R
R
Institut für Verhaltenswissenschaft, Eidgenössische Technische Hochschule Zürich. roland.vonkaenel@ifv.gess.ethz.ch
D000818:Animals; D001143:Arousal / Q000235:genetics / Q000502:physiology; D005075:Biological Evolution; D001777:Blood Coagulation / Q000235:genetics* / Q000502:physiology; D003328:Coronary Thrombosis / Q000097:blood / Q000523:psychology; D003866:Depressive Disorder / Q000097:blood* / Q000523:psychology; D005342:Fibrinolysis / Q000235:genetics / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D013315:Stress, Psychological / Q000097:blood / Q000150:complications*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D019851:Thrombophilia / Q000097:blood / Q000235:genetics*