von Känel R
Institut für Verhaltenswissenschaft, Eidgenössische Technische Hochschule Zürich.
Ther Umsch. 2003 Nov;60(11):682-8. doi: 10.1024/0040-5930.60.11.682.
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).
精神压力和抑郁的特征是高凝状态,这可能介导了感到压力或抑郁的个体冠心病风险的增加。压力和抑郁导致的血液凝固和纤维蛋白溶解变化很大程度上由交感神经系统通过儿茶酚胺和肾上腺素能受体活性介导。压力也可能通过影响凝血和纤维蛋白溶解分子编码基因的调控来影响凝血活性。有证据表明,非选择性β受体阻滞剂可降低急性应激引起的高凝性。选择性5-羟色胺再摄取抑制剂似乎可使抑郁症中增加的血小板活性恢复正常。前瞻性研究需要表明,压力和抑郁中的凝血异常与严重心血管终点之间是否存在关联,以及这种关联是否受到治疗干预(如药物治疗、心理治疗、压力管理)的有利影响。