Schroeder Verena, Borner Urs, Gutknecht Stefan, Schmid Jean-Paul, Saner Hugo, Kohler Hans P
Laboratory for Thrombosis Research, Department of Clinical Research, University of Bern, Bern, Switzerland.
Eur J Cardiovasc Prev Rehabil. 2007 Dec;14(6):782-7. doi: 10.1097/HJR.0b013e32828622e8.
It has been suggested that changes in blood coagulation and fibrinolysis might explain the observed association between depression and coronary artery disease (CAD). So far, only a few coagulation factors have been investigated in this regard, and the results were not consistent.
The aim of our study was to analyse a broad range of coagulation and fibrinolytic factors, with emphasis on factors directly involved in clot formation and degradation or reflecting coagulation activation, in patients with CAD and controls without CAD, as assessed by coronary angiography, who also underwent a diagnostic procedure for depression.
We screened 306 patients with CAD and controls without CAD for depression using the Hospital Anxiety and Depression Scale and Allgemeine Depressions Skala-L questionnaires. In participants with positive screening result, diagnosis of major depression was confirmed or excluded by a structured interview. We analysed the following coagulation and fibrinolytic factors: fibrinogen, prothrombin fragment F1+2, factor XIII A-subunit, factor XIII B-subunit, tissue plasminogen activator, plasminogen activator inhibitor-1, thrombin-activable fibrinolysis inhibitor, and D-dimer.
We did not observe significant associations between depression and CAD, nor between depression and cardiovascular risk factors. Coagulation and fibrinolytic factors showed no differences between patients with CAD and controls, but they were associated with several cardiovascular risk factors. Depression was not associated with coagulation and fibrinolytic factors. No associations were found either when both CAD and depression were taken into account.
Our study gives no evidence that there is a significant relation among depression, CAD, and blood coagulation and fibrinolysis.
有人提出，凝血和纤维蛋白溶解的变化可能解释了抑郁症与冠状动脉疾病（CAD）之间观察到的关联。到目前为止，在这方面仅对少数凝血因子进行了研究，结果并不一致。
我们研究的目的是分析广泛的凝血和纤维蛋白溶解因子，重点是直接参与血栓形成和降解或反映凝血激活的因子，这些因子来自经冠状动脉造影评估的CAD患者和无CAD的对照组，他们也接受了抑郁症诊断程序。
我们使用医院焦虑和抑郁量表以及一般抑郁量表-L问卷对306例CAD患者和无CAD的对照组进行抑郁症筛查。对于筛查结果呈阳性的参与者，通过结构化访谈确认或排除重度抑郁症的诊断。我们分析了以下凝血和纤维蛋白溶解因子：纤维蛋白原、凝血酶原片段F¹+₂、因子XIII A亚基、因子XIII B亚基、组织纤溶酶原激活剂、纤溶酶原激活剂抑制剂-1、凝血酶激活的纤维蛋白溶解抑制剂和D-二聚体。
我们未观察到抑郁症与CAD之间、抑郁症与心血管危险因素之间存在显著关联。CAD患者和对照组之间的凝血和纤维蛋白溶解因子无差异，但它们与几种心血管危险因素相关。抑郁症与凝血和纤维蛋白溶解因子无关。当同时考虑CAD和抑郁症时，也未发现关联。
我们的研究没有证据表明抑郁症、CAD与凝血和纤维蛋白溶解之间存在显著关系。
