Department of Consultation-Liaison Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Max Planck Institute of Psychiatry, Munich, Germany.
Ann Behav Med. 2020 Aug 8;54(8):611-618. doi: 10.1093/abm/kaaa001.
Depressed patients have an increased risk of myocardial infarction, for which acute stress is a frequent trigger. Prothrombotic changes could be one involved mechanism that can be modulated by psychological coping.
We examined the effects of remitted major depression and situation-specific coping strategies on stress-induced coagulation activation.
Forty patients with remitted depression and 23 healthy controls underwent the Trier Social Stress Test, rating applied coping strategies thereafter. Blood was sampled at baseline and 15 and 45 min poststress to measure fibrinogen, von Willebrand factor (VWF) and D-dimer. Coagulation activation over time was quantified as area under the curve (AUC) with respect to baseline activity. Standardized z-scores of individual coagulation AUC measures were added up to a prothrombotic index.
Stress provoked significant VWF (p = .024) and D-dimer (p = .002) responses. Remitted depressed patients used positive distraction coping more frequently than controls did (p = .030). Coagulation AUC measures were similar in both groups. In all participants, higher positive coping total (p = 0.009), driven by devaluation/defense (p = .022) and distraction (p = .004) coping, was associated with a lower prothrombotic index. In controls, but not in remitted depressed patients, higher positive coping total (p = .008), driven by higher devaluation/defense (p = .010) and distraction (p = .023) coping, was associated with lower VWF AUC.
Despite the use of favorable coping strategies in a specific stress situation, remitted depressed patients may benefit less from a positive effect of positive situational coping on coagulation activation than controls. Such a mechanism could partially explain the increased risk of myocardial infarction in depressed individuals.
抑郁患者发生心肌梗死的风险增加，急性应激是常见的诱因。促血栓形成改变可能是一种相关机制，可以通过心理应对进行调节。
我们研究了缓解期抑郁症和特定情境应对策略对应激诱导的凝血激活的影响。
40 例缓解期抑郁症患者和 23 例健康对照者接受特里尔社会应激测试，随后对应用的应对策略进行评分。在基线和应激后 15 分钟和 45 分钟采血，以测量纤维蛋白原、血管性血友病因子（VWF）和 D-二聚体。用相对于基线活性的曲线下面积（AUC）来量化凝血激活随时间的变化。将个体凝血 AUC 测量的标准化 z 分数相加得到一个促血栓形成指数。
应激引起了 VWF（p =.024）和 D-二聚体（p =.002）的显著反应。缓解期抑郁症患者比对照组更频繁地使用积极的分散注意力应对策略（p =.030）。两组的凝血 AUC 测量值相似。在所有参与者中，更高的积极应对总分（p = 0.009），主要由贬低/防御（p =.022）和分散注意力（p =.004）应对驱动，与较低的促血栓形成指数相关。在对照组中，但在缓解期抑郁症患者中并非如此，更高的积极应对总分（p =.008），主要由更高的贬低/防御（p =.010）和分散注意力（p =.023）应对驱动，与较低的 VWF AUC 相关。
尽管在特定的应激情况下使用了有利的应对策略，但缓解期抑郁症患者可能不像对照组那样从积极的情境应对对凝血激活的积极影响中获益更多。这种机制可能部分解释了抑郁个体心肌梗死风险增加的原因。
