Department of Psychiatry and Behavioral Sciences.
Department of Medicine.
Health Psychol. 2019 Oct;38(10):910-924. doi: 10.1037/hea0000742. Epub 2019 Aug 5.
Coronary artery disease (CAD) patients with comorbid depression show an increase in mortality compared to cardiac patients without depression, but the mechanisms mediating this effect remain obscure. One possible explanation for this finding is that depressed patients with CAD exhibit an increased vulnerability to stress. The purpose of this study was to assess the effects of stress and depression on brain function and to explore its relationship with myocardial ischemia in CAD patients.
Patients with CAD and depression ( = 13) and CAD without depression ( = 15) underwent imaging of the brain with positron emission tomography and [O-15] water and imaging of the heart with single photon emission computed tomography (SPECT) and [Tc-99] sestamibi under mental stress task and control conditions.
CAD patients with depression compared to nondepressed showed decreased function with mental stress in the rostral anterior cingulate, the hippocampus, parts of the dorsolateral temporal and parietal cortex, the cerebellum, and the uncus, with increased blood flow in the parahippocampus, visual association cortex, and posterior cingulate. Depressed CAD patients who became ischemic during a mental stress task had relative decreases in the caudal and posterior cingulate, orbitofrontal cortex, and cerebellum, and increased activation in the parietal cortex and precuneus/visual association cortex compared to nonischemic depressed CAD patients.
These findings are consistent with dysfunction in a network of brain regions involved in the stress response in patients with comorbid CAD and depression that has direct and indirect links to the heart, suggesting a pathway by which stress and depression could lead to increased risk of heart disease related morbidity and mortality. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
与无抑郁的心脏病患者相比,合并抑郁的冠心病患者的死亡率增加,但介导这种效应的机制仍不清楚。这一发现的一个可能解释是,合并 CAD 的抑郁患者对压力的易感性增加。本研究旨在评估压力和抑郁对大脑功能的影响,并探讨其与 CAD 患者心肌缺血的关系。
对 13 例合并抑郁的 CAD 患者和 15 例无抑郁的 CAD 患者进行正电子发射断层扫描和[O-15]水以及单光子发射计算机断层扫描(SPECT)和[Tc-99] sestamibi 进行心脏成像,在心理应激任务和对照条件下进行。
与非抑郁组相比,抑郁的 CAD 患者在额前扣带回、海马、背外侧颞叶和顶叶皮质的部分、小脑和钩回在精神应激时功能下降,而在海马旁回、视觉联合皮质和后扣带回血流增加。在心理应激任务中发生缺血的抑郁性 CAD 患者与非缺血性抑郁性 CAD 患者相比,后扣带回、眶额皮质和小脑相对减少,顶叶皮质和楔前叶/视觉联合皮质激活增加。
这些发现与合并 CAD 和抑郁的患者中参与应激反应的大脑区域网络功能障碍一致,这些区域与心脏有直接和间接的联系,提示应激和抑郁可能导致与心脏病相关的发病率和死亡率增加的途径。(PsycINFO 数据库记录(c)2019 APA,保留所有权利)。