Depressions and Mental Stress Ischemia: Brain Mechanisms

精神应激性缺血（MSI）的潜在机制尚未阐明， 哪些患者发生MSI的风险增加。特别是，利特菲是众所周知的心理 MSI相关。抑郁症通常与压力有关，影响约20%的CAD患者，是一种常见的疾病。 死亡和随后心脏事件的重要危险因素。抑郁症与未能 激活神经回路，包括前扣带回，内侧前额叶皮层的其他区域和 海马体，其具有对杏仁核的抑制性输入。杏仁核抑制的失败可能会导致 通过下丘脑-垂体-肾上腺的心血管和神经激素反应的外周激活 (HPA)轴和交感神经系统（SNS）。这些途径可能会增加 MSI与冠心病伴抑郁患者内皮损伤和血管阻力的关系。 我们提出了一种综合的方法来研究CAD患者的大脑和 抑郁症中涉及的神经激素途径导致对精神压力的异常心血管反应， 包括MSI和外周血管功能障碍。我们的中心假设是抑郁症， 与抑郁症相关的神经生物学途径在精神应激诱导的缺血中发挥着重要作用。我们 我还假设这些相同的神经生物学通路参与外周血管功能障碍 在精神压力下。本研究的目的是：1）评估MSI与抑郁症的关系。（二） 使用正电子发射断层扫描（PET）和0-15水，评估CAD患者中MSI的脑部相关性。第三章 使用正电子发射断层扫描（PET）和0-15水，评估周围血管的脑相关性 在精神压力下的功能（血管收缩，动脉僵硬和反应性充血）。我们假设 抑郁症在患有MSI的患者中比那些没有患MSI的患者更常见， 在抑郁症（前扣带、海马）中，对应激激素系统具有抑制功能， 在患有MSI的患者中， 在精神压力下发生外周血管功能障碍的患者。对于目标1， MSI和抑郁症将在我们的PPG中对所有650名参与者进行评估。对于目标2和3，我们将选择80个 来自650名患者的汇总中的患有MSI的受试者和80名没有MSI的受试者。每例受试者将接受PET 大脑扫描结合精神压力和计数控制使用既定的方法。

The mechanisms underlying mental stress ischemia (MSI) have not yet been elucidated, and it is not known which pafients are at increased risk of developing MSI. In particular, litfie is known about the psychological correlates of MSI. Depression, which is often linked to stress, affects about 20% of patients with CAD and is an important risk factor for death and subsequent cardiac events. Depression is associated with a failure to activate a neural circuit including the anterior cingulate, other areas of the medial prefrontal cortex and the hippocampus, which have inhibitory inputs to the amygdala. Failure of inhibition of the amygdala could result in peripheral activation of cardiovascular and neurohormonal responses through the hypothalamus-pituitaryadrenal (HPA) axis and the sympathetic nervous system (SNS). These pathways could increase the risk of MSI and contribute to endothelial damage and vascular resistance in CAD patients with depression. We propose a comprehensive approach to study the mechanisms by which, in CAD patients, the brain and neurohormonal pathways involved in depression lead to abnormal cardiovascular responses to mental stress, including MSI and peripheral vascular dysfuncfion. Our central hypothesis is that depression, and neurobiological pathways linked to depression, play an important role in mental stress-induced ischemia. We also hypothesize that these same neurobiological pathways are involved in peripheral vascular dysfunction during mental stress. The aims of this project are: 1) Assess the relationship between MSI and depression. 2) Using positron emission tomography (PET) and 0-15 water, assess brain correlates of MSI in CAD patients. 3) Using positron emission tomography (PET) and 0-15 water, assess brain correlates of peripheral vascular function during mental stress (vasoconstriction, arterial stiffness and reactive hyperemia). We hypothesize that depression is more common in patients who develop MSI than those who do not, and that brain areas involved in depression (anterior cingulate, hippocampus) that have inhibitory function on stress hormonal systems with pathways to the heart, will show decreased function during mental stress in patients who develop MSI and patients who develop peripheral vascular dysfunction during mental stress. For Aim 1, the relationship between MSI and depression will be assessed in all 650 participants in our PPG. For Aims 2 and 3, we will select 80 subjects with MSI and 80 subjects without MSI from the pool of 650 patients. Each subject will undergo PET scanning of the brain in conjunction with mental stress and a counting control using established methods.