The Association of Autonomic Dysfunction with the Relationship between Depression and Coronary Disease

A3.项目摘要 并发抑郁症和冠状动脉疾病(CAD)导致心血管疾病增加三倍 死亡，但这种病理背后的机制仍然知之甚少。这是重大的公共卫生问题 抑郁症仍然是全球残疾的主要原因，而冠心病是导致死亡的主要原因。向上 每5名冠心病患者中就有1名患有共病抑郁，但增加筛查的干预措施 抑郁和通过传统方法进行治疗并没有显示出对总体结果的任何影响。一个 抑郁症和冠心病的潜在机制是自主神经系统(ANS)功能障碍。 例如，迷走神经刺激可以改善顽固性抑郁，减轻缺血引起的胸痛。 心脏病，这表明存在着强烈的共同生物关系。心率变异性(HRV)服务 作为自主神经功能的心电生物标志物，通过测量交感神经和 副交感神经流出至心脏的窦房结。心率变异性低代表自主神经功能障碍。我们 已经表明，一种新的心率变异性测量方法DYX有望成为预测心肌异常的指标 血流灌注，并在初步分析表明与抑郁有关。我们致力于发掘 心率变异性作为研究抑郁和抑郁等中枢过程功能障碍的一种手段 外周心血管反射与阻塞性冠心病的关系。我们假设低心率变异性将是 与抑郁症和冠状动脉疾病呈剂量-反应关系，而这 关系将根据年龄和性别进行修改。在对这一队列的初步研究中，初步数据表明 协会是存在的。为了充分描述抑郁症、冠心病和ANS功能障碍之间的这种联系，我们 将研究200名同时患有抑郁症和冠心病的参与者的心率变异性变化， 或者两者都不是。目的1将DYX测量的抑郁症状负担与ANS功能障碍进行比较 在其他HRV措施中。目标2将比较阻塞性冠心病和ANS功能障碍的存在 由DYX测量。年龄、性别和心率变异测量的时间与结果的交互作用将是 考虑过了。拟议的分析将提供可信的证据，证明ANS功能障碍与这两种疾病有关 抑郁症和冠心病，长期目标是确定针对ANS功能障碍的干预措施，以减少 死亡率。

A3. PROJECT ABSTRACT Comorbid depression and coronary artery disease (CAD) lead to a three-fold increase in cardiovascular mortality, but the mechanisms behind this pathology remain poorly understood. This is major public health issue as depression remains a leading cause of disability globally and CAD is the leading cause of death. Up to 1 of every 5 patients with CAD have comorbid depression, yet interventions from increased screening for depression and treatment through traditional methods have not shown any impact on overall outcomes. A potential mechanistic pathway for depression and CAD is dysfunction of the autonomic nervous system (ANS). Vagal nerve stimulation, for example, improves refractory depression and reduces chest pain from ischemic heart disease, suggesting that strong shared biological relationships exist. Heart rate variability (HRV) serves as an electrocardiographic biomarker of autonomic function, by measuring the sympathetic and parasympathetic outflow to the sinoatrial node of the heart. Low HRV represents autonomic dysfunction. We have shown that that a novel HRV measure, Dyx, shows promise as a predictor of abnormal myocardial perfusion, and in preliminary analysis shows a relationship with depression. We seek to explore the potential of HRV to serve as a means of investigating dysfunction of both central processes such as depression and peripheral cardiovascular reflexes as they relate to obstructive CAD. We hypothesize that low HRV will be associated with both depression and coronary artery disease in a dose-response manner, and that this relationship will be modified by age and sex. In the pilot study on this cohort, preliminary data that these associations exist. To fully characterize this association between depression, CAD, and ANS dysfunction, we will examine the changes in HRV in a cohort of 200 participants with both depression and CAD, either disease, or neither. Aim 1 will compare the depressive symptom burden with ANS dysfunction as measured by Dyx amongst other HRV measures. Aim 2 will compare the presence of obstructive CAD with ANS dysfunction as measured by Dyx. The interaction of age, sex, and time of day of HRV measurement with the findings will be considered. The proposed analyses will provide plausible evidence that the ANS dysfunction links both depression and CAD, with the long-term goal of identifying interventions that target ANS dysfunction to reduce mortality.