Bremner J Douglas, Piccinelli Marina, Garcia Ernest V, Moncayo Valeria M, Elon Lisa, Nye Jonathon A, Cooke C David, Washington Brianna P, Ortega Rebeca Alvarado, Desai Shivang R, Okoh Alexis K, Cheung Brian, Soyebo Britt O, Shallenberger Lucy H, Raggi Paolo, Shah Amit J, Daaboul Obada, Jajeh Mohamed Nour, Ziegler Carrie, Driggers Emily G, Murrah Nancy, De Cecco Carlo N, van Assen Marly, Krafty Robert T, Quyyumi Arshed A, Vaccarino Viola
Department of Psychiatry & Behavioral Sciences, Emory University School of Medicine, Atlanta, GA.
Department Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, GA.
Med Res Arch. 2023 Apr;11(4). doi: 10.18103/mra.v11i4.3787. Epub 2023 Apr 25.
Coronary heart disease is a leading cause of death and disability. Although psychological stress has been identified as an important potential contributor, mechanisms by which stress increases risk of heart disease and mortality are not fully understood. The purpose of this study was to assess mechanisms by which stress acts through the brain and heart to confer increased CHD risk.
Coronary Heart Disease patients (N=10) underwent cardiac imaging with [Tc-99m] sestamibi single photon emission tomography at rest and during a public speaking mental stress task. Patients returned for a second day and underwent positron emission tomography imaging of the brain, heart, bone marrow, aorta (indicating inflammation) and subcutaneous adipose tissue, after injection of [F]2-fluoro-2-deoxyglucose for assessment of glucose uptake followed mental stress. Patients with (N=4) and without (N=6) mental stress-induced myocardial ischemia were compared for glucose uptake in brain, heart, adipose tissue and aorta with mental stress.
Patients with mental stress-induced ischemia showed a pattern of increased uptake in the heart, medial prefrontal cortex, and adipose tissue with stress. In the heart disease group as a whole, activity increase with stress in the medial prefrontal brain and amygdala correlated with stress-induced increases in spleen (r=0.69, p=0.038; and r=0.69, p=0.04 respectfully). Stress-induced frontal lobe increased uptake correlated with stress-induced aorta uptake (r=0.71, p=0.016). Activity in insula and medial prefrontal cortex was correlated with post-stress activity in bone marrow and adipose tissue. Activity in other brain areas not implicated in stress did not show similar correlations. Increases in medial prefrontal activity with stress correlated with increased cardiac glucose uptake with stress, suggestive of myocardial ischemia (r=0.85, p=0.004).
These findings suggest a link between brain response to stress in key areas mediating emotion and peripheral organs involved in inflammation and hematopoietic activity, as well as myocardial ischemia, in Coronary Heart Disease patients.
冠心病是导致死亡和残疾的主要原因。虽然心理压力已被确认为一个重要的潜在因素，但压力增加心脏病风险和死亡率的机制尚未完全明确。本研究的目的是评估压力通过大脑和心脏增加冠心病风险的机制。
10名冠心病患者在静息状态下以及在公众演讲心理应激任务期间接受了[锝-99m]甲氧基异丁基异腈单光子发射断层扫描心脏成像。患者在第二天返回，在注射[氟]2-氟-2-脱氧葡萄糖后接受大脑、心脏、骨髓、主动脉（显示炎症）和皮下脂肪组织的正电子发射断层扫描成像，以评估心理应激后的葡萄糖摄取情况。比较了有（N = 4）和无（N = 6）心理应激诱导的心肌缺血的患者在心理应激状态下大脑、心脏、脂肪组织和主动脉的葡萄糖摄取情况。
有心理应激诱导缺血的患者在应激状态下心脏、内侧前额叶皮质和脂肪组织的摄取呈现增加模式。在整个心脏病组中，内侧前额叶脑区和杏仁核应激时的活动增加与应激诱导的脾脏增加相关（分别为r = 0.69，p = 0.038；r = 0.69，p = 0.04）。应激诱导的额叶摄取增加与应激诱导的主动脉摄取相关（r = 0.71，p = 0.016）。岛叶和内侧前额叶皮质的活动与应激后骨髓和脂肪组织的活动相关。其他与应激无关的脑区活动未显示类似的相关性。内侧前额叶活动随应激增加与应激时心脏葡萄糖摄取增加相关，提示心肌缺血（r = 0.85，p = 0.004）。
这些发现表明，在冠心病患者中，大脑在介导情绪的关键区域对应激的反应与参与炎症和造血活动的外周器官以及心肌缺血之间存在联系。
