Mind the Heart: Stress-Associated Neural Activity Associates With Perivascular Coronary Inflammation and Vulnerable Plaque Features.
Mind the Heart: Stress-Associated Neural Activity Associates With Perivascular Coronary Inflammation and Vulnerable Plaque Features.
复制标题
注意心脏：压力相关的神经活动与血管周围冠状动脉炎症和易损斑块特征相关。
DOI：
10.1016/j.jcmg.2023.05.004
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Tawakol,Ahmed
中科院分区：
文献类型：
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作者：
Osborne,MichaelT;Tawakol,Ahmed
慢性社会心理压力对心血管疾病（CVD）的归因风险与主要的经典CVD风险因素（如高血压和糖尿病）相似。最近的研究已经阐明了将慢性压力和应激条件与心血管疾病联系起来的脑-心联系的重要机制。这种联系涉及一条神经免疫通路，它是由与压力感知相关的神经结构的改变引发的，这种改变导致交感神经系统（SNS）和下丘脑-垂体-肾上腺轴的激活。由于SNS直接支配骨髓和动脉，SNS活动增加导致白细胞生成和炎症增加，以及血管功能受损和凝血升高，这些共同加剧动脉粥样硬化和心血管疾病。需要对这种心脑联系进行更多的研究。神经成像技术已被应用于研究这些机制。在18f -氟脱氧葡萄糖-正电子发射断层扫描（18F-FDG-PET）成像中，一种反复被证明可以预测心血管疾病的神经测量方法包括评估杏仁核（边缘系统中一个重要的恐惧中心）与皮层（一个调节恐惧反应的大脑区域）代谢活动的平衡。考虑到皮质活动在压力信号传递中所起的重要作用，这个比值以前被称为“杏仁核活动”，现在更适合称为“压力相关神经活动”（SNA）。SNA与感知压力、社会经济压力源和交通噪声暴露有关。4-7此外，SNA与CVD危险因素（即糖尿病和内脏脂肪）、全身炎症升高、骨髓活性（BMA）和18F-FDGPET动脉炎症、冠状动脉计算机断层血管造影（CCTA）非钙化斑块负担以及不良CVD事件（包括心肌梗死、中风和takotsubo综合征）相关。4,7 -11此外，中介分析表明，SNA与CVD风险通过一系列途径相关，包括更大的BMA和动脉炎症。尽管这些发现支持慢性应激与CVD之间存在神经免疫通路，但仍存在一个重要的知识缺口，例如应激神经生物学改变是否会增强冠状动脉炎症，以及这是否通过驱动高风险冠状动脉斑块（HRP）特征导致CVD。CCTA为无创评估几种冠状动脉特征提供了独特的机会。除了可以量化斑块负担外，CCTA还可以测量冠状动脉周围脂肪衰减指数（FAI）和评估HRP特征。12-14 FAI提供了血管周围脂肪组织（PVAT）炎症的评估，这与HRP特征的后续发展有关。因此，更完整地描述在SNA增加的情况下冠状动脉粥样硬化的变化，将对慢性应激和心血管疾病之间的炎症机制产生新的见解。
Chronic psychosocial stress carries a similar attributable risk for cardiovascular disease (CVD) as major classical CVD risk factors, such as hypertension and diabetes. 1 Recent research has illuminated important mechanisms underlying the brain-heart connection that links chronic stress and stress conditions to CVD. This connection involves a neuroimmune pathway that is triggered by alterations of neural structures related to stress perception that result in activation of the sympathetic nervous system (SNS) and hypothalamicpituitary-adrenal axis. 2 Because the SNS directly innervates the bone marrow and arteries, increased SNS activity results in greater leukopoiesis and inflammation as well as impaired vascular function and heightened coagulation, which together potentiate atherosclerosis and CVD. 2, 3 More research into this heart-brain connection is needed. Neuroimaging techniques have been applied to study these mechanisms. One neural measure that has repeatedly been shown to predict CVD involves an assessment of the balance of metabolic activity of the amygdala, an important fear center within the limbic system, to that of the cortex, a regulatory brain region that modulates the fear response, on 18F-fluorodeoxyglucose–positron emission tomography (18F-FDG-PET) imaging. 4 This ratio, which was previously named “amygdalar activity,” is better referred to as stress-associated neural activity (SNA), given the important role that cortical activity plays in stress signaling. SNA is related to perceived stress, socioeconomic stressors, and transportation noise exposure. 4-7 Furthermore, SNA associates with CVD risk factors (ie, diabetes and visceral adiposity), heightened systemic inflammation, bone marrow activity (BMA) and arterial inflammation on 18F-FDGPET, noncalcified plaque burden on coronary computed tomographic angiography (CCTA), and adverse CVD events including myocardial infarctions, strokes, and takotsubo syndrome. 4, 7-11 Moreover, mediation analyses suggest that SNA associates with CVD risk through a serial path involving greater BMA and arterial inflammation. 4 Although these findings support the existence of a neuroimmune pathway linking chronic stress to CVD, an important knowledge gap remains, such as whether altered stress neurobiology potentiates coronary artery inflammation and whether this leads to CVD by driving highrisk coronary plaque (HRP) features. CCTA provides a unique opportunity to noninvasively evaluate several coronary features. Beyond allowing quantification of plaque burden, CCTA enables measurement of peri-coronary fat attenuation index (FAI) and evaluation of HRP features. 12-14 FAI provides an assessment of inflammation in perivascular adipose tissue (PVAT) that associates with the subsequent development of HRP features. 13 Accordingly, a more complete characterization of the coronary atherosclerotic changes present in the setting of increased SNA would yield novel insights into the inflammatory mechanisms linking chronic stress and CVD.