Mechanistic Understanding of Socioeconomic Disparities in Cardiovascular Disease.
Mechanistic Understanding of Socioeconomic Disparities in Cardiovascular Disease.
复制标题
对心血管疾病社会经济差异的机制理解。
DOI：
10.1016/j.jacc.2019.04.043
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发表时间：
2019
影响因子：
24
通讯作者：
Shimbo,Daichi
中科院分区：
文献类型：
--
作者：
Miller,GregoryE;Chen,Edith;Shimbo,Daichi
一个多世纪以来，人口统计学家一直注意到发病率和死亡率方面的社会经济差异。但是，直到 Marmot 对英国公务员的开创性研究在 20 世纪 80 年代开始出现 (1, 2)，社会经济地位 (SES) 作为心血管危险因素才开始受到认真关注。在接下来的几年里，我们对这些差异的范围和规模有了很多了解 (3, 4)。差距很大，而且还在扩大。最近一项针对 2200 万成年人的荟萃分析显示，受教育程度低与心血管疾病 (CVD) 风险增加 42% 至 66% 有关(5, 6)。我们还深入了解了造成这些差异的各种机制的相对重要性。遗传变异和生活方式差异都发挥了作用，获得医疗保健的机会也起到了一定作用。然而，这些因素都不能完全解释这些差距 (7)。这些观察结果与表明对服从存在强烈、持久的生理反应的动物研究相结合，使得关注健康差异的研究人员推测，与低 SES 相关的压力源可能直接导致 CVD 发病机制 (8, 9)。与这一观点一致的是，研究发现低 SES 人群中多种 CVD 生物标志物的水平较高，包括内皮功能障碍、炎症和血小板活化 (9)。但是，这一假设缺乏令人信服的证据。在此背景下，本期杂志刊登了 Tawakol 等人 (10) 发表的一篇引人入胜且重要的报告，研究了将低 SES 与 CVD 风险联系起来的推定压力相关神经生物学途径。该论文利用一种称为中介路径分析的统计技术来整合有关邻近条件、全身 18F-氟脱氧葡萄糖正电子发射断层扫描/计算机断层扫描成像和 CVD 结果的数据。在此过程中，它提供了迄今为止最详细的机制解释，说明低SES（一种压力暴露）如何“进入体内”加速CVD进展。简而言之，结果表明，不利的社区社会经济地位因素，例如低中位收入和高犯罪率，会引起杏仁核的持续激活，杏仁核是一个主要参与判断外部刺激所构成威胁程度的大脑区域。反过来，杏仁核激活程度越高，骨髓中的代谢活动越强。根据之前的证据，作者认为这种联系是由交感神经系统介导的，交感神经系统在受到威胁的情况下会导致造血干细胞和祖细胞从骨髓中流出 (11-13)。这种与压力相关的祖细胞动员是有选择性的，并且以具有强烈促炎倾向的未成熟骨髓细胞为主 (14)。一旦进入循环，这些细胞就会迁移到创伤和感染部位，包括动脉粥样硬化病变。这一系列事件有助于解释 Tawakol 等人 (10) 的研究结果，即骨髓摄取较高 18F-氟脱氧葡萄糖的个体在主动脉壁和整个血管中表现出更高的代谢活动。
Demographers have noted socioeconomic disparities in morbidity and mortality for more than a century. But, it was not until Marmot’s pioneering studies of British civil servants began to appear in the 1980s (1, 2) that socioeconomic status (SES) started to receive serious attention as a cardiovascular risk factor. In the ensuing years, we have learned a great deal about the scope and scale of these disparities (3, 4). The gap is large, and it is growing. In a recent meta-analysis of 22 million adults, low education was associated with a 42% to 66% increased risk of cardiovascular disease (CVD)(5, 6). We have also learned a great deal about the relative importance of various mechanisms thought to underlie these disparities. Genetic variations and lifestyle differences both play a role, and so does access to health care. Yet, none of these factors can fully explain the gaps (7). These observations, coupled with animal studies indicating that there is a robust, lasting physiological response to subordination, have led researchers with a focus on health disparities to hypothesize that stressors associated with low SES may contribute directly to CVD pathogenesis (8, 9). Consistent with that view, research has found higher levels of multiple CVD biomarkers in low-SES populations, including endothelial dysfunction, inflammation, and platelet activation (9). But, convincing evidence for this hypothesis is lacking. Against that backdrop, this issue of the Journal features a fascinating and important report from Tawakol et al.(10), examining a putative stressassociated neurobiological pathway connecting low SES with CVD risk. The paper leverages a statistical technique called mediation path analysis to integrate data on neighborhood conditions, whole-body 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging, and CVD outcomes. In doing so, it offers the most detailed mechanistic account to date of how low SES, a stress exposure,“gets inside of the body” to accelerate CVD progression. Briefly, the results suggest that adverse neighborhood SES factors, such as low median income and high crime rate, induce persistent activation of the amygdala, a brain region that is centrally involved in judging the degree of threat posed by external stimuli. In turn, higher amygdala activation is associated with greater metabolic activity in the bone marrow.Based on previous evidence, the authors suggest that this connection is mediated by the sympathetic nervous system, which, under conditions of threat, causes hematopoietic stem and progenitor cells to egress from bone marrow (11–13). This stress-related mobilization of progenitor cells is selective, and it is dominated by immature myeloid cells with a strong pro-inflammatory skew (14). Once in circulation, these cells migrate to sites of trauma and infection, including atherosclerotic lesions. This chain of events helps to explain the findings in the study by Tawakol et al.(10) that individuals with higher 18F-fluorodeoxyglucose bone marrow uptake show greater metabolic activity in the aortic wall, and over the
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影响因子：
82.9
作者：
通讯作者：
--
黑人中产阶级社区
DOI：
10.1146/annurev.soc.29.010202.095956
发表时间：
2005
期刊：
Review of Sociology
影响因子：
--
作者：
Mary Pattillo
通讯作者：
Mary Pattillo
1969-2013 年美国心血管疾病死亡率的社会经济和种族差异不断扩大
影响因子：
--
作者：
Gopal K Singh;M. Siahpush;R. Azuine;Shanita D. Williams
通讯作者：
Shanita D. Williams
影响因子：
3.7
作者：
Gianaros, Peter J.;Manuck, Stephen B.;Hariri, Ahmad R.
通讯作者：
Hariri, Ahmad R.
影响因子：
3.7
作者：
Gianaros, Peter J.;Marsland, Anna L.;Verstynen, Timothy D.
通讯作者：
Verstynen, Timothy D.