炎症作为种族与心房颤动关联的介导因素：健康、衰老和身体成分研究的结果
Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation: Results from the Health, Aging, and Body Composition Study.
作者信息
Dewland Thomas A, Vittinghoff Eric, Harris Tamara B, Magnani Jared W, Liu Yongmei, Hsu Fang-Chi, Satterfield Suzanne, Wassel Christina, Marcus Gregory M
机构信息
Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California, San Francisco ; Knight Cardiovascular Institute, Oregon Health & Science University, Portland.
Department of Epidemiology and Biostatistics, University of California, San Francisco.
出版信息
JACC Clin Electrophysiol. 2015 Aug;1(4):248-255. doi: 10.1016/j.jacep.2015.04.014. Epub 2015 Jun 22.
BACKGROUND
Despite a lower prevalence of established atrial fibrillation (AF) risk factors, Whites exhibit substantially higher rates of this arrhythmia compared to Blacks. The mechanism underlying this observation is not known. Both inflammation and obesity are risk factors for AF, and adipose tissue is a known contributor to systemic inflammation.
OBJECTIVES
We sought to determine the degree to which racial differences in AF risk are explained by differences in inflammation and adiposity.
METHODS
Baseline serum inflammatory biomarker concentrations and abdominal adiposity (assessed by computed tomography) were quantified in a subset of Black and White participants without prevalent AF in the Health, Aging, and Body Composition (Health ABC) Study. Participants were prospectively followed for the diagnosis of AF using study ECGs and Medicare claims data. Cox proportional hazards models were used to determine the adjusted relative hazard of incident AF between races before and after biomarker adjustment.
RESULTS
Among 2,768 participants (43% Black), 721 developed incident AF over a median follow up of 10.9 years. White race was associated with a heightened adjusted risk of incident AF (HR 1.55, 95% CI 1.30 to 1.84, p < 0.001). Abdominal adiposity was not associated with AF when added to the adjusted model. Among the studied biomarkers, adiponectin, TNF-α, TNF-α SR I, and TNF-α SR II concentrations were each higher among Whites and independently associated with a greater risk of incident AF. Together, these inflammatory cytokines mediated 42% (95% CI 15 to 119%, p = 0.004) of the adjusted race-AF association.
CONCLUSIONS
Systemic inflammatory pathways significantly mediate the heightened risk of AF among Whites. The higher level of systemic inflammation and concomitant increased AF risk in Whites is not explained by racial differences in abdominal adiposity or the presence of other pro-inflammatory cardiovascular comorbidities.
背景
尽管已确诊的心房颤动（AF）危险因素的患病率较低，但与黑人相比，白人的这种心律失常发生率要高得多。这一现象背后的机制尚不清楚。炎症和肥胖都是房颤的危险因素，而脂肪组织是全身炎症的已知促成因素。
目的
我们试图确定炎症和肥胖差异在多大程度上解释了房颤风险的种族差异。
方法
在健康、衰老和身体成分（Health ABC）研究中，对一组无房颤病史的黑人和白人参与者的基线血清炎症生物标志物浓度和腹部肥胖情况（通过计算机断层扫描评估）进行了量化。通过研究心电图和医疗保险理赔数据，对参与者进行前瞻性随访以诊断房颤。采用Cox比例风险模型确定生物标志物调整前后种族间房颤发病的校正相对风险。
结果
在2768名参与者（43%为黑人）中，721人在中位随访10.9年期间发生了房颤。白人种族与房颤发病的校正风险增加相关（风险比1.55，95%置信区间1.30至1.84，p<0.001）。在调整后的模型中，腹部肥胖与房颤无关。在所研究的生物标志物中，脂联素、肿瘤坏死因子-α（TNF-α）、TNF-α受体I（TNF-α SR I）和TNF-α受体II（TNF-α SR II）的浓度在白人中均较高，且各自与房颤发病风险增加独立相关。这些炎症细胞因子共同介导了42%（95%置信区间15%至119%，p = 0.004）的校正种族-房颤关联。
结论
全身炎症途径显著介导了白人中房颤风险的增加。白人中全身炎症水平较高以及随之增加的房颤风险，并非由腹部肥胖的种族差异或其他促炎性心血管合并症的存在所解释。
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