Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation: Results from the Health, Aging, and Body Composition Study.
Inflammation as a Mediator of the Association Between Race and Atrial Fibrillation: Results from the Health, Aging, and Body Composition Study.
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炎症作为种族与心房颤动之间关联的中介：健康、衰老和身体成分研究的结果。
DOI：
10.1016/j.jacep.2015.04.014
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发表时间：
2015
期刊：
影响因子：
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通讯作者：
Marcus,GregoryM
中科院分区：
文献类型：
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作者：
Dewland,ThomasA;Vittinghoff,Eric;Harris,TamaraB;Magnani,JaredW;Liu,Yongmei;Hsu,Fang-Chi;Satterfield,Suzanne;Wassel,Christina;Marcus,GregoryM
本研究试图确定炎症和肥胖的差异在多大程度上解释了房颤风险的种族差异。背景尽管白人房颤危险因素的发生率较低，但这种心律失常的发生率明显高于黑人。这一观察结果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贡献者。方法在Health ABC(Health，Aging，and Body Compostion，健康、老龄化和身体成分)研究中，对没有普遍存在房颤的黑人和白人参与者的基线血清炎性生物标志物浓度和腹部肥胖(通过计算机断层扫描进行评估)进行了量化。使用研究心动图和医疗保险索赔数据对参与者进行前瞻性跟踪，以诊断房颤。结果在2768名参与者(43%为黑人)中，721名参与者在10.9年的中位时间内发生了房颤。白人种族与调整后的房颤事件风险增加相关(HR：1.55；95%可信区间：1.3至1.84，P<；0.001)。当添加到调整后的模型中时，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、肿瘤坏死因子-α可溶性受体(SR)I和肿瘤坏死因子-αSR II浓度在白人中均较高，且与发生房颤的风险独立相关。这些炎性细胞因子共同介导了42%(95%CI：15%至119%，P=0.004)的种族与房颤之间的调整关联。结论系统性炎症途径显著介导白人房颤风险的增加。白人全身炎症水平较高和伴随的房颤风险增加不能用腹部肥胖的种族差异或其他促炎心血管合并症的存在来解释。
ObjectivesThis study sought to determine the degree to which racial differences in atrial fibrillation (AF) risk are explained by differences in inflammation and adiposity.BackgroundDespite having a lower prevalence of established AF risk factors, whites exhibit substantially higher rates of this arrhythmia than 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.MethodsBaseline 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 ABC (Health, Aging, and Body Composition) study. Participants were prospectively followed for the diagnosis of AF, using study electrocardiography 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.ResultsAmong 2,768 participants (43% black), 721 participants 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% confidence interval [CI]: 1.30 to 1.84, p < 0.001). Abdominal adiposity was not associated with AF when added to the adjusted model. Among the biomarkers studied, adiponectin, tumor necrosis factor (TNF)-α, TNF-α soluble receptor (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 association between race and AF.ConclusionsSystemic 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 proinflammatory cardiovascular comorbidities.