Hughes-Austin Jan M, Wassel Christina L, Jiménez Jessica, Criqui Michael H, Ix Joachim H, Rasmussen-Torvik Laura J, Budoff Matthew J, Jenny Nancy S, Allison Matthew A
Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, CA, USA
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA.
Vasc Med. 2014 Aug;19(4):264-271. doi: 10.1177/1358863X14537545. Epub 2014 Jun 6.
Adipokines regulate metabolic processes linked to coronary artery (CAC) and abdominal aorta calcification (AAC). Because adipokine and other adiposity-associated inflammatory marker (AAIM) secretions differ between visceral and subcutaneous adipose tissue, we hypothesized that central adiposity modifies associations between AAIMs and CAC and AAC. We evaluated 1878 MESA participants with complete measures of AAIMs, anthropometry, CAC, and AAC. Associations of AAIMs with CAC and AAC prevalence and severity were analyzed per standard deviation of predictors (SD) using log binomial and linear regression models. The waist-to-hip ratio (WHR) was dichotomized at median WHR values based on sex/ethnicity. CAC and AAC prevalence were defined as any calcium (Agatston score >0). Severity was defined as ln (Agatston score). Analyses examined interactions with WHR and were adjusted for traditional cardiovascular disease risk factors. Each SD higher interleukin-6 (IL-6), fibrinogen and CRP was associated with 5% higher CAC prevalence; and each SD higher IL-6 and fibrinogen was associated with 4% higher AAC prevalence. Associations of IL-6 and fibrinogen with CAC severity, but not CAC prevalence, were significantly different among WHR strata. Median-and-above WHR: each SD higher IL-6 was associated with 24.8% higher CAC severity. Below-median WHR: no association (p =0.012). Median-and-above WHR: each SD higher fibrinogen was associated with 19.6% higher CAC severity. Below-median WHR: no association (p =0.034). Adiponectin, leptin, resistin, and tumor necrosis factor-alpha were not associated with CAC or AAC prevalence or severity. These results support findings that adiposity-associated inflammation is associated with arterial calcification, and further add that central adiposity may modify this association.
脂肪因子调节与冠状动脉钙化(CAC)和腹主动脉钙化(AAC)相关的代谢过程。由于内脏脂肪组织和皮下脂肪组织中脂肪因子及其他肥胖相关炎症标志物(AAIM)的分泌存在差异,我们推测中心性肥胖会改变AAIM与CAC和AAC之间的关联。我们评估了1878名参加多民族动脉粥样硬化研究(MESA)的参与者,他们具备AAIM、人体测量学、CAC和AAC的完整测量数据。使用对数二项式和线性回归模型,按预测因子的标准差(SD)分析AAIM与CAC和AAC患病率及严重程度的关联。根据性别/种族,将腰臀比(WHR)在中位数WHR值处进行二分。CAC和AAC患病率定义为存在任何钙化(阿加斯顿评分>0)。严重程度定义为ln(阿加斯顿评分)。分析研究了与WHR的相互作用,并对传统心血管疾病危险因素进行了校正。白细胞介素-6(IL-6)、纤维蛋白原和C反应蛋白(CRP)每升高1个标准差,CAC患病率分别升高5%;IL-6和纤维蛋白原每升高1个标准差,AAC患病率分别升高4%。IL-6和纤维蛋白原与CAC严重程度的关联(而非与CAC患病率的关联)在WHR分层之间存在显著差异。WHR处于中位数及以上:IL-6每升高1个标准差,CAC严重程度升高24.8%。WHR低于中位数:无关联(p =0.012)。WHR处于中位数及以上:纤维蛋白原每升高1个标准差,CAC严重程度升高19.6%。WHR低于中位数:无关联(p =0.