Varma Bhavya, Ogunmoroti Oluseye, Ndumele Chiadi E, Zhao Di, Szklo Moyses, Sweeney Ty, Allison Matthew A, Budoff Matthew J, Subramanya Vinita, Bertoni Alain G, Michos Erin D
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD.
Diabet Epidemiol Manag. 2022 Apr-Jun;6. doi: 10.1016/j.deman.2021.100047. Epub 2021 Dec 23.
Adipokines play a role in cardiometabolic pathways. Coronary artery calcium (CAC) progression prognosticates cardiovascular disease (CVD) risk. However, the association of adipokines with CAC progression is not well established. We examined the association of adipokines with CAC progression in a multi-ethnic cohort free of CVD at baseline.
We included 1,904 randomly-selected adults enrolled in the Multi-Ethnic Study of Atherosclerosis who had both adipokine levels [leptin, resistin, adiponectin] and CAC by CT measured at either exam 2 (2002-2004) or exam 3 (2004-2005). CAC was previously measured at exam 1 (2000-2002) and a subset (n=566) had CAC measured at exam 5 (2010-2012). We used logistic regression to examine odds of CAC progression between exam 1 and 2/3 (defined as >0 Agatston units of change/year). We used linear mixed effect models to examine CAC progression from exam 2/3 to 5.
At exam 2/3, the mean age was 65(10) yrs; 50% women. In models adjusted for sociodemographic factors and BMI, the highest tertile of leptin, compared to lowest, was associated with an increased odds of CAC progression over the preceding 2.6yrs [OR 1.60 (95% CI: 1.10-2.33)]. In models further adjusted for visceral fat and CVD risk factors, the highest tertile of leptin was statistically significantly associated with a 4% (1-7%) greater CAC progression over an average of 7yrs. No associations were seen for resistin and adiponectin.
Higher leptin levels were independently, but modestly, associated with CAC progression. Atherosclerosis progression may be one mechanism through which leptin confers increased CVD risk.
脂肪因子在心脏代谢途径中发挥作用。冠状动脉钙化(CAC)进展可预测心血管疾病(CVD)风险。然而,脂肪因子与CAC进展之间的关联尚未完全明确。我们在一个基线时无CVD的多民族队列中研究了脂肪因子与CAC进展的关联。
我们纳入了1904名随机选择的参加动脉粥样硬化多民族研究的成年人,他们在第2次检查(2002 - 2004年)或第3次检查(2004 - 2005年)时通过CT测量了脂肪因子水平[瘦素、抵抗素、脂联素]和CAC。CAC先前在第1次检查(2000 - 2002年)时进行了测量,并且有一个子集(n = 566)在第5次检查(2010 - 2012年)时测量了CAC。我们使用逻辑回归来检查第1次和第2/3次检查之间CAC进展的几率(定义为每年变化>0阿加斯顿单位)。我们使用线性混合效应模型来检查从第2/3次检查到第5次检查的CAC进展情况。
在第2/3次检查时,平均年龄为65(10)岁;50%为女性。在根据社会人口统计学因素和BMI进行调整的模型中,与最低三分位数相比,瘦素最高三分位数与前2.6年中CAC进展几率增加相关[比值比1.60(95%置信区间:1.10 - 2.33)]。在进一步根据内脏脂肪和CVD危险因素进行调整的模型中,瘦素最高三分位数与平均7年期间CAC进展增加4%(1 - 7%)在统计学上显著相关。未发现抵抗素和脂联素存在关联。
较高的瘦素水平与CAC进展独立但适度相关。动脉粥样硬化进展可能是瘦素增加CVD风险的一种机制。