Bittencourt Marcio S, Santos Raul D, Staniak Henrique, Sharovsky Rodolfo, Kondapally Rao, Vallejo-Vaz Antonio J, Ray Kausik K, Bensenor Isabela, Lotufo Paulo
Center for Clinical and Epidemiological Research, University Hospital, University of São Paulo School of Medicine, São Paulo, Brazil.
Center for Clinical and Epidemiological Research, University Hospital, University of São Paulo School of Medicine, São Paulo, Brazil; Lipid Clinic Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil.
Am J Cardiol. 2017 May 1;119(9):1352-1358. doi: 10.1016/j.amjcard.2017.01.033. Epub 2017 Feb 10.
Although low-density lipoprotein cholesterol (LDL-C) is widely accepted as the principal lipid fraction associated with atherosclerosis, emerging evidence suggests a causal relation between lifelong elevations in triglyceride-rich lipoprotein cholesterol (TRL-C) and cardiovascular disease (CVD) in genetic studies. To provide further evidence for the potential relevance of TRL-C and atherosclerosis, we have evaluated the relation between TRL-C and coronary artery calcium (CAC) score. We included 3,845 subjects (49.9 ± 8.4 years, 54% women) who had no history of CVD, were not using lipid-lowering medications, and underwent CAC evaluation. We assessed the relation between increasing fasting TRL-C and the graded increase in CAC and to what extent TRL-C were independently associated with CAC over and above LDL-C using logistic regression models. Overall, 973 (25%) of the participants had a CAC >0 and 308 (8%) had a CAC >100. The median TRL-C level was 22 mg/dL (IQR 16 to 32). Subjects with CAC >0 had higher TRL-C levels than those with CAC = 0 (p <0.001). Similarly, subjects with CAC >0 had higher levels of LDL-C, non-high-density lipoprotein cholesterol, and lower high-density lipoprotein cholesterol (all p <0.001). After multivariate adjustment, log-transformed TRL-C remained associated with the presence and severity of CAC (all p <0.05). When TRL-C was added to models that contained demographic factors and conventional lipids, it significantly improved the model to predict the presence of CAC >0 (p = 0.01). In conclusion, in a large cohort of asymptomatic subjects, TRL-C was associated with subclinical atherosclerosis supporting a potentially causal role in CVD.
尽管低密度脂蛋白胆固醇（LDL-C）被广泛认为是与动脉粥样硬化相关的主要脂质成分，但新出现的证据表明，在基因研究中，富含甘油三酯的脂蛋白胆固醇（TRL-C）终身升高与心血管疾病（CVD）之间存在因果关系。为了进一步证明TRL-C与动脉粥样硬化潜在相关性的证据，我们评估了TRL-C与冠状动脉钙化（CAC）评分之间的关系。我们纳入了3845名受试者（年龄49.9±8.4岁，54%为女性），他们无CVD病史，未使用降脂药物，并接受了CAC评估。我们使用逻辑回归模型评估空腹TRL-C升高与CAC分级增加之间的关系，以及TRL-C在LDL-C之外与CAC独立相关的程度。总体而言，973名（25%）参与者的CAC>0，308名（8%）参与者的CAC>100。TRL-C的中位数水平为22mg/dL（四分位间距16至32）。CAC>0的受试者TRL-C水平高于CAC=0的受试者（p<0.001）。同样，CAC>0的受试者LDL-C、非高密度脂蛋白胆固醇水平较高，高密度脂蛋白胆固醇水平较低（均p<0.001）。多变量调整后，经对数转换的TRL-C仍与CAC的存在和严重程度相关（均p<0.05）。当将TRL-C添加到包含人口统计学因素和传统脂质的模型中时，它显著改善了预测CAC>0存在的模型（p=0.01）。总之，在一大群无症状受试者中，TRL-C与亚临床动脉粥样硬化相关，支持其在CVD中可能的因果作用。
