Relation of Fasting Triglyceride-Rich Lipoprotein Cholesterol to Coronary Artery Calcium Score (from the ELSA-Brasil Study)

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 g...

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Published inThe American journal of cardiology Vol. 119; no. 9; pp. 1352 - 1358
Main Authors Bittencourt, Marcio S., Santos, Raul D., Staniak, Henrique, Sharovsky, Rodolfo, Kondapally, Rao, Vallejo-Vaz, Antonio J., Ray, Kausik K., Bensenor, Isabela, Lotufo, Paulo
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.05.2017
Elsevier Limited
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Summary: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.
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ISSN:0002-9149
1879-1913
1879-1913
DOI:10.1016/j.amjcard.2017.01.033