Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5595612 | The American Journal of Cardiology | 2017 | 7 Pages |
Abstract
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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Authors
Marcio S. MD, MPH, PhD, Raul D. MD, MSc, PhD, Henrique MD, PhD, Rodolfo MD, PhD, Rao MD, Antonio J. MD, Kausik K. MD, Isabela MD, PhD, Paulo MD, MPH, DPH,