Association between postprandial triglycerides and coronary artery disease detected by coronary computed tomography angiography Henrique L. Staniak a, b , Wilson Salgado Filho b , Márcio H. Miname b , Isabela M. Benseñor a , Paulo A. Lotufo a , Rodolfo Sharovsky a , Carlos E. Rochitte b , Márcio S. Bittencourt a , Raul D. Santos b, * a Hospital Universitário, University of São Paulo, São Paulo, Brazil b Lipid Clinic Heart Institute (InCor), University of São Paulo Medical School Hospital, São Paulo, Brazil article info Article history: Received 16 September 2013 Received in revised form 12 November 2013 Accepted 3 December 2013 Available online 18 January 2014 Keywords: Triglycerides Postprandial lipemia Coronary computed tomography angiography Atherosclerosis abstract Background: Studies have demonstrated the association of severe anatomical coronary artery disease (CAD) with postprandial triglycerides (TG) concentrations. Nevertheless the relationship between less severe atherosclerosis plaque burden and postprandial TG is less established. Objective: to study the relationship between postprandial TG and CAD detected by coronary computed tomographic angiography (CTA). Material and methods: 130 patients who underwent an oral fat tolerance test were enrolled (85 with CAD detected by CTA and 45 without). Postprandial lipemia was studied by measuring TG from T0h to T6h with 2-h intervals, and analyzed the TG change over time using a longitudinal multivariable linear mixed effects model with the log normal of the TG as the primary outcome. Results: The majority of individuals with CAD had non-obstructive disease (63.3%) Patients with CAD had a slower clearance of postprandial TG change from 4 h to 6 h (p < 0.05) compared to patients without CAD. These results remained significant after adjustment for fasting TG and glucose, age, gender, body mass index, and waist circumference. However, those differences did not reach statistical significance after adjustment for fasting HDL-C. Conclusion: Patients with mild (<25% lumen obstruction) and moderate CAD (25e50% lumen obstruc- tion) detected by coronary CTA had an impaired postprandial metabolism, with a delayed TG clearance, when compared to individuals with no CAD. This difference was partially explained by the lower HDL-C. Thus, though postprandial TG may contribute to the development of CAD, this association is partially related to low HDL-C. Ó 2014 Elsevier Ireland Ltd. All rights reserved. 1. Introduction Atherosclerotic cardiovascular disease accounts for more than 19 million deaths each year [1], mainly due to coronary artery disease (CAD). Although traditional risk factors, such as cigarette smoking, diabetes, hypertension and hypercholesterolemia can explain up to 90% of the excess risk for CAD [2], individuals with no traditional risk factors may still experience cardiovascular events. This may be explained by several factors such as prothrombotic factors [3], inflammatory biomarkers [4e6] and atherogenic lipo- protein phenotypes which comprise increased concentrations of triglyceride-rich-lipoproteins (TRLs), increased low density lipo- protein (LDL) particle number and decreased concentration of high density lipoprotein cholesterol (HDL-C) [4]. Fasting triglycerides (TG) are an indirect measure of TRLs. However, the TRLs represent a heterogeneous population of parti- cles with different origins and composition. Their atherogenic po- tential is different and partially explained by their size and ability to enter into the arterial intima and induce atherosclerosis [7]. It has been demonstrated that patients with fasting TG levels >25 mmol/ L(>2214 mg/dL) and familial chylomicronemia syndrome rarely develop atherosclerosis [8], whereas patients with moderate hypertriglyceridemia such as in familial hypertriglyceridemia, fa- milial combined hyperlipidemia, remnant hyperlipidemia and metabolic syndrome often develop severe atherosclerosis [9]. Although TG is routinely measured after overnight fasting to allow more stable values, most individuals eat regular meals * Corresponding author. Unidade Clínica de Lípides-InCor HCFMUSP, Av Dr Eneas C. Aguiar, 44 Bloco 2 Segundo Andar sala 4, Cep-05403-900 Sao Paulo, Brazil. E-mail addresses: rdsf@uol.com.br, raul.santos@incor.usp.br (R.D. Santos). Contents lists available at ScienceDirect Atherosclerosis journal homepage: www.elsevier.com/locate/atherosclerosis 0021-9150/$ e see front matter Ó 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.atherosclerosis.2013.12.036 Atherosclerosis 233 (2014) 381e386