Abstract P269: Fasting HDL-C Partially Explains the Association of Postprandial Triglycerides and Coronary Artery Disease Detected by Computed Tomography Angiography

Background: Postprandial triglycerides (TG) are associated with severe coronary artery disease (CAD), though the underlying mechanisms remain unclear. In this study, we have investigated the effect of clinical and laboratory parameters on the association between postprandial TG and CAD detected by coronary computed tomographic angiography (CTA). Methods: We enrolled 130 patients without previous diagnosis of CAD, (85 with CAD detected by CTA and 45 without); who underwent an oral fat tolerance test. We studied the postprandial lipemia measuring TG from time 0h, 2h, 4h and 6h to analyze the TG change over time. We used a longitudinal multivariable linear mixed effects model with the log of the TG (lnTG) as the primary outcome due to non normal distribution of TG. To evaluate the effect of the other parameters on the longitudinal changes in the TG, each variable has been individually included in the model to evaluate for changes in the lnTG over time. Results: Patients with CAD were older (56.5 ± 6.8 vs 50.4 ± 7.1 years, p<0.001), predominantly male (68.2% vs. 37.8%, p< 0.001) and had lower fasting HDL-C (49 ± 14 vs. 54 ± 12 mg/dL, p=0.015). The majority of individuals with CAD had non-obstructive atherosclerosis (65.6%). The patients with CAD had similar fasting lnTG (2.08 ± 0.20 vs. 2.02 ± 0.18, p=0.069)and increase in lnTG from 0 to 4 hours (p=0.54), but a significantly slower clearance of postprandial lnTG change from 4h to 6h (p=0.040) compared to patients without CAD. Interestingly, although age, gender, fasting glucose, and abdominal circumference did not influence those findings, after the inclusion of fasting HDL-C in the model, the change in the lnTG clearance after 4 hours did not reach statistical significance (Table 1). Conclusion: Patients with CAD had an impaired postprandial metabolism, due to a delayed TG clearance. This association was partially explained by the lower fasting HDL-C. Thus, the contribution of postprandial TG metabolism to the development of CAD, may be partially, related to the low fasting HDL-C concentrations.