Objective Excessive levels of triglyceride-rich lipoproteins during postprandial lipemia (PPL) have been reported to be atherogenic. However, it is unclear whether the degree of PPL independently predicts cardiovascular disease (CVD) given the scarcity of longitudinal data with standardised measures of postprandial change. We reexamined associations of PPL with incident CVD events in a population-based cohort using detailed measures of postprandial change from a standardised fat challenge.
Research design and methods Postprandial triglycerides, TG-rich lipoprotein triglycerides, retinyl palmitate and apolipoprotein B48 to B100 ratio were measured before (following a 12-hour fasting period) and after a fat-tolerance test meal in a middle-aged, biracial subcohort without CVD (coronary heart disease (CHD) or stroke) from the community-based Atherosclerosis Risk in Communities (ARIC) Study in 1990–1993. Using these measures, we estimated associations of postprandial change with incident CVD (CHD, stroke) through 2012. Stratified analyses by race, obesity and carotid atherosclerotic severity were also conducted.
Results Of 559 participants, 127 (23%) developed CHD and 27 (5%) experienced a stroke over more than 20 years of follow-up. None of the measures of postprandial change were associated with incident CVD events in the overall sample, or by subgroups of race, obesity or carotid atherosclerotic severity (all p>0.3).
Conclusions The degree of PPL was not shown to predict excess CVD risk in extended follow-up of a population-based sample. While our study is the largest to examine the association between PPL and incident CVD using standardised postfat challenge measures, prospective investigation with similar assessment of PPL in more powered samples is warranted.
- Postprandial Lipemia
- CHD Coronary Heart Disease
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Contributors DK performed the statistical evaluation of the data and wrote the manuscript. ARS designed the original study protocol, directed the study and provided input throughout the manuscript preparation. HNG, VN, CMB and RCH provided expert input and critical review throughout the manuscript preparation. GH coordinated the study, provided input during manuscript preparation and provided funding. All authors approved the final manuscript.
Funding This work was supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C and HHSN268201100012C).
Disclaimer The views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs.
Competing interests HNG reports grants from National Institutes of Health USA, during the conduct of the study. VN reports personal fees from Siemens Laboratory, other from Roche, outside the submitted work; and Coinvestigator on a provisional patent filed along with Baylor College of Medicine and Roche for ‘Biomarkers to improve prediction of heart failure.’ CMB reports personal fees from AstraZeneca, grants and personal fees from Amarin, grants and personal fees from Amgen, grants and personal fees from Eli Lilly, grants and personal fees from Esperion, personal fees from Matinas BioPharma, personal fees from Merck, grants and personal fees from Novartis, grants and personal fees from Pfizer, grants and personal fees from Regeneron, grants and personal fees from Sanofi-Synthelabo, grants from National Institutes of Health, grants from American Heart Association, grants from American Diabetes Association, grants and personal fees from Ionis, outside the submitted work. RCH reports grants from Denka Seiken Co, outside the submitted work; In addition, RCH has a patent ‘Biomarkers to Improve Prediction of Heart Failure Risk’ (patent no. 61721475) pending.
Ethics approval Institutional Review Boards from all participating institutions approved the study.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data are available.
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