Remnant Cholesterol and Triglyceride-Rich Lipoproteins in Atherosclerosis Progression and Cardiovascular Disease
2016; Lippincott Williams & Wilkins; Volume: 36; Issue: 11 Linguagem: Inglês
10.1161/atvbaha.116.308305
ISSN1524-4636
AutoresAnette Varbo, Børge G. Nordestgaard,
Tópico(s)Diabetes, Cardiovascular Risks, and Lipoproteins
ResumoHomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 36, No. 11Remnant Cholesterol and Triglyceride-Rich Lipoproteins in Atherosclerosis Progression and Cardiovascular Disease Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBRemnant Cholesterol and Triglyceride-Rich Lipoproteins in Atherosclerosis Progression and Cardiovascular Disease Anette Varbo and Børge G. Nordestgaard Anette VarboAnette Varbo From the Department of Clinical Biochemistry (A.V., B.G.N.) and The Copenhagen General Population Study (A.V., B.G.N.), Herlev and Gentofte Hospital, Copenhagen University Hospital, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Denmark (A.V., B.G.N.); and The Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen University Hospital, Denmark (B.G.N.). and Børge G. NordestgaardBørge G. Nordestgaard From the Department of Clinical Biochemistry (A.V., B.G.N.) and The Copenhagen General Population Study (A.V., B.G.N.), Herlev and Gentofte Hospital, Copenhagen University Hospital, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Denmark (A.V., B.G.N.); and The Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen University Hospital, Denmark (B.G.N.). Originally published1 Nov 2016https://doi.org/10.1161/ATVBAHA.116.308305Arteriosclerosis, Thrombosis, and Vascular Biology. 2016;36:2133–2135In this issue of the journal, Puri et al1 examines the association of on-treatment concentrations of non–high-density lipoprotein (non-HDL) cholesterol and triglycerides with coronary atheroma progression and clinical events. They used data from 9 clinical trials, originally designed to examine effects of different medical therapies on regression of coronary atheroma burden, assessed by intravascular ultrasound. The main finding was that achieved concentrations of non-HDL cholesterol and achieved concentrations of triglycerides were closely associated with coronary atheroma progression and regression, irrespective of achieved concentrations of low-density lipoprotein (LDL) cholesterol, C-reactive protein concentration, and diabetes mellitus status.See accompanying article on page 2220Non-HDL cholesterol is a combined measure of the cholesterol content of LDL, lipoprotein(a), and triglyceride-rich lipoproteins, the latter also known as remnants (Figure). Remnants are here a combined term for intermediate-density lipoproteins, very-low-density lipoproteins, and chylomicron remnants. These lipoproteins likely are atherogenic by penetrating the arterial wall, leading to accumulation of cholesterol in the intimal space, foam cell formation, and atherosclerosis2–5 (Figure). Triglycerides are primarily carried by remnants, and concentrations of triglycerides are highly correlated with the cholesterol content of remnants, that is, remnant cholesterol.6 It is most likely that the cholesterol content of remnants, and not triglycerides, causes atherosclerosis because most cells can degrade triglycerides but not cholesterol2,5 and because cholesterol, and not triglycerides, accumulates in the intima.7Download figureDownload PowerPointFigure. Definition of lipoprotein categories and proposed mechanism of how lipoproteins cause atherosclerosis in the arterial wall. Low-density lipoproteins, lipoprotein (a), and remnants are small enough to enter the arterial wall, get trapped, and cause plaque formation. Chylomicrons are too large to enter the arterial wall27,28 until they are hydrolyzed by lipoprotein lipase and become remnants, which is a process that in most individuals happens rapidly, and therefore, large chylomicrons normally are only present in plasma in minute amounts. HDL indicates high-density lipoprotein; IDL, intermediate-density lipoprotein; LDL, low-density lipoprotein; Lp(a), lipoprotein (a); and VLDL, very low-density lipoprotein.The findings of Puri et al1 are in line with previous studies by us and others showing associations between concentrations of remnant cholesterol (or the highly correlated triglycerides) and increased risk of cardiovascular disease, both in observational8–16 and genetic studies,6,17–19 indicating remnant cholesterol as a causal risk factor for cardiovascular disease. It was therefore a limitation to the study, and a missed opportunity, that Puri et al1 did not report on the direct association between remnant cholesterol and coronary atheroma regression, because this could have added to the understanding of the relative importance of the different parts of cholesterol in non-HDL, that is, LDL cholesterol and remnant cholesterol. But perhaps, a head-to-head comparison of remnant cholesterol with LDL cholesterol can be reported on in a follow-up publication, similar to what we have reported previously for individuals in the general population15 and in patients with ischemic heart disease.20 Nevertheless, Puri et al1 found a stronger association between achieved non-HDL cholesterol concentrations and atheroma progression compared with achieved LDL cholesterol concentrations, indirectly indicating that additional predictive information lies in the remnant cholesterol part of non-HDL cholesterol. This is important for the design of future lipid-lowering studies to most effectively reduce the residual risk of cardiovascular disease seen after LDL cholesterol lowering.There is strong evidence suggesting that high concentrations of remnant cholesterol cause atherosclerosis and ischemic heart disease, with important differences in how remnants cause atherosclerosis compared with LDL. Remnants pass into the arterial wall3,4 and are taken up by macrophages and smooth muscle cells without modification, which is unlike LDL, that needs to be modified before uptake.21 Also, remnant particles are larger than LDL and carry ≤40 times as much cholesterol per particle, perhaps making them even more atherogenic than LDL.7 Also, we have previously found that high remnant cholesterol concentrations were associated with low-grade inflammation and with ischemic heart disease, whereas LDL cholesterol concentrations were not associated with low-grade inflammation, despite an association with ischemic heart disease.22 This indicates that remnant cholesterol causes atherosclerosis with an inflammatory component, whereas LDL cholesterol causes atherosclerosis without. These differences in mechanism make it interesting to examine remnant cholesterol and LDL cholesterol separately.Unfortunately, among some lipid experts, there is resistance toward using the easily calculated remnant cholesterol, determined as total cholesterol minus HDL cholesterol minus LDL cholesterol, as we have done previously.5,6,10,15,20,22–24 Remnant cholesterol can be calculated from a standard lipid profile without additional cost and can probably add to the risk evaluation of cardiovascular disease in an individual. Arguments against using calculated remnant cholesterol are mainly that it is in fact calculated; however, LDL cholesterol is also calculated often, and non-HDL cholesterol likewise, and there is no doubt that lowering LDL cholesterol is beneficial, despite the fact that some of the evidence is based on calculated LDL cholesterol.There is an urgent need for future randomized clinical intervention trials examining whether lowering remnant cholesterol and triglycerides in those with high concentrations can reduce the risk of cardiovascular disease. Previous studies with triglyceride-lowering drugs have had conflicting results5; however, this can partly be explained by the way participants were recruited. No study to date have selectively recruited individuals with mild to moderately elevated or high concentrations of triglycerides, and the present study from Puri et al1 showed that atheroma progression was only associated with triglycerides >200 mg/dL (2.27 mmol/L). This is in line with previous post hoc analyses of triglyceride-lowering studies, showing that in the subgroup of individuals with high baseline triglycerides, the risk of cardiovascular disease was reduced after triglyceride lowering.5,13,25 Fortunately, 2 randomized, placebo-controlled trials of triglyceride-lowering therapy added to statin therapy in individuals with elevated triglyceride concentrations with the aim of reducing cardiovascular disease are ongoing (NCT01492361 and NCT02104817), and one is planned to start relatively soon.26The findings of Puri et al1 contribute valuable information about non-HDL cholesterol, triglycerides, and atherosclerosis. In Kaplan–Meier sensitivity analyses, the study also demonstrated greater major adverse cardiovascular event rates in those with higher versus lower non-HDL cholesterol and triglycerides, with earlier separation for the non-HDL cholesterol curve compared with the LDL cholesterol curve. Their interesting, well-performed, and timely study warrants future studies examining whether lowering of non-HDL cholesterol, triglycerides, and remnant cholesterol can reduce the considerable residual risk of cardiovascular disease seen after lowering of LDL cholesterol with statins.DisclosuresB.G. Nordestgaard has received lecture and/or consultancy honoraria from AstraZeneca, Merck, Omthera, Sanofi, Regeneron, IONIS, Aegerion, Dezima, Amgen, Kowa, and Denka Seiken. The other author reports no conflicts.FootnotesCorrespondence to Børge G. Nordestgaard, MD, DMSc, Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev Ringvej 75, 2730 Herlev, Denmark. E-mail [email protected]References1. Puri R, Nissen SE, Shao M, Elshazly MB, Kataoka Y, Kapadia SR, Tuzcu EM, Nicholls SJ. 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Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women.JAMA. 2007; 298:309–316. doi: 10.1001/jama.298.3.309.CrossrefMedlineGoogle Scholar17. Do R, Willer CJ, Schmidt EM, et al. Common variants associated with plasma triglycerides and risk for coronary artery disease.Nat Genet. 2013; 45:1345–1352. doi: 10.1038/ng.2795.CrossrefMedlineGoogle Scholar18. Thomsen M, Varbo A, Tybjærg-Hansen A, Nordestgaard BG. Low nonfasting triglycerides and reduced all-cause mortality: a mendelian randomization study.Clin Chem. 2014; 60:737–746. doi: 10.1373/clinchem.2013.219881.CrossrefMedlineGoogle Scholar19. Helgadottir A, Gretarsdottir S, Thorleifsson G, et al. Variants with large effects on blood lipids and the role of cholesterol and triglycerides in coronary disease.Nat Genet. 2016; 48:634–639. doi: 10.1038/ng.3561.CrossrefMedlineGoogle Scholar20. Jepsen AM, Langsted A, Varbo A, Bang LE, Kamstrup PR, Nordestgaard BG. Increased remnant cholesterol explains part of residual risk of all-cause mortality in 5414 patients with ischemic heart disease.Clin Chem. 2016; 62:593–604. doi: 10.1373/clinchem.2015.253757.CrossrefMedlineGoogle Scholar21. Nakajima K, Nakano T, Tanaka A. The oxidative modification hypothesis of atherosclerosis: the comparison of atherogenic effects on oxidized LDL and remnant lipoproteins in plasma.Clin Chim Acta. 2006; 367:36–47. doi: 10.1016/j.cca.2005.12.013.CrossrefMedlineGoogle Scholar22. Varbo A, Benn M, Tybjærg-Hansen A, Nordestgaard BG. Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation.Circulation. 2013; 128:1298–1309. doi: 10.1161/CIRCULATIONAHA.113.003008.LinkGoogle Scholar23. Jørgensen AB, Frikke-Schmidt R, West AS, Grande P, Nordestgaard BG, Tybjærg-Hansen A. 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