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Published on: October 12, 2017
Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated
Anette Varbo1, Marianne Benn, Anne Tybjærg-Hansen
1Department of Clinical Biochemistry ( A.V., B.G.N.) and Copenhagen General Population Study (A.V., M.B., A.T.-H., B.G.N.), Herlev Hospital, Copenhagen University Hospital, Copenhagen, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark (A.V., M.B., A.T.-H., B.G.N.); Department of Clinical Biochemistry, Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark (M.B.); Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen University Hospital, Denmark (A.T.-H., B.G.N.); and Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark (A.T.-H.).
Elevated nonfasting remnant cholesterol causally increases inflammation and ischemic heart disease (IHD) risk. Elevated low-density lipoprotein (LDL) cholesterol also causes IHD, but independently of inflammation.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Elevated nonfasting remnant cholesterol and low-density lipoprotein (LDL) cholesterol are linked to ischemic heart disease (IHD).
- The role of these lipoproteins in causing low-grade inflammation remains unclear.
Purpose of the Study:
- To investigate the causal associations between nonfasting remnant cholesterol, LDL cholesterol, and low-grade inflammation.
- To determine the causal relationship between these lipoproteins and ischemic heart disease (IHD).
Main Methods:
- Utilized a multidirectional Mendelian randomization design.
- Analyzed data from 60,608 individuals across three large Danish population studies.
- Genotyped participants for variants affecting lipid levels and C-reactive protein.
Main Results:
- A 1-mmol/L increase in nonfasting remnant cholesterol causally increased C-reactive protein (inflammation marker) by 28%.
- LDL cholesterol showed no causal association with increased C-reactive protein levels.
- Both nonfasting remnant cholesterol (causal risk ratio 3.3) and LDL cholesterol (causal risk ratio 1.8) were causally associated with IHD.
Conclusions:
- Nonfasting remnant cholesterol is causally linked to both low-grade inflammation and IHD.
- LDL cholesterol is causally associated with IHD, but not through an inflammatory pathway.
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