De atherogene rol van triglyceriden, LDL- en HDL-subfracties - NVKC

51. Miller NE. Associations of high-density lipoprotein subclasses
and apolipoproteins with ischaemic heart disease
and coronary atherosclerosis. Am Heart J 1987; 113: 589-
597.
52. Buring JE, O'Connor GT, Goldhaber SZ, Rosner B, Herbert
PN, Blum CB, Breslow JL et al. Decreased HDL2
and HDL3 cholesterol, apo A-I and apo A-II, and increased
risk of myocardial infarction. Circulation 1992; 85:
22-29.
53. Stampfer MJ, Sacks FM, Salvini S, Willett WC, Hennekes
CH. A prospective study of cholesterol, apolipoproteins,
and the risk of myocardial infarction. N Engl J Med 1991;
325: 373-381.
54. Demacker PNM, Baadenhuysen H, Stuyt PMJ, Laar A
van 't . Studies on the relationship between the cholesterol
content in total high density lipoprotein and its subfractions,
HDL 2 and HDL 3 in normo- and hyperlipidemic subjects.
Atherosclerosis 1986; 61: 225-229.
Summary
The atherogenic role of triglycerides and the subfractions of
LDL and HDL. Swinkels DW and Demacker PNM. Ned Tijdschr
Klin Chem 1996; 21: 41-46.
Epidemiologic studies using multivariate techniques seldomly
recognize plasma-triglycerides as an independent risk factor
for coronary heart disease (CHD). However, diverse potential
mechanisms could explain a causal role of triglycerides in the
pathogenesis of atherosclerosis. Especially the postprandial
triglycerides, enriched with cholesterylesters, in the form of
chylomicron- and VLDL-remnants, appear to be atherogenic.
In addition, elevated triglyceride levels are associated with the
predominance of small LDL particles and a low concentration
of HDL cholesterol. Both small LDL particles and low HDL
cholesterol concentration are associated with premature CHD.
Whether this association is an independent relation remains
unclear. Small LDL has diminished affinity for the LDL-receptor
and is more susceptible to oxidative modification, as
compared to large LDL. This might implicate that not triglycerides
but (small) LDL plays the essential role in the pathogenesis
of CHD. The same holds true for HDL, whether it is related
to the risk for CHD, and if so which HDL subfraction
might be responsible. Although epidemiological data are not
unequivocal, the relationship between decreased HDL 2 levels,
as determined by ultracentrifugation and gradient gel electrophoresis,
and the susceptibility for CHD has been emphasized.
Also, the HDL subfraction enriched with apoA-I, isolated by
immuno-affinity chromatography, is decreased in CHD.
The methods for determination of LDL and HDL subfractions
will be reviewed. The possible role of both LDL and HDL
subfractions in the pathogenesis of atherosclerosis, either direct
or indirect through the triglyceride metabolism, will be
discussed upon.
Key-words: atherosclerosis; triglycerides; postprandial triglycerides;
LDL subfractions; HDL subfractions
46 Ned Tijdschr Klin Chem 1996, vol. 21, no. 1