Chapter 3. Lipids and Low-Density Lipoproteins in Intima in Relation to Its Morphological Characteristics
- Ruth Porter and
- Julie Knight
Published Online: 30 MAY 2008
Copyright © 1973 Ciba Foundation
Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors
How to Cite
Smith, E. B. and Slater, R. S. (2008) Lipids and Low-Density Lipoproteins in Intima in Relation to Its Morphological Characteristics, in Ciba Foundation Symposium 12 - Atherogenesis: Initiating Factors (eds R. Porter and J. Knight), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470719954.ch3
- Published Online: 30 MAY 2008
- Published Print: 1 JAN 1973
Print ISBN: 9789021940137
Online ISBN: 9780470719954
- low-density lipoproteins;
- fatty acids;
- fibrous lesions
The lipids in human aortic intima occur in two chemically and morphologically distinct forms. In typical fatty streaks the lipid is within fat-filled cells and the cholesterol ester fatty acids are characterized by a very high proportion of oleic (18 : 1) acid, suggesting that the cholesterol has been esterified by the cells in situ. In normal intima and early fibrous lesions the lipid is in the form of fine, extracellular droplets orientated along collagen and elastic fibres, with a cholesterol ester fatty acid pattern in which linoleic (18 : 2) is the predominant fatty acid. This closely resembles the cholesterol ester in serum low-density lipoprotein, and is probably derived directly from it.
The atheroma lipid pool underlying large plaques contains the linoleic acid rich, low-density lipoprotein type of cholesterol ester, and it is concluded that most of the lipid in large human plaques is derived directly from plasma lipoprotein.
The amount of immunologically intact lipoprotein in the intima has been measured by electrophoresis directly from the minced tissue into an antibody-containing gel. In normal intinia the concentration of low-dmsity lipoprotein is highly correlated with the serum cholesterol level during the week before death (r= 0.965; P< 0.001). The volume of the patient's own serum in the intima is independent of cholesterol level, but is increased in hypertension. In the ‘gelatinous’ precursors of plaques and at the edges of developing plaques the lipoprotein concentrations are respectively 2 and 3 1/2 times greater than normal. There is a particularly marked increase in lipoprotein concentration in the deep layers, where in young plaques it exceeds the concentration in the superficial layers, thus providing a substantial pool of lipoprotein from which lipid could be split.