We isolated and characterized immunoreactive apolipoprotein B (apoB) -containing lipoproteins from human atherosclerotic plaque and plasma to determine whether verylow-density lipoprotein (VLDL) can enter and become incorporated into the atherosclerotic lesion and how plaque apoBcontaining lipoproteins differ from apoB-containing lipoproteins isolated from plasma. Atherosclerotic plaques were obtained during aortic surgery and processed immediately. Lipoproteins were extracted from minced plaque in a buffered saline solution (extract A). In selected cases a second extraction was done after plaque was incubated with collagenase (extract B). Lipoproteins were then isolated from the extracts by anti-apoB immunosorption and separated into VLDL+intermediate-density lipoprotein (IDL) (d< 1.019 g/mL) and low-density lipoprotein (LDL) (1.019«f< 1.070 g/mL) fractions by ultracentrifugation. The VLDL+IDL fractions from plaque contained more than one third of the total apoB-associated lipoprotein cholesterol in both extracts A and B. The lipid composition of VLDL+IDL in both extracts was related to that of plasma VLDL+IDL By electron microscopy L ipoprotein infiltration into the artery wall is an essential event in the pathogenesis of atherosclerosis, but little is known about the process of lipoprotein infiltration and eventual entrapment in plaque. Even the identity of the lipoproteins involved has not been conclusively determined. It is generally agreed that low-density lipoproteins (LDL) have access to the artery wall, but very-low-density lipoproteins (VLDL) also may infiltrate the artery wall and directly contribute to atherogenesis. VLDL, particularly VLDL remnants, certainly have atherogenic potential.1 -2 Particles resembling VLDL remnants can be taken up by macrophages to produce foam cells, 3 -3 stimulate endothelial cells to express a monocyte-specific chemotactic factor, 6 and increase monocyte adherence to the endothelium. 7 Furthermore, varying amounts of labeled © 1994 American Heart Association, Inc.mean particle diameters of VLDL+IDL from extracts A and B were 9% and 23%, respectively, greater than VLDL+IDL diameters from plasma. Mean diameters of LDL from extracts A and B were 11% and 31% greater than LDL diameters from plasma. The apoE-apoB ratio of extract A VLDL+IDL was nearly twice that of plasma VLDL+IDL and severalfold higher than that of extract A LDL. Immunoblots of both VLDL+IDL and LDL from extract A demonstrated minimal fragmentation of apoB. These results demonstrate that (1) VLDL, VLDL remnants, or both, can enter human atherosclerotic plaque and become bound to the connective tissue matrix; (2) apoB-containing lipoproteins from plaque differ from plasma lipoproteins in size and apoE content; and (3) there appears to be minimal fragmentation of buffer-extractable apoB in plaque lipoproteins. (Arterioscler Thromb.

Elevated lipid levels usually associated with an increased risk of atherosclerosis may predispose patients to an increased incidence of intimal hyperplasia after endarterectomy.

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