Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease

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Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease

MC Cheung, BG Brown, AC Wolf and JJ Albers
Department of Medicine, School of Medicine, University of Washington, Seattle 98103.

Plasma high density lipoproteins (HDL) can be separated into two subpopulations of apolipoprotein A-I-containing particles: those that also contain apoA-II [Lp(AI w AII)] and those that do not [Lp(AI w/o AII)]. These particles were isolated by immunoaffinity chromatography from 17 men (9 normolipidemic (NL), 8 hyperlipidemic (HL) with symptomatic coronary artery disease (CAD), from 17 NL men without any symptoms of CAD (healthy controls), and from 10 NL men with entirely normal coronary arteriograms (CAD-free controls). The distributions of particle size in these two subpopulations were determined by gradient gel electrophoresis and densitometric scanning. Approximately half of the Lp(AI w AII) particles in all subjects were distributed in the 8.2- 9.2 nm interval. For patients with CAD, a greater fraction of the particles were small, in the 7.0-8.2 nm interval [33% in CAD vs. 26% in CAD-free controls (P less than 0.01) and 19% in healthy controls (P less than 0.0001)], and a smaller fraction of the particles were in the 9.2-11.2 nm interval (14% in CAD vs. 24% in CAD-free control (P less than 0.002) and healthy control groups (P less than 0.001). The Lp(AI w/o AII) of both control groups were primarily composed of two discrete subpopulations in the 8.2-9.2 nm and the 9.2-11.2 nm intervals. In CAD patients there were fewer particles in the 9.2-11.2 nm size interval (23% in CAD vs. 33% in CAD-free controls (P less than 0.005) and 36% in healthy controls (P less than 0.0001), and more particles in the smallest 7.0-8.2 nm size interval (32% in CAD vs. 23% in CAD-free controls (P less than 0.01) and 18% in healthy controls (P less than 0.001]. Thus, the spectrum of HDL particle sizes in patients with CAD tends to be shifted toward the smaller particle when compared with the two control groups. This was observed in both NL and HL patients with HDL cholesterol (CH) values in the normal range. As a group, CAD patients had lower HDL (42 +/- 7 mg/dl) and HDL2 (6 +/- 4 mg/dl) CH than healthy (HDL: 49 +/- 7, HDL2: 12 +/- 6 mg/dl) and CAD-free (HDL: 51 +/- 9, HDL2: 12 +/- 6 mg/dl) controls. When controls and patients were compared for their frequencies of abnormal HDL CH levels and particle sizes, abnormalities in HDL and HDL2 CH levels were not significantly more frequent (twofold) among CAD patients than among controls.(ABSTRACT TRUNCATED AT 400 WORDS)
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				B. F. Asztalos, K. V. Horvath, J. R. McNamara, P. S. Roheim, J. J. Rubinstein, and E. J. Schaefer Effects of atorvastatin on the HDL subpopulation profile of coronary heart disease patients J. Lipid Res., October 1, 2002; 43(10): 1701 - 1707. [Abstract] [Full Text] [PDF]

				W. A. Pitman, R. Korstanje, G. A. Churchill, E. Nicodeme, J. J. Albers, M. C. Cheung, M. A. Staton, S. S. Sampson, S. Harris, and B. Paigen Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice Physiol Genomics, May 10, 2002; 9(2): 93 - 102. [Abstract] [Full Text] [PDF]

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				B. G. Brown, X.-Q. Zhao, A. Chait, L. D. Fisher, M. C. Cheung, J. S. Morse, A. A. Dowdy, E. K. Marino, E. L. Bolson, P. Alaupovic, et al. Simvastatin and Niacin, Antioxidant Vitamins, or the Combination for the Prevention of Coronary Disease N. Engl. J. Med., November 29, 2001; 345(22): 1583 - 1592. [Abstract] [Full Text] [PDF]

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ARTICLES

Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease

				B. F. Asztalos, M. Lefevre, T. A. Foster, R. Tulley, M. Windhauser, L. Wong, and P. S. Roheim Normolipidemic Subjects With Low HDL Cholesterol Levels Have Altered HDL Subpopulations Arterioscler. Thromb. Vasc. Biol., October 1, 1997; 17(10): 1885 - 1893. [Abstract] [Full Text]

				P. T. Williams, D. M. Dreon, P. J. Blanche, and R. M. Krauss Variability of Plasma HDL Subclass Concentrations in Men and Women Over Time Arterioscler. Thromb. Vasc. Biol., April 1, 1997; 17(4): 702 - 706. [Abstract] [Full Text]

				P. Alaupovic, W. J. Mack, C. Knight-Gibson, and H. N. Hodis The Role of Triglyceride-Rich Lipoprotein Families in the Progression of Atherosclerotic Lesions as Determined by Sequential Coronary Angiography From a Controlled Clinical Trial Arterioscler. Thromb. Vasc. Biol., April 1, 1997; 17(4): 715 - 722. [Abstract] [Full Text]

				L. Lagrost, A. Athias, B. Herbeth, V. Guyard-Dangremont, Y. Artur, F. Paille, P. Gambert, and C. Lallemant Opposite Effects of Cholesteryl Ester Transfer Protein and Phospholipid Transfer Protein on the Size Distribution of Plasma High Density Lipoproteins. PHYSIOLOGICAL RELEVANCE IN ALCOHOLIC PATIENTS J. Biol. Chem., August 9, 1996; 271(32): 19058 - 19065. [Abstract] [Full Text] [PDF]

				E. A. Brinton Oral Estrogen Replacement Therapy in Postmenopausal Women Selectively Raises Levels and Production Rates of Lipoprotein A-I and Lowers Hepatic Lipase Activity Without Lowering the Fractional Catabolic Rate Arterioscler. Thromb. Vasc. Biol., March 1, 1996; 16(3): 431 - 440. [Abstract] [Full Text]

				E. Cavallero, F. Brites, B. Delfly, N. Nicolaiew, C. Decossin, C. De Geitere, J.-C. Fruchart, R. Wikinski, B. Jacotot, and G. Castro Abnormal Reverse Cholesterol Transport in Controlled Type II Diabetic Patients : Studies on Fasting and Postprandial LpA-I Particles Arterioscler. Thromb. Vasc. Biol., December 1, 1995; 15(12): 2130 - 2135. [Abstract] [Full Text]

				T. Murakami, S. Michelagnoli, R. Longhi, G. Gianfranceschi, F. Pazzucconi, L. Calabresi, C. R. Sirtori, and G. Franceschini Triglycerides Are Major Determinants of Cholesterol Esterification/Transfer and HDL Remodeling in Human Plasma Arterioscler. Thromb. Vasc. Biol., November 1, 1995; 15(11): 1819 - 1828. [Abstract] [Full Text]

				J. Coresh, T.H. Beaty, V.L. Prenger, J. Xu, and P.O. Kwiterovich Jr Segregation Analysis of HDL3-C Levels in Families of Patients Undergoing Coronary Arteriography at an Early Age Arterioscler. Thromb. Vasc. Biol., September 1, 1995; 15(9): 1307 - 1313. [Abstract] [Full Text]

				M. Bouly, D. Masson, B. Gross, X.-c. Jiang, C. Fievet, G. Castro, A. R. Tall, J.-C. Fruchart, B. Staels, L. Lagrost, et al. Induction of the Phospholipid Transfer Protein Gene Accounts for the High Density Lipoprotein Enlargement in Mice Treated with Fenofibrate J. Biol. Chem., July 6, 2001; 276(28): 25841 - 25847. [Abstract] [Full Text] [PDF]