High-density lipoprotein metabolism and progression of atherosclerosis: New insights from the HDL Atherosclerosis Treatment Study

Current Opinion in Cardiology

Volumn 19, Issue 4, 2004, Pages 385-391

  Asztalos, Bela F ^a  

^a TUFTS UNIVERSITY   (United States)

Author keywords

Anti atherogenicity; Atherosclerosis; High density lipoprotein; High density lipoprotein subspecies

Indexed keywords

APOLIPOPROTEIN A1; CHOLESTEROL ESTER TRANSFER PROTEIN; FIBRIC ACID DERIVATIVE; GEMFIBROZIL; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; NICOTINIC ACID; PROTEIN INHIBITOR; SIMVASTATIN;

ATHEROSCLEROSIS; CELL HETEROGENEITY; CHOLESTEROL TRANSPORT; CLINICAL TRIAL; CORONARY ARTERY OBSTRUCTION; ENDOTHELIUM; HUMAN; INFLAMMATION; ISCHEMIC HEART DISEASE; LIPID OXIDATION; LIPOPROTEIN METABOLISM; PRIORITY JOURNAL; PROTEIN ANALYSIS; REVIEW; RISK FACTOR; TANGIER DISEASE;

ANIMALS; ANTILIPEMIC AGENTS; ANTIOXIDANTS; ARTERIOSCLEROSIS; BIOLOGICAL TRANSPORT, ACTIVE; CHOLESTEROL; CORONARY ARTERIOSCLEROSIS; ENDOTHELIUM, VASCULAR; HUMANS; INFLAMMATION; LIPOPROTEINS, HDL;

EID: 3142768382     PISSN: 02684705     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.hco.0000126979.41946.7e     Document Type: Review

References (87)

1. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). Circulation 2002, 106:3143-3421.
2. Robins SJ, Collins D, Wittes JT, et al.: For the VA-Hit Study Group: Relation of gemfibrozil treatment and lipid levels with major coronary events. VA-HIT: A randomized controlled trial. JAMA 2001, 285:1585-1591.
3. Bersot TP, Pepin GM, Mahley RW: Risk determination of dyslipidemia in populations characterized by low levels of high-density lipoprotein cholesterol. Am Heart J 2003, 146:1052-1059. The authors demonstrated that the total cholesterol/HDL-C ratio predicts CHD risk regardless of the absolute LDL-C and HDL-C levels in the Turkish Heart Study.
4. Mowri HO, Patsch W, Smith LC, et al.: Different reactivities of high-density lipoprotein2 subfractions with hepatic lipase. J Lipid Res 1992, 33:1269-1279.
5. Castro GR, Fielding CJ: Early incorporation of cell-derived cholesterol into preβ-migrating high density lipoprotein. Biochemistry (Mosc) 1988, 27:25-29.
6. Miida T, Kawano M, Fielding PE, et al.: Regulation of the concentration of preβ high-density lipoprotein in normal plasma by cell membranes and lecithin-cholesterol acyltransferase activity. Biochemistry (Mosc) 1992, 31:11112-11117.
7. von Eckardstein A, Huang Y, Assmann G: Physiological role and clinical relevance of high-density lipoprotein subclasses. Curr Op Lipidol 1994, 5:404-416.
8. Puchois P, Kandoussi A, Fievet P, et al.: Apolipoprotein A-I-containing lipoproteins in coronary artery disease. Atherosclerosis 1987, 68:35-40.
9. Stampfer MJ, Sacks FM, Salvini S, et al.: A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. N Engl J Med 1991, 325:373-381.
10. Sweetnam PM, Bolton CH, Yarnel IW, et al.: Associations of HDL2 and HDL3 cholesterol subfractions with the development of ischemic heart disease in British men. Circulation 1994, 90:769-774.
11. Montali A, Vega GL, Grundy SM: Concentrations of apoA-I-containing particles in patients with hypoalphalipoproteinemia. Arterioscler Thromb Vasc Biol 1994, 14:511-517.
12. Buring JE, O'Connor GT, Goldhaber SZ, et al.: Decreased HDL2 and HDL3 cholesterol, apoA-I and apoA-II, and increased risk of myocardial infarction. Circulation 1992, 85:22-29.
13. Fruchart JC, Ailhaud G: Apolipoprotein A-containing lipoprotein particles: physiological role, quantification, and clinical significance. Clin Chem 1992, 38:793-797.
14. Schultz JR, Verstuyft JG, Gong EL, et al.: Protein composition determines the anti-atherogenic properties of HDL in transgenic mice. Nature 1993, 365:762.
15. Asztalos BF, Roheim PS, Milani RL, et al.: Distribution of apoA-I-containing HDL subpopulations in patients with coronary heart disease. Arterioscler Thromb Vasc Biol 2000, 20:2670-2676.
16. Miida T, Ozaki K, Murakami T, et al.: Preβ1-high-density lipoprotein (preβ1-HDL) concentration can change with low low-density lipoprotein concentration independent of cholesteryl ester transfer protein. Clin Chim Acta 2000, 292:69-80.
17. Fielding PE, Kawano M, Catapano AL, et al.: Unique epitope of apolipoprotein A-I expressed in Preβ-1 high-density lipoprotein and its role in the catalyzed efflux of cellular cholesterol. Biochemistry (Mosc) 1994, 33:6981-6985.
18. Miida T, Nakamura Y, Inano K: Preβ high-density lipoprotein increases in coronary artery disease. Clin Chem 1996, 42:1992-1995.
19. Otvos JD, Jeyarajah EJ, Cromwell WC: Measurement issues related to lipoprotein heterogeneity. Am J Cardiol 2002, 90:22i-29i.
20. Kuller L, Arnold A, Tracy R, et al.: Nuclear magnetic resonance spectroscopy of lipoproteins and risk of coronary heart disease in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 2002, 22:1175-1180.
21. Asztalos BF, Lefevre M, Foster TA, et al.: Normolipidemic subjects with low HDL cholesterol levels have altered HDL subpopulations. Arterioscler Thromb Vasc Biol 1997, 17:1885-1893.
22. Asztalos BF, Batista M, Horvath KV, et al.: Change in α-1 HDL concentration predicts progression in coronary artery stenosis. Arterioscler Thromb Vasc Biol 2003, 23:847-852. The authors demonstrated the association between large LpA-I α-1 and progression of coronary stenosis as well as the effects of simvastatin-niacin and antioxidants on the HDL subpopulation profile of CHD patients.
23. Brown GB, Zhao XQ, Chait A, et al.: Lipid altering or antioxidant vitamins for patients with coronary disease and low HDL cholesterol? The HDL-Atherosclerosis Treatment Study design. Can J Cardiol 1998, 14:6a-13a.
24. Brown GB, Zhao XQ, Chait A, et al.: Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med 2001, 345:1583-1592.
25. Cheung MC, Zhao XQ, Chait A, et al.: Antioxidant supplements block the response of HDL to simvastatin-niacin therapy in patients with coronary artery disease and low HDL. Arterioscler Thromb Vasc Biol 2001, 21:1320-1326.
26. Asztalos BF, Horvath KV, McNamara JR, et al.: Effects of atorvastatin on the HDL subpopulation profile of coronary heart disease patients. J Lipid Res 2002, 43:1701-1707.
27. Asztalos BF, Horvath KV, McNamara JR, et al.: Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients. Atherosclerosis 2002, 164:361-369.
28. Barter PJ, Rye K: Molecular mechanisms of reverse cholesterol transport. Curr Op Lipidol 1996, 7:82-87.
29. Hattori H, Kujiraoka T, Egashira T, et al.: Association of coronary heart disease with preβ-HDL concentrations in Japanese men. Clin Chem 2004, 50:589-595. The authors illustrated the associations between CHD and preβ HDL concentrations in Japanese men as well as the role of preβ in reverse cholesterol transport.
30. Curb JD, Abbott RD, Rodriguez BL, et al.: A prospective study of HDL cholesterol and cholesteryl ester transfer protein gene mutations and the risk of coronary heart disease in the elderly. J Lipid Res 2004, Feb. 16 (Epub). The authors investigated genetic variations of CETP and their role in determining HDL-C levels in the elderly in the Honolulu Heart Study.
31. Oram JF: HDL apolipoproteins and ABCA1 : partners in the removal of excess cellular cholesterol. Arterioscler Thromb Vasc Biol 2003, 23:720-727. Overview of the ATP-binding cassette transporter A1 pathway and its importance as a therapeutic target for treating cardiovascular disease.
32. Okuhira KI, Tsujita M, Yamauchi Y, et al.: Potential involvement of dissociated apolipoprotein A-I in the ABCA1-dependent cellular lipid release by high density lipoprotein. J Lipid Res 2004, 45. In vitro study demonstrating that ABCA1-dependent cholesterol release to HDL is mediated by apoA-I dissociated from HDL.
33. Brousseau ME, Eberhart GP, Dupuis J, et al.: Cellular cholesterol efflux in heterozygotes for Tangier disease is markedly reduced and correlates with high density lipoprotein cholesterol concentration and particle size. J Lipid Res 2000, 41:1125-1135.
34. Asztalos BF, Brousseau ME, McNamara JR, et al.: Subpopulations of high-density lipoproteins in homozygous and heterozygous Tangier disease. Atherosclerosis 2001, 156:217-225.
35. Assman G, Nofer JR: Athero-protective effects of high-density lipoproteins. Ann Rev Med 2003, 54:321-341. A review summarizing current views on the molecular mechanisms underlying the atheroprotective effects of HDL.
36. Ohta T, Nakamura R, Frohlich JJ, et al.: Characterization of subspecies of lipoprotein containing apolipoprotein A-I in heterozygotes for familial lecithin-cholesterol acyltransferase deficiency. Atherosclerosis 1995, 114:147-155.
37. Homma S, Murayama N, Yoshida I, et al.: Marked atherosclerosis in a patient with familiar lecithin:cholesterol acyltransferase deficiency associated with end-stage renal disease and diabetes mellitus. Am J Nephrol 2001, 5:415-419.
38. Kuivenhoven JA, Pritchard H, Hill J, et al.: The molecular pathology of lecithin-cholesterol acyltransferase deficiency syndromes. J Lipid Res 1997, 38:191-205.
39. Tall AR: Plasma high density lipoproteins; metabolism and relationship to atherogenesis. J Clin Invest 1990, 86:379-384.
40. Inazu A, Brown ML, Hesler CB, et al.: Increased high density lipoprotein levels caused by a common cholesteyl-ester transfer protein mutation. N Engl J Med 1990, 323:1234-1238.
41. Asztalos BF, Horvath KV, Kajinami K, et al.: Apolipoprotein composition of HDL in cholesteryl-ester transfer protein deficiency. J Lipid Res 2004, 45:448-455. This report compared the HDL subpopulation profiles of study participants either heterozygous or homozygous for CETP deficiency with those of control participants.
42. DeBeer MC, Durbin DM, Cai L, et al.: Apolipoprotein A-II modulates the binding and selective lipid uptake of reconstituted high density lipoprotein by scavenger receptor BI. J Biol Chem 2001, 276:15832-15839.
43. Hirano K, Yamashita S, Kuga Y, et al.: Atherosclerotic disease in marked hyper-alphalipoproteinemia. Arterioscler Thromb Vasc Biol 1995, 15:1849-1856.
44. Moriyama Y, Okamura T, Inazu A, et al.: A low prevalence of coronary heart disease among subjects with increased high density lipoprotein cholesterol levels including those with plasma cholesteryl ester transfer protein deficiency. Prev Med 1998, 27:659-667.
45. Sviridov D, Nestel P: Dynamics of reverse cholesterol transport: protection against atherosclerosis. Atherosclerosis 2002, 161:245-254.
46. de Grooth GJ, Kuivenhoven JA, Stalenhoef AF, et al.: Efficacy and safety of a novel cholesteryl ester transfer protein inhibitor, JTT-705, in humans: a randomized phase II dose-response study. Circulation 2002, 105:2159-2165.
47. Clark RW, Sutfin TA, Ruggeri RB, et al.: Raising high-density lipoprotein in humans through inhibition of cholesteryl ester transfer protein: an initial multidose study of torcetrapib. Arterioscler Thromb Vasc Biol 2004, 24:490-497. The first complete report on the effects of different doses of CETP inhibitor, torcetrapid, compared with placebo in humans.
48. Jolley CD, Woollett LA, Turley SD, et al.: Centripetal cholesterol flux to the liver is dictated by events in the peripheral organs and not by the plasma high density lipoprotein and apolipoprotein A-I concentration. J Lipid Res 1998, 39:2143-2149.
49. Groen AK, Bloks VW, Bandsma RH, et al.: Hepatobiliary cholesterol transport is not impaired in ABCA1-null mice lacking HDL. J Clin Invest 2001, 108:843-850.
50. Tall AR, Wang N, Mucksavage P: Is it time to modify the reverse cholesterol transport model? J Clin Invest 2001, 108:1273-1275.
51. Kujiraoka T, Nanjee MN, Oka T, et al.: Effects of intravenous apolipoprotein A-I/phosphatidylcholine discs on LCAT, PLTP, and CETP in plasma and peripheral lymph in humans. Arterioscler Thromb Vasc Biol 2003, 23:1653-1659. A report on the effects of intravenous injection of apoA-I/phosphatidylcholine discs on three HDL components that play key roles in reverse cholesterol transport.
52. Eriksson M, Carlson LA, Miettinen TA, et al.: Stimulation of fecal steroid excretion after infusion of recombinant proapolipoprotein A-I: potential reverse cholesterol transport in humans. Circulation 1999, 100:594-598.
53. Zhang Y, Zanotti I, Reilly MP, et al.: Overexpression of apolipoprotein A-I promotes reverse cholesterol transport of cholesterol from macrophages to feces in vivo. Circulation 2003, 108:661-663. The authors investigated the ability of apoA-I overexpression to promote macrophage-specific reverse cholesterol transport in mice.
54. Nissen SE, Tsunoda T, Tuzcu EM, et al.: Effect of recombinant apoA-IMilano on coronary atherosclerosis in patients with acute coronary syndrome. JAMA 2003, 290:2292-2300. A pilot study demonstrating that administration of an exogenously produced HDL mimetic resulted in a significant regression of coronary atherosclerosis. This finding may lead to an entirely new approach to atherosclerosis treatment.
55. Paromov VM, Morton RE: Lipid transfer inhibition protein denies the participation of high density lipoprotein subfractions in lipid transfer reactions mediated by cholesteryl ester transfer protein. J Biol Chem 2003, 278:40859-40866. The authors investigated the role of lipid transfer inhibitor protein in CETP-facilitated lipid flux among HDL subfractions indicating that LTIP is a regulator of HDL metabolism.
56. Van Lanten BJ, Navab M, Shih D, et al.: The role of high density lipoproteins in oxidation and inflammation. Trends Cardiovasc Med 2001, 1:155-161.
57. Garner B, Waldeck AR, Witting PK, et al.: Oxidation of high density lipoproteins: evidence for direct reduction of lipid hydroperoxides by methionine residues of apolipoproteins A-I and A-II. J Biol Chem 1998, 273:6088-6095.
58. Navab M, Berliner JA, Subbanagounder G, et al.: HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb Vasc Biol 2001, 21:481-488.
59. Watson AD, Berliner SY, Hama BN, et al.: Protective effect of high density lipoprotein associated paraoxonase: inhibition of the biological activity of minimally oxidized low density lipoprotein. J Clin Invest 1995, 96:2882-2891.
60. Stremler KE: An oxidized derivative of phosphatidylcholine is a substrate for the platelet-activating factor acetylhydrolase from human plasma. J Biol Chem 1989, 264:5331-5334.
61. Goyal J, Wang K, Liu M, Subbaiah PV: Novel function of lecithin-cholesterol acyltransferase: hydrolysis of oxidized polar phospholipids generated during lipoprotein oxidation. J Biol Chem 1997, 272:16231-16239.
62. Navab M, Hama SY, Anantharamaiah GM, et al.: Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoproteins. J Lipid Res 2000, 41:1495-1508.
63. Boisfer E, Stengel D, Pastier D, et al.: Antioxidant properties of HDL in transgenic mice overexpressing human apolipoprotein A-II. J Lipid Res 2002, 43:732-741.
64. Klimov AN, Gurevich VS, Nikiforova AA, et al.: Antioxidative activity of high density lipoproteins in vivo. Atherosclerosis 1993, 100:13-18.
65. Kontush A, Chantepie S, Chapman MJ: Small, dense HDL particles exert potent protection of atherogenic LDL against oxidative stress. Arterioscler Thromb Vasc Biol 2003, 23:1881-1888. This study examined the capacity of HDL subfractions to protect LDL from oxidation, indicating that small dense HDL exhibits more antioxidant activity than the larger more lipidated HDL particles.
66. Kontush A, de Faria EC, Chantepie S, et al.: Antioxidative activity of HDL particle subspecies is impaired in hyperalphalipoproteinemia: relevance of enzymatic and physicochemical properties. Arterioscler Thromb Vasc Biol 2004, 24:1-9. The authors investigated the impact of hyperalphalipoproteinemia on the antioxidative activities of HDL subfractions and concluded that the intrinsic antioxidative activity of HDL particles is decreased in persons with hyperalphalipoproteinemia with low hepatic lipase activity.
67. Shih DM, Gu L, Hama S, et al.: Genetic-dietary regulation of serum paroxonase expression and its role in atherogenesis in a mouse model. J Clin Invest 1996, 97:1630-1639.
68. Cockerill GW, McDonald MC, Mota-Filipe H, et al.: High density lipoproteins reduce organ injury and organ dysfunction in a rat model of hemorrhagic shock. FASEB J 2001, 15:1941-1952.
69. Quarck R, De Geest B, Stengel D, et al.: Adenovirus-mediated gene transfer of human platelet-activating factor-acetylhydrolase prevents injury-induced neointima formation and reduces spontaneous atherosclerosis in apolipoprotein E-deficient mice. Circulation 2001, 103:2495-2500.
70. Brown BG, Cheung MC, Lee AC, et al.: Antioxidant vitamins and lipid therapy: end of a long romance? Arterioscler Thromb Vasc Biol 2002, 22:1535-1546.
71. Dwyer JH, Paul-Labrador MJ, Fan J, et al.: Progression of carotid intima-media thickness and plasma antioxidants: The Los Angeles Atherosclerosis Study. Arterioscler Thromb Vasc Biol 2004, 24:313-319. This study suggests that higher plasma levels of oxygenated carotenoids and α-carotene may be protective against early atherosclerosis.
72. O'Connell BJ, Genest J Jr: High density lipoproteins and endothelial function. Circulation 2001, 104:1978-1983.
73. Yuhanna IS, Zhu Y, Cox BE, et al.: High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat Med 2001, 7:853-857.
74. Li XA, Titlow WB, Jackson BA, et al.: High density lipoprotein binding to scavenger receptor Class B type I activates endothelial nitric-oxide synthase in a ceramide-dependent manner. J Biol Chem 2002, 277:11058-11063.
75. Rämet ME, Rämet M, Lu Q, et al.: High-density lipoprotein increases the abundance of eNOS protein in human vascular endothelial cells by increasing its half-life. J Am Coll Cardiol 2003, 41:2288-2297. The authors investigated the effects of HDL on eNOS protein concentration in cultured human endothelial cells and demonstrated a previously unrecognized mechanism for regulating eNOS.
76. Cockerill GW, Huehns TY, Weerasinghe A, et al.: Elevation of plasma high-density lipoprotein concentration reduces interleukin-1-induced expression of E-selectin in an in vivo model of acute inflammation. Circulation 2001, 103:108-112.
77. Dimayuga P, Zhu J, Oguchi S, et al.: Reconstituted HDL containing human apolipoprotein A-I reduces VCAM-1 expression and neointima formation following periadventitial cuff-induced carotid injury in apoE null mice. Biochem Biophys Res Commun 1999, 264:465-468.
78. Barter PJ, Baker PW, Rye KA: Effect of high-density lipoproteins on the expression of adhesion molecules in endothelial cells. Curr Opin Lipidol 2002, 13:285-288.
79. Calabresi L, Franceschini G, Sirtori CR, et al.: Inhibition of VCAM-1 expression in endothelial cells by reconstituted high density lipoproteins. Biochem Biophys Res Commun 1997, 238:61-65.
80. Libby P, Ridker PM, Masery A: Inflammation and atherosclerosis. Circulation 2002, 105:1135-1143.
81. Pearson TA, Mensah GA, Alexander RW, et al.: Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation 2003, 107:499-511. A good review of the importance of inflammatory markers and recommendations for the use of inflammatory markers in clinical and public health practice.
82. Van Lenten BJ, Wagner AC, Navab M, et al.: Oxidized phospholipids induce changes in hepatic paraoxonase and apoJ but not monocyte chemoattractant protein-1 via interleukin-6. J Biol Chem 2001, 276:1923-1929.
83. Six DA, Dennis EA: The expanding superfamily of phospholipase A2 enzymes: classification and characterization. Biochem Biophys Acta 2000, 1488:1-19.
84. McMurray HF, Parthasarathy S, Steinberg D: Oxidatively modified low density lipoprotein is a chemoattractant for human T lymphocytes. J Clin Invest 1993, 92:1004-1008.
85. Ansell BJ, Navab M, Hama S, et al.: Inflammatory/anti-inflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment. Circulation 2003, 108:2751-2756. In this study, the inflammatory/antiinflammatory properties of HDL were determined by the ability of the study participant's HDL to alter LDL-induced monocyte chemotactic activity in a human artery wall coculture. The authors concluded that the inflammatory/antiinflammatory properties of HDL distinguished patients from control participant better than HDL-C, and this parameter was improved with simvastatin.
86. Ridker PM: On evolutionary biology, inflammation, infection and the causes of atherosclerosis. Circulation 2002, 105:2-4.
87. Sampietro T, Bigazzi F, Dal Pino B, et al.: Increased plasma C-reactive protein in familial hypoalphalipoproteinemia: a proinflammatory condition? Circulation 2002, 105:11-14.