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Erschienen in: Herz 1/2017

14.11.2016 | Koronare Herzerkrankung | Übersichten

Klinische Bedeutung des HDL-Cholesterins

Erschienen in: Herz | Ausgabe 1/2017

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Zusammenfassung

Einleitung

In Deutschland werden pro Jahr 16–17 Mio. Bestimmungen des HDL („high-density lipoprotein“)-Cholesterins (HDL‑C) durchgeführt und interpretiert. Aktuelle Daten haben zu einer fundamentalen Neubewertung der klinischen Bedeutung des HDL‑C geführt.

Methode

Diese Übersichtsarbeit basiert auf einer selektiven Literaturrecherche.

Ergebnisse

Niedriges HDL‑C ist in der Regel ein Hinweis auf ein erhöhtes kardiovaskuläres Risiko, insbesondere in der Primärprävention, die epidemiologische Beziehung zwischen HDL‑C und dem Risiko ist jedoch komplex. HDL spielt eine Rolle für den Rücktransport und die Ausscheidung von Cholesterin. Die biologischen Funktionen von HDL sind dabei von der Protein- und Lipidzusammensetzung abhängig, die nicht durch den HDL-C-Gehalt erfasst werden. In pathologischer Zusammensetzung kann HDL auch negative vaskuläre Effekte ausüben.

Schlussfolgerung

Im Vergleich zum LDL („low-density lipoprotein“)-Cholesterin (LDL-C) kommt dem HDL‑C eine nachrangige Bedeutung für die kardiovaskuläre Risikostratifizierung zu, die generelle Berechnung von Quotienten aus LDL- und HDL‑C ist nicht sinnvoll. Niedriges HDL‑C sollte dazu veranlassen, die betroffene Person bezüglich metabolischer und inflammatorischer Pathologien zu untersuchen. Eine Anhebung des HDL‑C durch Lebensstilumstellung (Rauchstopp, körperliche Bewegung) hat positive Auswirkungen und ist empfehlenswert. Das HDL‑C stellt jedoch aktuell kein valides Ziel für eine medikamentöse Therapie dar.
Literatur
1.
Zurück zum Zitat Gordon DJ, Probstfield JL, Garrison RJ et al (1989) High density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation 79:8–15CrossRefPubMed Gordon DJ, Probstfield JL, Garrison RJ et al (1989) High density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies. Circulation 79:8–15CrossRefPubMed
2.
Zurück zum Zitat Genest JJ, McNamara JR, Salem DN, Schaefer EJ (1991) Prevalence of risk factors in men with premature coronary artery disease. Am J Cardiol 67:1185–1189CrossRefPubMed Genest JJ, McNamara JR, Salem DN, Schaefer EJ (1991) Prevalence of risk factors in men with premature coronary artery disease. Am J Cardiol 67:1185–1189CrossRefPubMed
3.
Zurück zum Zitat Di Angelantonio E, Sarwar N, Perry P et al (2009) Major lipids, apolipoproteins, and risk of vascular disease. JAMA 302:1993–2000CrossRefPubMed Di Angelantonio E, Sarwar N, Perry P et al (2009) Major lipids, apolipoproteins, and risk of vascular disease. JAMA 302:1993–2000CrossRefPubMed
4.
Zurück zum Zitat van der Steeg WA, Holme I, Boekholdt SM et al (2008) High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A‑I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies. J Am Coll Cardiol 51:634–642CrossRefPubMed van der Steeg WA, Holme I, Boekholdt SM et al (2008) High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A‑I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies. J Am Coll Cardiol 51:634–642CrossRefPubMed
5.
Zurück zum Zitat Bartlett J, Predazzi IM, Williams SM et al (2016) Is isolated low high-density lipoprotein cholesterol a cardiovascular disease risk factor? New insights from the Framingham offspring study. Circ Cardiovasc Qual Outcomes 9:206–212CrossRefPubMed Bartlett J, Predazzi IM, Williams SM et al (2016) Is isolated low high-density lipoprotein cholesterol a cardiovascular disease risk factor? New insights from the Framingham offspring study. Circ Cardiovasc Qual Outcomes 9:206–212CrossRefPubMed
7.
Zurück zum Zitat Quintao EC, Cazita PM (2010) Lipid transfer proteins: past, present and perspectives. Atherosclerosis 209:1–9CrossRefPubMed Quintao EC, Cazita PM (2010) Lipid transfer proteins: past, present and perspectives. Atherosclerosis 209:1–9CrossRefPubMed
8.
Zurück zum Zitat Bodzioch M, Orso E, Klucken J et al (1999) The gene encoding ATP-binding cassette transporter 1 is mutated in Tangier disease. Nat Genet 22:347–351CrossRefPubMed Bodzioch M, Orso E, Klucken J et al (1999) The gene encoding ATP-binding cassette transporter 1 is mutated in Tangier disease. Nat Genet 22:347–351CrossRefPubMed
9.
Zurück zum Zitat Rust S, Rosier M, Funke H et al (1999) Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1. Nat Genet 22:352–355CrossRefPubMed Rust S, Rosier M, Funke H et al (1999) Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1. Nat Genet 22:352–355CrossRefPubMed
10.
Zurück zum Zitat Bachorik PS, Ross JW (1995) National Cholesterol Education Program recommendations for measurement of low-density lipoprotein cholesterol: executive summary. The National Cholesterol Education Program Working Group on Lipoprotein Measurement. Clin Chem 41:1414–1420PubMed Bachorik PS, Ross JW (1995) National Cholesterol Education Program recommendations for measurement of low-density lipoprotein cholesterol: executive summary. The National Cholesterol Education Program Working Group on Lipoprotein Measurement. Clin Chem 41:1414–1420PubMed
11.
Zurück zum Zitat Warnick GR, Nauck M, Rifai N (2001) Evolution of methods for measurement of HDL-cholesterol: from ultracentrifugation to homogeneous assays. Clin Chem 47:1579–1596PubMed Warnick GR, Nauck M, Rifai N (2001) Evolution of methods for measurement of HDL-cholesterol: from ultracentrifugation to homogeneous assays. Clin Chem 47:1579–1596PubMed
12.
Zurück zum Zitat van den Broek I, Romijn FP, Nouta J et al (2016) Automated multiplex LC-MS/MS assay for quantifying serum apolipoproteins A‑I, B, C‑I, C‑II, C‑III, and E with qualitative apolipoprotein E phenotyping. Clin Chem 62:188–197CrossRefPubMed van den Broek I, Romijn FP, Nouta J et al (2016) Automated multiplex LC-MS/MS assay for quantifying serum apolipoproteins A‑I, B, C‑I, C‑II, C‑III, and E with qualitative apolipoprotein E phenotyping. Clin Chem 62:188–197CrossRefPubMed
13.
Zurück zum Zitat Kaess B, Fischer M, Baessler A et al (2008) The lipoprotein subfraction profile: heritability and identification of quantitative trait loci. J Lipid Res 49:715–723CrossRefPubMed Kaess B, Fischer M, Baessler A et al (2008) The lipoprotein subfraction profile: heritability and identification of quantitative trait loci. J Lipid Res 49:715–723CrossRefPubMed
14.
Zurück zum Zitat Khera AV, Cuchel M, de la Llera-Moya M et al (2011) Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N Engl J Med 364:127–135CrossRefPubMedPubMedCentral Khera AV, Cuchel M, de la Llera-Moya M et al (2011) Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N Engl J Med 364:127–135CrossRefPubMedPubMedCentral
15.
16.
Zurück zum Zitat Ritsch A, Scharnagl H, Marz W (2015) HDL cholesterol efflux capacity and cardiovascular events. N Engl J Med 372:1870–1871PubMed Ritsch A, Scharnagl H, Marz W (2015) HDL cholesterol efflux capacity and cardiovascular events. N Engl J Med 372:1870–1871PubMed
17.
Zurück zum Zitat Marz W, Ritsch A (2016) Cholesterol efflux capacity: choke point of reverse cholesterol traffic? J Am Coll Cardiol 67:2488–2491CrossRefPubMed Marz W, Ritsch A (2016) Cholesterol efflux capacity: choke point of reverse cholesterol traffic? J Am Coll Cardiol 67:2488–2491CrossRefPubMed
18.
Zurück zum Zitat Vergeer M, Korporaal SJ, Franssen R et al (2011) Genetic variant of the scavenger receptor BI in humans. N Engl J Med 364:136–145CrossRefPubMed Vergeer M, Korporaal SJ, Franssen R et al (2011) Genetic variant of the scavenger receptor BI in humans. N Engl J Med 364:136–145CrossRefPubMed
19.
Zurück zum Zitat Ljunggren SA, Levels JH, Hovingh K et al (2015) Lipoprotein profiles in human heterozygote carriers of a functional mutation P297S in scavenger receptor class B1. Biochim Biophys Acta 1851:1587–1595CrossRefPubMed Ljunggren SA, Levels JH, Hovingh K et al (2015) Lipoprotein profiles in human heterozygote carriers of a functional mutation P297S in scavenger receptor class B1. Biochim Biophys Acta 1851:1587–1595CrossRefPubMed
20.
Zurück zum Zitat Zanoni P, Khetarpal SA, Larach DB et al (2016) Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease. Science 351:1166–1171CrossRefPubMedPubMedCentral Zanoni P, Khetarpal SA, Larach DB et al (2016) Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease. Science 351:1166–1171CrossRefPubMedPubMedCentral
21.
Zurück zum Zitat Zhang Y, Da Silva JR, Reilly M, Billheimer JT, Rothblat GH, Rader DJ (2005) Hepatic expression of scavenger receptor class B type I (SR-BI) is a positive regulator of macrophage reverse cholesterol transport in vivo. J Clin Invest 115:2870–2874CrossRefPubMedPubMedCentral Zhang Y, Da Silva JR, Reilly M, Billheimer JT, Rothblat GH, Rader DJ (2005) Hepatic expression of scavenger receptor class B type I (SR-BI) is a positive regulator of macrophage reverse cholesterol transport in vivo. J Clin Invest 115:2870–2874CrossRefPubMedPubMedCentral
22.
Zurück zum Zitat Huby T, Doucet C, Dachet C et al (2006) Knockdown expression and hepatic deficiency reveal an atheroprotective role for SR-BI in liver and peripheral tissues. J Clin Invest 116:2767–2776CrossRefPubMedPubMedCentral Huby T, Doucet C, Dachet C et al (2006) Knockdown expression and hepatic deficiency reveal an atheroprotective role for SR-BI in liver and peripheral tissues. J Clin Invest 116:2767–2776CrossRefPubMedPubMedCentral
23.
Zurück zum Zitat Voight BF, Peloso GM, Orho-Melander M et al (2012) Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 380:572–580CrossRefPubMedPubMedCentral Voight BF, Peloso GM, Orho-Melander M et al (2012) Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 380:572–580CrossRefPubMedPubMedCentral
24.
Zurück zum Zitat Ference BA, Majeed F, Penumetcha R, Flack JM, Brook RD (2015) Effect of naturally random allocation to lower low-density lipoprotein cholesterol on the risk of coronary heart disease mediated by polymorphisms in NPC1L1, HMGCR, or both: a 2 x 2 factorial Mendelian randomization study. J Am Coll Cardiol 65:1552–1561CrossRefPubMed Ference BA, Majeed F, Penumetcha R, Flack JM, Brook RD (2015) Effect of naturally random allocation to lower low-density lipoprotein cholesterol on the risk of coronary heart disease mediated by polymorphisms in NPC1L1, HMGCR, or both: a 2 x 2 factorial Mendelian randomization study. J Am Coll Cardiol 65:1552–1561CrossRefPubMed
26.
Zurück zum Zitat Taskinen MR, Boren J (2015) New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis 239:483–495CrossRefPubMed Taskinen MR, Boren J (2015) New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis 239:483–495CrossRefPubMed
27.
Zurück zum Zitat Badimon JJ, Badimon L, Fuster V (1990) Regression of atherosclerostic lesions by high density lipoprotein lasma fraction in the cholesterol-fed rabbit. J Clin Invest 85:1234–1241CrossRefPubMedPubMedCentral Badimon JJ, Badimon L, Fuster V (1990) Regression of atherosclerostic lesions by high density lipoprotein lasma fraction in the cholesterol-fed rabbit. J Clin Invest 85:1234–1241CrossRefPubMedPubMedCentral
28.
Zurück zum Zitat Ameli S, Hultgardh-Nilsson A, Cercek B et al (1994) Recombinant apolipoprotein A‑I Milano reduces intimal thickening after balloon injury in hypercholesterolemic rabbits. Circulation 90:1935–1941CrossRefPubMed Ameli S, Hultgardh-Nilsson A, Cercek B et al (1994) Recombinant apolipoprotein A‑I Milano reduces intimal thickening after balloon injury in hypercholesterolemic rabbits. Circulation 90:1935–1941CrossRefPubMed
29.
Zurück zum Zitat Shah PK, Nilsson J, Kaul S et al (1998) Effects of recombinant apolipoprotein A‑I(Milano) on aortic atherosclerosis in apolipoprotein E‑deficient mice. Circulation 97:780–785CrossRefPubMed Shah PK, Nilsson J, Kaul S et al (1998) Effects of recombinant apolipoprotein A‑I(Milano) on aortic atherosclerosis in apolipoprotein E‑deficient mice. Circulation 97:780–785CrossRefPubMed
30.
Zurück zum Zitat Cockerill GW, Rye KA, Gamble JR, Vadas MA, Barter PJ (1995) High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol 15:1987–1994CrossRefPubMed Cockerill GW, Rye KA, Gamble JR, Vadas MA, Barter PJ (1995) High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler Thromb Vasc Biol 15:1987–1994CrossRefPubMed
31.
Zurück zum Zitat Yuhanna IS, Zhu Y, Cox BE et al (2001) High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat Med 7:853–857CrossRefPubMed Yuhanna IS, Zhu Y, Cox BE et al (2001) High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat Med 7:853–857CrossRefPubMed
32.
Zurück zum Zitat Mineo C, Yuhanna IS, Quon MJ, Shaul PW (2003) High density lipoprotein-induced endothelial nitric-oxide synthase activation is mediated by Akt and MAP kinases. J Biol Chem 278:9142–9149CrossRefPubMed Mineo C, Yuhanna IS, Quon MJ, Shaul PW (2003) High density lipoprotein-induced endothelial nitric-oxide synthase activation is mediated by Akt and MAP kinases. J Biol Chem 278:9142–9149CrossRefPubMed
33.
Zurück zum Zitat Nofer JR, van der Giet M, Tolle M et al (2004) HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3. J Clin Invest 113:569–581CrossRefPubMedPubMedCentral Nofer JR, van der Giet M, Tolle M et al (2004) HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3. J Clin Invest 113:569–581CrossRefPubMedPubMedCentral
34.
Zurück zum Zitat Vaisar T, Pennathur S, Green PS et al (2007) Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL. J Clin Invest 117:746–756CrossRefPubMedPubMedCentral Vaisar T, Pennathur S, Green PS et al (2007) Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL. J Clin Invest 117:746–756CrossRefPubMedPubMedCentral
35.
Zurück zum Zitat Besler C, Heinrich K, Rohrer L et al (2011) Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease. J Clin Invest 121:2693–2708CrossRefPubMedPubMedCentral Besler C, Heinrich K, Rohrer L et al (2011) Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease. J Clin Invest 121:2693–2708CrossRefPubMedPubMedCentral
36.
Zurück zum Zitat Riwanto M, Rohrer L, Roschitzki B et al (2013) Altered activation of endothelial anti- and proapoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of high-density lipoprotein-proteome remodeling. Circulation 127:891–904CrossRefPubMed Riwanto M, Rohrer L, Roschitzki B et al (2013) Altered activation of endothelial anti- and proapoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of high-density lipoprotein-proteome remodeling. Circulation 127:891–904CrossRefPubMed
37.
38.
Zurück zum Zitat Davidson WS, Silva RA, Chantepie S, Lagor WR, Chapman MJ, Kontush A (2009) Proteomic analysis of defined HDL subpopulations reveals particle-specific protein clusters: relevance to antioxidative function. Arterioscler Thromb Vasc Biol 29:870–876CrossRefPubMedPubMedCentral Davidson WS, Silva RA, Chantepie S, Lagor WR, Chapman MJ, Kontush A (2009) Proteomic analysis of defined HDL subpopulations reveals particle-specific protein clusters: relevance to antioxidative function. Arterioscler Thromb Vasc Biol 29:870–876CrossRefPubMedPubMedCentral
39.
Zurück zum Zitat Vickers KC, Palmisano BT, Shoucri BM, Shamburek RD, Remaley AT (2011) MicroRNAs are transported in plasma and delivered to recipient cells by high-density lipoproteins. Nat Cell Biol 13:423–433CrossRefPubMedPubMedCentral Vickers KC, Palmisano BT, Shoucri BM, Shamburek RD, Remaley AT (2011) MicroRNAs are transported in plasma and delivered to recipient cells by high-density lipoproteins. Nat Cell Biol 13:423–433CrossRefPubMedPubMedCentral
40.
Zurück zum Zitat Mackness MI, Durrington PN, Mackness B (2000) How high-density lipoprotein protects against the effects of lipid peroxidation. Curr Opin Lipidol 11:383–388CrossRefPubMed Mackness MI, Durrington PN, Mackness B (2000) How high-density lipoprotein protects against the effects of lipid peroxidation. Curr Opin Lipidol 11:383–388CrossRefPubMed
41.
Zurück zum Zitat Regieli JJ, Jukema JW, Doevendans PA et al (2009) Paraoxonase variants relate to 10-year risk in coronary artery disease: impact of a high-density lipoprotein-bound antioxidant in secondary prevention. J Am Coll Cardiol 54:1238–1245CrossRefPubMed Regieli JJ, Jukema JW, Doevendans PA et al (2009) Paraoxonase variants relate to 10-year risk in coronary artery disease: impact of a high-density lipoprotein-bound antioxidant in secondary prevention. J Am Coll Cardiol 54:1238–1245CrossRefPubMed
42.
Zurück zum Zitat Besler C, Luscher TF, Landmesser U (2012) Molecular mechanisms of vascular effects of High-density lipoprotein: alterations in cardiovascular disease. EMBO Mol Med 4:251–268CrossRefPubMedPubMedCentral Besler C, Luscher TF, Landmesser U (2012) Molecular mechanisms of vascular effects of High-density lipoprotein: alterations in cardiovascular disease. EMBO Mol Med 4:251–268CrossRefPubMedPubMedCentral
43.
Zurück zum Zitat Sorrentino SA, Besler C, Rohrer L et al (2010) Endothelial-vasoprotective effects of high-density lipoprotein are impaired in patients with type 2 diabetes mellitus but are improved after extended-release niacin therapy. Circulation 121:110–122CrossRefPubMed Sorrentino SA, Besler C, Rohrer L et al (2010) Endothelial-vasoprotective effects of high-density lipoprotein are impaired in patients with type 2 diabetes mellitus but are improved after extended-release niacin therapy. Circulation 121:110–122CrossRefPubMed
44.
Zurück zum Zitat Griffin JH, Kojima K, Banka CL, Curtiss LK, Fernandez JA (1999) High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C. J Clin Invest 103:219–227CrossRefPubMedPubMedCentral Griffin JH, Kojima K, Banka CL, Curtiss LK, Fernandez JA (1999) High-density lipoprotein enhancement of anticoagulant activities of plasma protein S and activated protein C. J Clin Invest 103:219–227CrossRefPubMedPubMedCentral
45.
Zurück zum Zitat Drew BG, Duffy SJ, Formosa MF et al (2009) High-density lipoprotein modulates glucose metabolism in patients with type 2 diabetes mellitus. Circulation 119:2103–2111CrossRefPubMed Drew BG, Duffy SJ, Formosa MF et al (2009) High-density lipoprotein modulates glucose metabolism in patients with type 2 diabetes mellitus. Circulation 119:2103–2111CrossRefPubMed
46.
Zurück zum Zitat Barter PJ, Rye KA, Tardif JC et al (2011) Effect of torcetrapib on glucose, insulin, and hemoglobin A1c in subjects in the investigation of lipid level management to understand its impact in atherosclerotic events (ILLUMINATE) trial. Circulation 124:555–562CrossRefPubMed Barter PJ, Rye KA, Tardif JC et al (2011) Effect of torcetrapib on glucose, insulin, and hemoglobin A1c in subjects in the investigation of lipid level management to understand its impact in atherosclerotic events (ILLUMINATE) trial. Circulation 124:555–562CrossRefPubMed
47.
Zurück zum Zitat Siebel AL, Natoli AK, Yap FY et al (2013) Effects of high-density lipoprotein elevation with cholesteryl ester transfer protein inhibition on insulin secretion. Circ Res 113:167–175CrossRefPubMed Siebel AL, Natoli AK, Yap FY et al (2013) Effects of high-density lipoprotein elevation with cholesteryl ester transfer protein inhibition on insulin secretion. Circ Res 113:167–175CrossRefPubMed
48.
Zurück zum Zitat Mortensen SP, Boushel R (2013) High-density lipoprotein: a new therapeutic target for glucose intolerance? Circulation 128:2349–2350CrossRefPubMed Mortensen SP, Boushel R (2013) High-density lipoprotein: a new therapeutic target for glucose intolerance? Circulation 128:2349–2350CrossRefPubMed
49.
Zurück zum Zitat von Eckardstein A, Widmann C (2014) High-density lipoprotein, beta cells, and diabetes. Cardiovasc Res 103:384–394CrossRef von Eckardstein A, Widmann C (2014) High-density lipoprotein, beta cells, and diabetes. Cardiovasc Res 103:384–394CrossRef
50.
Zurück zum Zitat Lehti M, Donelan E, Abplanalp W et al (2013) High-density lipoprotein maintains skeletal muscle function by modulating cellular respiration in mice. Circulation 128:2364–2371CrossRefPubMedPubMedCentral Lehti M, Donelan E, Abplanalp W et al (2013) High-density lipoprotein maintains skeletal muscle function by modulating cellular respiration in mice. Circulation 128:2364–2371CrossRefPubMedPubMedCentral
51.
Zurück zum Zitat Speer T, Rohrer L, Blyszczuk P et al (2013) Abnormal high-density lipoprotein induces endothelial dysfunction via activation of Toll-like receptor-2. Immunity 38:754–768CrossRefPubMed Speer T, Rohrer L, Blyszczuk P et al (2013) Abnormal high-density lipoprotein induces endothelial dysfunction via activation of Toll-like receptor-2. Immunity 38:754–768CrossRefPubMed
52.
Zurück zum Zitat Zewinger S, Speer T, Kleber ME et al (2014) HDL cholesterol is not associated with lower mortality in patients with kidney dysfunction. J Am Soc Nephrol 25:1073–1082CrossRefPubMedPubMedCentral Zewinger S, Speer T, Kleber ME et al (2014) HDL cholesterol is not associated with lower mortality in patients with kidney dysfunction. J Am Soc Nephrol 25:1073–1082CrossRefPubMedPubMedCentral
53.
54.
Zurück zum Zitat Silbernagel G, Schottker B, Appelbaum S et al (2013) High-density lipoprotein cholesterol, coronary artery disease, and cardiovascular mortality. Eur Heart J 34:3563–3571CrossRefPubMed Silbernagel G, Schottker B, Appelbaum S et al (2013) High-density lipoprotein cholesterol, coronary artery disease, and cardiovascular mortality. Eur Heart J 34:3563–3571CrossRefPubMed
55.
Zurück zum Zitat Zewinger S, Drechsler C, Kleber ME et al (2015) Serum amyloid A: high-density lipoproteins interaction and cardiovascular risk. Eur Heart J 36:3007–3016PubMed Zewinger S, Drechsler C, Kleber ME et al (2015) Serum amyloid A: high-density lipoproteins interaction and cardiovascular risk. Eur Heart J 36:3007–3016PubMed
56.
Zurück zum Zitat Li XM, Tang WH, Mosior MK et al (2013) Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks. Arterioscler Thromb Vasc Biol 33:1696–1705CrossRefPubMedPubMedCentral Li XM, Tang WH, Mosior MK et al (2013) Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks. Arterioscler Thromb Vasc Biol 33:1696–1705CrossRefPubMedPubMedCentral
57.
Zurück zum Zitat Singh IM, Shishehbor MH, Ansell BJ (2007) High-density lipoprotein as a therapeutic target: a systematic review. JAMA 298:786–798CrossRefPubMed Singh IM, Shishehbor MH, Ansell BJ (2007) High-density lipoprotein as a therapeutic target: a systematic review. JAMA 298:786–798CrossRefPubMed
58.
Zurück zum Zitat Eckel RH, Jakicic JM, Ard JD et al (2013) AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014(129):76–99 Eckel RH, Jakicic JM, Ard JD et al (2013) AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014(129):76–99
59.
Zurück zum Zitat Adams V, Besler C, Fischer T et al (2013) Exercise training in patients with chronic heart failure promotes restoration of high-density lipoprotein functional properties. Circ Res 113:1345–1355CrossRefPubMed Adams V, Besler C, Fischer T et al (2013) Exercise training in patients with chronic heart failure promotes restoration of high-density lipoprotein functional properties. Circ Res 113:1345–1355CrossRefPubMed
60.
Zurück zum Zitat Cai M, Zou Z (2016) Effect of aerobic exercise on blood lipid and glucose in obese or overweight adults: a meta-analysis of randomised controlled trials. Obes Res Clin Pract. doi:10.1016/j.orcp.2015.10.010 Cai M, Zou Z (2016) Effect of aerobic exercise on blood lipid and glucose in obese or overweight adults: a meta-analysis of randomised controlled trials. Obes Res Clin Pract. doi:10.​1016/​j.​orcp.​2015.​10.​010
61.
Zurück zum Zitat Ghafouri K, Cooney J, Bedford DK, Wilson J, Caslake MJ, Gill JM (2015) Moderate exercise increases affinity of large very low-density lipoproteins for hydrolysis by lipoprotein lipase. J Clin Endocrinol Metab 100:2205–2213CrossRefPubMed Ghafouri K, Cooney J, Bedford DK, Wilson J, Caslake MJ, Gill JM (2015) Moderate exercise increases affinity of large very low-density lipoproteins for hydrolysis by lipoprotein lipase. J Clin Endocrinol Metab 100:2205–2213CrossRefPubMed
62.
Zurück zum Zitat Briel M, Ferreira-Gonzalez I, You JJ et al (2009) Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis. BMJ 338:b92CrossRefPubMedPubMedCentral Briel M, Ferreira-Gonzalez I, You JJ et al (2009) Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis. BMJ 338:b92CrossRefPubMedPubMedCentral
63.
Zurück zum Zitat Jun M, Foote C, Lv J et al (2010) Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis. Lancet 375:1875–1884CrossRefPubMed Jun M, Foote C, Lv J et al (2010) Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis. Lancet 375:1875–1884CrossRefPubMed
64.
Zurück zum Zitat Keech A, Simes RJ, Barter P et al (2005) Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 366:1849–1861CrossRefPubMed Keech A, Simes RJ, Barter P et al (2005) Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 366:1849–1861CrossRefPubMed
65.
Zurück zum Zitat Ginsberg HN, Elam MB, Lovato LC et al (2010) Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med 362:1563–1574CrossRefPubMed Ginsberg HN, Elam MB, Lovato LC et al (2010) Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med 362:1563–1574CrossRefPubMed
66.
Zurück zum Zitat Rajamani K, Colman PG, Li LP et al (2009) Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet 373:1780–1788CrossRefPubMedPubMedCentral Rajamani K, Colman PG, Li LP et al (2009) Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet 373:1780–1788CrossRefPubMedPubMedCentral
67.
Zurück zum Zitat Fruchart JC, Sacks FM, Hermans MP (2010) Implications of the ACCORD lipid study: perspective from the Residual Risk Reduction Initiative (R(3)i). Curr Med Res Opin 26:1793–1797CrossRefPubMed Fruchart JC, Sacks FM, Hermans MP (2010) Implications of the ACCORD lipid study: perspective from the Residual Risk Reduction Initiative (R(3)i). Curr Med Res Opin 26:1793–1797CrossRefPubMed
68.
Zurück zum Zitat Bruckert E, Labreuche J, Deplanque D, Touboul PJ, Amarenco P (2011) Fibrates effect on cardiovascular risk is greater in patients with high triglyceride levels or atherogenic dyslipidemia profile: a systematic review and meta-analysis. J Cardiovasc Pharmacol 57:267–272CrossRefPubMed Bruckert E, Labreuche J, Deplanque D, Touboul PJ, Amarenco P (2011) Fibrates effect on cardiovascular risk is greater in patients with high triglyceride levels or atherogenic dyslipidemia profile: a systematic review and meta-analysis. J Cardiovasc Pharmacol 57:267–272CrossRefPubMed
69.
Zurück zum Zitat Bruckert E, Labreuche J, Amarenco P (2010) Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis. Atherosclerosis 210:353–361CrossRefPubMed Bruckert E, Labreuche J, Amarenco P (2010) Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis. Atherosclerosis 210:353–361CrossRefPubMed
70.
Zurück zum Zitat Boden WE, Probstfield JL, Anderson T et al (2011) Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 365:2255–2267CrossRefPubMed Boden WE, Probstfield JL, Anderson T et al (2011) Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 365:2255–2267CrossRefPubMed
71.
Zurück zum Zitat Lavigne PM, Karas RH (2013) The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression. J Am Coll Cardiol 61:440–446CrossRefPubMed Lavigne PM, Karas RH (2013) The current state of niacin in cardiovascular disease prevention: a systematic review and meta-regression. J Am Coll Cardiol 61:440–446CrossRefPubMed
72.
Zurück zum Zitat Landray MJ, Haynes R, Hopewell JC et al (2014) Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 371:203–212CrossRefPubMed Landray MJ, Haynes R, Hopewell JC et al (2014) Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med 371:203–212CrossRefPubMed
73.
Zurück zum Zitat Administration FaD (2016) Withdrawal of approval of indications related to the coadministration with statins in applications for niacin extended-release tablets and fenofibric acid delayed-release capsules. Federal Register Administration FaD (2016) Withdrawal of approval of indications related to the coadministration with statins in applications for niacin extended-release tablets and fenofibric acid delayed-release capsules. Federal Register
74.
Zurück zum Zitat Administration FaD (2016) Withdrawal of approval of new drug applications for Advicor and Simcor. Federal Register Administration FaD (2016) Withdrawal of approval of new drug applications for Advicor and Simcor. Federal Register
75.
Zurück zum Zitat Fielding CJ, Fielding PE (1995) Molecular physiology of reverse cholesterol transport. J Lipid Res 36:211–228PubMed Fielding CJ, Fielding PE (1995) Molecular physiology of reverse cholesterol transport. J Lipid Res 36:211–228PubMed
76.
Zurück zum Zitat Tall AR (1993) Plasma cholesteryl ester transfer protein. J Lipid Res 34:1255–1274PubMed Tall AR (1993) Plasma cholesteryl ester transfer protein. J Lipid Res 34:1255–1274PubMed
77.
Zurück zum Zitat Johannsen TH, Frikke-Schmidt R, Schou J, Nordestgaard BG, Tybjaerg-Hansen A (2012) Genetic inhibition of CETP, ischemic vascular disease and mortality, and possible adverse effects. J Am Coll Cardiol 60:2041–2048CrossRefPubMed Johannsen TH, Frikke-Schmidt R, Schou J, Nordestgaard BG, Tybjaerg-Hansen A (2012) Genetic inhibition of CETP, ischemic vascular disease and mortality, and possible adverse effects. J Am Coll Cardiol 60:2041–2048CrossRefPubMed
78.
Zurück zum Zitat Li YY, Wu XY, Xu J, Qian Y, Zhou CW, Wang B (2013) Apo A5 −1131 T/C, FgB −455 G/A, −148 C/T, and CETP TaqIB gene polymorphisms and coronary artery disease in the Chinese population: a meta-analysis of 15,055 subjects. Mol Biol Rep 40:1997–2014CrossRefPubMed Li YY, Wu XY, Xu J, Qian Y, Zhou CW, Wang B (2013) Apo A5 −1131 T/C, FgB −455 G/A, −148 C/T, and CETP TaqIB gene polymorphisms and coronary artery disease in the Chinese population: a meta-analysis of 15,055 subjects. Mol Biol Rep 40:1997–2014CrossRefPubMed
79.
Zurück zum Zitat Niu W, Qi Y (2015) Circulating cholesteryl ester transfer protein and coronary heart disease: mendelian randomization meta-analysis. Circ Cardiovasc Genet 8:114–121CrossRefPubMed Niu W, Qi Y (2015) Circulating cholesteryl ester transfer protein and coronary heart disease: mendelian randomization meta-analysis. Circ Cardiovasc Genet 8:114–121CrossRefPubMed
80.
Zurück zum Zitat Ritsch A, Scharnagl H, Eller P et al (2010) Cholesteryl ester transfer protein and mortality in patients undergoing coronary angiography: the Ludwigshafen Risk and Cardiovascular Health study. Circulation 121:366–374CrossRefPubMedPubMedCentral Ritsch A, Scharnagl H, Eller P et al (2010) Cholesteryl ester transfer protein and mortality in patients undergoing coronary angiography: the Ludwigshafen Risk and Cardiovascular Health study. Circulation 121:366–374CrossRefPubMedPubMedCentral
81.
Zurück zum Zitat Hovingh GK, Ray KK, Boekholdt SM (2015) Is cholesteryl ester transfer protein inhibition an effective strategy to reduce cardiovascular risk? CETP as a target to lower CVD risk: suspension of disbelief? Circulation 132:433–440CrossRefPubMed Hovingh GK, Ray KK, Boekholdt SM (2015) Is cholesteryl ester transfer protein inhibition an effective strategy to reduce cardiovascular risk? CETP as a target to lower CVD risk: suspension of disbelief? Circulation 132:433–440CrossRefPubMed
82.
Zurück zum Zitat Brousseau ME, Schaefer EJ, Wolfe ML et al (2004) Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N Engl J Med 350:1505–1515CrossRefPubMed Brousseau ME, Schaefer EJ, Wolfe ML et al (2004) Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N Engl J Med 350:1505–1515CrossRefPubMed
83.
Zurück zum Zitat Kastelein JJ (2007) Refocusing on use of cholesteryl ester transfer protein inhibitors. Am J Cardiol 100:S47–S52CrossRef Kastelein JJ (2007) Refocusing on use of cholesteryl ester transfer protein inhibitors. Am J Cardiol 100:S47–S52CrossRef
84.
Zurück zum Zitat Barter PJ, Caulfield M, Eriksson M et al (2007) Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 357:2109–2122CrossRefPubMed Barter PJ, Caulfield M, Eriksson M et al (2007) Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 357:2109–2122CrossRefPubMed
85.
Zurück zum Zitat Schwartz GG, Olsson AG, Abt M et al (2012) Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 367:2089–2099CrossRefPubMed Schwartz GG, Olsson AG, Abt M et al (2012) Effects of dalcetrapib in patients with a recent acute coronary syndrome. N Engl J Med 367:2089–2099CrossRefPubMed
86.
Zurück zum Zitat Morton RE, Izem L (2015) Modification of CETP function by changing its substrate preference: a new paradigm for CETP drug design. J Lipid Res 56:612–619CrossRefPubMedPubMedCentral Morton RE, Izem L (2015) Modification of CETP function by changing its substrate preference: a new paradigm for CETP drug design. J Lipid Res 56:612–619CrossRefPubMedPubMedCentral
87.
Zurück zum Zitat Parhofer KG (2015) Increasing HDL-cholesterol and prevention of atherosclerosis: a critical perspective. Atheroscler Suppl 18:109–111CrossRefPubMed Parhofer KG (2015) Increasing HDL-cholesterol and prevention of atherosclerosis: a critical perspective. Atheroscler Suppl 18:109–111CrossRefPubMed
88.
Zurück zum Zitat Kingwell BA, Chapman MJ, Kontush A, Miller NE (2014) HDL-targeted therapies: progress, failures and future. Nat Rev Drug Discov 13:445–464CrossRefPubMed Kingwell BA, Chapman MJ, Kontush A, Miller NE (2014) HDL-targeted therapies: progress, failures and future. Nat Rev Drug Discov 13:445–464CrossRefPubMed
89.
Zurück zum Zitat Siddiqi HK, Kiss D, Rader D (2015) HDL-cholesterol and cardiovascular disease: rethinking our approach. Curr Opin Cardiol 30:536–542CrossRefPubMed Siddiqi HK, Kiss D, Rader D (2015) HDL-cholesterol and cardiovascular disease: rethinking our approach. Curr Opin Cardiol 30:536–542CrossRefPubMed
Metadaten
Titel
Klinische Bedeutung des HDL-Cholesterins
Publikationsdatum
14.11.2016
Erschienen in
Herz / Ausgabe 1/2017
Print ISSN: 0340-9937
Elektronische ISSN: 1615-6692
DOI
https://doi.org/10.1007/s00059-016-4499-0

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