#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#
CS
proLékaře.cz / Journals / Athero Review / 2021 - 1

Second consensus statement of European Atherosclerosis Society on low-density lipoproteins: statement of Czech Society for Atherosclerosis

Czech version

Authors: Pavel Kraml 1;  Michal Vrablík 2;  Vladimír Bláha 3;  Renata Cífková 4;  Tomáš Freiberger 5;  David Karásek 6;  Jan Piťha 7;  Hana Rosolová 8;  Vladimír Soška 9;  Tomáš Štulc 1;  Zuzana Urbanová Za Výbor Čsat 10
Authors‘ workplace: Interní klinika 3. LF a FN Královské Vinohrady, Praha 1;  III. interní klinika – endokrinologie a metabolismu 1. LF UK a VFN v Praze 2;  III. interní gerontometabolická klinika LF UK a FN Hradec Králové 3;  Centrum kardiovaskulární prevence 1. LF UK a Thomayerova nemocnice, Praha 4;  Centrum kardiovaskulární a transplantační chirurgie, Brno 5;  III. interní klinika – nefrologická, revmatologická a endokrinologická LF UP a FN Olomouc 6;  Interní klinika 2. LF UK a FN Motol a Laboratoř pro výzkum aterosklerózy IKEM, Praha 7;  II. interní klinika LF UK a FN Plzeň 8;  Oddělení klinické biochemie, II. interní klinika LF MU a FN u sv. Anny v Brně 9;  Klinika dětského a dorostového lékařství 1. LF UK a VFN v Praze 10
Published in: AtheroRev 2021; 6(1): 9-16
Category: Guidelines

Overview

In January 2020, the expert panel of the European Atherosclerosis Society released already its second consensus regarding Low Density Lipoproteins (LDL) and their relation to cardiovascular diseases based on atherosclerosis (ASCVD) [1]. This process begins in childhood and it has been proven that 71 % middle-aged males and 43 % middle-aged females already present the signs of subclinical atherosclerosis [1–3]. This statement discusses the causal role of LDL in the pathogenesis of atherosclerosis, their direct effect on the arterial wall with a cascade of processes leading to plaque formation, at the molecular, cellular and tissue levels. The mechanisms involved in the penetration of LDL through the arterial intima, their retention within the wall, as well as the subsequent factors of the immuno-inflammatory response have not been fully eluci­dated yet. The authors further note that the other lipoproteins containing apoprotein B including Triglyceride rich lipoproteins (TGRL) and their remnants – lipoproteins of intermediate density (IDL), and also Lp(a), have a causal relationship to the pathogenesis of atherosclerosis, however their significance is not part of this statement [5–8].

Keywords:

cardiovascular diseases based on atherosclerosis – low-density lipoproteins – intermediate-density lipoproteins – cardiovascular diseases based on atherosclerosis – low density lipoproteins – intermediate density lipoproteins

Sources

  1. Borén J, Chapman MJ, Krauss RM et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2020; 41(24): 2313–2330. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehz962>.

  2. Berenson GS, Srinivasan SR, Bao W et al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. N Engl J Med 1998; 338(23): 1650–1656. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJM199806043382302>.

  3. Newman WP, Freedman DS, Voors AW et al. Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study. N Engl J Med 1986; 314(3): 138–144.Dostupné z DOI: <http://dx.doi.org/10.1056/NEJM198601163140302>.

  4. Fernandez-Friera L, Penalvo JL, Fernandez-Ortiz A et al. Prevalence, vascular distribution, and multi territorial extent of subclinical atherosclerosis in a middle-aged cohort: the PESA (Progression of Early Subclinical Atherosclerosis) study. Circulation 2015; 131(24): 2104–2113.Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCULATIONAHA.114.014310>.

  5. Nordestgaard BG. Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology. Circ Res 2016; 118(4): 547–563. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCRESAHA.115.306249>.

  6. Chapman MJ, Ginsberg HN, Amarenco P et al. European Atherosclerosis Society Consensus Panel. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J 2011; 32(11): 1345–1361.Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehr112>.

  7. Nordestgaard BG, Chapman MJ, Ray K et al. European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J 2010; 31(23): 2844–2853. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehq386>.

  8. Laufs U, Parhofer KG, Ginsberg HN et al. Clinical review on triglycerides. Eur Heart J 2020; 41(1): 99–109. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehz785>.

  9. Tabas I, Williams KJ, Borén J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: update and therapeutic implications. Circulation 2007; 116(16): 1832–1844. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCULATIONAHA.106.676890>.

  10. Williams KJ, Tabas I. The response-to-retention hypothesis of early atherogenesis. Arterioscler Thromb Vasc Biol 1995; 15(5): 551–561. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.15.5.551>.

  11. Nordestgaard BG, Zilversmit DB. Large lipoproteins are excluded from the arterial wall in diabetic cholesterol-fed rabbits. J Lipid Res 1988; 29(11): 1491–1500.

  12. Nordestgaard BG, Tybjaerg-Hansen A, Lewis B. Influx in vivo of low density, intermediate density, and very low density lipoproteins into aortic intimas of genetically hyperlipidemic rabbits. Roles of plasma concentrations, extent of aortic lesion, and lipoprotein particle size as determinants. Arterioscler Thromb 1992; 12(1): 6–18. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.12.1.6>.

  13. Zhang X, Sessa WC, Fernandez-Hernando C. Endothelial transcytosis of lipoproteins in atherosclerosis. Front Cardiovasc Med 2018; 5: 130. Dostupné z DOI: <http://dx.doi.org/10.3389/fcvm.2018.00130>.

  14. Armstrong SM, Sugiyama MG, Levy A et al. Novel assay for detection of LDL transcytosis across coronary endothelium reveals an unexpected role for SR-B1. Circulation 2014; 130(Suppl 2): A11607.

  15. Kraehling JR, Chidlow JH, Rajagopal C et al. Genome-wide RNAi screen reveals ALK1 mediates LDL uptake and transcytosis in endothelial cells. Nat Commun 2016; 7: 13516. Dostupné z DOI: <http://dx.doi.org/10.1038/ncomms13516>.

  16. Ghaffari S, Naderi Nabi F, Sugiyama MG et al. Estrogen inhibits LDL (Low-Density Lipoprotein) transcytosis by human coronary artery endothelial cells via GPER (G-Protein-Coupled Estrogen Receptor) and SR-BI (Scavenger Receptor Class B Type 1). Arterioscler Thromb Vasc Biol 2018; 38(10): 2283–2294. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.118.310792>.

  17. Bai X, Yang X, Jia X et al. CAV1-CAVIN1-LC3B-mediated autophagy regulates high glucose-stimulated LDL transcytosis. Autophagy 2020; 16(6): 1111–1129. Dostupné z DOI: <http://dx.doi.org/10.1080/15548627.2019.1659613>.

  18. Bartels ED, Christoffersen C, Lindholm MW et al. Altered metabolism of LDL in the arterial wall precedes atherosclerosis regression. Circ Res 2015; 117(11): 933–942. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCRESAHA.115.307182>.

  19. Boren J, Olin K, Lee I et al. Identification of the principal proteoglycan-binding site in LDL. A single-point mutation in apo-B100 severely affects proteoglycan interaction without affecting LDL receptor binding. J Clin Invest 1998; 101(12): 2658–2664. Dostupné z DOI: <http://dx.doi.org/10.1172/JCI2265>.

  20. Nakashima Y, Wight TN, Sueishi K. Early atherosclerosis in humans: role of diffuse intimal thickening and extracellular matrix proteoglycans. Cardiovasc Res 2008; 79(1): 14–23. Dostupné z DOI: <http://dx.doi.org/10.1093/cvr/cvn099>.

  21. Steffensen LB, Mortensen MB, Kjolby M et al. Disturbed laminar blood flow vastly augments lipoprotein retention in the artery wall: a key mechanism distinguishing susceptible from resistant sites. Arterioscler Thromb Vasc Biol 2015; 35(9): 1928–1935. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.115.305874>.

  22. Kalan JM, Roberts WC. Morphologic findings in saphenous veins used as coronary arterial bypass conduits for longer than 1 year: necropsy analysis of 53 patients, 123 saphenous veins, and 1865 five-millimeter segments of veins. Am Heart J 1990; 119(5): 1164–1184. Dostupné z DOI: <http://dx.doi.org/10.1016/s0002–8703(05)80249–2>.

  23. Berneis KK, Krauss RM. Metabolic origins and clinical significance of LDL heterogeneity. J Lipid Res 2002; 43(9): 1363–1379. Dostupné z DOI: <http://dx.doi.org/10.1194/jlr.r200004-jlr200>.

  24. Diffenderfer MR, Schaefer EJ. The composition and metabolism of large and small LDL. Curr Opin Lipidol 2014; 25(3): 221–226. Dostupné z DOI: <http://dx.doi.org/10.1097/MOL.0000000000000067>.

  25. Krauss RM. Lipoprotein subfractions and cardiovascular disease risk. Curr Opin Lipidol 2010; 21(4): 305–311. <Dostupné z DOI: http://dx.doi.org/10.1097/MOL.0b013e32833b7756>.

  26. Packard CJ, Shepherd J. Lipoprotein heterogeneity and apolipoprotein B metabolism. Arterioscler Thromb Vasc Biol 1997; 17(12): 3542–3556. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.17.12.3542>.

  27. Li KM, Wilcken DE, Dudman NP. Effect of serum lipoprotein(a) on estimation of low-density lipoprotein cholesterol by the Friedewald formula. Clin Chem 1994; 40(4): 571–573.

  28. Adiels M, Olofsson S-O, Taskinen MR et al. Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome. Arterioscler Thromb Vasc Biol 2008; 28(7): 1225–1236. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.107.160192>.

  29. Adiels M, Taskinen MR, Packard C et al. Overproduction of large VLDL particles is driven by increased liver fat content in man. Diabetologia 2006; 49(4): 755–765. Dostupné z DOI: <http://dx.doi.org/10.1007/s00125–005–0125-z>.

  30. Boren J, Watts GF, Adiels M et al. Kinetic and related determinants of plasma triglyceride concentration in abdominal obesity: multicenter Tracer Kinetic Study. Arterioscler Thromb Vasc Biol 2015; 35(10): 2218–2224. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.115.305614>.

  31. Taskinen MR, Boren J. Why is apolipoprotein CIII emerging as a novel therapeutic target to reduce the burden of cardiovascular disease? Curr Atheroscler Rep 2016; 18(10): 59. Dostupné z DOI: <http://dx.doi.org/10.1007/s11883–016–0614–1>.

  32. Tremblay AJ, Lamarche B, Ruel IL et al. Increased production of VLDL apoB-100 in subjects with familial hypercholesterolemia carrying the same null LDL receptor gene mutation. J Lipid Res 2004; 45(5): 866–872. Dostupné z DOI: <http://dx.doi.org/10.1194/jlr.M300448-JLR200>.

  33. Guerin M, Dolphin PJ, Chapman MJ. Preferential cholesterol-ester acceptors among the LDL subspecies of subjects wth familial hypercholesterolemia. Arterioscler Thromb 1994; 14(5): 679–685. Dostupné z doi: <http://dx.doi.org/10.1161/01.atv.14.5.679>.

  34. Krauss RM. Lipids and lipoproteins in patients with type 2 diabetes. Diabetes Care 2004; 27(6): 1496–1504. Dostupné z DOI: <http://dx.doi.org/10.2337/diacare.27.6.1496>.

  35. Krauss RM. Lipids and lipoproteins in patients with type 2 diabetes. Diabetes Care 2004; 27(6): 1496–1504. Dostupné z DOI: <http://dx.doi.org/10.2337/diacare.27.6.1496>.

  36. Taskinen MR, Boren J. New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis 2015; 239(2): 483–495. Dostupné z DOI: <http://dx.doi.org/10.1016/j.atherosclerosis.2015.01.039>.

  37. Taskinen MR, Adiels M, Westerbacka J et al. Dual metabolic defects are required to produce hypertriglyceridemia in obese subjects. Arterioscler Thromb Vasc Biol 2011; 31(9): 2144–2150. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.111.224808>.

  38. Guerin M, Le Goff W, Lassel TS et al. Atherogenic role of elevated CE transfer from HDL to VLDL(1) and dense LDL in type 2 diabetes: impact of the degree of triglyceridemia. Arterioscler Thromb Vasc Biol 2001; 21(2): 282–288. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.21.2.282>.

  39. Lada AT, Rudel LL. Associations of low density lipoprotein particle composition with atherogenicity. Curr Opin Lipidol 2004; 15(1): 19–24. Dostupné z DOI: <http://dx.doi.org/10.1097/00041433–200402000–00005>.

  40. Ruuth M, Nguyen SD, Vihervaara T et al. Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths. Eur Heart J 2018; 39(27): 2562–2573. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehy319>.

  41. Witztum JL, Lichtman AH. The influence of innate and adaptive immune responses on atherosclerosis. Annu Rev Pathol 2014; 9: 73–102. Dostupné z DOI: <http://dx.doi.org/10.1146/annurev-pathol-020712–163936>.

  42. Steinberg D, Witztum JL. Oxidized low-density lipoprotein and atherosclerosis. Arterioscler Thromb Vasc Biol 2010; 30(12): 2311–2316. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.108.179697>.

  43. Mora S, Caulfield MP, Wohlgemuth J et al. Atherogenic lipoprotein subfractions determined by ion mobility and first cardiovascular events after random allocation to high-intensity statin or placebo: the Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial. Circulation 2015; 132(23): 2220–2229. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCULATIONAHA.115.016857>.

  44. Chancharme L, Thérond P, Nigon F et al. Cholesteryl ester hydroperoxide lability is a key feature of the oxidative susceptibility of small, dense LDL. Arterioscler Thromb Vasc Biol 1999; 19(3): 810–820. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.19.3.810>.

  45. Shin MJ, Krauss RM. Apolipoprotein CIII bound to apoB-containing lipoproteins is associated with small, dense LDL independent of plasma triglyceride levels in healthy men. Atherosclerosis 2010; 211(1): 337–341. Dostupné z DOI: <http://dx.doi.org/10.1016/j.atherosclerosis.2010.02.025>.

  46. Younis N, Charlton-Menys V, Sharma R et al. Glycation of LDL in non-diabetic people: small dense LDL is preferentially glycated both in vivo and in vitro. Atherosclerosis 2009; 202(1): 162–168. Dostupné z DOI: <http://dx.doi.org/10.1016/j.atherosclerosis.2008.04.036>.

  47. Nigon F, Lesnik P, Rouis M et al. Discrete subspecies of human low density lipoproteins are heterogeneous in their interaction with the cellular LDL receptor. J Lipid Res 1991; 32(11): 1741–1753.

  48. Campos H, Arnold KS, Balestra ME et al. Differences in receptor binding of LDL subfractions. Arterioscler Thromb Vasc Biol 1996; 16(6): 794–801. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.16.6.794>.

  49. Skalen K, Gustafsson M, Rydberg EK et al. Subendothelial retention of atherogenic lipoproteins in early atherosclerosis. Nature 2002; 417(6890): 750–754. Dostupné z DOI: <http://dx.doi.org/10.1038/nature00804>.

  50. Binder CJ, Papac-Milicevic N, Witztum JL. Innate sensing of oxidation-specific epitopes in health and disease. Nat Rev Immunol 2016; 16(8): 485–497. Dostupné z DOI: <http://dx.doi.org/10.1038/nri.2016.63>.

  51. Bochkov VN, Oskolkova OV, Birukov KG et al. Generation and biological activities of oxidized phospholipids. Antioxid Redox Signal 2010; 12(8): 1009–1059. Dostupné z DOI: <http://dx.doi.org/10.1089/ars.2009.2597>.

  52. Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med 2011; 17(11): 1410–1422. Dostupné z DOI: <http://dx.doi.org/10.1038/nm.2538>.

  53. Moore KJ, Koplev S, Fisher EA et al. Macrophage trafficking, inflammatory resolution, and genomics in atherosclerosis: JACC macrophage in CVD series (Part 2). J Am Coll Cardiol 2018; 72(18): 2181–2197. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2018.08.2147>.

  54. Kruth HS, Jones NL, Huang W et al. Macropinocytosis is the endocytic pathway that mediates macrophage foam cell formation with native low density lipoprotein. J Biol Chem 2005; 280(3): 2352–2360. Dostupné z DOI: <http://dx.doi.org/10.1074/jbc.M407167200>.

  55. Anzinger JJ, Chang J, Xu Q et al. Native low-density lipoprotein uptake by macrophage colony-stimulating factor-differentiated human macrophages is mediated by macropinocytosis and micropinocytosis. Arterioscler Thromb Vasc Biol 2010; 30(10): 2022–2031. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.110.210849>.

  56. Williams JW, Giannarelli C, Rahman A et al. Macrophage biology, classification, and phenotype in cardiovascular disease: JACC macrophage in CVD series (Part 1). J Am Coll Cardiol 2018;72(18):2166–2180. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2018.08.2148>.

  57. Pourcet B, Staels B. Alternative macrophages in atherosclerosis: not always protective! J Clin Invest 2018; 128(3): 910–912. Dostupné z DOI: <http://dx.doi.org/10.1172/JCI120123>.

  58. Stewart CR, Stuart LM, Wilkinson K et al. CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer. Nat Immunol 2010; 11(2): 155–161. Dostupné z DOI: <http://dx.doi.org/10.1038/ni.1836>.

  59. Shankman LS, Gomez D, Cherepanova OA et al. KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis. Nat Med 2015; 21(6): 628–637. Dostupné z DOI: <http://dx.doi.org/10.1038/nm.3866>.

  60. Duewell P, Kono H, Rayner KJ et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 2010; 464(7293): 1357–1361. Dostupné z DOI: <http://dx.doi.org/10.1038/nature08938>.

  61. Baumer Y, McCurdy S, Weatherby TM et al. Hyperlipidemia-induced cholesterol crystal production by endothelial cells promotes atherogenesis. Nat Commun 2017; 8(1): 1129. Dostupné z DOI: <http://dx.doi.org/10.1038/s41467–017–01186-z>.

  62. Tabas I, Lichtman AH. Monocyte-macrophages and T cells in atherosclerosis. Immunity 2017; 47(4): 621–634. Dostupné z DOI: <http://dx.doi.org/10.1016/j.immuni.2017.09.008>.

  63. Wolf D, Ley K. Immunity and inflammation in atherosclerosis. Circ Res 2019; 124(2): 315–327. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCRESAHA.118.313591>.

  64. Ait-Oufella H, Sage AP, Mallat Z et al. Adaptive (T and B cells) immunity and control by dendritic cells in atherosclerosis. Circ Res 2014; 114(10): 1640–1660. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCRESAHA.114.302761>.

  65. Sage AP, Tsiantoulas D, Binder CJ et al. The role of B cells in atherosclerosis. Nat Rev Cardiol 2019; 16(3): 180–196. Dostupné z DOI: <http://dx.doi.org/10.1038/s41569–018–0106–9>.

  66. Tsiantoulas D, Diehl CJ, Witztum JL et al. B cells and humoral immunity in atherosclerosis. Circ Res 2014; 114(11): 1743–1756. Dostupné z DOI: <http://dx.doi.org/10.1161/CIRCRESAHA.113.301145>.

  67. Ridker PM, Everett BM, Thuren T et al. [Glynn RJCANTOS Trial Group]. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 2017; 377(12): 1119–1131. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJMoa1707914>.

  68. Arandjelovic S, Ravichandran KS. Phagocytosis of apoptotic cells in homeostasis. Nat Immunol 2015; 16(9): 907–917. Dostupné z DOI: <http://dx.doi.org/10.1038/ni.3253>.

  69. Poon IK, Lucas CD, Rossi AG et al. Apoptotic cell clearance: basic biology and therapeutic potential. Nat Rev Immunol 2014; 14(3): 166–180. Dostupné z DOI: <http://dx.doi.org/10.1038/nri3607>.

  70. Dalli J, Serhan CN. Specific lipid mediator signatures of human phagocytes: microparticles stimulate macrophage efferocytosis and pro-resolving mediators. Blood 2012; 120(15): e60–e72. Dostupné z DOI: <http://dx.doi.org/10.1182/blood-2012–04–423525>.

  71. Vengrenyuk Y, Nishi H, Long X et al. Cholesterol loading reprograms the microRNA-143/145-myocardin axis to convert aortic smooth muscle cells to a dysfunctional macrophage-like phenotype. Arterioscler Thromb Vasc Biol 2015; 35(3): 535–546. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.114.304029>.

  72. Wirka RC, Wagh D, Paik DT et al. Atheroprotective roles of smooth muscle cell phenotypic modulation and the TCF21 disease gene as revealed by single-cell analysis. Nat Med 2019; 25(8): 1280–1289. Dostupné z DOI: <http://dx.doi.org/10.1038/s41591–019–0512–5>.

  73. Abela GS, Aziz K, Vedre A et al. Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes. Am J Cardiol 2009; 103(7): 959–968. Dostupné z DOI: <http://dx.doi.org/10.1016/j.amjcard.2008.12.019>.

  74. Dai J, Xing L, Jia H et al. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study. Eur Heart J 2018; 39(22): 2077–2085. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehy101>.

  75. Iannaccone M, Quadri G, Taha S et al. Prevalence and predictors of culprit plaque rupture at OCT in patients with coronary artery disease: a meta-analysis. Eur Heart J Cardiovasc Imaging 2016; 17(10): 1128–1137. Dostupné z DOI: <http://dx.doi.org/10.1093/ehjci/jev283>.

  76. Pasterkamp G, den Ruijter HM, Libby P. Temporal shifts in clinical presentation and underlying mechanisms of atherosclerotic disease. Nat Rev Cardiol 2017; 14(1): 21–29. Dostupné z DOI: <http://dx.doi.org/10.1038/nrcardio.2016.166>.

  77. Virmani R, Burke AP, Farb A et al. Pathology of the vulnerable plaque. J Am Coll Cardiol 2006; 47(8 Suppl): C13–C18. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2005.10.065>.

  78. Falk E, Nakano M, Bentzon JF et al. Update on acute coronary syndromes: the pathologists’ view. Eur Heart J 2013; 34(10): 719–728. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehs411>.

  79. Vervueren PL, Elbaz M, Dallongeville J et al. Relationships between chronic use of statin therapy, presentation of acute coronary syndromes and one-year mortality after an incident acute coronary event. Int J Cardiol 2013; 163(1): 102–104. Dostupné z DOI: <http://dx.doi.org/10.1016/j.ijcard.2012.06.112>.

  80. Stary HC, Chandler AB, Dinsmore RE et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995; 92(5): 1355–1374. Dostupné z DOI: <http://dx.doi.org/10.1161/01.cir.92.5.1355>.

  81. Burke AP, Farb A, Malcom GT et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997; 336(18): 1276–1282. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJM199705013361802>.

  82. Kataoka Y, Hammadah M, Puri R et al. Plaque microstructures in patients with coronary artery disease who achieved very low low-density lipoprotein cholesterol levels. Atherosclerosis 2015; 242(2): 490–495. Dostupné z DOI: <http://dx.doi.org/10.1016/j.atherosclerosis.2015.08.005>.

  83. Johnson JL. Metalloproteinases in atherosclerosis. Eur J Pharmacol 2017; 816: 93–106. Dostupné z DOI: <http://dx.doi.org/10.1016/j.ejphar.2017.09.007>.

  84. Dykun I, Lehmann N, Kalsch H et al. Statin medication enhances progression of coronary artery calcification: the Heinz Nixdorf Recall Study. J Am Coll Cardiol 2016; 68(19): 2123–2125. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2016.08.040>.

  85. DeFina LF, Radford NB, Barlow CE et al. Association of all-cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiol 2019; 4(2): 174. Dostupné z DOI: <http://dx.doi.org/10.1001/jamacardio.2018.4628>.

  86. Mauriello A, Servadei F, Zoccai GB et al. Coronary calcification identifies the vulnerable patient rather than the vulnerable plaque. Atherosclerosis 2013; 229(1): 124–129. Dostupné z DOI: <http://dx.doi.org/10.1016/j.atherosclerosis.2013.03.010>.

  87. Motoyama S, Kondo T, Sarai M et al. Multislice computed tomographic characteristics of coronary lesions in acute coronary syndromes. J Am Coll Cardiol 2007; 50(4): 319–326. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2007.03.044>.

  88. Erdman J, Kessler T, Munoz Venegas L et al. A decade of genome wide association studies for coronary artery disease: the challenges ahead. Cardiovasc Res 2018; 114(9): 1241–1257. Dostupné z DOI: <http://doi: 10.1093/cvr/cvy084>.

  89. Erdmann J, Kessler T, Munoz Venegas L et al. A decade of genome-wide association studies for coronary artery disease: the challenges ahead. Cardiovasc Res 2018; 114(9): 1241–1257. Dostupné z DOI: <http://dx.doi.org/10.1093/cvr/cvy084>.

  90. Ntalla I, Kanoni S, Zeng L et al. [Biobank CardioMetabolic Consortium CHD Working Group]. Genetic risk score for coronary disease identifies predispositions to cardiovascular and noncardiovascular diseases. J Am Coll Cardiol 2019; 73(23): 2932–2942. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2019.03.512>.

  91. Chen S, Wang X, Wang J et al. Genomic variant in CAV1 increases susceptibility to coronary artery disease and myocardial infarction. Atherosclerosis 2016; 246:148–156. Dostupné z DOI i: <http://dx.doi.org/10.1016/j.atherosclerosis.2016.01.008>.

  92. Samani NJ, Erdmann J, Hall AS et al. [HWTCCC and the Cardiogenics Consortium]. Genomewide association analysis of coronary artery disease. N Engl J Med 2007; 357(5): 443–453. Dostupné z DOI: <http://dx.doi.org/10.1056/NEJMoa072366>.

  93. Klarin D, Damrauer SM, Cho K et al. Genetics of blood lipids among ∼300,000 multi-ethnic participants of the Million Veteran Program. Nat Genet 2018; 50(11): 1514–1523. Dostupné z DOI: <http://dx.doi.org/10.1038/s41588–018–0222–9>.

  94. Schaar JA, Muller JE, Falk E et al. Terminology for high-risk and vulnerable coronary artery plaques. Report of a meeting on the vulnerable plaque, June 17 and 18, 2003, Santorini, Greece. Eur Heart J 2004; 25(12): 1077–1082. Dostupné z DOI: <http://dx.doi.org/10.1016/j.ehj.2004.01.002.

  95. Virmani R, Kolodgie FD, Burke AP et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2000; 20(5): 1262–1275. Dostupné z DOI: <http://dx.doi.org/10.1161/01.atv.20.5.1262>.

  96. Owens AP, Passam FH, Antoniak S et al. Monocyte tissue factor-dependent activation of coagulation in hypercholesterolemic mice and monkeys is inhibited by simvastatin. J Clin Invest 2012; 122(2): 558–568. Dostupné z DOI: <http://dx.doi.org/10.1172/JCI58969>.

  97. Obermayer G, Afonyushkin T, Binder CJ. Oxidized low-density lipoprotein in inflammation-driven thrombosis. J Thromb Haemost 2018;16(3):418–428. Dostupné z DOI: <http://dx.doi.org/10.1111/jth.13925>.

  98. Doi H, Kugiyama K, Oka H et al. Remnant lipoproteins induce proatherothrombogenic molecules in endothelial cells through a redox-sensitive mechanism. Circulation 2000; 102(6): 670–676. Dostupné z DOI: <http://dx.doi.org/10.1161/01.cir.102.6.670>.

  99. Chan HC, Ke LY, Chu CS et al. Highly electronegative LDL from patients with ST-elevation myocardial infarction triggers platelet activation and aggregation. Blood 2013; 122(22): 3632–3641. Dostupné z DOI: <http://dx.doi.org/10.1182/blood-2013–05–504639>.

  100. Otsuka F, Finn AV, Yazdani SK et al. The importance of the endothelium in atherothrombosis and coronary stenting. Nat Rev Cardiol 2012; 9(8): 439–453. Dostupné z DOI: <http://dx.doi.org/10.1038/nrcardio.2012.64>.

  101. Chen YC, Huang AL, Kyaw TS et al. Atherosclerotic plaque rupture: identifying the straw that breaks the Camel’s back. Arterioscler Thromb Vasc Biol 2016; 36(8): e63–e72. Dostupné z DOI: <http://dx.doi.org/10.1161/ATVBAHA.116.307993>.

  102. Ference BA, Ginsberg HN, Graham I et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2017; 38(32): 2459–2472. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehx144>.

  103. Goldstein JL, Brown MS. A century of cholesterol and coronaries: from plaques to genes to statins. Cell 2015; 161(1): 161–172. Dostupné z DOI: <http://dx.doi.org/10.1016/j.cell.2015.01.036>.

  104. Crisby M, Nordin-Fredriksson G, Shah PK et al. Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques: implications for plaque stabilization. Circulation 2001; 103(7): 926–933. Dostupné z DOI: <http://dx.doi.org/10.1161/01.cir.103.7.926>.

  105. Nissen SE, Nicholls SJ, Sipahi I et al. [ASTEROID Investigators]. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the trial. JAMA 2006; 295(13): 1556–1565. Dostupné z DOI: <http://dx.doi.org/10.1001/jama.295.13.jpc60002>.

  106. Almeida SO, Budoff M. Effect of statins on atherosclerotic plaque. Trends Cardiovasc Med 2019; 29(8): 451–455. Dostupné z DOI: <http://dx.doi.org/10.1016/j.tcm.2019.01.001>.

  107. Andelius L, Mortensen MB, Norgaard BL et al. Impact of statin therapy on coronary plaque burden and composition assessed by coronary computed tomographic angiography: a systematic review and meta-analysis. Eur Heart J Cardiovasc Imaging 2018; 19(8): 850–858. Dostupné z DOI: <http://dx.doi.org/10.1093/ehjci/jey012>.

  108. Hattori K, Ozaki Y, Ismail TF et al. Impact of statin therapy on plaque characteristics as assessed by serial OCT, grayscale and integrated backscatter-IVUS. JACC Cardiovasc Imaging 2012; 5(2): 169–177. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jcmg.2011.11.012>.

  109. Nordestgaard BG, Langsted A. Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology. J Lipid Res 2016;57(11):1953–1975. Dostupné z DOI: <http://dx.doi.org/10.1194/jlr.R071233>.

  110. Nordestgaard BG, Nicholls SJ, Langste0d A et al. Advances in lipid-lowering therapy through gene-silencing technologies. Nat Rev Cardiol 2018; 15(5): 261–272. Dostupné z DOI: <http://dx.doi.org/10.1038/nrcardio.2018.3>.

  111. Baigent C, Catapano AL, Koskinas KC et al. [Mach FESC Scientific Document Group]. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification, to reduce cardiovascular risk: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). Eur Heart J 2020; 41(1): 111–188. Dostupné z DOI: <http://dx.doi.org/10.1093/eurheartj/ehz455>

  112. Klarin D, Zhu QM, Emdin CA et al. Genetic analysis in UK Biobank links insulin resistance and transendothelial migration pathways to coronary artery 000disease. Nat Genet 2017; 49(9): 1392–1397. Dostupné z DOI: <http://dx.doi.org/10.1038/ng.3914>.

  113. Schwartz GG, Bessac L, Berdan LG et al. Effect of alirocumab, a monoclonal antibody to PCSK9, on long-term cardiovascular outcomes following acute coronary syndromes: rationale and design of the ODYSSEY outcomes trial. Am Heart J 2014; 168(5): 682–689. Dostupné z DOI: <http://dx.doi.org/10.1016/j.ahj.2014.07.028>.

  114. Koren MJ, Sabatine MS, Giugliano RP et al. Long-term efficacy and safety of evolocumab in patients with hypercholesterolemia. J Am Coll Cardiol 2019; 74(17): 2132–2146. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacc.2019.08.1024>.

Labels
Angiology Diabetology Internal medicine Cardiology General practitioner for adults
Úvodník
Important current information of consensus statement of EAS on low-density lipoproteins: editorial
Liečba dyslipidémií počas pandémie COVID-19
Antiatherosclerotic and antiinflammatory activities of SGLT2 inhibitors
Early cardiovascular risk intervention means cummulation of positive impacts in time
Why we need to improve serum levels of cholesterol after percutanneous coronary intervention
Low concentration of plasma cholesterol and type 2. diabetes mellitus
Comment on Low concentration of plasma cholesterol and type 2. diabetes mellitus
How we are (un)successful in the managing of dyslipidemia and why
Inclisiran: the first siRNA approved by European Medicines Agency for treatment of dyslipidemias
Rešerše zajímavých článků ze zahraniční literatury
24. virtuální kongres o ateroskleróze
Article was published in

Athero Review

Issue 1
2021 Issue 1
Most read in this issue
Topics Journals
Login
Forgotten password

Enter the email address that you registered with. We will send you instructions on how to set a new password.

Login

Don‘t have an account?  Create new account

#ADS_BOTTOM_SCRIPTS#