Гипертриглицеридемия (триглицерид-богатые липопротеины и их ремнанты): роль в развитии атеросклеротических сердечно-сосудистых заболеваний и стратегия контроля. Заключение Комитета экспертов Российского кардиологического общества (РКО), Национального общества по изучению атеросклероза (НОА), Российского общества кардиосоматической реабилитации и вторичной профилактики (РосОКР)

Обложка

Цитировать

Полный текст

Аннотация

В представленном экспертном документе обсуждается проблема высокой распространённости сердечно-сосудистых заболеваний (ССЗ), обусловленных атеросклерозом. Сегодня очевидно, что причины и генез атеросклеротических ССЗ (АССЗ) не всегда можно объяснить с позиции нарушения липидного обмена, основанного исключительно на липопротеинах низкой плотности (ЛНП). В последние годы наблюдается рост количества исследований, посвящённых гипертриглицеридемии (ГТГ), обсуждаются механизмы ее формирования и значимость в атеротромбогенезе. В этой связи возникает необходимость актуализации ключевых вопросов, определяющих первопричину развития АССЗ при ГТГ и роль компонентов триглицерид-богатых липопротеинов (ТГ-богатых ЛП) и их ремнантов в этом процессе. К настоящему времени завершены эпидемиологические и генетические исследования, свидетельствующие о причинно-следственной связи ГТГ с развитием АССЗ независимо от уровня холестерина (ХС) ЛНП; определена значимость ТГ-богатых ЛП в формировании высокого остаточного сердечно-сосудистого риска на фоне контроля уровня ХС ЛНП; получены доказательства профилактической пользы при снижении повышенного уровня ТГ в крови.

Об авторах

Марина Геннадьевна Бубнова

Национальный медицинский исследовательский центр терапии и профилактической медицины

Автор, ответственный за переписку.
Email: mbubnova@gnicpm.ru
ORCID iD: 0000-0003-2250-5942
SPIN-код: 6733-1430

д-р мед. наук, профессор

Россия, Москва

Марат Владиславович Ежов

Национальный медицинский исследовательский центр кардиологии им. акад. Е.И. Чазова

Email: MVEzhov@cardio.ru
ORCID iD: 0000-0002-1518-6552
SPIN-код: 7623-2135

д-р мед. наук, профессор

Россия, Москва

Давид Меерович Аронов

Национальный медицинский исследовательский центр терапии и профилактической медицины

Email: daronov@gnicPM.ru
ORCID iD: 0000-0003-0484-9805
SPIN-код: 5094-6509

д-р мед. наук, профессор

Россия, Москва

Альберт Сарварович Галявич

Казанский государственный медицинский университет

Email: agalyavich@mail.ru
ORCID iD: 0000-0002-4510-6197
SPIN-код: 4694-0795

д-р мед. наук, профессор

Россия, Казань

Виктор Савельевич Гуревич

Санкт-Петербургский государственный университет; Северо-Западный государственный медицинский университет им. И.И. Мечникова

Email: ater@med122.com
ORCID iD: 0000-0002-6815-444X
SPIN-код: 3267-2301

д-р мед. наук, профессор

Россия, Санкт-Петербург; Санкт-Петербург

Дмитрий Викторович Дупляков

Самарский государственный медицинский университет

Email: duplyakov@yahoo.com
ORCID iD: 0000-0002-6453-2976
SPIN-код: 5665-9578

д-р мед. наук, профессор

Россия, Самара

Виталий Константинович Зафираки

Кубанский государственный медицинский университет

Email: vzaphir@mail.ru
ORCID iD: 0000-0003-3883-8696
SPIN-код: 9844-3747

д-р мед. наук, профессор

Россия, Краснодар

Наталья Станиславовна Карамнова

Национальный медицинский исследовательский центр терапии и профилактической медицины

Email: nkaramnova@gnicpm.ru
ORCID iD: 0000-0002-8604-712X
SPIN-код: 2878-3016

д-р мед. наук

 

Россия, Москва

Василий Васильевич Кашталап

Кемеровский государственный медицинский университет

Email: v_kash@mail.ru
ORCID iD: 0000-0003-3729-616X
SPIN-код: 8816-7409

д-р мед. наук, профессор

Россия, Кемерово

Геннадий Александрович Коновалов

Клинико-диагностический центр «МЕДСИ на Белорусской»

Email: mbubnova@gnicpm.ru
ORCID iD: 0000-0001-6644-3064

д-р мед. наук, профессор

Россия, Москва

Алексей Николаевич Мешков

Национальный медицинский исследовательский центр терапии и профилактической медицины

Email: eleno4ka_g@mail.ru
ORCID iD: 0000-0001-5989-6233
SPIN-код: 6340-5187

д-р мед. наук, профессор

Россия, Москва

Андрей Григорьевич Обрезан

Санкт-Петербургский государственный университет

Email: obrezan1@yandex.ru
ORCID iD: 0000-0001-6115-7923
SPIN-код: 4790-3880

д-р мед. наук, профессор

Россия, Санкт-Петербург

Александр Анатольевич Семенкин

Омский государственный медицинский университет

Email: asemyonkin@mail.ru
ORCID iD: 0000-0002-3786-9995
SPIN-код: 5836-8365

д-р мед. наук, профессор

Россия, Омск

Игорь Владимирович Сергиенко

Национальный медицинский исследовательский центр кардиологии им. акад. Е.И. Чазова

Email: igorcardio@mail.ru
ORCID iD: 0000-0003-1534-3965
SPIN-код: 1643-1586

д-р мед. наук, профессор

Россия, Москва

Александр Евгеньевич Филиппов

Санкт-Петербургский государственный университет

Email: AEFilippov@hse.ru
ORCID iD: 0000-0002-4413-5068
SPIN-код: 9717-0103

д-р мед. наук, профессор

Россия, Санкт-Петербург

Список литературы

  1. Ezhov MV, Kukharchuk VV, Sergienko IV, et al. Disorders of lipid metabolism. Clinical Guidelines 2023. Russian Journal of Cardiology. 2023;28(5):5471. doi: 10.15829/1560-4071-2023-5471 EDN: YVZOWJ
  2. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41:111–88. doi: 10.1093/eurheartj/ehz455
  3. Visseren FLJ, Mach F, Smulders YM, et al. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. Eur Heart J. 2021;42:3227–337. doi: 10.1093/eurheartj/ehab484
  4. Hegele RA, Ginsberg HN, Chapman MJ, et al. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management. Lancet Diabetes Endocrinol. 2014;2(8):655–66. doi: 10.1016/S2213-8587(13)70191-8
  5. Langsted A, Freiberg JJ, Nordestgaard BG. Fasting and nonfasting lipid levels: influence of normal food intake on lipids, lipoproteins, apolipoproteins, and cardiovascular risk prediction. Circulation. 2008;118:2047–56. doi: 10.1161/CIRCULATIONAHA.108.804146
  6. Nordestgaard BG, Langsted A, Mora S, et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points — a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Eur Heart J. 2016;37(25):1944–58. doi: 10.1093/eurheartj/ehw152
  7. Nordestgaard BG. Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease New Insights From Epidemiology, Genetics, and Biology. Circ Res. 2016;118:547–63. doi: 10.1161/CIRCRESAHA.115.306249
  8. Ginsberg HN, Packard CJ, Chapman MJ, et al. Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies-a consensus statement from the European Atherosclerosis Society. Eur Heart J. 2021;42(47):4791–806. doi: 10.1093/eurheartj/ehab551
  9. Castelli WP. Epidemiology of triglycerides: a view from Framingham. American J Cardiol. 1992;70(19):H3–H9. doi: 10.1016/0002-9149(92)91083-g
  10. Carr RA, Rejowski BJ, Cote GA, et al. Systematic review of hypertriglyceridemia-induced acute pancreatitis: a more virulent etiology? Pancreatology. 2016;16:469–76. doi: 10.1016/j.pan.2016.02.011
  11. Pedersen SB, Langsted A, Nordestgaard BG. Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis. JAMA Intern Med. 2016;176:1834–42. doi: 10.1001/jamainternmed.2016.6875
  12. Murphy M, Shemg X, MacDonald TM. Hypertriglyceridemia and acute pancreatitis. JAMA Intern Med. 2013;173(2):162–4. doi: 10.1001/2013.jamaintermed.477
  13. Faghih M, Singh VK. Do elevated triglycerides truly trigger acute pancreatitis? Dig Dis Sci. 2019;64:616–8. doi: 10.1007/s10620-019-05501-0
  14. Virani SS, Morris PB, Agarwala A, et al. 2021 ACC expert consensus decision pathway on the management of ASCVD risk reduction in patients with persistent hypertriglyceridemia: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2021;78(9):960–93. doi: 1016/j.jacc.2021.06.011
  15. Stürzebecher PE, Katzmann JL, Laufs U. What is ‘remnant cholesterol’? Eur Heart J. 2023;44:1446–8. doi: 10.1093/eurheartj/ehac783
  16. Remaley AT, Otvos JD. Methodological issues regarding: "A third of nonfasting plasma cholesterol is in remnant lipoproteins: lipoprotein subclass profiling in 9293 individuals". Atherosclerosis. 2020;302:55–6. doi: 10.1016/j.atherosclerosis.2020.01.020
  17. Tybjærg-Hansen A, Nordestgaard BG, Christoffersen M. Triglyceride-rich remnant lipoproteins are more atherogenic than LDL per particle: is this important? Eur Heart J. 2023;44:4196–8. doi: 10.1093/eurheartj/ehad419
  18. White KT, Moorthy MV, Akinkuolie AO, et al. Identifying an optimal cutpoint for the diagnosis of hypertriglyceridemia in the nonfasting state. Clin Chem. 2015;61:1156–63. doi: 10.1373/clinchem.2015.241752
  19. Raja V, Aguiar C, Alsayed N, et al. Non-HDL-cholesterol in dyslipidemia: Review of the state-of-the-art literature and outlook. Atherosclerosis. 2023;383:117312. doi: 10.1016/j.atherosclerosis.2023.117312
  20. Fredrickson DS. An international classification of hyperlipidemias and hyperlipoproteinemias. Ann Intern Med. Ann Intern Med. 1971;75(3):471–2. doi: 10.7326/0003-4819-75-3-471
  21. Gill PK, Dron JS, Berberich AJ, et al. Combined hyperlipidemia is genetically similar to isolated hypertriglyceridemia. J Clin Lipidol. 2021;15(1):79–87. doi: 10.1016/j.jacl.2020.11.006
  22. Laufs U, Parhofer KG, Ginsberg HN, Hegele RA. Clinical review on triglycerides. Eur Heart J. 2020;41:99–109. doi: 10.1093/eurheartj/ehz785
  23. Cohen JD, Cziraky MJ, Cai Q, et al. 30-year trends in serum lipids among United States adults: results from the National Health and Nutrition Examination Surveys II, III, and 1999-2006. Am J Cardiol. 2010;106(7):969–75. doi: 10.1016/j.amjcard.2010.05.030
  24. Simha V. Management of hypertriglyceridemia. BMJ. 2020;371:m3109. doi: 10.1136/bmj.m3109
  25. Chyzhyk V, Kozmic S, Brown AS, et al. Extreme hypertriglyceridemia: genetic diversity, pancreatitis, pregnancy, and prevalence. J Clin Lipidol. 2019;13(1):89–99. doi: 10.1016/j.jacl.2018.09.007
  26. Gitt A.K, Drexel H, Feely J, et al. DYSIS Investigators. Persistent lipid abnormalities in statin-treated patients and predictors of LDL-cholesterol goal achievement in clinical practice in Europe and Canada. Eur J Prev Cardiol. 2012;19(2):221–30. doi: 10.1177/1741826711400545
  27. Drapkina OM, Imaeva AE, Kutsenko VA, et al. Dyslipidemia in the Russian Federation: population data, associations with risk factors. Cardiovascular Therapy and Prevention. 2023;22(8S):3791. doi: 10.15829/1728-8800-2023-3791 EDN DGYJLA
  28. Karpov Y, Khomitskaya Y. PROMETHEUS: an observational, cross-sectional, retrospective study of hypertriglyceridemia in Russia. Cardiovasc Diabetol. 2015;14:115. doi: 10.1186/s12933-015-0268-2
  29. Ghandehari H, Kamal-Bahl S, Wong ND. Prevalence and extent of dyslipidemia and recommended lipid levels in US adults with and without cardiovascular comorbidities: The National Health and Nutrition Examination Survey 2003-2004. Am Heart J. 2008;156(1):112–9. doi: 10.1016/j.ahj.2008.03.005
  30. Chait A, Eckel RH. The chylomicronemia syndrome is most often multifactorial: a narrative review of causes and treatment. Ann Intern Med. 2019;170:626–34. doi: 10.7326/M19-0203
  31. Gugliucci A. The chylomicron saga: time to focus on postprandial metabolism. Front Endocrinol. 2023;14:1322869. doi: 10.3389/fendo.2023.1322869
  32. Nordestgaard BG, Zilversmit DB. Large lipoproteins are excluded from the arterial wall in diabetic cholesterol-fed rabbits. J Lipid Res. 1988;29:1491–500.
  33. Bubnova MG, Oganov RG. Impaired edible fats tolerance and its contribution to atherothrombogenesis. Terapevticheskiy arkhiv. 2004;1:73–8. (In Russ.)
  34. Sylvers-Davie KL, Davies BSJ. Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8. Am J Physiol Endocrinol Metab. 2021;321(4):E493–508. doi: 10.1152/ajpendo.00195.2021
  35. Williams KJ, Chen K. Recent insights into factors affecting remnant lipoprotein uptake. Curr Opin Lipidol. 2010;21(3):218–28. doi: 10.1097/MOL.0b013e328338cabc
  36. Veniant MM, Zlot CH, Walzem RL, et al. Lipoprotein clearance mechanisms in LDL receptor-deficient "Apo-B48-only" and "Apo-B100-only" mice. J Clin Invest. 1998;102(8):1559–68. doi: 10.1172/JCI4164
  37. Salinas CAA, Chapman MJ. Remnant lipoproteins: are they equal to or more atherogenic than LDL? Curr Opin Lipidol. 2020;31:132–9. doi: 10.1097/MOL.0000000000000682
  38. Botham K, Bravo E, Elliott J, Wheeler-Jones C. Direct interaction of dietary lipids carried in chylomicron remnants with cells of the artery wall: implications for atherosclerosis development. Curr Pharm Des. 2005;11(28):3681–95. doi: 10.2174/138161205774580732
  39. Dalla-Riva J, Garonna E, Elliott J, et al. Botham KM, Wheeler-Jones CP. Endothelial cells as targets for chylomicron remnants. Atheroscler Suppl. 2010;11(1):31–7. doi: 10.1016/j.atherosclerosissup.2010.04.001
  40. Liberale L, Dallegri F, Montecucco F, Carbone F. Pathophysiological relevance of macrophage subsets in atherogenesis. Thromb Haemost. 2017;117:7–18. doi: 10.1160/TH16-08-0593
  41. Pal S, Semorine K, Watts GF, Mamo J. Identification of lipoproteins of intestinal origin in human atherosclerotic plaque. Clin Chem Lab Med. 2003;41:792–5. doi: 10.1515/CCLM.2003.120
  42. Rapp JH, Lespine A, Hamilton RL, et al. Triglyceride-rich lipoproteins isolated by selected-affinity anti-apolipoprotein B immunosorption from human atherosclerotic plaque. Arterioscler Thromb. 1994;14:1767–74. doi: 10.1161/01.atv.14.11.1767
  43. Rosenson RS, Davidson MH, Hirsh BJ, et al. Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardio-vascular disease. J Am Coll Cardiol. 2014;64:2525–40. doi: 10.1016/j.jacc.2014.09.042
  44. Nakano T, Nakajima K, Niimi M, et al. Detection of apolipoproteins B-48 and B-100 carrying particles in lipoprotein fractions extracted from human aortic atherosclerotic plaques in sudden cardiac death cases. Clin Chim Acta. 2008;390:38–43. doi: 10.1016/j.cca.2007.12.012
  45. Davidson MH. Triglyceride-rich lipoprotein cholesterol (TRL-C): the ugly stepsister of LDL-C. Eur Heart J. 2018;39:620–2. doi: 10.1093/eurheartj/ehx741
  46. Örni K, Lehti S, Sjövall P, Kovanen PT. Triglyceride-rich lipoproteins as a source of proinflammatory lipids in the arterial wall. Curr Med Chem. 2018;26(9):1701–10. doi: 10.2774/0929867325666180530094819
  47. Varbo A, Benn M, Tybjærg-Hansen A, Nordestgaard BG. Elevated remnant cholesterol causes both low-grade inflammation and ischemic heart disease, whereas elevated low-density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation. 2013;128:1298–309. doi: 10.1161/CIRCULATIONAHA.113.003008
  48. Raposeiras-Roubin S, Rosselló X, Oliva B, et al. Triglycerides and residual atherosclerotic risk. J Am Coll Cardiol. 2021;77:3031–41. doi: 10.1016/j.jacc.2021.04.059
  49. Lin A, Nerlekar N, Rajagopalan A, et al. Remnant cholesterol and coronary atherosclerotic plaque burden assessed by computed tomography coronary angiography. Atherosclerosis. 2029;284:24–30. doi: 10.1016/j.atherosclerosis.2019.02.019
  50. Bubnova MG, Aronov DM, Perova NV, Mazaev VP. Relationship between the level of lipemia after fat load and the severity of coronary artery atherosclerosis. Therapeutic archive. 2004;76(6):62–7. (In Russ.)
  51. Elshazly MB, Mani P, Nissen S, et al. Remnant cholesterol, coronary atheroma progression and clinical events in statin-treated patients with coronary artery disease. Eur J Prev Cardiol. 2020;27:1091–100. doi: 10.1177/2047487319887578
  52. Krauss RM, Williams PT, Brensike J, et al. Intermediate-density lipoproteins and progression of coronary artery disease in hypercholesterolemic men. Lancet. 1987;2:62–6. doi: 10.1016/s0140-6736(87)92734-6
  53. Karpe F, Steiner G, Uffelman K, et al. Postprandial lipoproteins and progression of coronary atherosclerosis. Atherosclerosis. 1994;106:83–97. doi: 10.1016/0021-9150(94)90085-x
  54. Phillips NR, Water D, Havel RJ. Plasma lipoproteins and progression of coronary artery disease evaluated by angiography and clinical events. Circulation. 1993;88:2762–70. doi: 10.1161/01.cir.88.6.2762
  55. 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;41:2313–30. doi: 10.1093/eurheartj/ehz962
  56. Borén J, Matikainen N, Adiels M, Taskinen MR. Postprandial hypertriglyceridemia as a coronary risk factor. Clin Chim Acta. 2014;431:131–42. doi: 10.1016/j.cca.2014.01.015
  57. Björnson E, Packard CJ, Adiels M, et al. Investigation of human apoB48 metabolism using a new, integrated non-steady-state model of apoB48 and apoB100 kinetics. J Intern Med. 2019;285:562–77. doi: 10.1111/joim.12877
  58. Austin MA. Plasma triglyceride and coronary heart disease. Arterioscler Thromb. 1991;11:2–14. doi: 10.1161/01.atv.11.1.2
  59. Stavenow L, Kjellström T. Influence of serum triglyceride levels on the risk for myocardial infarction in 12,510 middle aged males: interaction with serum cholesterol. Atherosclerosis. 1999;147(2):243–7. doi: 10.1016/s0021-9150(99)00190-2
  60. Austin MA, Hokanson JE, Edwards KL. Hypertriglyceridemia as a cardiovascular risk factor. Am J Cardiol. 1998;81:7B–12B. doi: 10.1016/s0002-9149(98)00031-9
  61. Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007;115(4):450–8. doi: 10.1161/CIRCULATIONAHA.106.637793
  62. Di Angelantonio E, Sarwar N, Perry P, et al. Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302:1993–2000. doi: 10.1001/jama.2009.1619
  63. Nordestgaard BG, Varbo A. Triglycerides and cardiovascular disease. Lancet. 2014;384:626-35. doi: 10.1016/S0140-6736(14)61177-6
  64. Varbo A, Nordestgaard BG. Remnant cholesterol and risk of ischemic stroke in 112,512 individuals from the general population. Ann Neurol. 2019;85:550–9. doi: 10.1002/ana.25432
  65. Ference BA, Kastelein JJP, Ray KK, et al. Association of triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants with risk of coronary heart disease. JAMA. 2019;321:364–73. doi: 10.1001/jama.2018.20045
  66. Kalthoft M, Langsted A, Nordestgaard BG. Triglycerides and remnant cholesterol associated with risk of aortic valve stenosis: Mendelian randomization in the Copenhagen General Population Study. Eur Heart J. 2020;41:2288–99. doi: 10.1093/eurheartj/ehaa172
  67. Park H-B, Arsanjani R, Hong S-J, et al. Impact of hypertriglyceridaemia on cardiovascular mortality according to low-density lipoprotein cholesterol in a 15.6-million population. Eur J Prevent Cardiol. 2024;31:280–90. doi: 10.1093/eurjpc/zwad330
  68. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk. 1996;3:213–9.
  69. Patel A, Barzi F, Jamrozik K, et al. Asia Pacific Cohort Studies Collaboration. Serum triglycerides as a risk factor for cardiovascular diseases in the Asia-Pacific region. Circulation. 2004;110:2678–86. doi: 10.1161/01.CIR.0000145615.33955.83
  70. Arca M, Veronesi C, D’Erasmo L, et al. Association of Hypertriglyceridemia with All-Cause Mortality and Atherosclerotic Cardiovascular Events in a Low-Risk Italian Population: The TG-REAL Retrospective Cohort Analysis. J Am Heart Assoc. 2020;9:e015801. doi: 10.1161/JAHA.119.015801
  71. Patel RS, Pasea L, Soran H, et al. Elevated plasma triglyceride concentration and risk of adverse clinical outcomes in 1.5 million people: a CALIBER linked electronic health record study. Cardiovasc Diabetol. 2022;21(1):102. doi: 10.1186/s12933-022-01525-5
  72. Lee H, Park J-B, Hwang I-C, et al. Association of four lipid components with mortality, myocardial infarction, and stroke in statin-naïve young adults: A nationwide cohort study. Eur J Prevent Cardiol. 2020;27(8):870–81. doi: 10.1177/2047487319898571
  73. Pletcher MJ, Bibbins-Domingo K, Liu K, et al. Nonoptimal lipids commonly present in young adults and coronary calcium later in life: the CARDIA (Coronary Artery Risk Development in Young Adults) study. Ann Intern Med. 2010;153(3):137–46. doi: 10.7326/0003-4819-153-3-201008030-00004
  74. Jeppesen J, Hein HO, Suadicani P, et al. Relation of high TG-low HDL cholesterol and LDL cholesterol to the incidence of ischemic heart disease. An 8-year follow-up in the Copenhagen Male Study. Arterioscler Thromb Vasc Biol. 1997;17(6):1114–20. doi: 10.1161/01.atv.17.6.1114
  75. Kivioja R, Pietila A, Martinez-Majander N, et al. Risk factors for early-onset ischemic stroke: a case-control study. J Am Heart Assoc. 2018;7(21):e009774. doi: 10.1161/JAHA.118.009774
  76. Nordestgaard BG, Benn M, Schnohr P, Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007;298(3):299–308. doi: 10.1001/jama.298.3.299
  77. Freiberg JJ, Tybjærg-Hansen A, Jensen JS, Nordestgaard BG. Nonfasting triglycerides and risk of ischemic stroke in the general population. JAMA. 2008;300(18):2142–52. doi: 10.1001/jama.2008.621
  78. Bansal S, Buring JE, Rifai N, et al. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007;298(3):309–16. doi: 10.1001/jama.298.3.309
  79. Varbo A, Nordestgaard BG. Nonfasting triglycerides, low-density lipoprotein cholesterol, and heart failure risk: two cohort studies of 113 554 individuals. Arterioscler Thromb Vasc Biol. 2018;38(2):464-72. doi: 10.1161/ATVBAHA.117.310269
  80. Toth PP, Sephy P, Hull M, Granowitz C. Elevated Triglycerides (≥150 mg/dL) and High Triglycerides (200-499 mg/dL) Are Significant Predictors of New Heart Failure Diagnosis: A Real-World Analysis of High-Risk Statin-Treated Patients. Vascular Health and Risk Management. 2019;15:533–8. doi: 10.2147/VHRM.S221289
  81. Varbo A, Benn M, Tybjærg-Hansen A, et al. Remnant cholesterol as a causal risk factor for ischemic heart disease. J Am Coll Cardiol. 2013;61(4):427–36. doi: 10.1016/j.jacc.2012.08.1026
  82. Goliasch G, Wiesbauer F, Blessberger H, et al. Premature myocardial infarction is strongly associated with increased levels of remnant cholesterol. J Clin Lipidol. 2015;9:801–6. doi: 10.1016/j.jacl.2015.08.009
  83. Varbo A, Freiberg JJ, Nordestgaard BG. Extreme nonfasting remnant cholesterol vs extreme LDL cholesterol as contributors to cardiovascular disease and all-cause mortality in 90000 individuals from the general population. Clin Chem. 2015;61(3):533–43. doi: 10.1373/clinchem.2014.234146
  84. Jepsen AM, Langsted A, Varbo A, et al. Increased remnant cholesterol explains part of residual risk of all-cause mortality in 5414 patients with ischemic heart disease. Clin Chem. 2016;62(4):593–604. doi: 10.1373/clinchem.2015.253757
  85. Bittencourt MS, Santos RD, Staniak H, et al. Relation of fasting triglyceride-rich lipoprotein cholesterol to coronary artery calcium score (from the ELSA-Brasil Study). Am J Cardiol. 2017;119(9):1352–8. doi: 10.1016/j.amjcard.2017.01.033
  86. Doi T, Langsted A, Nordestgaard BG. Dual elevated remnant cholesterol and C-reactive protein in myocardial infarction, atherosclerotic cardiovascular disease, and mortality. Atherosclerosis. 2023;379:117141. doi: 10.1016/j.atherosclerosis.2023.05.010
  87. Quispe R, Martin SS, Michos ED, et al. Remnant cholesterol predicts cardiovascular disease beyond LDL and ApoB: a primary prevention study. Eur Heart J. 2021;42:4324–32. doi: 10.1093/eurheartj/ehab432
  88. Lee SJ, Kim S-E, Go T-H, et al. Remnant cholesterol, low-density lipoprotein cholesterol, and incident cardiovascular disease among Koreans: a national population-based study. Eur J Prevent Cardiol. 2023;30:1142–50. doi: 10.1093/eurjpc/zwad036
  89. Wadström BN, Wulff AB, Pedersen KM, et al. Elevated remnant cholesterol increases the risk of peripheral artery disease, myocardial infarction, and ischaemic stroke: a cohort-based study. Eur Heart J. 2022;43:3258–69. doi: 10.1093/eurheartj/ehab705
  90. Yang XH, Zhang BL, Cheng Y, et al. Association of remnant cholesterol with risk of cardiovascular disease events, stroke, and mortality: A systemic review and meta-analysis. Atherosclerosis. 2023;371:21–31. doi: 10.1016/j.atherosclerosis.2023.03.012
  91. Cordero A, Alvarez-Alvarez B, Escribano D, et al. Remnant cholesterol in patients admitted for acute coronary syndromes. Eur J Prevent Cardiol. 2023;30:340–8. doi: 10.1093/eurjpc/zwac286
  92. Langsted A, Freiberg JJ, Tybjaerg-Hansen A, et al. Nonfasting cholesterol and triglycerides and association with risk of myocardial infarction and total mortality: the Copenhagen City Heart Study with 31 years of follow-up. J Intern Med. 2011;270:65–75. doi: 10.1111/j.1365-2796.2010.02333.x
  93. Wadström BN, Pedersen KM, Wulff AB, et al. Elevated remnant cholesterol, plasma triglycerides, and cardiovascular and non-cardiovascular mortality. Eur. Heart J. 2023;44:1432–45. doi: 10.1093/eurheartj/ehac822
  94. Jørgensen AB, Frikke-Schmidt R, West AS, et al. Genetically elevated non-fasting triglycerides and calculated remnant cholesterol as causal risk factors for myocardial infarction. Eur Heart J. 2013;34:1826–33. doi: 10.1093/eurheartj/ehs431
  95. Chapman MJ, Ginsberg HN, Amarenco P, et al. the 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;32:1345–61. doi: 10.1093/eurheartj/ehr112
  96. Boullart AC, de Graaf J, Stalenhoef AF. Serum triglycerides and risk of cardiovascular disease. Biochim Biophys Acta. 2012;1821:867–75. doi: 10.1016/j.bbalip.2011.10.002
  97. Björnson E, Adiels M, Taskinen M-R, et al. Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of coronary heart disease: a UK Biobank study. Eur Heart J. 2023;44:4186–95. doi: 10.1093/eurheartj/ehad337
  98. Do R, Stitziel NO, Won HH, et al. Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction. Nature. 2015;518:102–6. doi: 10.1038/nature13917
  99. Jørgensen AB, Frikke-Schmidt R, Nordestgaard BG, Tybjærg-Hansen A. Loss-of function mutations in APOC3 and risk of ischemic vascular disease. N Engl J Med. 2014;371:32–41. doi: 10.1056/NEJMoa1308027
  100. Khera AV, Won HH, Peloso GM, et al. Myocardial Infarction Genetics Consortium, DiscovEHR Study Group, CARDIoGRAM Exome Consortium, and Global Lipids Genetics Consortium. Association of rare and common variation in the lipoprotein lipase gene with coronary artery disease. JAMA. 2017;317:937–46. doi: 10.1001/jama.2017.0972
  101. Stitziel NO, Khera AV, Wang X, et al. PROMIS and Myocardial Infarction Genetics Consortium Investigators. ANGPTL3 deficiency and protection against coronary artery disease. J Am Coll Cardiol. 2017;69:2054–63. doi: 10.1016/j.jacc.2017.02.030
  102. Dewey FE, Gusarova V, O’Dushlaine C, et al. Inactivating variants in ANGPTL4 and risk of coronary artery disease. N Engl J Med. 2016;374:1123–33. doi: 10.1056/NEJMoa1510926
  103. Stitziel NO, Stirrups KE, Masca NG, et al. Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia Investigators; Coding variation in ANGPTL4, LPL, and SVEP1 and the risk of coronary disease. N Engl J Med. 2016;374:1134–44. doi: 10.1056/NEJMoa1507652
  104. Helkkula P, Kiiskinen T, Havulinna AS, et al. ANGPTL8 protein-truncating variant associated with lower serum triglycerides and risk of coronary disease. PLoS Genet. 2021;17:e1009501. doi: 10.1371/journal.pgen.1009501
  105. Thomsen M, Varbo A, Tybjaerg-Hansen A, Nordestgaard BG. Low nonfasting triglycerides and reduced all-cause mortality: a mendelian randomization study. Clin Chem. 2014;60:737–46. doi: 10.1373/clinchem.2013.219881
  106. Crosby J, Peloso GM, Auer PL, et al. Loss-of-function mutations in APOC3, triglycerides, and coronary disease. N Engl J Med. 2014;371:22–31. doi: 10.1056/NEJMoa1307095
  107. Dhindsa DS, Sandesara PB, Shapiro MD, Wong ND. The evolving understanding and approach to residual cardiovascular risk management. Front Cardiovasc Med. 2020;7:88. doi: 10.3389/fcvm.2020.00088
  108. Toth Peter P, Fazio S, Wong ND. Risk of cardiovascular events in patients with hypertriglyceridaemia: A review of real-world evidence. Diabetes Obes Metab. 2020;22:279–89. doi: 10.1111/dom.13921
  109. Marston NA, Giugliano RP, Im KAh, et al. Association between triglyceride lowering and reduction of cardiovascular risk across multiple lipid-lowering therapeutic classes: a systematic review and meta-regression analysis of randomized controlled trials. Circulation. 2019;140:1308–17. doi: 10.1161/CIRCULATIONAHA.119.041998
  110. Schwartz GG, Abt M, Bao W, et al. Fasting triglycerides predict recurrent ischemic events in patients with acute coronary syndrome treated with statins. J Am Coll Cardiol. 2015;65(21):2267–75. doi: 10.1016/j.jacc.2015.03.544
  111. Sacks FM, Tonkin AM, Shepherd J, et al. Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: the Prospective Pravastatin Pooling Project. Circulation. 2000;102:1893–900. doi: 10.1161/01.cir.102.16.1893
  112. Miller M, Cannon CP, Murphy SA, et al. PROVE IT-TIMI 22 Investigators. Impact of triglyceride levels beyond low-density lipoprotein cholesterol after acute coronary syndrome in the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2008;51:724–30. doi: 10.1016/j.jacc.2007.10.038
  113. Faergeman O, Holme I, Fayyad R, et al. Steering Committees of IDEAL and TNT Trials. Plasma triglycerides and cardiovascular events in the Treating to New Targets and Incremental Decrease in End-Points through Aggressive Lipid Lowering trials of statins in patients with coronary artery disease. Am J Cardiol. 2009;104(4):459–63. doi: 10.1016/j.amjcard.2009.04.008
  114. Anderson JW, Konz EC. Obesity and disease management: effects of weight loss on comorbid conditions. Obes Res. 2001;9(Suppl 4):326S–334S. doi: 10.1038/oby.2001.138
  115. Couillard C, Després JP, Lamarche B, et al. Effects of endurance exercise training on plasma HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. Arterioscler Thromb Vasc Biol. 2001;21(7):1226–32. doi: 10.1161/hq0701.092137
  116. Bubnova MG, Aronov DM, Olferyev AM, Bondarenko IZ. Modification of blood lipoprotein and apolipoprotein levels by physical exercise of various type and intensity in healthy men with normo- and hyperlipidemia. Cardiovascular Therapy and Prevention. 2005;4(2):74–83. (In Russ.)
  117. Aronov DM, Bubnova MG, Perova NV, et al. The effect of maximal versus submaximal exertion on postprandial lipid levels in individuals with and without coronary heart disease. J Clin Lipidol. 2017;11:369–76. doi: 10.1016/j.jacl.2017.01.007
  118. Kirkpatrick CF, Sikand G, Petersen KS, et al. Nutrition interventions for adults with dyslipidemia: A Clinical Perspective from the National Lipid Association. J Clin Lipidol. 2023;17(4):428–51. doi: 10.1016/j.jacl.2023.05.099
  119. Williams L, Rhodes KS, Karmally W, et al. Familial chylomicronemia syndrome: Bringing to life dietary recommendations throughout the life span. J Clin Lipidol. 2018;12(4):908–19. doi: 10.1016/j.jacl.2018.04.010
  120. Fechner E, Smeets ETHC, Schrauwen P, Mensink RP. The Effects of Different Degrees of Carbohydrate Restriction and Carbohydrate Replacement on Cardiometabolic Risk Markers in Humans-A Systematic Review and Meta-Analysis. Nutrients. 2020;12(4):991. doi: 10.3390/nu12040991
  121. Stoernell CK, Tangney CC, Rockway SW. Short-term changes in lipoprotein subclasses and C-reactive protein levels of hypertriglyceridemic adults on low-carbohydrate and low-fat diets. Nutr Res. 2008;28(7):443–9. doi: 10.1016/j.nutres.2008.03.013
  122. Wycherley TP, Moran LJ, Clifton PM, et al. Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials. Am J Clin Nutr. 2012;96(6):1281–98. doi: 10.3945/ajcn.112.044321
  123. Stanhope KL, Schwarz JM, Keim NL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009;119(5):1322-34. doi: 10.1172/JCI37385
  124. Kodama S, Horikawa C, Fujihara K, et al. Relationship between intake of fruit separately from vegetables and triglycerides – A meta-analysis. Clin Nutr ESPEN. 2018;27:53–8. doi: 10.1016/j.clnesp.2018.07.001
  125. Leslie MA, Cohen DJA, Liddle DM, et al. A review of the effect of omega-3 polyunsaturated fatty acids on blood triacylglycerol levels in normolipidemic and borderline hyperlipidemic individuals. Lipids Health Dis. 2015;14:53. doi: 10.1186/s12944-015-0049-7
  126. Liu YX, Yu JH, Sun JH, et al. Effects of Omega-3 Fatty Acids Supplementation on Serum Lipid Profile and Blood Pressure in Patients with Metabolic Syndrome: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Foods. 2023;12(4):725. doi: 10.3390/foods12040725
  127. Khorshidi M, Hazaveh ZS, Alimohammadi-kamalabadi M, et al. Effect of omega-3 supplementation on lipid profile in children and adolescents: a systematic review and meta-analysis of randomized clinical trials. Nutr J. 2023;22:9. doi.10.1186/s12937-022-00826-5
  128. Jones PH, Davidson MH, Stein EA, et al.; STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92(2):152–60. doi: 10.1016/s0002-9149(03)00530-7
  129. Arutyunov GP, Boytsov SA, Voyevoda MI, et al. Correction of Hypertriglyceridemia as the Way to Reduce Residual Risk in Diseases Caused by Atherosclerosis. Conclusion of the Advisory Board of the RussianSociety of Cardiology, the Russian Scientific Medical Society of Therapists, the Eurasian Association of Therapists, the Russian National Atherosclerosis Society, the Russian Association of Endocrinologists, and the National League of Cardiologic Genetics. Rational Pharmacotherapy in Cardiology. 2019;15(2):282–8. doi: 10.20996/1819-6446-2019-15-2-282-288
  130. Staels B, Dallongeville J, Auwerx J, et al. Mechanism of Action of Fibrates on Lipid and Lipoprotein Metabolism. Circulation. 1998;98:2088–93. doi: 10.1161/01.cir.98.19.2088
  131. Kim NH, Kim SG. Fibrates Revisited: Potential Role in Cardiovascular Risk Reduction. Diabetes Metab J. 2020;44:213–21. doi.10.4093/dmj.2020.0001
  132. Fruchart JC, Duriez P. Mode of action of fibrates in the regulation of triglyceride and HDL-cholesterol metabolism. Drugs Today (Barc). 2006;42(1):39–64. doi: 10.1358/dot.2006.42.1.963528
  133. Keating GM, Croom KF. Fenofibrate: a review of its use in primary dyslipidaemia, the metabolic syndrome and type 2 diabetes mellitus. Drugs. 2007;67(1):121–53. doi: 10.2165/00003495-200767010-00013
  134. Feher MD, Caslake M, Foxton J, et al. Atherogenic lipoprotein phenotype in type 2 diabetes: reversal with micronised fenofibrate. Diabetes Metab Res Rev. 1999;15:395. doi: 10.1002/(SICI)1520-7560(199911/12)15:6<395:AID-DMRR65>3.0.CO;2-N
  135. Ezhov MV, Arutyunov GP. Effectiveness and Safety of Fenofibrate in Routine Treatment of Patients with Hypertriglyceridemia and Metabolic Syndrome. Diseases. 2023;11:140. doi: 10.3390/diseases11040140
  136. DAIS investigators. Effect of fenofibrate on progression of coronary-artery disease in type 2 diabetes: the Diabetes Atherosclerosis Intervention Study, a randomised study. Lancet. 2001;357:905–10. doi: 10.1016/S0140-6736(00)04209-4
  137. Keech A, Simes RJ, Barter P, et al. The FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005;366(9500):1849–61. doi: 10.1016/S0140-6736(05)67667-2
  138. Ginsberg HN, Elam MB, Lovato LС, et al. The ACCORD Study Group. Effects of Combination Lipid Therapy in Type 2 Diabetes Mellitus. N Engl J Med. 2010;362:1563–74. doi: 10.1056/NEJMoa1001282
  139. Wierzbicki AS. FIELD of dreams, fields of tears: a perspective on the fibrate trials. Int J Clin Pract. 2006;60(4):442–9. doi: 10.1111/j.1368-5031.2006.00882.x
  140. Jo SH, Nam H, Lee J, Park S, et al. Fenofibrate Use Is Associated With Lower Mortality and Fewer Cardiovascular Events in Patients With Diabetes: Results of 10,114 Patients From the Korean National Health Insurance Service Cohort. Diabetes Care. 2021;44:1868–76. doi: 10.2337/dc20-1533
  141. Kim NH, Han KH, Choi J, et al. Use of fenofibrate on cardiovascular outcomes in statin users with metabolic syndrome: propensity matched cohort study. BMJ. 2019;366:5125. doi: 10.1136/bmj.l5125
  142. Das Pradhan A, Glynn RJ, Fruchart JC, et al. PROMINENT Investigators. Triglyceride lowering with pemafibrate to reduce cardiovascular risk. N Engl J Med. 2022;387:1923–34. doi: 10.1056/NEJMoa2210645
  143. Ku EJ, Kim B, Han K, et al. Fenofibrate to prevent amputation and reduce vascular complications in patients with diabetes: FENO-PREVENT. Cardiovascular Diabetology. 2024;23:329. doi: 10.1186/s12933-024-02422-9
  144. Elam M, Lovato L, Ginsberg H. The ACCORD-Lipid study: implications for treatment of dyslipidemia in Type 2 diabetes mellitus Clin Lipidol. 2011;6(1):9–20. doi: 10.2217/clp.10.84
  145. Li J, Shi L, Zhao G, et al. High triglyceride levels increase the risk of diabetic microvascular complications: a cross-sectional study. Lipids Health Dis. 2023;22(1):109. doi: 10.1186/s12944-023-01873-5
  146. Gitay MN, Sohail A, Arzoo Y, Shakir MA. Changes in serum lipids with the onset and progression of Diabetic Retinopathy in Type-II Diabetes Mellitus. Pak J Med Sci. 2023;39(1):188–91. doi: 10.12669/pjms.39.1.6265
  147. Franssen R, Vergeer M, Stroes ES, Kastelein JJ. Combination statin-fibrate therapy: safety aspects. Diabetes Obes Metab. 2009;11(2):89–94. doi: 10.1111/j.1463-1326.2008.00917.х
  148. Jones PH, Cusi K, Davidson MH, et al. Efficacy and safety of fenofibric acid co-administered with low- or moderate-dose statin in patients with mixed dyslipidemia and type 2 diabetes mellitus: results of a pooled subgroup analysis from three randomized, controlled, double-blind trials. Am J Cardiovasc Drugs. 2010;10(2):73–84. doi: 10.2165/10061630-000000000-00000
  149. Roth EM, McKenney JM, Kelly MT, et al. Efficacy and safety of rosuvastatin and fenofibric acid combination therapy versus simvastatin monotherapy in patients with hypercholesterolemia and hypertriglyceridemia: a randomized, double-blind study. Am J Cardiovasc Drugs. 2010;10(3):175–86. doi: 10.2165/11533430-000000000-00000
  150. Kim NH, Kim JY, Choi J, Kim SG. Associations of omega-3 fatty acids vs. fenofibrate with adverse cardiovascular outcomes in people with metabolic syndrome: propensity matched cohort study. Eur Heart J Cardiovascular Pharmacotherapy. 2024;10(2):118–27. doi: 10.1093/ehjcvp/pvad090
  151. Oscarsson J, Hurt-Camejo E. Omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and their mechanisms of action on apolipoprotein B-containing lipoproteins in humans: a review. Lipids in Health and Disease. 2017;16(1):149. doi: 10.1186/s12944-017-0541-3
  152. Drexel H, Tamargo J, Kaski JC, et al. Triglycerides revisited: is hypertriglyceridaemia a necessary therapeutic target in cardiovascular disease? Eur Heart J Cardiovascular Pharmacotherapy. 2023;9(6):570–82. doi: 10.1093/ehjcvp/pvad044
  153. Kaur Gurleen, Mason RP, Steg PhG, Bhatt DL. Omega-3 fatty acids for cardiovascular event lowering. Eur J Prevent Cardiol. 2024;31:1005–14. doi: 10.1093/eurjpc/zwae003
  154. Banaszak M, Dobrzyńska M, Kawka A, et al. Role of Omega-3 fatty acids eicosapentaenoic (EPA) and docosahexaenoic (DHA) as modulatory and anti-inflammatory agents in noncommunicable diet-related diseases — Reports from the last 10 years. Clin Nutr ESPEN. 2024;63:240–58. doi: 10.1016/j.clnesp.2024.06.053
  155. Sezai A, Unosawa S, Taoka M, et al. Long-Term Comparison of Ethyl Icosapentate vs. Omega-3-Acid Ethyl in Patients With Cardiovascular Disease and Hypertriglyceridemia (DEFAT Trial). Circ J. 2019;83(6):1368–76. doi: 10.1253/circj.CJ-18-076
  156. Wang T, Zhang X, Zhou N, et al. Association between omega-3 fatty acid intake and dyslipidemia: a continuous dose-response meta-analysis of randomized controlled trials. J Am Heart Assoc. 2023;12(11):e029512. doi: 10.1161/JAHA.123.029512
  157. Budoff MJ, Muhlestein JB, Bhatt DL, et al. Effect of icosapent ethyl on progression of coronary atherosclerosis in patients with elevated triglycerides on statin therapy: a prospective, placebo-controlled randomized trial (EVAPORATE): interim results. Cardiovascular Research. 2021;117(4):1070–7. doi: 10.1093/cvr/cvaa184
  158. Bernasconi AA, Wiest MM, Lavie CJ, et al. Effect of Omega-3 Dosage on Cardiovascular Outcomes: An Updated Meta-Analysis and Meta-Regression of Interventional Trials. Mayo Clinic Proceedings. 2021;96(2):304–13. doi: 10.1016/j.mayocp.2020.08.034.
  159. Yokoyama M, Origasa H, Matsuzaki M, et al. Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet. 2007;369(9567):1090–8 doi: 10.1016/S0140-6736(07)60527-3
  160. Bhatt DL, Steg PG, Miller M, et al.; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380(1):11–22. doi: 10.1056/NEJMoa1812792
  161. Bhatt DL, Steg PG, Miller M, et al. REDUCE-IT Investigators. Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT. J Am Coll Cardiol. 2019;73(22):2791–802. doi: 10.1016/j.jacc.2019.02.032
  162. Nicholls SJ, Lincoff AM, Garcia M, et al. Effect of high-dose Omega-3 fatty acids vs corn oil on Major adverse cardiovascular events in patients at high cardiovascular risk: the STRENGTH randomized clinical trial. JAMA. 2020;324:2268–80. doi: 10.1001/jama.2020.22258
  163. Barbarawi M, Lakshman H, Barbarawi O, et al. Omega-3 supplementation and heart failure: A meta-analysis of 12 trials including 81,364 participants. Contemporary Clinical Trials. 2021;107:106458. doi: 10.1016/j.cct.2021.106458
  164. Sarker J, Kim M, Munger MA, Kim K. Icosapent Ethyl-Associated New Atrial Fibrillation Incidence compared to Omega-3 Fatty Acids: An Observational Cohort Study. Circulation. 2024;150(Suppl 1):A4140072-A4140072. doi: 10.1101/2024.09.16.24313779
  165. Valdivielso P, Ramirez-Bueno A, Ewald N. Current knowledge of hypertriglyceridemic pancreatitis. Eur J Intern Med. 2014;25:689–94. doi: 10.1016/j.ejim.2014.08.008
  166. Berberich AJ, Ziada A, Zou GY, Hegele RA. Conservative management in hypertriglyceridemia-associated pancreatitis. J Intern Med. 2019;286:644–50. doi: 10.1111/joim.12925
  167. Konovalov GA, Filonenko IV, Akopyan VS, et al. Rheopheresis in clinical practice. Kremlin medicine. Clinical Bulletin. 2004;3:48–53. (In Russ.)
  168. Konovalov GA, Chebyshev AN, Zvezdkin PV, et al. Extracorporeal methods in the treatment of severe forms of atherosclerosis, metabolic syndrome and dilated cardiomyopathy. Kremlin medicine. Clinical Bulletin. 2001;4:48–54. (In Russ.)

Дополнительные файлы

Доп. файлы
Действие
1. JATS XML
2. Приложение 1. Рекомендации по питанию для лиц с гипертриглицеридэмией
Скачать (25KB)
3. Рис. 1. Липопротеины: размеры и плотность [адаптирована из 8]: апо — аполипопротеин, ЛВП — липопротеины высокой плотности, ЛНП — липопротеины низкой плотности, ЛОНП — липопротеины очень низкой плотности, ЛП — липопротеины, ЛПП — липопротеины промежуточной плотности, ТГ — триглицериды.

Скачать (259KB)
4. Рис. 2. Поэтапное обследование и маршрутизация пациента с гипертриглицеридемией: ЛНП — липопротеины низкой плотности, ГТГ — гипертриглицеридемия, ТГ — триглицериды, ХС — холестерин.

Скачать (291KB)
5. Рис. 3. Алгоритм ведения пациентов с гипертриглицеридемией (согласованная позиция экспертов): АССЗ — атеросклеротические сердечно-сосудистые заболевания, ГТГ — гипертриглицеридемия, ЛНП — липопротеины низкой плотности, СД — сахарный диабет, ТГ — триглицериды, ХС — холестерин.

Скачать (327KB)
6. Рис. 4. Терапия гипертриглицеридемии [адаптировано из 1]. * — с учётом клинического фенотипа пациента, ** — омега 3 пнжк — омега 3 полиненасыщенных жирных кислот этиловые эфиры 90 в дозе 2–4 г/сут. ПНЖК — полиненасыщенные жирные кислоты, ТГ — триглицериды.

Скачать (140KB)

© ООО "Эко-Вектор", 2025

Creative Commons License
Эта статья доступна по лицензии Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Согласие на обработку персональных данных с помощью сервиса «Яндекс.Метрика»

1. Я (далее – «Пользователь» или «Субъект персональных данных»), осуществляя использование сайта https://journals.rcsi.science/ (далее – «Сайт»), подтверждая свою полную дееспособность даю согласие на обработку персональных данных с использованием средств автоматизации Оператору - федеральному государственному бюджетному учреждению «Российский центр научной информации» (РЦНИ), далее – «Оператор», расположенному по адресу: 119991, г. Москва, Ленинский просп., д.32А, со следующими условиями.

2. Категории обрабатываемых данных: файлы «cookies» (куки-файлы). Файлы «cookie» – это небольшой текстовый файл, который веб-сервер может хранить в браузере Пользователя. Данные файлы веб-сервер загружает на устройство Пользователя при посещении им Сайта. При каждом следующем посещении Пользователем Сайта «cookie» файлы отправляются на Сайт Оператора. Данные файлы позволяют Сайту распознавать устройство Пользователя. Содержимое такого файла может как относиться, так и не относиться к персональным данным, в зависимости от того, содержит ли такой файл персональные данные или содержит обезличенные технические данные.

3. Цель обработки персональных данных: анализ пользовательской активности с помощью сервиса «Яндекс.Метрика».

4. Категории субъектов персональных данных: все Пользователи Сайта, которые дали согласие на обработку файлов «cookie».

5. Способы обработки: сбор, запись, систематизация, накопление, хранение, уточнение (обновление, изменение), извлечение, использование, передача (доступ, предоставление), блокирование, удаление, уничтожение персональных данных.

6. Срок обработки и хранения: до получения от Субъекта персональных данных требования о прекращении обработки/отзыва согласия.

7. Способ отзыва: заявление об отзыве в письменном виде путём его направления на адрес электронной почты Оператора: info@rcsi.science или путем письменного обращения по юридическому адресу: 119991, г. Москва, Ленинский просп., д.32А

8. Субъект персональных данных вправе запретить своему оборудованию прием этих данных или ограничить прием этих данных. При отказе от получения таких данных или при ограничении приема данных некоторые функции Сайта могут работать некорректно. Субъект персональных данных обязуется сам настроить свое оборудование таким способом, чтобы оно обеспечивало адекватный его желаниям режим работы и уровень защиты данных файлов «cookie», Оператор не предоставляет технологических и правовых консультаций на темы подобного характера.

9. Порядок уничтожения персональных данных при достижении цели их обработки или при наступлении иных законных оснований определяется Оператором в соответствии с законодательством Российской Федерации.

10. Я согласен/согласна квалифицировать в качестве своей простой электронной подписи под настоящим Согласием и под Политикой обработки персональных данных выполнение мною следующего действия на сайте: https://journals.rcsi.science/ нажатие мною на интерфейсе с текстом: «Сайт использует сервис «Яндекс.Метрика» (который использует файлы «cookie») на элемент с текстом «Принять и продолжить».