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Противовоспалительная терапия при атеросклерозе – новое перспективное направление?
Противовоспалительная терапия при атеросклерозе – новое перспективное направление?
Кириченко А.А. Противовоспалительная терапия при атеросклерозе – новое перспективное направление? Consilium Medicum. 2018; 20 (5): 18–22. DOI: 10.26442/2075-1753_2018.5.18-22
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Аннотация
Повышенное содержание в крови маркеров воспаления является независимым прогностическим признаком коронарных событий у лиц со стабильным или бессимптомным течением ишемической болезни сердца. Активация локального воспалительного процесса в атеросклеротической бляшке приводит к деструкции фиброзной капсулы и риску ее разрыва с формированием артериального тромбоза. Индукторами воспалительных реакций могут выступать вирусы и бактерии. Синергичное действие нескольких патогенов увеличивает риск развития воспалительного процесса в сосудистой стенке, что отражено в концепции «бремени инфекций». Высоким риском развития сердечно-сосудистых осложнений характеризуются иммуновоспалительные ревматические заболевания. Хроническое воспаление как ключевой элемент патогенеза атеросклероза может быть обусловлено не только инфекционными и иммунными, но и метаболическими факторами. Индуцированная кристаллами холестерина активация инфламмасом в макрофагах является важным связующим звеном между метаболизмом холестерина и воспалением в атеросклеротических бляшках. Подтверждением важной патогенетической роли воспаления считается снижение риска сердечно-сосудистых осложнений на фоне противовоспалительной терапии, в том числе данные закончившегося в 2017 г. исследования CANTOS (Canakinumab ANtiinflammatory Trombosis Outcomes Study): вторичная профилактика сердечно-сосудистых осложнений человеческими моноклональными антителами к интерлейкину-1b (канакинумаб) пациентов со стабильной ишемической болезнью сердца, у которых наблюдалось увеличение концентрации высокочувствительного С-реактивного белка (более 2 мг/л), привела к достоверному снижению риска сердечно-сосудистых осложнений независимо от пола, курения, уровня липидов.
Ключевые слова: ишемическая болезнь сердца, воспаление, атеросклероз, атеротромбоз.
Ключевые слова: ишемическая болезнь сердца, воспаление, атеросклероз, атеротромбоз.
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Elevated level of inflammatory markers in blood is an independent prognostic factor for cardiovascular events in patients with stable or asymptomatic IHD. Local inflammation activation in atheromatous plaque results in fibrous capsule destruction and risk of its rupture with arterial thrombosis formation. Viruses and bacteriophages can be inductors for inflammatory response. Synergistic action of several pathogens increases risk of inflammatory process development in vessel wall that is reflected in “infection burden” conception. Immunoinflammatory rheumatic disorders are characterized by high risk of cardiovascular events development. Chronic inflammation as a core aspect of atherosclerosis pathogenesis can be explained not only by infectious and immune, but also by metabolic factors. Macrophage inflammasomes activation induced with cholesterol crystals is an important link between cholesterol metabolism and atheromatous plaque inflammation. Reduction of cardiovascular events risk on the background of anti-inflammatory therapy confirms the important pathogenic role of inflammation. It is also supported by CANTOS trial results acquired in 2017: secondary cardiovascular events prophylaxis with human monoclonal antibodies to interleukin 1β (canakinumab) in patients with stable IHD in whom an increase of hsCRP (more than 2 mg/l) was found resulted in significant cardiovascular risk reduction irrespective of sex, smoking and serum lipid level.
Key words: IHD, inflammation, atherosclerosis, atherothrombosis.
Key words: IHD, inflammation, atherosclerosis, atherothrombosis.
Полный текст
Список литературы
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________________________________________________
2. Baigent C et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366: 1267–78.
3. Greenland P et al. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA 2003; 290: 891–7.
4. Ridker PM, Cushman M, Stampfer MJ et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973–81.
5. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000; 342: 836–43.
6. The Emerging Risk Factors Collaboration. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet 2010; 375: 132–40.
7. Yarullina D.R., Il'inskaya O.N., Silkin N.I. i dr. Infekcionnaya priroda ateroskleroza: fakty i gipotezy. Uchenye zapiski Kazanskogo gosudarstvennogo universiteta, 2010. T. 152. Kn. 1; s. 136–54. [in Russian]
8. Adam E, Melnick JL, Probtsfield JL et al. High levels of CMV antibody in patients requiring vascular surgery for atherosclerosis. Lancet 1987; 2: 291–3.
9. Benditt EP, Barret I, McDougall JK. Viruses in the citology of atherosclerosis. Proc Natl Acad Sci USA 1983; 80: 6386–9.
10. Grattan MT, Moreno-Cabral CE, Starnes VA et al. Cytomegalovirus infection is associated with cardiac allograft rejection and atherosclerosis. JAMA 1989; 261 (4): 3561–6.
11. Hajjar DF. Viral pathogenesis of atherosclerosis. Am J Pathol 1991; 139: 1993–211.
12. Kenina V, Auce P, Priede Z et al. Cytomegalovirus chronic infection as a risk factor for stroke: a prospective study. Proceedings of the Latvian academi of sciences. 2010. Section b; 64 (3/4): 133–6.
13. Morre SA, Stooker W, Lagrand WK et al. Microorganisms in the aetiology of atherosclerosis. J Clin Pathol 2000; 53 (9): 647–54.
14. Mrochek A.G., Gorbachev V.V. Ateroskleroz. Minsk: Knizhnyj dom, 2005. [in Russian]
15. Grahame-Clarke С. Human cytomegalovirus, endothelial function and atherosclerosis. Herpes 2005; 12 (2): 42–5.
16. Beck JD, Elter JR, Heiss G et al. Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study. Arterioscler Thromb Vasc Biol 2001; 21 (11): 1816–22.
17. Grudyanov A.I. Terapiya vospalitel'nyh zabolevanij. Lechashchij vrach. 2012; 7: 106–8. [in Russian]
18. Saikku P, Leinonen M, Mattila K et al. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet 1988; 2 (8618): 983–6.
19. Saikku P, Leinonen M, Tenkanen L et al. ChronicChlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study. Ann Intern Med 1992; 116: 273–8.
20. Saikku P. Chlamydia pneumoniae infection as a risk factor in acute myocardial infarction Eur Heart J 1993; 14: 62–5.
21. Linnanmaki E, Leinonen M, Mattila K et al. Chlamydia pneumoniae-spedfic circulating immune complexes in patients with chronic heart disease. Circulation 1993; 87: 1130–4.
22. Molestina RE, Miller RD, Ramirez JA, Summersgill JT. Infection of human endothelial cells with Chlamydia pneumoniae stimulates transendothelial migration of neutrophils and monocytes. Infect Immun 1999; 67: 1323–30.
23. Coombes BK, Mahony JB. Chlamydia pneumoniae infection of human endothelial cells induces proliferation of smooth muscle cells via an endothelial cell-derived soluble factors). Infect Immun 1999; 67: 2909–15.
24. Fryer RH, Schwobe EP, Woods ML, Rodgers GM. Chlamydia species infect human vascular endothelial cells and induce procoagulant activity. J Investig Med 1997; 45: 168–74.
25. Dechend R, Maass M, Gieffers J et al. Chlamydia pneumoniae infection of vascular smooth muscle and endothelial cells activates NF-kappa B and induces tissue factor and PAI-1 expression: a potential link to accelerated arteriosclerosis. Circulation 1999; 100: 1369–73.
26. Kol A, Sukhova GK, Lichtman AH, Libby P. Chlamydial heat shock protein 60 localizes in human atheroma and regulates macrophage tumor necrosis factor-alpha and matrix metalloproteinase expression. Circulation 1998; 98: 300–7.
27. Vatutin H.T., Chupina V.A. Infekciya kak faktor razvitiya ateroskleroza i ego oslozhnenij. Kardiologiya. 2000; 2: 67–71. [in Russian]
28. Nikitin Yu.P., Reshetnikov O.V., Kurilovich S.A. i dr. Ishemicheskaya bolezn' serdca, hlamidijnaya i helikobakternaya infekcii: populyacionnoe issledovanie. Kardiologiya. 2000; 8: 4–7. [in Russian]
29. Gupta S, Leatham EW, Carrington D et al. Elevated CMamydhi pneumoniae antiboties, cardiovascular events, and azitromycin in male survivors of myocardial infarction. Circulation 1997; 96: 404–7.
30. Ridker PM, Hennekens CH, Stampfer MJ, Wang F. Prospective study of herpes simplex virus, cytomegalovirus, and the risk of future myocardial infarction and stroke. Circulation 1998; 98: 2796–9.
31. Zhu J, Quyyumi AA, Norman JE et al. Effects of total pathogen burden on coronary artery disease risk and C-reactive protein levels. Am J Cardiol 2000; 85 (2): 140–6.
32. Kiechl S, Egger G, Mayr M et al. Chronic infections and the risk of carotid atherosclerosis: Prospective studies result from a large population study. Circulation 2001; 103: 1064–70.
33. Auer JW, Berent R, Weber I, Eber B. Immunopathogenesis of atherosclerosis (Response). Circulation 2002; 105 (10): 64.
34. Espinola-Klein C, Rupprecht HJ, Blankenberg S et al. Impact of infectious burden on extent and long-term prognosis of atherosclerosis. Circulation 2002; 105 (1): 15–21.
35. Prasad A, Zhu J, Halcox JP et al. Predisposition to atherosclerosis by infections: role of endothelial dysfunction. Circulation 2002; 106 (2): 184–90.
36. Zebrack JS, Anderson JL. The role of inflammation and infection in the pathogenesis and evolution of coronary artery disease. Curr Cardiol Rep 2002; 4 (4): 278–88.
37. Vorob'ev A.A., Abakumova Yu.V. Rol' virusno-gerpeticheskoj infekcii v razvitii ateroskleroza: klinicheskie, virusologicheskie, immunologicheskie dokazatel'stva. Vesti RAMN. 2003; 4: 3–10. [in Russian]
38. Nasonov EL., Popkova T.V. Protivovospalitel'naya terapiya ateroskleroza – vklad i uroki revmatologii. Nauchno-prakticheskaya revmatologiya. 2017; 55 (5): 465–73. [in Russian]
39. Meune C, Touze E, Trinquart L, Allanore Y. High risk of clinical cardiovascular events in RA: levels of associations of myocardial infarction and stroke through a systematic review and meta-analysis. Arch Cardiovasc Dis 2010; 103: 253–61.
40. Popkova T.V., Novikova D.S., Nasonov E.L. Serdechno-sosudistye zabolevaniya pri revmatoidnom artrite: novye dannye. Nauchno-prakticheskaya revmatologiya. 2016; 54 (2): 122–8. [in Russian]
41. Rajamäki K, Lappalainen J, Oörni K et al. Cholesterol crystals activate the NLRP3 inflammasome in human macrophages: a novel link between cholesterol metabolism and inflammation. PLoS One 2010; 5 (7): e11765.
42. Kovalenko V.N., Talaeva T.V., Bratus' V.V. Holesterin i ateroskleroz: tradicionnye vzglyady i sovremennye predstavleniya. Ukr. kardіol. zhurn. 2010; 3: 7–35. [in Russian]
43. Moreno PR, Purushothaman RK, Fuster V, O’Connor WN. Increased incidence of internal elastic lamina rupture and intimal changes in complex atherosclerotic lesions: Understanding the remodeling paradox and plaque disruption. J Am Coll Cardiol 2002; 39: 249–51.
44. Maseri A, Cianflone D. Inflammation in acute coronary syndromes. Eur Heart J 2002; 4 (Suppl. B): 8–13, 60.
45. Liuzzo G, Goronzy JJ, Yang H et al. Monoclonal T-cell proliferation and plaque instability in acute coronary syndromes. Circulation 2000; 101: 2883–8.
46. Stefanadis C, Diamantopoulos L, Dernellis J et al. Heat production of atherosclerotic plaques and inflammation assessed by the acute phase proteins in acute coronary syndromes. J Mol Cel Cardiol 2000; 32: 43–52.
47. Stefanadis C, Diamantopoulos L, Vlachopoulos C et al. Thermal geterogenity within human atherosclerotic coronary arteries detected in vivo: a new method of detection by application of a special thermography catheter. Circulation 1999; 99: 1965–71.
48. Lutaj M.I. Razryv ateroskleroticheskoj blyashki i ego klinicheskie posledstviya. Mozhno li predotvratit' koronarnuyu katastrofu? Ukr. kardіol. zhurn. 2002; 5: 45–9. [in Russian]
49. Tardif JC, L’Allier PL, Ibiahim R et al. Treatment with 5-lipoxygenase inhibitor VIA-2291 (Atre-leuton) in patients with recent acute coronary syndrome. Circ Cardiovasc Imaging 2010; 3: 298–307.
50. Nidorf M. Low dose colchicine for secondary prevention of cardiovascular disease (The LoDoCo Trial). J Am Coll Cardiol 2013; 61: 404–10.
51. Ridker PM. Testing the inflammatory hypothesis of atherothrombosis: scientific rationale for the cardiovascular inflammation reduction trial (CIRT). J Thromb Hemostasis 2009; 7 (Suppl. 1): 332–9.
52. Solov'eva A.E., Kobalava Zh.D. Perspektivy protivovospalitel'noj terapii ateroskleroza. Klin. farmakologiya i terapiya. 2014; 23 (3): 28–38. [in Russian]
Авторы
А.А.Кириченко
ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России. 125993, Россия, Москва, ул. Баррикадная, д. 2/1
andrey.apollonovich@yandex.ru
ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России. 125993, Россия, Москва, ул. Баррикадная, д. 2/1
andrey.apollonovich@yandex.ru
________________________________________________
A.A.Kirichenko
Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation. 125995, Russian Federation, Moscow, ul. Barrikadnaia, d. 2/1
andrey.apollonovich@yandex.ru
Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation. 125995, Russian Federation, Moscow, ul. Barrikadnaia, d. 2/1
andrey.apollonovich@yandex.ru
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