Anti-inflammatory therapy in atherosclerosis - is it a new promising trend?

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Abstract

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.

About the authors

A. A Kirichenko

Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation

Email: andrey.apollonovich@yandex.ru
д-р мед. наук, проф., зав. каф. терапии №2 125995, Russian Federation, Moscow, ul. Barrikadnaia, d. 2/1

References

  1. Рекомендации ЕОК/ЕОА по диагностике и лечению дислипидемий 2016. Рос. кардиологич. журн. 2017; 5 (145): 7-77.
  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 P.M, Cushman M, Stampfer M.J et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973-81.
  5. Ridker P.M, Hennekens C.H, Buring J.E, 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. Яруллина Д.Р., Ильинская О.Н., Силкин Н.И. и др. Инфекционная природа атеросклероза: факты и гипотезы. Ученые записки Казанского государственного университета, 2010. Т. 152. Кн. 1; с. 136-54.
  8. Adam E, Melnick J.L, Probtsfield J.L et al. High levels of CMV antibody in patients requiring vascular surgery for atherosclerosis. Lancet 1987; 2: 291-3.
  9. Benditt E.P, Barret I, McDougall J.K. Viruses in the citology of atherosclerosis. Proc Natl Acad Sci USA 1983; 80: 6386-9.
  10. Grattan M.T, Moreno-Cabral C.E, Starnes V.A et al. Cytomegalovirus infection is associated with cardiac allograft rejection and atherosclerosis. JAMA 1989; 261 (4): 3561-6.
  11. Hajjar D.F. 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 S.A, Stooker W, Lagrand W.K et al. Microorganisms in the aetiology of atherosclerosis. J Clin Pathol 2000; 53 (9): 647-54.
  14. Мрочек А.Г., Горбачев В.В. Атеросклероз. Минск: Книжный дом, 2005. / 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 J.D, Elter J.R, 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. Грудянов А.И. Терапия воспалительных заболеваний. Лечащий врач. 2012; 7: 106-8.
  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 R.E, Miller R.D, Ramirez J.A, Summersgill J.T. Infection of human endothelial cells with Chlamydia pneumoniae stimulates transendothelial migration of neutrophils and monocytes. Infect Immun 1999; 67: 1323-30.
  23. Coombes B.K, Mahony J.B. 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 R.H, Schwobe E.P, Woods M.L, Rodgers G.M. 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 G.K, Lichtman A.H, 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. Ватутин H.T., Чупина В.А. Инфекция как фактор развития атеросклероза и его осложнений. Кардиология. 2000; 2: 67-71.
  28. Никитин Ю.П., Решетников О.В., Курилович С.А. и др. Ишемическая болезнь сердца, хламидийная и хеликобактерная инфекции: популяционное исследование. Кардиология. 2000; 8: 4-7.
  29. Gupta S, Leatham E.W, 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 P.M, Hennekens C.H, Stampfer M.J, 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 A.A, Norman J.E 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 J.W, Berent R, Weber I, Eber B. Immunopathogenesis of atherosclerosis (Response). Circulation 2002; 105 (10): 64.
  34. Espinola-Klein C, Rupprecht H.J, 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 J.P et al. Predisposition to atherosclerosis by infections: role of endothelial dysfunction. Circulation 2002; 106 (2): 184-90.
  36. Zebrack J.S, Anderson J.L. The role of inflammation and infection in the pathogenesis and evolution of coronary artery disease. Curr Cardiol Rep 2002; 4 (4): 278-88.
  37. Воробьев A.A., Абакумова Ю.В. Роль вирусно-герпетической инфекции в развитии атеросклероза: клинические, вирусологические, иммунологические доказательства. Вести РАМН. 2003; 4: 3-10.
  38. Насонов Е.Л., Попкова Т.В. Противовоспалительная терапия атеросклероза - вклад и уроки ревматологии. Научно-практическая ревматология. 2017; 55 (5): 465-73.
  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. Попкова Т.В., Новикова Д.С., Насонов Е.Л. Сердечно-сосудистые заболевания при ревматоидном артрите: новые данные. Научно-практическая ревматология. 2016; 54 (2): 122-8.
  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. Коваленко В.Н., Талаева Т.В., Братусь В.В. Холестерин и атеросклероз: традиционные взгляды и современные представления. Укр. кардіол. журн. 2010; 3: 7-35.
  43. Moreno P.R, Purushothaman R.K, Fuster V, O’Connor W.N. 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 J.J, 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. Лутай М.И. Разрыв атеросклеротической бляшки и его клинические последствия. Можно ли предотвратить коронарную катастрофу? Укр. кардіол. журн. 2002; 5: 45-9.
  49. Tardif J.C, L’Allier P.L, 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 P.M. 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. Соловьева А.Е., Кобалава Ж.Д. Перспективы противовоспалительной терапии атеросклероза. Клин. фармакология и терапия. 2014; 23 (3): 28-38.

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