Тромбоз, гемостаз и реология №02 2015

Значение инфекции и воспаления в развитии атеросклероза. Диагностика и лечение

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Инфекция и воспаление играют ведущую роль в индукции и прогрессировании атеросклероза. Инфекция способствует процессу атерогенеза и развитию осложнений атеросклероза, вызванных разрывом атеросклеротической бляшки. Уязвимые атеросклеротические бляшки имеют признаки локального воспаления. Атеросклеротические бляшки с подобными особенностями могут разорваться и способствовать развитию тромбоза. Современные исследования показывают целесообразность противоспалительной терапии для достижения стабильности атеросклеротической бляшки. Разработка лабораторной и неинвазивной инструментальной диагностики и новых противоспалительных терапевтических подходов для предотвращения атеротромбоза является важным приоритетом исследований в сердечно-сосудистой сфере.

Инфекция и воспаление играют ведущую роль в индукции и прогрессировании атеросклероза. Инфекция способствует процессу атерогенеза и развитию осложнений атеросклероза, вызванных разрывом атеросклеротической бляшки. Уязвимые атеросклеротические бляшки имеют признаки локального воспаления. Атеросклеротические бляшки с подобными особенностями могут разорваться и способствовать развитию тромбоза.

Современные исследования показывают целесообразность противоспалительной терапии для достижения стабильности атеросклеротической бляшки. Разработка лабораторной и неинвазивной инструментальной диагностики и новых противоспалительных терапевтических подходов для предотвращения атеротромбоза является важным приоритетом исследований в сердечно-сосудистой сфере.

Ключевые слова: атеросклероз — диагностика и лечение — воспаление — инфекционные заболевания.

Для корреспонденции

Аршинов Андрей Владимирович — д.м.н., профессор кафедры пропедевтики внутренних болезней ГБОУ ВПО ЯГМА МЗ РФ.

Адрес: 150000, Россия, Ярославль, ул. Революционная, д. 5.

E-mail: a_arshinov@mail.ru

Статья поступила 27.03.2014, принята к печати 30.01.2015.

IMPORTANCE OF INFECTION AND INFLAMMATION IN ATHEROSCLEROSIS DEVELOPMENT. DIAGNOSTICS AND TREATMENT

A. V. Arshinov, Yu.A. Goncharova, I. G. Maslova

Yaroslavl State Medical Academy, Health Ministry of Russian Federation, Yaroslavl, Russia

Yaroslavl State Medical Academy, Health Ministry of Russian Federation, Yaroslavl, Russia Infection and inflammation play the leading role in induction and progression of atherosclerosis. Infection promotes the development of atherogenesis and its complications caused by rupture of atherosclerotic plaque. Vulnerable atherosclerotic plaques have symptoms of local inflammation. Atherosclerotic plaques with such characteristics may rupture and promote thrombosis.

Current studies show appropriateness of anti-inflammatory therapy for achieving stability of atherosclerotic plaque. Elaboration of laboratory and noninvasive instrumental diagnostics and new anti-inflammatory therapeutic approaches for atherothrombosis prevention is important priority in cardiovascular researches.

Key words: atherosclerosis — diagnostics and treatment — inflammation — infectious diseases.

Список исп. литературыСкрыть список
1. Davies M. J. Coronary disease: the pathophysiology of acute coronary syndromes // Heart. — 2000. — Vol. 83. — Р. 361— 366.
2. Burke A. P., Kolodgie F. D., Farb A. et al. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression // Circulation. — 2001. — Vol. 103, № 7. — Р. 934–940.
3. Kanse S. M., Parahuleva M., Muhl L. et al. Factor VII-activating protease (FSAP): vascular functions and role in atherosclerosis. Review // Thromb. Haemost. — 2008. — Vol. 99. — Р. 286–289.
4. Naruko T., Furukawa A., Yunoki K. et al. Increased expression and plasma levels of myeloperoxidase are closely related to the presence of angiographically-detected complex lesion morphology in unstable angina // Heart. — 2010. — Vol. 96. — Р. 1716–1722.
5. Ridker P. M., Danielson E., Fonseca F. A. et al. JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein // N. Engl. J. Med. — 2008. — Vol. 359, № 2. — Р. 2195–2207.
6. Kaptoge S., Di Angelantonio E., Lowe G. et al. 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. — Vol. 375. — Р. 132–140.
7. Everett B. M., Glynn R. J., MacFadyen J.G., Ridker P. M. Rosuvastatin in the prevention of stroke among men and women with elevated levels of C-reactive protein: justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) // Circulation. — 2010. — Vol. 121. — Р. 143–150.
8. Genest J., McPherson R., Frohlich J. et al. 2009 Canadian Cardiovascular Society/Canadian guidelines for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease in the adult — 2009 recommendations // Can. J. Cardiol. — 2009. — Vol. 25, № 10. — Р. 567–579.
9. NACB LMPG Committee Members, Myers G. L., Christenson R. H., Cushman M. et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice guidelines: emerging biomarkers for primary prevention of cardiovascular disease // Clin. Chem. — 2009. — Vol. 55, № 2. — Р. 378–384.
10. Camerlingo M., Valente L., Tognozzi M. et al. C-reactive protein levels in the first three hours after acute cerebral infarction // Neurosci. Int. J. Neurosci. — 2011. — Vol. 121, № 2. — Р. 65–68.
11. Youn C. S., Choi S. P., Kim S. H. et al. Serum highly selective C-reactive protein concentration is associated with the volume of ischemic tissue in acute ischemic stroke // Am. J. Emerg. Med. — 2012. — Vol. 30, № 1. — Р. 124–128 (doi: 10.1016/j.ajem.2010.11.006).
12. Ormstad H., Aass H. C., Lund-Sørensen N. et al. Serum lev els of cytokines and C-reactive protein in acute ischemic stroke patients, and their relationship to stroke lateralization, type, and infarct volume // J. Neurol. — 2011. — Vol. 258, № 4. — Р. 677–685.
13. Chei C. L., Yamagishi K., Kitamura A. et al. C-reactive protein levels and risk of stroke and its subtype in Japanese: The Circulatory Risk in Communities Study (CIRCS) // Atherosclerosis. — 2011. — Vol. 217, № 1. — Р. 187–193.
14. Ridker P. M. High-sensitivity C-reactive protein, vascular imaging, and vulnerable plaque. More evidence to support trials of antiinflammatory therapy for cardiovascular risk reduction // Circ. Cardiovasc. Imaging. — 2011. — Vol. 4, № 3. — Р. 195–197.
15. Gupta M., Singh N., Tsigoulis M. et al. Perceptions of Canadian primary care physicians towards cardiovascular risk assessment and lipid management // Can. J. Cardiol. — 2012. — Vol. 28, № 1. — Р. 14–19.
16. Rosa G. M., Bauckneht M., Masoero G. et al. The vulnerable coronary plaque: update on imaging technologies // Thromb. Haemost. — 2013. — Vol. 110, № 4. — Р. 706–722.
17. Lavi S., Bae J. H., Rihal C. S. et al. Segmental coronary endothelial dysfunction in patients with minimal atherosclerosis is associated with necrotic core plaques // Heart. — 2009. — Vol. 95, № 18. — Р. 1525–1530.
18. Kawasaki M., Takatsu H., Noda T. et al. In vivo quantitative tissue characterization of human coronary arterial plaques by use of integrated backscatter intravascular ultrasound and comparison with angioscopic findings // Circulation. — 2002. — Vol. 105. — Р. 2487–2492.
19. Kubo T., Imanishi T., Takarada S. et al. Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy // J. Am. Coll. Cardiol. — 2007. — Vol. 50. — Р. 933–939.
20. Nadkarni S. K., Pierce M. C., Park B. H. et al. Measurement of collagen and smooth muscle cell content in atherosclerotic plaques using polarization-sensitive optical coherence tomography // J. Am. Coll. Cardiol. — 2007. — Vol. 49, № 13. — Р. 1474–1481.
21. Wu J.C., Ylä-Herttuala S. Human gene therapy and imaging: cardiology // Eur. J. Nucl. Med. Mol. Imaging. — 2005. — Vol. 32. — Р. 346–357.
22. Anderson J. L., Muhlestein J. B. Antibiotic trials for coronary heart disease // Tex. Heart Inst. J. — 2004. — Vol. 31, № 1. — Р. 33–38.
23. Dunne M. WIZARD and the design of trials for secondary prevention of atherosclerosis with antibiotics // Am. Heart J. — 1999. — Vol. 138 (5 Pt 2). — Р. 542–544.
24. Neumann F., Kastrati A., Miethke T. et al. Treatment of Chlamydia pneumoniae infection with roxithromycin and effect on neointima proliferation after coronary stent placement (ISAR-3): a randomised, double-blind, placebo-controlled trial // Lancet. — 2001. — Vol. 357. — Р. 2085–2089.
25. Gu Y., Lee H. M., Sorsa T. et al. Non-antibacterial tetracyclines modulate mediators of periodontitis and atherosclerotic cardiovascular disease: A mechanistic link between local and systemic inflammation // Pharmacol. Res. — 2011. — Vol. 64, № 6. — Р. 573–579.
26. Reichert T. A., Simonsen L., Sharma A. et al. Influenza and the winter increase in mortality in the United States, 1959–1999 // Am. J. Epidemiol. — 2004. — Vol. 160, № 5. — Р. 492–502.
27. Haidari M., Wyde P. R., Litovsky S. et al. Influenza virus directly infects, inflames, and resides in the arteries of atherosclerotic and normal mice // Atherosclerosis. — 2010. — Vol. 208, № 1. — Р. 90–96.
28. Gurfinkel E. P., de la Fuente R. L. Two-year follow-up of the FLU Vaccination Acute Coronary Syndromes (FLUVACS) Registry // Tex. Heart. Inst. J. — 2004. — Vol. 31, № 1. — Р. 28–32.
29. Phrommintikul A., Kuanprasert S., Wongcharoen W. et al. Influenza vaccination reduces cardiovascular events in patients with acute coronary syndrome // Eur. Heart J. — 2011. — Vol. 32, № 14. — Р. 1730–1735.
30. Zhu T., Carcaillon L., Martinez I. et al. Association of in- fluenza vaccination with reduced risk of venous thromboembolism // Thromb. Haemost. — 2009. — Vol. 102. — Р. 1259–1264.
31. Davis M. M., Taubert K., Benin A. L. et al. American Heart Association; American College of Cardiology. Influenza vaccination as secondary prevention for cardiovascular disease: a science advisory from the American Heart Association/ American College of Cardiology // Circulation. — 2006. — Vol. 114, № 14. — Р. 1549–1553.
32. Elkind M. S. Inflammatory mechanisms of stroke // Stroke. — 2010. — Vol. 41, № 10. — Р. 3–8.
33. Ridker P. M. The Time for Cardiovascular Inflammation Reduction Trials Has Arrived. How Low to Go for hsCRP? // Arterioscler Thromb Vasc Biol. — 2008. — Vol. 28, № 7. — Р. 1222–1224.
34. Ridker P. M., MacFadyen J.G., Fonseca F. A. et al. JUPITER Study Group. Number needed to treat with rosuvastatin to prevent first cardiovascular events and death among men and women with low low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin (JUPITER) // Circ. Cardiovasc. Qual. Outcomes. — 2009. — Vol. 2, № 6. — Р. 616–623.
35. O’Riordan M. FDA advisory panel votes in favor of broadened rosuvastatin indication // Heart. — 2009. — Available at: www.theheart.org/article/1035155/print.do.
36. Yoneda H., Miura K., Matsushima H. et al. Aspirin inhibits Chlamydia pneumoniae-induced NF-kappa B activation, cyclooxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth // J. Med. Microbiol. — 2003. — Vol. 52. — Р. 409–415.
37. Jagielska J., Salguero G., Schieffer B., Bavendiek U. Digitoxin elicits anti-inflammatory and vasoprotective properties in endothelial cells: Therapeutic implications for the treatment of atherosclerosis? // Atherosclerosis. — 2009. — Vol. 206, № 2. — Р. 390–396.
38. Doostzadeh J., Clark L. N., Bezenek S. et al. Recent progress in percutaneous coronary intervention: evolution of the drugeluting stents, focus on the XIENCE V drug-eluting stent // Coron. Artery Dis. — 2010. — Vol. 21, № 1. — Р. 46–56.
39. Simsek C., Onuma Y., Magro M. et al. Four-year clinical outcome of sirolimus- and paclitaxel-eluting stents compared to bare-metal stents for the percutaneous treatment of stable coronary artery disease // Catheter Cardiovasc. Interv. — 2010. — Vol. 76, № 3. — Р. 41–49.
40. Karanasos A., Simsek C., Serruys P. et al. Five-year optical coherence tomography follow-up of an everolimus-eluting bioresorbable vascular scaffold: changing the paradigm of coronary stenting? // Circulation. — 2012. — Vol. 126, № 7. — Р. 89–91.
41. Nauta S. T., Van Mieghem N. M., Magro M. et al. Seven-year safety and efficacy of the unrestricted use of drug-eluting stents in saphenous vein bypass grafts // Catheter Cardiovasc. Interv. — 2012. — Vol. 79, № 6. — Р. 912–918.
42. Ma K. L., Varghese Z., Ku Y. et al. Sirolimus inhibits endogenous cholesterol synthesis induced by inflammatory stress in human vascular smooth muscle cells // Am. J. Physiol. Heart. Circ. Physiol. — 2010. — Vol. 298, № 6. — Р. 1646— 1651.
43. Chen W. Q., Zhong L., Zhang L. et al. Oral rapamycin attenuates inflammation and enhances stability of atherosclerotic plaques in rabbits independent of serum lipid levels // Br. J. Pharmacol. — 2009. — Vol. 156, № 6. — Р. 941–951.
44. Schanberg L. E., Sandborg C., Barnhart H. X. et al. Atherosclerosis Prevention in Pediatric Lupus Erythematosus Investigators. Premature atherosclerosis in pediatric systemic lupus erythematosus: risk factors for increased carotid intima-media thickness in the atherosclerosis prevention in pediatric lupus erythematosus cohort // Arthritis Rheum. — 2009. — Vol. 60, № 5. — Р. 1496–1507.
45. Lobatto M. E., Fayad Z. A., Silvera S. et al. Multimodal Clinical Imaging To Longitudinally Assess a Nanomedical Anti- Inflammatory Treatment in Experimental Atherosclerosis // Mol. Pharm. — 2010. — Vol. 7, № 6. — Р. 2020–2029.
46. Van Halm V. P., Nurmohamed M. T., Twisk J. W. et al. Diseasemodifying antirheumatic drugs are associated with a reduced risk for cardiovascular disease in patients with rheumatoid arthritis: a case control study // Arthritis Res. Ther. — 2006. — Vol. 8, № 5. — R151.
47. Ruiz-Irastorza G., Ramos-Casals M., Brito-Zeron P., Khamashta M. A. Clinical efficacy and side effects of antimalarials in systemic lupus erythematosus: a systematic review // Ann. Rheum. Dis. — 2010. — Vol. 69, № 1. — Р. 20–28.
48. Belizna C. C., Richard V., Thuillez C. et al. Insights into atherosclerosis therapy in antiphospholipid syndrome // Autoimmun. Rev. — 2007. — Vol. 7, № 1. — Р. 46–51.
49. Westlake S. L., Colebatch A. N., Baird J. et al. The effect of methotrexate on cardiovascular disease in patients with rheumatoid arthritis: a systematic literature review // Rheumatology (Oxford). — 2010. — Vol. 49, № 2. — Р. 295–307.
50. Ridker P. M. Testing the inflammatory hypothesis of atherothrombosis: scientific rationale for the cardiovascular inflammation reduction trial (CIRT) // J. Thromb. Haemost. — 2009. — Vol. 7 (Suppl 1). — Р. 332–339.
51. Ridker P. M. Moving beyond JUPITER: will inhibiting inflammation reduce vascular event rates? // Curr. Atheroscler. Rep. — 2013. — Vol. 15, № 1. — Р. 295–297.
52. Murdaca G., Spanò F., Puppo F. Use of leflunomide plus TNF-α inhibitors in rheumatoid arthritis // Expert. Opin. Drug Saf. — 2013. — Vol. 12, № 6. — Р. 801–804.
53. Suissa S., Bernatsky S., Hudson M. Antirheumatic drug use and the risk of acute myocardial infarction // Arthritis Rheum. — 2006. — Vol. 55, № 4. — Р. 531–536.
54. Gajanayake T., Sawitzki B., Matozan K. et al. Dextran sulfate facilitates anti-CD4 mAb-induced long-term rat cardiac allograft survival after prolonged cold ischemia // Am. J. Transplant. — 2008. — Vol. 8, № 6. — Р. 1151–1162.
55. Мansell A., Reinicke A., Worrall D. M., O’Neill L. A. The serine protease inhibitor antithrombin III inhibits LPS-mediated NF-κB activation by TLR-4 // FEBS Letters. — 2001. — Vol. 508, № 3. — Р. 313–317.
56. Ballow M., Allen C. Intravenous immunoglobulin modulates the maturation of TLR4-primed peripheral blood monocytes // J. Clin. Immunol. — 2011. — Vol. 139, № 2. — Р. 208–214.
57. Kessel A., Peri R., Haj T. et al. IVIg attenuates TLR-9 activation in B cells from SLE patients // J. Clin. Immunol. — 2011. — Vol. 32. — Р. 30–38.
58. Toldo S., Seropian I. M., Mezzaroma E. et al. Alpha-1 antitrypsin inhibits caspase-1 and protects from acute myocardial ischemia-reperfusion injury // J. Mol. Cell. Cardiol. — 2011. — Vol. 51, № 2. — Р. 244–251.
59. Johnson G. B., Brunn G. J., Platt J. L. Cutting edge: an endogenous pathway to systemic inflammatory response syndrome (SIRS)-like reactions through Toll-like receptor 4 // J. Immunol. — 2004. — Vol. 172, № 1. — Р. 20–24.
60. Monaco C., Gregan S. M., Navin T. J. et al. Toll-like receptor-2 mediates inflammation and matrix degradation in human atherosclerosis // Circulation. — 2009. — Vol. 120, № 24. — Р. 2462–2469.
61. Arslan F., Houtgraaf J. H., Keogh B. et al. Treatment with OPN-305, a humanized anti-Toll-Like receptor-2 antibody, reduces myocardial ischemia/reperfusion injury in pigs // Circ. Cardiovasc. Interv. — 2012. — Vol. 5. — Р. 279–287.
62. Spirig R., Tsui J., Shaw S. et al. The Emerging Role of TLR and Innate Immunity in Cardiovascular Disease // Cardiol. Res. Pract. — 2012. — Vol. 2012. — Р. 181394.
63. Franco C., Ho B., Mulholland D. et al. Doxycycline alters vascular smooth muscle cell adhesion, migration, and reorganisation of fibrillar collagen matrices // Am. J. Pathol. — 2006. — Vol. 168. — Р. 1697–1709.
64. Dalvi P. S., Singh A., Trivedi H. R. et al. Effect of doxycycline in patients of moderate to severe chronic obstructive pulmonary disease with stable symptoms // Ann. Thorac. Med. — 2011 — Vol. 6, № 4. — Р. 221–226 (doi: 10.4103/1817—1737.84777).
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