N.А. TSIBULKIN¹, G.V. TUKHVATULLINA², V.N. TSIBULKINA^3,4, А.I. АBDRAKHMANOVA¹

¹Kazan State Medical Academy, 36 Butlerov Str., Kazan, Russian Federation, 420012

²Occupational health facility of the Ministry of Internal Affairs of the Russian Federation of the Republic of Tatarstan, Clinical hospital, 132 Orenburgskiy Trakt, Kazan, Russian Federation, 420064

³Kazan State Medical University, 49 Butlerov Str., Kazan, Russian Federation, 420012 

Tsybulkin N.A. ― Cand. Med. Sc., Associate Professor of the Department of cardiology, roentgen-endovascular and cardiovascular surgery, tel. (843) 261-74-11, e-mail: [email protected]

Galina V.T. ― Head of the Clinical and Diagnostic Laboratory, tel. +7-917-904-41-28, e-mail: [email protected]

Tsybulkina V.N. ― D. Med. Sc., Professor, Head of the Department of clinical immunology and allergology, tel. (843) 231-20-87, e-mail: [email protected]

Abdrakhmanova A.I. ― Cand. Med.S c., Associate Professor of the Department of cardiology, roentgen-endovascular and cardiovascular surgery, tel. +7-917-922-6629, e-mail: [email protected]

Atherosclerosis is one of the most widespread diseases in developed countries. It is characterised by a typical picture of structural changes in walls of arteries, which can be diagnosed by morphological, ultrasonic and roentgen contrast methods. The results of the last experimental and clinical studies show that except for characteristic morphological picture, atherosclerosis indicates an important component of pathogenesis that unites all the clinical forms and that is reflected in profile of laboratory parameters. This is the inflammatory process that is present on site of an atherosclerotic plaque and also has systemic symptoms. Inflammation represents the key pathogenetic mechanism which mediates realization of risk factors in morphological changes and clinical symptoms. As for contemporary situation, atherosclerosis is a chronic inflammatory disease that eventually leads to a variety of development of organo-specific complications. These complications are considered as independent nosological forms.

Key words: atherosclerosis, pathogenesis, inflammation, inflammatory mediators.

REFERENCES

1. Raieian-Kopaei M., Setorki M., Doudi M. et al. Atherosclerosis: process, indicators, risk factors and new hopes. International Journal of Preventive Medicine, 2014, no. 8 (5), rr. 927-946.
2. Campbell K., Lipinski M., Doran A., Skaflen M. et al. Lymphocytes and the adventitial immune response in atherosclerosis. Circ Res, 2012, no. 110, pp. 889-900.
3. Fogelstrand P., Boren J. Retention of atherogenic lipoproteins in the artery wall and its role in atherogenesis. Nutr. Metab. Cardiovasc. Dis, 2012, no. 22, P. 1-7.
4. Throne R., Mhaidat N., Ralston K., Burns J. CD36 is a receptor for oxidized high density lipoprotein: implications for the development of atherosclerosis. FEBS Lett, 2007, no. 581, pp. 1227-1232.
5. Redgrave J., Gallagher P., Lovett J., Rothwell P. Critical cap thickness and rupture in symptomatic carotid plaque: the oxford plaque study. Stroke, 2008, no. 39, pp. 1722-1729.
6. Agmon-Levin N., Bat-sheva P., Barzilai O. et al. Antitreponemal antibodies leading to autoantibody production and protection from atherosclerosis in Kitavans from Papua New Guinea. Ann N Y Acad. Sci, 2009, no. 1173, pp. 675-682.
7. Rosenfeld M., Campbell L. Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis. Thromb Haemost, 2011, no. 106, pp. 858-867.
8. Campbell L., Lee A., Rosenfeld M., Kuo C. Chlamydia pneumoniae induces expression of pro-atherogenic factors through activation of the lectin-like oxidized LDL receptor-1. Pathogens and Disease, 2013, no. 1 (69), pp. 1-6.
9. Kamei M., Carman C. New observations on the trafficking and diapedesis of monocytes. Curr. Opin. Hematol, 2010, no. 17, pp. 43-52.
10. Pant S., Deshmukh A., Gurumurthy G. et al. Inlammation and atherosclerosis ― revisited. Journal of Cardiovascular Pharmacology and therapeutics, 2014, no. 2 (19), pp. 170-178.
11. Zheng Y., Gardner S., Clarke M. Cell death, damage-associated molecular patterns, and sterile inflammation in cardiovascular disease. Arterioscler. Thromb. Vasc. Biol, 2011, no. 31, pp. 2781-2786.