SUBCLINICAL CARDIOVASCULAR SYSTEM INVOLVEMENT IN RHEUMATIC DISEASES

Aim. Assessment of patients with different rheumatic diseases and studying of markers of subclinical course of involvement of target organs (the heart, vessels, kidneys), with consequent analysis of their relation to the level of ADMA. Material and methods. Totally 162 patients included in the study, with RD (RA, SSD, AS), 63 without rheumatic pathology with more than 2 factors of cardiovascular risk, and 10 healthy volunteers. All patients were examined by rheumatologist and cardiologist, the anamnesis was collected and physical examination with anthropometry. Of laboratory tests we performed creatinine measurement, glucose, total cholesterol, C-reactive protein (C-RP), ADMA. Estimated glomerular filtration rate was calculated by MDRD equation. Functional assessment included EchOCG, ultrasound visualization of carotid arteries and vessel stiffness evaluation. Data processing was done using the software Statistica 8.0 (StatSoft Inc., USA), and Prism 5 for Windows, version 5,03, GraphPad Software, Inc., USA).
Results. Analyzing subclinical involvement of target organs in it found that, as in R D, in the comparison group patients the parameters of the pulse wave velocity, glomerular filtration rate, left ventricle hypertrophy were not out of normal range. The main changes affected intima-media complex thickness, thatwas the highest in rheumatoid arthritis, and the beginning renal disease was characteristic for systemic sclerodermia patients. These same subgroups of ADMA were the highest and correlated with the studied parameters the same way as in the group of patients with more prominent atherosclerotic disease.
Conclusion. The earliest sign of subclinical involvement of target organs in rheumatic diseases is remodeling of vessel wall. ADMA can be a mediator of atherosclerosis progression in rheumatic diseases as in patients with the combination of traditional risk factors of cardiovascular diseases.

1. .Roifman I, Beck PL, Anderson TJ, et al. Chronic inflammatory diseases and cardiovascular risk: a systematic review. Can J Cardiol, 2011; 27(2): 174-82.

2. Rebrov AP, Gajdukova IZ., Poddubnyj DA. Cardiovascular pathology in patients with ankylosing spondylitis. Scientific and Practical Rheumatology 2012; (2): 100-5. Russian (Ребров, А.П., Гайдукова И.3., Поддубный Д.А. Кардиоваскулярная патология у больных анкилозирующим спондилитом. Научно-практическая ревматология 2012; (2): 100-5).

3. Novikova DS, Popkova TV, Gerasimov AN, et al. Relationship between cardiovascular risk factors and arterial wall rigidity in womans with hight activity of rheumatoid artritis. Rational pharmacotherapy in cardiology, 2012; 8(6): 756-65. Russian (Новикова, Д.С, Т.В.Попкова, А.Н.Герасимов, и др. Взаимосвязь кардиоваскулярных факторов риска с ригидностью артериальной стенки у женщин с высокой активностью ревматоидного артрита. Рациональная фармакотерапия в кардиологии, 2012; 8(6): 756-65).

4. FrostegardJ. Rheumatic diseases: insights into inflammation and atherosclerosis. ArteriosclerThroinb Vase Biol, 2010; 30(5): 892-3.

5. Chen ХМ, Ни СР, Li YJ, et al. Cardiovascular risk in autoimmune disorders: role of asymmetric dimethylarginine. Eur J Pharmacol, 2012; 696(1-3): 5-11.

6. Soltesz P, Kerekes G, Der H, et al. Comparative assessment of vascular function in autoimmune rheumatic diseases: considerations of prevention and treatment. Autoimmun Rev, 2011; 10(7): 416-25.

7. Nussinovitch U, ShoenfeldY Atherosclerosis and macrovascular involvement in systemic sclerosis: myth or reality. Autoimmun Rev, 2011; 10(5): 259-66.

8. Tyrrell PN, Beyene J, Feldman BM, et al. Rheumatic disease and carotid intima-media thickness: a systematic review and meta-analysis. Arterioscler Thromb Vase Biol, 2010; 30(5): 1014-26.

9. Gupta N, Saigal R, Goyal L, et al. Carotid intima media thickness as a marker of atherosclerosis in ankylosing spondylitis. Int J Rheumatol, 2014: ID 839135, http://dx.doi. org/10.1155/2014/839135.

10. Riccioni G, Bucciarelli V, Scotti L, et al. Relationship between asymmetric dimethylarginine and asymptomatic carotid atherosclerosis. J Biol Regul Homeost Agents, 2010. 24(3): 351-8.

11. Surdacki A, Martens-Lobenhoffer J, Wloch A, et al. Elevated plasma asymmetric dimethyl-L-arginine levels are linked to endothelial progenitor cell depletion and carotid atherosclerosis in rheumatoid arthritis. Arthritis Rheum, 2007; 56(3): 809-19.

12. Masljanskij AL, Penin IN, Cheshuina MD, et al. General patterns of cytokines and chemokines production in patients with chronic inflammatory diseases, inflammatory arthropathy and atherosclerosis. Cytokines and Inflammation 2014; 13, 3: 9-21. Russian (Маслянский А.Л., Пенин И.Н., Чешуина М.Д., и др. Общие закономерности продукции цитокинов и хемокинов у больных диффузными заболеваниями соединительной ткани, воспалительными артропатиями и атеросклерозом. Цитокины и воспаление 2014; 13,3:9-21).

13. Sandoo AT, Dimitroulas JJ, van Zanten V, et al. Lack of association between asymmetric dimethylarginine and in vivo microvascular and macrovascular endothelial function in patients with rheumatoid arthritis. Clin Exp Rheumatol, 2012; 30(3): 388-96.

14. Erre GL, Sanna P, Zinellu A, et al. Plasma asymmetric dimethylarginine (ADMA) levels and atherosclerotic disease in ankylosing spondylitis: a cross-sectional study. Clin Rheumatol, 2011; 30(1): 21-7.

15. Kemeny-Beke A, Gesztelyi R, Bodnar N, et al. Increased production of asymmetric dimethylarginine (ADMA) in ankylosing spondylitis: association with other clinical and laboratory parameters. Joint Bone Spine, 2011; 78(2): 184-7.