INFLAMMATORY MEDIATORS ROLE IN ATHEROSCLEROTIC LESION DEVELOPMENT IN THE LARGE ARTERIES IN PATIENTS WITH SYSTEMIC SCLERODERMIA
https://doi.org/10.15829/1728-8800-2015-3-4-11
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Abstract
Aim. To evaluate the prevalence of atherosclerosis, to define the type of atherosclerotic lesion of brachiocephalic arteries in patients with systemic sclerodermia (SSD); to reveal the main factors influencing that process.
Material and methods. Totally 38 patients with SSD studied. We measured vessel stiffness on the area between carotid and femoral arteries; instrumental and laboratory characteristics of endothelial function, morphology of carotid arteries, lipid profile parameters, as glucose, uric acid, N-terminal brain natriuretic peptide (NT-proBNP), antinuclear autoantibodies spectrum, cytokines concentration and chemokines of serum.
Results. The increase of intima-media thickness (IMT) was found in 79% (n=30/38) of the patients studied with SSD. In one of the patients there was occluded carotid artery. Different level of arterial stenosis (20- 70%) — in 52,6% (n=20/38) of patients. We also measured relation of IMT and several classic risk factors (RF) of atherosclerosis (age, glyciemia level). Among non-classical risk factors there was relation of IMT and levels of asymmetrical dimethyl arginine (ADMA), soluble adhesion endothelium molecule (sVCAM), uric acid, NT-proBNP, autoantibodies to centromeres proteines. In multiple regression analysis the most informative predictors of IMT were age, uric acid, sVCAM, granulocytic colony- stimulating factor (G-CSF) and interleucine-1 (IL-1). Conclusion. In SSD patients atherosclerosis develops partially through non-classic factors influence, primarily inflammatory mediators and common for SSD metabolic disruptions (uricemia). This can point on the specific interrelation of pathogenetic mechanisms of arterial wall involvement in SSD, and might require repeated assessment of IMT in SSD, using larger patients selection and additional investigation methods.
About the Authors
A. L. MaslyanskyRussian Federation
E. P. Kolesova
Russian Federation
A. V. Kozlenok
Russian Federation
E. Yu. Vasilieva
Russian Federation
I. N. Penin
Russian Federation
O. P. Rotar
Russian Federation
N. M. Lazareva
Russian Federation
S. V. Lapin
Russian Federation
K. A. Sysoev
Russian Federation
V. N. Solntsev
Russian Federation
A. N. Bazhenov
Russian Federation
A. O. Konradi
Russian Federation
References
1. Katsumoto TR, Whitfield ML, Connolly MK. The pathogenesis of systemic sclerosis. Annu Rev Pathol 2011; 6: 509-37.
2. Man A, Zhu Y Zhang Y et al. The risk of cardiovascular disease in systemic sclerosis: a population-based cohort study. Ann Rheum Dis 2013; 72(7): 1188-93.
3. Muller-Ladner U, Distler O, Ibba-Manneschi L, et al. Mechanisms of vascular damage in systemic sclerosis. Autoimmunity 2009; 42(7): 587-95.
4. Pattanaik D, Brown M, Postlethwaite AE. Vascular involvement in systemic sclerosis (scleroderma). J Inflamm Res 2011; 4: 105-25.
5. Pencina MJ, D'Agostino RB, Larson MG, et al. Predicting the 30-year risk of cardiovascular disease: the framingham heart study. Circulation 2009; 119(24): 3078-84.
6. Culleton BF, Larson MG, Kannel WB, et al. Serum uric acid and risk for cardiovascular disease and death: the Framingham Heart Study. Ann Intern Med 1999; 131(1): 7-13.
7. Kim SY Guevara JP, Kim KM, et al. Hyperuricemia and coronary heart disease: a systematic review and meta-analysis. Arthritis Care Res (Hoboken) 2010; 62(2): 170-80.
8. Sabio JM, Vargas-Hitos J, Zamora-Pasadas M, et al. Metabolic syndrome is associated with increased arterial stiffness and biomarkers of subclinical atherosclerosis in patients with systemic lupus erythematosus. J Rheumatol 2009; 36(10): 2204-11.
9. Elshamy HA, Ibrahim SE, Farouk HM, et al. N-terminal pro-brain natriuretic peptide in systemic sclerosis: new insights. Eur J Dermatol 2011; 21(5): 686-90.
10. Hu Z, Zhang J, Guan A, et al. Granulocyte colony-stimulating factor promotes atherosclerosis in high-fat diet rabbits. Int J Mol Sci 2013; 14(3): 4805-16.
11. Ait-Oufella H, Taleb S, Mallat Z, et al. Recent advances on the role of cytokines in atherosclerosis. Arterioscler Thromb Vasc Biol 2011; 31(5): 969-79.
12. Colaci M, Giuggioli D, Manfredi A, et al. Aortic pulse wave velocity measurement in systemic sclerosis patients. Reumatismo 2012; 64(6): 360-7.
13. Constans J, Germain C, Gosse P, et al. Arterial stiffness predicts severe progression in systemic sclerosis: the ERAMS study. J Hypertens 2007; 25(9): 1900-6.
14. Maslyanskiy AL, Kolesova EP, Penin IN, et al. The impact of anti-V cell therapy on the rigidity of the vascular wall in patients with systemic scleroderma. Arterial hypertension 2013; 19(3): 212-20. Russian (Maslyanskii A. L., Kolesova E. P., Penin I. N. i dr. Vliyanie anti V-kletochnoi terapii na zhestkost' sosudistoi stenki u bol'nykh sistemnoi sklerodermiei. Arterial'naya gipertenziya 2013; 19(3): 212-20).
15. Chen XM, Hu CP, Li YJ, et al. Cardiovascular risk in autoimmune disorders: role of asymmetric dimethylarginine. Eur J Pharmacol 2012; 696(3): 5-11.
Review
For citations:
Maslyansky A.L., Kolesova E.P., Kozlenok A.V., Vasilieva E.Yu., Penin I.N., Rotar O.P., Lazareva N.M., Lapin S.V., Sysoev K.A., Solntsev V.N., Bazhenov A.N., Konradi A.O. INFLAMMATORY MEDIATORS ROLE IN ATHEROSCLEROTIC LESION DEVELOPMENT IN THE LARGE ARTERIES IN PATIENTS WITH SYSTEMIC SCLERODERMIA. Cardiovascular Therapy and Prevention. 2015;14(3):4-11. (In Russ.) https://doi.org/10.15829/1728-8800-2015-3-4-11
ISSN 2619-0125 (Online)