1. Ketlinskij, S.A. Citokiny. / S.A. Ketlinskij. S-Pb.: Foliant, 2008.550 р.
2. Marchenko Zh.A. Rol’ sosudistogo jendotelial’nogo faktora rosta v patogeneze revmatoidnogo artrita / Zh.A. Marchenko, Lukina G.V. // Nauchno-prakticheskaja revmatologija. 2005 no. 1. рр. 57-61.
3. Nasonov, E.L. Immunologicheskie markery ateroskleroza / E.L. Nasonov // Antifosfolipidnyj sindrom. M.: Litera, 2004. 298 p.
4. Nasonov, E.L. Problema aterotromboza v revmatologii / E.L. Nasonov // Vestn. RAMN. – 2003. no. 7. pp. 6–10.
5. Nedogoda S.V. Sosudistaja zhestkost’ i skorost’ rasprostranenija pul’sovoj volny: novye faktory riska serdechno-sosudistyh oslozhnenij i misheni dlja farmakoterapii / S.V. Nedogoda // Consilium Medicum: Bolezni serdca i sosudov. 2006. no. 4. pp. 25–29.
6. Novikov, A.A. Rol’ citokinov v patogeneze revmatoidnogo artrita / A.A. Novikov, E.N. Aleksandrova, M.A. Diatroptova // Nauchno-prakticheskaja revmatologija. 2010. no. 2. pp. 71–82.
7. Revmatologija: nacional’noe rukovodstvo / pod red. E.L. Nasonova, V.A. Nasonovoj. M.: GJeOTAR-Media, 2008. 852 p.
8. Juwuk, E.N. Jendotelial’naja disfunkcija pri zabolevanijah serdechno-sosudistoj sistemy i metody ee korrekcii / E.N. Juwuk, Ju.A. Vasjuk, A.B. Hadzegova, P.G. Filippov // Klinich. farmakologija i farmakoterapija. 2005. T. 1, no. 5. pp. 85–87.
9. Firestein G., Panayiand G., Wollheim F. Rheumatoid Arthritis. Oxford University Press, 2006;173–92.
10. Furst D.E., Keystone E.C., Fleischmann R. et al. Updated consensus statement on biological agents for the treatment of rheumatic diseases, 2010 //Ann. Rheum. Dis. 2010; 69 (Suppl II): i2-i29.
11. Infanger M., Kossmehl P., Shakibaei M., et al.Vascular endothelial growth factor inhibits programmed cell death of endothelial cells induced by clinorotation. J GravitPhysiol 2004; 11: pp. 199–200.
12. Kaplan M.J. Cardiovascular disease in rheumatoid arthritis. Curr. Opin. Rheumatol. 2006;18:28997.
13. Maki-Petaja K.M., Hall F.C., Booth A.D. et al. Rheumatoid arthritis is associated with increased aortic pulse wave velocity, which is reduced by anti-tumor necrosis factor-alpha therapy. Circulation, 2006;114:1185–92.