The effect of ivabradine and ω-3 polyunsaturated fatty acids on the fibronectin plasma levels in patients with heart failure


  • S. V. Fedorov SHHE «Ivano-Frankivsk National Medical University», Ukraine



heart failure, treatment, ivabradine, ω-3 polyunsaturated fatty acids


Chronic heart failure (HF) is a highly prevalent chronic pathological condition with high morbidity and mortality rates. The cost for HF treatment is 2% of the national health expenditures each year. Fibronectin (Fn) has a crucial role in the process of tissue-specific morphogenesis and cell differentiation in embryogenesis; it stimulates fibroblasts and different growth factors during wound healing and tissue reparation. The aim of our study was to assess the possible effects of Ivabradine and ω-3 polyunsaturated fatty acids on the fibronectin plasma level in patients with heart failure. 357 Patients with ischemic HF and the sinus rhythm were observed. In accordance to treatment regimens all patients were divided into four groups: group I – basic treatment; group II – basic treatment and Ivabradine; group III – basic treatment and PUFA; group IV – basic treatment with Ivabradine and PUFA. The fibronectin levels were measured by ELISA method. The average value of the Fn concentration in HF patients was 1.25 times higher than in the control group (p<0.05). In patients with basic HF treatment the tendency to the Fn plasma level decrease (p>0.05) was observed. In the group with additional prescription of Ivabradine the concentration of this protein in the blood decreased by 14.5% (p<0.01). The same situation was observed in the group with additional use of PUFA – by 11.1% (p<0.05). In group IV the plasma concentration of Fn decreased by 12.9% (p<0.05). Thus, Ivabradine and ω-3 polyunsaturated fatty acids, either alone or in combination, decrease the plasma levels of fibronectin in patients with heart failure, and it shows a pronounced cardioprotective effect.


Сидорчук Л.П. // Український терапевтичний журнал. - 2007. - №3. - С. 33-39.

Chun L., Teng Z., Na-Dan Z. [et al.] //PLOS One. - 2012. –Vol. 7(6). – P. 1-13.

Deedwania P. //Drugs. -2013. –Vol.73. –P.1569-1586.

Ding L., Guo D., Homandberg G.A. //Osteoarthritis Cartilage. - 2009. – Vol.17. – P.1385–1392.

Ekman I., Cleland J.G., Andersson B. [et al.]// Eur. J. Heart Fail. - 2005. –Vol.7. – P.699–703.

Fox K., Ford I., Steg P.G. [et al.] //Lancet. - 2008. –Vol.372(9641). – P.817–821.

McMurrey J., Adamopoulus S., Anker S. [et al.] // European Heart Journal. – 2012. – Vol. 33. – P.1787–1847.

Mewton N., Liu C., Croisillie P. [et al.] //JACC. - 2011. –Vol.57. – P.891-903.

Moore K.J., Fisher E.A. (2012). The double-edged sword of fibronectin in atherosclerosis. EMBO Mol. Med., 4, 561-563.

Schultz G.S., Wysocki A. //Wound Repair Regen. - 2009. – Vol.17. – P.153–162.

Stewart S., Jenkins A., Buchan S. [et al.] // Eur. Heart Fail. – 2002. –Vol. 4. –P.361-371.

White E.S., Baralle E.F., Muro A.F. //J. Pathol. - 2008. –Vol.216. –P.1-14.






Experimental and Clinical Pharmacology