The effect of ivabradine and ω-3 polyunsaturated fatty acids on the cytokine levels in patients with ischemic heart failure
Keywords:heart failure, treatment, ivabradine, ω-3 polyunsaturated fatty acids, cytokines
The aim of our study was to evaluate of the possible effect of ivabradine and ω-3 polyunsaturated fatty acids on the levels of pro- and anti-inflammatory cytokines in patients with ischemic heart failure. 357 patients with ischemic HF and the sinus rhythm were observed. In accordance to treatment all patients were divided into four groups. The levels of interleukin 1β (IL-1β), interleukin 6 (IL-6), and interleukin 10 (IL-10 ) in the serum were determined using commercial ELISA kits according to the manufacturer’s instructions. During treatment we observed decrease of the serum IL-1β level in all groups of patients. The medicines of the basic treatment decreased of the serum IL-6 level by 30%. Dynamics in the second group was higher – 37.6%. The more intensive changes were caused by additional use of PUFA (for 45.9%) or their combination with ivabradin (for 48.6%). All therapeutic schemes caused the increase of IL-10 levels in the HF patients blood. But more intensive changes were observed in groups with PUFA: by 26%; and 26.1%, respectively. In the first group this value increased by 21.4%; in the second group – by 20.6%. Conclusions: 1. The PUFA medicines have the immunomodulatory effects: they decrease the levels of the serum pro-inflammatory cytokines (IL-1β, IL-6) and increase the level of the anti-inflammatory IL-10. 2. Ivabradine reduces the levels of proinflammarory IL-1β and IL-6 in the serum, but does not influence on the anti-inflammatory IL-10 concentration.
Прасолов А.В. // Аллергол. и иммунол. – 2009. – Т. 10, №1. – С. 99-109.
Dinarello C. // Blood. – 2011. – Vol. 117. – P. 3710-3732.
European Medicines Agency. ICH Harmonised Tripartite Guideline E6: Note for Guidance on Good Clinical Practice (PMP/ICH/135/95). – London: European Medicines Agency, 2002. – 46 p.
Ferrucci L., Cherubini A., Bandinelli S. et al. //J. Clin. Endocrinol. Metab. – 2006. – Vol. 91. – P. 439-446.
Gullestad L., Ueland T., Vinge L. et al. // Cardiol. – 2012. – Vol. 122. – P. 23-35.
Hofmann U., Frantz S. // Basic. Res. Cardiol. – 2013. – Vol. 108. – P. 2-19.
Lecour S., James R.W. // Eur. Heart J. – 2011. – Vol. 32. – P. 680-685.
McMurrey J., Adamopoulus S., Anker S. et al. // Eur. Heart J. – 2012. – Vol. 33. – P. 1787-1847.
Prabhakar U., Conway T.M., Murdock P. et al. // DNA Cell. Biol. – 2005. – Vol. 24. – P. 410-431.
Sola S., Mir M., Rajagopalan S. et al. // J. Card. Fail. – 2005. – Vol. 11. – P. 607-612.
Sheller J., Charalis A., Smidt-Arras D. et al. //BBA. – 2011. – Vol. 1813. – P. 878-888.
Tikiz C., Ufuk O., Pirildar T. et al. // The J. Rheum. – 2011. – Vol. 32. – P. 2095-2101.
Copyright (c) 2015 National University of Pharmacy
This work is licensed under a Creative Commons Attribution 4.0 International License.Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).