Russian Heart Failure Journal 2015year Natriuretic peptide and inflammation mediators in patients with different responses to cardiac resynchronization therapy


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2015/№2

Natriuretic peptide and inflammation mediators in patients with different responses to cardiac resynchronization therapy

Kuznetsov V. A., Soldatova A. M., Enina T. N., Petelina T. I.
Affiliate of the Federal State Budgetary Institution, "Research Institute of Cardiology" at the Siberian Branch of the Russian Academy of Medical Sciences, "Tyumen Cardiology Center", Melnikayte 111, Tyumen 625026

Keywords: N-terminal prohormone of brain natriuretic peptide (NT-proBNP), NT-proBNP, inflammation mediator, resynchronization therapy, CHF, EchoCG

DOI: 10.18087/rhfj.2015.2.2047

Background. Cardiac resynchronization therapy (CRT) is a current standard for the treatment of patients with severe CHF. A marker for beneficial response to CRT is being searched for. Aim. To evaluate time-related changes in levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and inflammation mediators in patients with different responses to CRT. Materials and methods. The study included 47 patients with CHF (78.7 % men, mean age 54.5±8.7) who were implanted with CRT devices. EchoCG was performed and levels of NT-proBNP, interleukin-6 (IL-6), С-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) were measured for all patients at baseline, 12 months and 24 months of follow-up. Patients were divided into three groups based on the time-related decrease in LV end systolic volume (ESV) following the CRT device implantation: patients with LV ESV reduced by >15 % constituted the responder group (n=29; 61.7 %); patients with LV ESV reduced from 5 to 15 % constituted the non-progressor group (n=9; 19.1 %); and patients with LV ESV reduced by <5 % constituted the non-responder group (n=9; 19.1 %). Results. In the responder group, significant decreases were observed for concentrations of NT-proBNP (р=0.039; р=0.018), IL-6 (р=0.035; р=0.028), and TNF-α (р=0.035; р=0.043) throughout the entire follow-up period. The CRP level was significantly decreased at 12 months but did not differ from baseline values at 24 months of observation (р=0.034; р=0.139). In the non-progressor group, NT-proBNP was decreasing during the first years. However at 24 months, the NT-proBNP level did not significantly differ from baseline (р=0.029; р=0.477), and changes in inflammation mediators were not observed. In the non-responder group, levels of NT-proBNP and inflammation mediators did not differ from baseline values during the entire follow-up period. Conclusion. A positive response to CRT is associated with reduced neuro-humoral activity and systemic inflammation. The neuro-humoral background decreases in the first year; however, further improvement and decreases in inflammation mediators were not observed in the remote period. Probably, the complex decrease in levels of NT-proBNP and inflammation mediators can be used as a marker for a beneficial response to CRT.
  1. Харченко Е. П. Сердечная недостаточность: патогенетический континуум и биомаркеры. Кардиология. 2012;52 (3):53–64.
  2. Gullestad L, Ueland T, Vingeet LE et al. Inflammatory cytokines in heart failure: mediators and markers. Cardiology. 2012;122 (1):23–35.
  3. Hofmann U, Frantz S. How can we cure a heart «in flame»? A translational view on inflammation in heart failure. Basic Res Cardiol. 2013 Jul;108 (4):356.
  4. Мареев В. Ю., Агеев Ф. Т., Арутюнов Г. П. и др. Рекомендации ВНОК и ОССН по диагностике и лечению хронической сердечной недостаточности (третий пересмотр). Журнал Сердечная Недостаточность. 2010;11 (1):3–62.
  5. Oikonomou E, Tousoulis D, Siasos G et al. The role of inflammation in heart failure: new therapeutic approaches. Hellenic J Cardiol. 2011 Jan-Feb;52 (1):30–40.
  6. Brignole M, Auricchio A, Baron-Esquiviaset G et al. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Eur Heart J. 2013 Aug;34 (29):2281–329.
  7. Кузнецов В. А. Сердечная ресинхронизирующая терапия: избранные вопросы. – М.: «Абис», 2007. – 128с.
  8. Кузнецов В. А., Виноградова Т. О., Енина Т. Н. и др. Влияние сердечной ресинхронизирующей терапии на выживаемость пациентов с кардиомиопатией ишемического и неишемического генеза в клинической практике. Терапевтический архив. 2012;84 (8):52–6.
  9. Yu CM, Sanderson JE, Gorsan J 3rd. Echocardiography, dyssynchrony, and the response to cardiac resynchronization therapy. Eur Heart J. 2010 Oct;31 (19):2326–37.
  10. Dong YХ, Burnett JCJr, Chen HH et al. Effect of cardiac resynchronization therapy on broad neurohormone biomarkers in heart failure. J Interv Card Electrophysiol. 2011 Apr;30 (3):241–9.
  11. Kuznetsov VA, Soldatova AM, Enina TN et al. Dynamics of natriuretic peptide and inflammatory markers in patients with different response to cardiac resynchronisation therapy. Eur J Heart Fail. 2014;16 (Suppl 2):242.
  12. Ding LG, Hua W, Zhang S et al. Decrease of plasma N-terminal pro В-type natriuretic peptide as a predictor of clinical improvement after cardiac resynchronization therapy for heart failure. Chin Med J. 2009 Mar 20;122 (6):617–21.
  13. Кузнецов В. А., Колунин Г. В., Харац В. Е. и др. «Регистр проведенных операций сердечной ресинхронизирующей терапии». Свидетельство о государственной регистрации базы данных № 2010620077 зарегистрировано в Реестре базы данных 1 февраля 2010 года.
  14. Rostagno C, Olivo G, Comeglio M et al. Prognostic value of 6‑min walk corridor test in patients with mild to moderate heart failure comparison with other methods of functional evalution. Eur J Heart Fail. 2003 Jun;5 (3):247–52.
  15. Tarquini R, Guerra CT, Porciani MC et al. Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure. Cardiol J. 2009;16 (6):545–52.
  16. Berger R, Shankar A, Fruhwald F et al. Relationships between cardiac resynchronization therapy and N-terminal pro-brain natriuretic peptide in patients with heart failure and markers of cardiac dyssynchrony: an analysis from the Cardiac Resynchronization in Heart Failure (CARE-HF) study. Eur Heart J. 2009 Sep;30 (17):2109–16.
  17. Braun MU, Rauwolf T, Zerm T et al. Long term biventricular resynchronisation therapy in advanced heart failure: effect on neurohormones. Heart. 2005 May;91 (5):601–5.
  18. Lappegård KT, Bjørnstad H. Anti inflammatory ffect of cardiac resynchronization therapy. Pacing Clin Electrophysiol. 2006 Jul;29 (7):753–8.
  19. Stanciu AE, Vatasescu RG, Stanciu MM et al. Cardiac resynchronization therapy in patients with chronic heart failure is associated with anti-inflammatory and anti-remodeling effects. Clin Biochem. 2013 Feb;46 (3):230–4.
  20. Orrego CM, Nasir N, Oliveira GH et al. Cellular evidence of reverse cardiac remodeling induced by cardiac resynchronization therapy. Congest Heart Fail. 2011 May-Jun;17 (3):140–6.
  21. Przybyła A, Czarnecka D, Kusiak A et al. The influence of cardiac resynchronization therapy on selected inflammatory markers and aldosterone levels in patients with chronic heart failure. Przegl Lek. 2011;68 (7):359–61.
  22. Boriani G, RegolI F, Saporito D et al. Neurohormones and inflammatory mediators in patients with heart failure undergoing cardiac resynchronization therapy: time courses and prediction of response. Peptides. 2006 Jul;27 (7):1776–86.
  23. Seifert M, Schlegl M, Hoersch W et al. Functional capacity and changes in the neurohormonal and cytokine status after long-term CRT in heart failure patients. Int J Cardiol. 2007 Sep 14;121 (1):68–73.
  24. Menardi E, Vado A, Rossetti G et al. Cardiac resynchronization therapy modifies the neurohormonal profile, hemodynamic and functional capacity in heart failure patients. Arch Med Res. 2008 Oct;39 (7):702–8.
  25. Osmancik P, Herman D, Stros P et al. Changes and prognostic impact of apoptotic and inflammatory cytokines in patients trea­ted with cardiac resynchronization therapy. Cardiology. 2013;124 (3):190–8.
  26. Shinohara T, Takahashi N, Saito S et al. Effect of cardiac resynchronization therapy on cardiac sympathetic nervous dysfunction and serum C-reactive protein level. Pacing Clin Electrophysiol. 2011 Oct;34 (10):1225–30
Kuznetsov V. A., Soldatova A. M., Enina T. N. et al. Natriuretic peptide and inflammation mediators in patients with different responses to cardiac resynchronization therapy. Russian Heart Failure Journal. 2015;16 (2):88–92

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