Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure

Roberto Tarquini, Cristina Tosti Guerra, Maria Cristina Porciani, Antonio Michelucci, Margherita Padeletti, Giuseppe Ricciardi, Marco Chiostri, Sania Jelic, Luigi Padeletti

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background: The effect of cardiac resynchronization therapy (CRT) on systemic inflammation and neurohormonal alterations associated with heart failure is not well characterized. Accordingly, we aimed to assess the long term effects of CRT on systemic inflammation and neurohormonal factors in heart failure patients. Methods and results: In 47 HF patients (NYHA III-IV) we evaluated, at baseline and after one year of CRT: TNF-α, TNF soluble receptors (sTNFR1 and sTNFR2), insulin-like growth factor-1a (IGF-1α), adiponectin, norepinephrine, pro-atrial natriuretic peptide (pro-ANP), N-terminal-pro-brain natriuretic peptide (NT-proBNP) and angiotensin II, NYHA functional class, quality of life (the Minnesota Living with Heart Failure questionnaire), a 6-minute walk test and an echocardiogram. Long-term CRT decreased activation of renin-angiotensin system (RAS) only in patients with reverse remodelling. It failed to prevent a decline in adiponectin levels, regardless of reverse remodelling. NT-proBNP remained unchanged in patients with reverse remodelling, whereas its levels increased in those without reverse remodelling. IGF-1α increased with CRT, whereas CRT had no effect on pro-ANP and inflammatory markers. Conclusions: Long-term CRT is associated with decreased RAS activation and stabilization of NT-proBNP in heart failure patients with reverse remodelling. Long-term CRT, with or without reverse remodelling, does not affect systemic inflammation and fails to prevent a decline in adiponectin.

Original languageEnglish
Pages (from-to)545-552
Number of pages8
JournalCardiology Journal
Volume16
Issue number6
Publication statusPublished - 2009

Fingerprint

Cardiac Resynchronization Therapy
Heart Failure
Inflammation
Brain Natriuretic Peptide
Adiponectin
Atrial Natriuretic Factor
Somatomedins
Renin-Angiotensin System
Tumor Necrosis Factor Receptors
Angiotensin II
Norepinephrine
Quality of Life

Keywords

  • Heart failure
  • Neuro-hormonal pattern
  • Resynchronization therapy

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Tarquini, R., Guerra, C. T., Porciani, M. C., Michelucci, A., Padeletti, M., Ricciardi, G., ... Padeletti, L. (2009). Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure. Cardiology Journal, 16(6), 545-552.

Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure. / Tarquini, Roberto; Guerra, Cristina Tosti; Porciani, Maria Cristina; Michelucci, Antonio; Padeletti, Margherita; Ricciardi, Giuseppe; Chiostri, Marco; Jelic, Sania; Padeletti, Luigi.

In: Cardiology Journal, Vol. 16, No. 6, 2009, p. 545-552.

Research output: Contribution to journalArticle

Tarquini, R, Guerra, CT, Porciani, MC, Michelucci, A, Padeletti, M, Ricciardi, G, Chiostri, M, Jelic, S & Padeletti, L 2009, 'Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure', Cardiology Journal, vol. 16, no. 6, pp. 545-552.
Tarquini R, Guerra CT, Porciani MC, Michelucci A, Padeletti M, Ricciardi G et al. Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure. Cardiology Journal. 2009;16(6):545-552.
Tarquini, Roberto ; Guerra, Cristina Tosti ; Porciani, Maria Cristina ; Michelucci, Antonio ; Padeletti, Margherita ; Ricciardi, Giuseppe ; Chiostri, Marco ; Jelic, Sania ; Padeletti, Luigi. / Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure. In: Cardiology Journal. 2009 ; Vol. 16, No. 6. pp. 545-552.
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AU - Ricciardi, Giuseppe

AU - Chiostri, Marco

AU - Jelic, Sania

AU - Padeletti, Luigi

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N2 - Background: The effect of cardiac resynchronization therapy (CRT) on systemic inflammation and neurohormonal alterations associated with heart failure is not well characterized. Accordingly, we aimed to assess the long term effects of CRT on systemic inflammation and neurohormonal factors in heart failure patients. Methods and results: In 47 HF patients (NYHA III-IV) we evaluated, at baseline and after one year of CRT: TNF-α, TNF soluble receptors (sTNFR1 and sTNFR2), insulin-like growth factor-1a (IGF-1α), adiponectin, norepinephrine, pro-atrial natriuretic peptide (pro-ANP), N-terminal-pro-brain natriuretic peptide (NT-proBNP) and angiotensin II, NYHA functional class, quality of life (the Minnesota Living with Heart Failure questionnaire), a 6-minute walk test and an echocardiogram. Long-term CRT decreased activation of renin-angiotensin system (RAS) only in patients with reverse remodelling. It failed to prevent a decline in adiponectin levels, regardless of reverse remodelling. NT-proBNP remained unchanged in patients with reverse remodelling, whereas its levels increased in those without reverse remodelling. IGF-1α increased with CRT, whereas CRT had no effect on pro-ANP and inflammatory markers. Conclusions: Long-term CRT is associated with decreased RAS activation and stabilization of NT-proBNP in heart failure patients with reverse remodelling. Long-term CRT, with or without reverse remodelling, does not affect systemic inflammation and fails to prevent a decline in adiponectin.

AB - Background: The effect of cardiac resynchronization therapy (CRT) on systemic inflammation and neurohormonal alterations associated with heart failure is not well characterized. Accordingly, we aimed to assess the long term effects of CRT on systemic inflammation and neurohormonal factors in heart failure patients. Methods and results: In 47 HF patients (NYHA III-IV) we evaluated, at baseline and after one year of CRT: TNF-α, TNF soluble receptors (sTNFR1 and sTNFR2), insulin-like growth factor-1a (IGF-1α), adiponectin, norepinephrine, pro-atrial natriuretic peptide (pro-ANP), N-terminal-pro-brain natriuretic peptide (NT-proBNP) and angiotensin II, NYHA functional class, quality of life (the Minnesota Living with Heart Failure questionnaire), a 6-minute walk test and an echocardiogram. Long-term CRT decreased activation of renin-angiotensin system (RAS) only in patients with reverse remodelling. It failed to prevent a decline in adiponectin levels, regardless of reverse remodelling. NT-proBNP remained unchanged in patients with reverse remodelling, whereas its levels increased in those without reverse remodelling. IGF-1α increased with CRT, whereas CRT had no effect on pro-ANP and inflammatory markers. Conclusions: Long-term CRT is associated with decreased RAS activation and stabilization of NT-proBNP in heart failure patients with reverse remodelling. Long-term CRT, with or without reverse remodelling, does not affect systemic inflammation and fails to prevent a decline in adiponectin.

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