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Tumour necrosis factor α blockade reduces circulating N-terminal pro-brain natriuretic peptide levels in patients with active rheumatoid arthritis: results from a prospective cohort study
  1. Mike J L Peters1,
  2. Paul Welsh2,
  3. Iain B McInnes2,
  4. Gertjan Wolbink3,
  5. Ben A C Dijkmans1,
  6. Naveed Sattar2,
  7. Michael T Nurmohamed1,3
  1. 1VU University Medical Centre, Amsterdam, The Netherlands
  2. 2University of Glasgow, Glasgow, UK
  3. 3Jan van Breemen Institute, Amsterdam, The Netherlands
  1. Correspondence to Dr Mike Peters, VU University Medical Centre, P O Box 7057, 1007 MB Amsterdam, The Netherlands; mjl.peters{at}vumc.nl

Abstract

Background Patients with rheumatoid arthritis (RA) are at increased risk of heart failure and vascular events. Small increases in circulating N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with an increased risk of a cardiovascular event, and high levels signal left ventricular dysfunction. Data on the effects of tumour necrosis factor α(TNFα) blocking agents on circulating NT-proBNP levels in patients with active RA are lacking but may be informative.

Methods 171 consecutive patients with RA (28-joint disease activity score >3.2) without congestive heart failure (NYHA class III or IV) were scheduled to receive adalimumab once every 2 weeks. Serum NT-proBNP concentrations were measured simultaneously on stored baseline and 16-week samples. Paired sample t tests were used to observe differences in biomarkers before and after adalimumab administration. Correlations between the biomarkers and changes in circulating log NT-proBNP levels were evaluated with the Pearson test and multivariable linear regression analyses of correlates were performed (forward selection procedure).

Results Circulating levels of NT-proBNP decreased significantly after 16 weeks of adalimumab administration (median NT-proBNP 83.0 pg/ml vs 69.5 pg/ml, p=0.004). Changes in NT-proBNP levels were associated with changes in pulse pressure (r=0.18, p=0.02), systolic blood pressure (r=0.16, p=0.04) and erythrocyte sedimentation rate (r=0.18, p=0.02). On multivariable analysis, changes in pulse pressure and erythrocyte sedimentation rate remained independently associated with changes in circulating NT-proBNP levels.

Conclusions These observations show that blocking TNFα in patients with RA without evident heart failure decreases NT-proBNP levels by about 18%. This suggests no treatment-induced deterioration in cardiac function and a potential cardiovascular risk benefit.

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Footnotes

  • MTN and NS contributed equally.

  • Funding The study was facilitated by the Clinical Research Bureau of the JBI which receives financial support from the Dutch Arthritis Association. MJP received a EULAR bursary and this research was conducted while he was an ARTICULUM Fellow.

  • Competing interests NS and PW have had reagents for the measurement of NT-proBNP donated for unrelated research projects by Roche International. There are no other conflicts of interest.

  • Ethics approval The study was approved by the local medical ethics committee and all patients gave written informed consent.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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