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TNFα blockade therapy reduces circulating NT-proBNP levels in RA patients with active disease: results from prospective cohort study
  1. Mike J L Peters1,*,
  2. Paul Welsh2,
  3. Iain B McInnes2,
  4. Gerrit Jan Wolbink3,
  5. Ben A C Dijkmans1,
  6. Michael T Nurmohamed1,
  7. Naveed Sattar2
  1. 1 VU University Medical Center, Netherlands;
  2. 2 Glasgow University, United Kingdom;
  3. 3 Jan van Breemen Instituut, Netherlands
  1. Correspondence to: Mike Johannes Leonardus Peters, Rheumatology, VU University medical center, De Boelelaan 1117, Amsterdam, 1081 HV, Netherlands; mjl.peters{at}vumc.nl

Abstract

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

Methods: 171 consecutive RA patients (disease activity score-28 above 3.2) without congestive HF (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. Pearson’s test evaluated biomarker correlations with changes in circulating log NT-proBNP levels, 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 versus 69.5 pg/ml, p = 0.004. Changes in NT-proBNP were associated with changes in pulse pressure (r = 0.18, p = 0.02), systolic blood pressure (r = 0.16, p = 0.04), and ESR (r = 0.18, p = 0.02). On multivariable analysis, changes in pulse pressure and ESR remained independently associated with changes in circulating NT-proBNP.

Discussion: Our novel observations demonstrate that blocking TNFα in RA patients without evident HF decreases NT-proBNP levels by around 18%. This suggests no treatment-induced deterioration in cardiac function, and a potential CV risk benefit.

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