Rheumatoid arthritis (RA) is associated with an increased risk for cardiovascular (CV) events including cardiac insufficiency, acute myocardial infarction and stroke.¹ It is assumed that the release of proinflammatory cytokines and acute-phase proteins furthers the progression of atherosclerosis.^2,3 This process seems to be further accelerated and aggravated by the administration of cyclooxygenase (Cox) inhibitors (coxibs and non-steroidal anti-inflammatory drugs (NSAIDs)). Therefore, without defining how this could be done, the Food and Drug Administration and European Agency for the Evaluation of Medicinal Products have recommended CV-risk stratification and individualised risk assessment in patients with RA before using coxibs or NSAIDs.

The B type natriuretic peptide (BNP) is a hormone synthesised by cardiomyocytes in response to increased wall tension. The plasma level of its stable, inactive breakdown product, N-terminal prohormone BNP (NT-proBNP), has been identified as a universal predictor of CV risks⁴ even in patients with clinically inapparent impaired CV function. Patients with RA are known to be burdened with an increased incidence of CV impairment.¹ There is preliminary evidence that the serum levels of NT-proBNP in these patients reflect this burden.⁵

Recently, we observed that the use of NSAIDs and coxibs goes …