Article Text

Download PDFPDF
BNP: not just for heart failure
  1. M G Nicholls,
  2. C M Frampton,
  3. T G Yandle
  1. Department of Medicine, Christchurch School of Medicine and Health Sciences, Christchurch Hospital, New Zealand
  1. Professor M G Nicholls, Department of Medicine, Christchurch School of Medicine and Health Sciences, Riccarton Avenue, PO Box 4345, Christchurch, New Zealand; gary.nicholls{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Measurement of circulating natriuretic peptides has found a secure place in the diagnosis and management of patients with heart failure. In this issue of Heart, Khan and colleagues report that plasma levels of immunoreactive N-terminal pro-B-type natriuretic peptide (NTproBNP) provide prognostic information better than that given by the TIMI risk score in patients with ST-segment elevation myocardial infarction (STEMI) (see article on page 40).1 The paper adds significantly to an already impressive literature describing the response of circulating natriuretic peptides, especially the B-type peptides, to acute coronary syndromes (ACS) and their potential use as prognostic indicators.

Circulating levels of the natriuretic peptides (BNP, NTproBNP and atrial natriuretic peptide (ANP)) exhibit a substantial and sustained increase after ACS, although the magnitude and pattern of change differs between the peptides.2 What accounts for this response? Enhanced cardiac secretion of the peptides results probably from increased mechanical stretch of the infarct and peri-infarct regions of the heart together with stimulatory effects from neurohormonal systems which are activated at the time of ACS. These include the sympathetic nervous system, the corticotrophin/ACTH/cortisol axis, renin–angiotensin systems (both systemic and cardiac) and endothelin, together with local tissue hypoxia and acidosis. Teleologically, this response can be viewed as protective through the actions of bioactive BNP and ANP, via cGMP, within cardiac tissue, to oppose the profibrotic and inflammatory effects of transforming growth factor β (TGFβ) and open KATP channels,3 for example, thereby …

View Full Text


  • Competing interests: None declared.

Linked Articles