B-type natriuretic peptide serum levels in acute heart failure.

We read with great interest the article by Cowie et al.1 on clinical applications of the assessment of B-type natriuretic peptide (BNP). This is an important subject and the article also helps to clarify which areas of BNP research need more attention. The authors conclude that in new patients presenting to emergency services with dyspnoea, if the BNP level is <100 pg/mL, then heart failure is highly unlikely to be present. BNP has been used in many clinical studies to exclude and/or identify congestive heart failure (HF) in patients with dyspnoea,2 however, in most published studies the time from symptom onset to BNP measurement is not reported, and likely BNP levels increase after a few hours. A patient with pulmonary oedema could have a “normal” BNP serum level if he/she presented to the emergency room very soon after symptoms onset. Would the authors advocate for repeated BNP assessments? Acute HF is usually caused by an acute change in LV performance or in structural cardiac integrity (i.e., acute myocardial infarct, papillary muscle rupture or fulminant myocarditis).3 The role of BNP in patients with HF symptoms because of mechanical complications after an acute myocardial infarct and in myocarditis has not yet been evaluated. It appears that the exact role of BNP measurement in the diagnostic algorithm of acute heart failure, a term including many different pathophysiological entities, remains to be fully clarified. We believe that more limitations of BNP assessment may become evident once it is used in everyday clinical practice. The authors report that BNP levels rise with age, are affected by gender and that several clinical circumstances can alter the clinical interpretation of BNP concentrations. Those states include ischaemia, infarction and renal failure, which are very common problems. What would the authors recommend here? Finally, we would like to comment that the metabolic effects of BNP include lipolytic effects that are at least as big as, but independent of, the effects of catecholamines.4 BNP may directly contribute to tissue wasting processes, in acute and in chronic heart failure. References