Coronary artery disease, heart failure, and cardiac natriuretic peptides in the middleThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

This editorial refers to ‘Plasma N-terminal pro-brain natriuretic peptide concentration predicts coronary events in men at work: a report from the BELSTRESS study’† by J. De Sutter et al., on page 2644 An experienced cardiologist recently reminded me that most heart failure patients have a medical history of arteriosclerosis and coronary artery disease (CAD) (Figure 1). With or without myocardial infarction, the ventricular myocardium becomes hypoxic during increased workload, which, in turn, strangulates cardiac performance and initiates pathological remodelling of the myocardium. In the course of reduced left ventricular systolic function, the endocrine heart compensates with increased production and secretion of natriuretic hormones, that is, the cardiac natriuretic peptides. In fact, the association between cardiac disease and increased concentrations of natriuretic peptides was reported more than 20 years ago.1 Since then, numerous clinical studies have established that the plasma concentrations of atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) reflect left ventricular systolic function and accordingly are helpful markers in heart failure diagnostics. However, the most feasible clinical application today seems to be as rule-out markers, which means that low plasma concentrations efficiently can exclude left ventricular systolic dysfunction.2 In contrast, the relatively low diagnostic specificity in heart failure diagnosis suggests that also other pathophysiological stimuli besides left ventricular systolic dysfunction can trigger increased production and secretion of natriuretic peptides from the cardiac myocytes.