Introducing a new role for BNP: as a general indicator of cardiac structural disease rather than a specific indicator of systolic dysfunction only.

In the early 1990s, the idea first arose that plasma concentrations of B type natriuretic peptide (BNP) might help target scarce cardiac investigations towards the most deserving. This mainly referred to the possibility that BNP could detect which patients had heart failure and which did not. This was based on the fact that echocardiography slots were limited, and that heart failure was hard to diagnose accurately on clinical grounds. The need for correct targeting of echocardiography increased when it was fully realised that clinical heart failure was a heterogeneous entity and that the treatments which produced major benefit (angiotensin converting enzyme (ACE) inhibitors and β blockers) were only of definite benefit in those with left ventricular (LV) systolic dysfunction. A huge amount of work then went in to establishing how well BNP identified either heart failure or LV systolic dysfunction. 4 The bottom line of this work is that a normal BNP is a very effective way of “ruling out” heart failure or LV systolic dysfunction in either a symptomatic or an asymptomatic patient. In this way, echocardiography could be reserved only for those with a high BNP concentration. However, it became patently clear that a high BNP in itself did not always indicate LV systolic dysfunction. Thus for diagnostic purposes BNP was sensitive but not specific—that is, although a high BNP was picking up nearly all LV systolic dysfunction, it appeared to also pick up some other patients. This begs the obvious question: what other patients were being identified by a high BNP concentration?