Activation of the renin–angiotensin–aldosterone system (RAAS) has a central role in the pathophysiology of congestive cardiac failure. Increased concentrations of RAAS neurohormones are associated with worse outcomes in patients with heart failure.¹ Blockade of this system with angiotensin converting enzyme (ACE) inhibitors, β blockers, and spironolactone is a cornerstone of treatment. Congestive cardiac failure is treated with a multiple drug approach limited by patient concordance, drug related side effects, and metabolic derangements. Despite chronic treatment RAAS activity can remain increased¹ and mortality of patients with congestive cardiac failure remains high.² Uncertainty concerning the combined role of ACE inhibitors and angiotensin II antagonists in heart failure has largely been resolved by the CHARM-Added (candesartan in heart failure assessment of reduction in mortality and morbidity for patients taking ACE inhibitors) study, which showed improvements in cardiovascular mortality and hospitalisations.² However, combination treatment in CHARM-Added did increase the risk of metabolic side effects. There may be a case for tailoring treatment for individual patients to maximise benefits.

Brain natriuretic peptide (BNP) concentrations are increased in congestive cardiac failure due to myocardial stretch and neuroendocrine interactions. BNP has potential for help in diagnosis …