Angiotensin-converting enzyme (ACE) inhibitors have long been the cornerstone of heart failure (HF) therapy thanks to their unique dual mechanism of action resulting in a reduction in angiotensin II and an increase in bradykinin. Bradykinin most likely contributes to a major extent to the well-established efficacy of the ACE inhibitors in the HF syndrome, since their beneficial effects, including attenuated cardiac remodeling and vasodilation, are fully reversed by bradykinin B2 receptor blockade. Whether other antagonists of the renin-angiotensin system will prove as effective as ACE inhibitors in chronic HF is as yet unknown. Although the combination of an angiotensin type I receptor antagonist and an ACE inhibitor would appear to provide more benefit than ACE inhibition alone, available studies comparing the two classes of agents show conflicting results. Consequently, guidelines on treatment of HF firmly confirm the central role of ACE inhibition in all phases of HF...