Two landmark clinical trials, CONSENSUS I and SOLVD-T, have shown, unequivocally, that angiotensin converting enzyme (ACE) inhibitors reduce all cause mortality in patients with chronic heart failure (CHF) and underlying left ventricular systolic dysfunction.1 ,2These and other trials have also confirmed that ACE inhibitors reduce morbidity, as manifest by hospital admission, in patients with CHF.3

A number of other key randomised, controlled, trials have also shown that ACE inhibitors reduce the risk of all cause mortality and major clinical events (sudden death, reinfarction, heart failure) after myocardial infarction.^w1–3 These benefits are most clearly seen in patients with left ventricular systolic dysfunction or clinical evidence of heart failure.^w4

The ATLAS study has shown that higher doses of ACE inhibitor give greater morbidity/mortality benefits.^w5

Recently, another drug known to block a component of the renin-angiotensin-aldosterone system (RAAS), spironolactone (an aldosterone antagonist), has also been shown to reduce mortality and morbidity in CHF, even when added to an ACE inhibitor (this was demonstrated in RALES).^w6

The question arises, therefore, as to what the role of the newest agents available for RAAS inhibition, the angiotensin II receptor antagonists or blockers (ARBs), might be in CHF and acute myocardial infarction?