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Angiotensin receptor blockers for chronic heart failure and acute myocardial infarction
  1. John J V McMurray
  1. Clinical Research Initiative in Heart Failure, Wolfson Building, University of Glasgow, Glasgow, UK
  1. Professor JJV McMurray, CRI in Heart Failure, Wolfson Building, University of Glasgow, Glasgow G12 8QQ, UKJ.McMurray{at}

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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?

ARB–ACE inhibitor comparison studies

Though, logically, the first question to ask of ARBs might be whether these new drugs are better than placebo, the first comparison actually made in a large scale trial was with an ACE inhibitor. The first of these—the ELITE-1 trial—addressed tolerability, whereas the hypothesis of the larger ELITE-2 trial was that losartan would be more efficacious than captopril. The approach of the ELITE trials was based on the belief that: (1) ARBs are more effective inhibitors of the RAAS than ACE inhibitors; and (2) bradykinin, the breakdown of which is blocked by ACE inhibitors, is directly or …

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