Aldosterone blockade over and above ACE-inhibitors in patients with coronary artery disease but without heart failure

Nimit C. Shah, Stuart Pringle, Allan Struthers

    Research output: Contribution to journalArticlepeer-review

    14 Citations (Scopus)


    Recent evidence points to a role for the renin-angiotensin-aldosterone system (RAAS) in the pathogenesis of atherosclerosis and its complications, including acute angina pectoris. Two large trials in heart failure have clearly demonstrated that blocking aldosterone improves mortality and that this benefit occurs over and above standard therapy with angiotensin-converting enzyme (ACE) inhibitors. The question that naturally arises from these landmark studies is whether aldosterone blockade would produce the same benefits in patients with coronary artery disease (CAD) but no heart failure. There are three reasons to believe this might be the case. Firstly, angiotensin II (Ang II) and aldosterone produce similar biological effects and Ang II withdrawal has been shown to benefit patients with angina; aldosterone blockade may therefore follow in the footsteps of ACE inhibitors, as it did in heart failure, and produce benefits in vascular patients without heart failure. Secondly, one of the main mechanisms which is thought to be responsible for the benefit of aldosterone blockade in the Randomised ALdactone Evaluation Study (RALES) and Eplerenone Post-AMI Heart Failure Survival Study (EPHESUS), is that it improves endothelial/vascular function and endothelial/vascular dysfunction is the fundamental abnormality in angina pectoris. Finally, aldosterone blockade has been shown to reduce atherosclerosis in animal studies of atherosclerosis without heart failure, which are analogous to CAD patients.
    Original languageEnglish
    Pages (from-to)20-30
    Number of pages11
    JournalJournal of the Renin-Angiotensin-Aldosterone System (JRAAS)
    Issue number1
    Publication statusPublished - Mar 2006


    Dive into the research topics of 'Aldosterone blockade over and above ACE-inhibitors in patients with coronary artery disease but without heart failure'. Together they form a unique fingerprint.

    Cite this