Tawfic Nessim Abu-Zahra, BSc, MSc

Presently, the standard therapy for heart failure consists of treatment with an angiotensin-converting enzyme (ACE) inhibitor, furosemide (Lasix) or other loop diuretic, and the possible use of a b-blocker or a positive inotropic agent such as digoxin (Lanoxin).¹ The goals of this therapy are to decrease blood volume, increase cardiac contractility and inhibit the neuroendocrine effects of the renin-angiotensin-aldosterone system (RAAS). Since ACE inhibition suppresses aldosterone release, treatment with ACE inhibitors was considered sufficient for blocking the effects of aldosterone in patients with heart failure.^1,2 Thus, the addition of the aldosterone receptor antagonist spironolactone (Aldactone) was considered unnecessary and, given the threat of hyperkalemia, continued to be contraindicated.1 However, contrary to this conventional view, results of the Randomized Aldactone Evaluation Study (RALES) have shown that spironolactone treatment can reduce morbidity and mortality in patients with severe heart failure.