Role of aldosterone in congestive heart failure

Abstract

Antialdosterone therapy in patients with secondary hyperaldosteronism due to myocardial failure must accomplish the following: (1) reduce or preferably normalize plasma aldosterone levels by blockade of excessive synthesis, (2) antagonize the renal and systemic effects of aldosterone at its receptor sites, and (3) minimize the presence of multiple stimuli to aldosterone secretion. Fulfillment of these goals likely requires the blockade of angiotensin II-induced aldosterone secretion (ie, angiotensin-converting enzyme inhibition) with an antagonist of aldosterone receptors (ie, spironolactone [Aldactone]). Despite the potential for hyperkalemia with this combined use of medications, particularly in patients with impaired renal function, such therapy is likely to attenuate the salt-acquisitive state that is characteristic of myocardial failure.