Heart failure with reduced ejection fraction is associated with decreased functional capacity, poor quality of life and increased mortality risk. The neurohormonal compensatory response to a reduced cardiac output is mainly comprised of the sympathetic nervous system, natriuretic peptides and the renin–angiotensin–aldosterone system, which attempt to maintain peripheral perfusion. The renin–angiotensin–aldosterone system is an integral mechanism in increasing afterload by promoting angiotensin II-mediated vasoconstriction and increasing preload via the secretion of aldosterone which causes sodium and water retention. Albeit compensatory mechanisms attempt to increase cardiac output and perfusion, their effects are maladaptive as left ventricular function deteriorates in response to an increased afterload, preload and ventricular remodelling. In an attempt to interrupt this vicious circle, first-line pharmacological therapy in the treatment of heart failure is beta blockade and inhibition of the renin–angiotensin–aldosterone system. Integral to this treatment strategy are mineralocorticoid receptor antagonists, also known as aldosterone antagonists. This class of drug inhibits the action of aldosterone, decreases preload and reduces left ventricular workload, thus preserving ventricular function. This translates into reduced mortality incidence, decreased episodes of hospitalisations for cardiac causes and improvement in clinical signs and symptoms. Although patient benefits are explicit, adverse effects such as hyperkalaemia and renal impairment are associated with this therapy. Regular patient follow up and monitoring for potential adverse effects and drug interactions are essential to the success of the therapy.
Hyperkalemia and management of renin-angiotensin-aldosterone system inhibitors in chronic heart failure with reduced ejection fraction: A systematic review
