The Metabolic Effects of Mineralocorticoid Receptor Antagonists in Heart Failure Patients

Heart failure (HF) remains a leading cause of cardiovascular morbidity and mortality worldwide. Mineralocorticod receptor (MR) antagonists (spironolactone and eplerenone) have been studied in HF patients and in patients with acute coronary syndrome or post-myocardial infarction and left ventricular (LV) dysfunction, as well as hypertensive subjects without HF symptoms. It has suggested that mineralocorticoid receptor antagonists provide cardiovascular protection beyond its diuretic and potassium-sparing capacities. Traditionally, progression of HF relates with not full blockade of renin-angiotensin system (RAS) activation and with so called “escape” phenomenon of neurohumoral activation from effects of angiotensin converting enzyme / angiotensin receptor blockers and beta-adrenoblockers. Circulating and local aldosteron over production is discussed a main cause of none adequate effect of RAS blockade contributed negative cardiovascular remodelling and worse survival. During the last decade, several studies have shown that completed control for RAS activation might be achieved through adding MR antagonists in contemporary treatment scheme. This approach raises survival and leads to a trend in declined mortality rate in patients with HF various etiologic causes. Therefore, there are increasing evidence that both MR antagonists spironolactone and eplerenone might have a different metabolic effect in HF patients and that this difference is required to pay attention in creating of optimal HF therapeutic program. The aim of the mini review is to evaluate clinically significance of metabolic effects of mineralocorticoid receptor antagonists in HF patients.