ALDOSTERONE BREAKTHROUGH (ABT) IN DOGS: PREVALANCE IN CLINICAL CARDIAC AND RENALPATIENTS RECEIVING ACE INHIBITORS

摘要

Chronic exposure to high concentrations of aldosterone results m excessive sodium retention with expansion of extracellular volume, favors potassium and magnesium wasting, inhibits myocardial norepinephrine uptake, diminishes heart rate variability (asign of cardiac health), produces cardiac arrhythmias, decreases baroreceptor sensitivity, contributes to endothelial dysfunction and vascular inflammation, and is independently associated with renal, vascular and cardiac remodelling and heart failure.1"5 The interruption of RAAS is a key therapeutic strategy in the therapy of chronic heart and kidney disease and is achieved via the administration of angiotensin converting enzyme-inhibitors (ACE-I), angiotensin II receptor blockers (ARB), and mineralocorticoid receptor blockers (MRB), alone or in combination. Incomplete pharmacologic blockade of the RAAS system by ACE-I (±ARB) has been referred to as both aldosterone escape and aldosterone breakthrough (ABT). The authors prefer the latter term, as itmore accurately reflects the phenomenon in which circulating aldosterone levels rise despite ACE-I or ARB therapy. Aldosterone escape refers to the physiologic phenomenon that allows the kidneys to 'escape' the sodium and water retaining effects of excessive aldosterone levels, preventing severe volume expansion and edema.