Role of Eplerenone in Reducing Recurrence of Atrial Fibrillation in Patient With Structural Heart Disease

Atrial fibrillation is the most common sustained arrhythmia, with a rising prevalence that substantially increases the risk of stroke and heart failure (1,2), The rate of recurrences without antiarrhythmic treatment is 71%-84%, and it can be reduced to 44%-67% with antiarrhythmic drug therapy(3) Mineralocorticoid receptor blockers (MRBs) are beneficial in systolic HF[ 4,5,6]. Specifically, the MRB eplerenone (EPL) has been shown to reduce new onset AF and recurrent AF in HF patients (7). Both angiotensin II and aldosterone elevations may lead to atrial fibrosis and contribute to human AF (8). Experimental results suggest that aldosterone may cause a substrate for atrial fibrosis and AF (9). Aldosterone increases the expression of 11β-hydroxysteroid dehydrogenase type 2 (11b-HSD2) leading to up-regulation of profibrotic mediators and collagen synthesis, which is prevented by MRBs (10).

The European Society of Cardiology (ESC) guidelines identify AF as secondary to Structural heart diseases (SHDs)when a left ventricle (LV) systolic or diastolic dysfunction is demonstrated or LV hypertrophy, valvular disease, and/or other SHDs are documented [11].currently, SHD includes: (a) heart failure with reduced ejection fraction (HFrEF, previously severe or moderate LV systolic dysfunction); (b) heart failure with preserved ejection fraction (HFpEF, previously LV diastolic dysfunction); (c) valvular heart disease (VHD) and (d) specific cardiomyopathies, such as hypertrophic cardiomyopathy (HCM) [12].

Electrical remodelling is the first mechanism that occurs at the onset of AF and promotes AF through a re-entry-prone substrate. Changes in atrial frequency are determined by changes in the physiology of ion channel activation[13] Amiodarone is an antiarrhythmic medication used to treat and prevent a number of types of cardiac dysrhythmias,it blocks the channels that are upregulated by remodelling such as inward-rectifying K1 current (IK1) or by stimulation of the sympathetic nervous system.[14]