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

Last updated: December 5, 2023
Sponsor: Assiut University
Overall Status: Active - Not Recruiting

Phase

4

Condition

Arrhythmia

Chest Pain

Cardiac Disease

Treatment

Eplerenone

Clinical Study ID

NCT06168994
Eplerenone in AF
  • All Genders

Study Summary

The aim of this study is to study synergistic effect of eplerenone as Selective aldosterone receptor antagonist with amiodarone compared with amiodarone only in reducing recurrence of atrial fibrillation in patient with structural heart disease

Eligibility Criteria

Inclusion

Inclusion Criteria:

  • paroxysmal AF who reverted to sinus rhythm either medically or electrically withoutappropriate secondary cause of primary AF

•AF attack should be documented with ECG

Exclusion

Exclusion Criteria:

  • 1-patients are currently on eplerenone or spironolactone 2-hyperkalemia 3-impairedrenal function(if CrCl <50ml/min or serum creatinine>2 mg/dl) 4-patient on betablocker and calcium channel blocker (non- dihydropyridine) 5-prosthetic valve 6-severemitral stenosis 7-thyroid dysfunction 8-WPW 9-severe liver disease 10-persistent orpermanent AF 11-pregnancy or breast feeding 12-LV EF<50% 13-known hypersensitivity ordrug reaction to amiodarone 14-acute coronary syndrome 15-refusal of consent

Study Design

Total Participants: 100
Treatment Group(s): 1
Primary Treatment: Eplerenone
Phase: 4
Study Start date:
February 01, 2024
Estimated Completion Date:
May 20, 2027

Study Description

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]