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Stanley Nattel, Aldosterone antagonism and atrial fibrillation: time for clinical assessment?
, European Heart Journal, Volume 26, Issue 20, October 2005, Pages 2079–2080, https://doi.org/10.1093/eurheartj/ehi477The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
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This editorial refers to ‘Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction’† by P. Milliez et al., on page 2193
Atrial fibrillation (AF) is the most common sustained clinical arrhythmia. Presently available therapy for AF is suboptimal: ‘rhythm control’ drugs are fraught with the risk of pro-arrhythmia and other adverse effects, ‘rate control’ leaves the atria fibrillating and fails to reproduce physiological heart rate adaptation, and ablation procedures are expensive, complex, and incompletely effective. Over the past few years, the notion of ‘upstream’ therapy, targeting signalling pathways involved in the development of the substrate that supports the arrhythmia,1 has gained increased interest, supported by experimental2 and clinical3 studies which indicate that suppression of the renin–angiotensin system can prevent AF. Such therapy is particularly effective in the context of left ventricular (LV) dysfunction,4 perhaps because congestive heart failure (CHF) engages angiotensin-dependent remodelling cascades.2 A potentially important component of the renin–angiotensin system that has not been previously investigated in AF prevention is the mineralocorticoid aldosterone.