LAUSR

Atrial fibrillation (AF) involves 1% to 2% of the adult general population, a rate that increases to 15% in those 80 years and above.1 Because of the aging of the general population, this epidemic of AF is expected to increase over the next decades2–4 and to impose an increasing burden on the healthcare system because of the need for life-long care and pharmacological treatment. Identification of the mechanisms underlying AF represents an unmet need and a first step toward developing more effective preventive measures. Arterial hypertension (HT) is tightly associated with AF, as originally reported in the Framingham Heart Study5 and thereafter confirmed by several studies.6–13 HT is a major predictor of AF, and 50% to 90% of AF patients have HT. Accumulating evidences point to a role for the renin–angiotensin–aldosterone system (RAAS) in the pathophysiology of cardiac inflammation, fibrosis, and hypertrophy.14–17 Aldosterone not only exerts well-known pressor effects, but also promotes inflammation, myocardial necrosis, cardiac collagen deposition, fibrosis, and left ventricular hypertrophy (LVH).18,19 Accordingly, there is renewed interest in aldosterone as one of the major culprits leading to chamber remodeling and ultimately creating the stage for AF in hypertensive patients.15,17,20–25 The evidence supporting a role for aldosterone in AF was, however, derived from observational studies performed in patients with heart diseases that are known to cause AF. This leaves open the question of whether aldosterone triggers AF per se or only in the presence of structural heart disease. In recent years, 3 reviews examined the relation between aldosterone and AF: one focused on the antiarrhythmic potential of mineralocorticoid receptor (MR) antagonists in AF patients;26 another on the role of the MR in arrhythmias;27 and the last …