Blockade of atrial angiotensin II type 1 receptors: a novel antiarrhythmic strategy to prevent atrial fibrillation?

Atrial fibrillation (AF) is known to cause significant changes in atrial tissue architecture and atrial electrophysiology (1). In recent years, it has become clear that preexisting alterations (autonomic dysbalance, degenerative tissue changes, fibrosis, and so forth) can provide an electrophysiologic and morphologic substrate, which increases the likelihood of AF onset in response to triggering events. Alterations of the interstitial matrix in atrial tissue seem to be especially significant contributing factors (1,2). Increased amounts of fibrous tissue in fibrillating human atria were described 30 years ago (3). However, only recently potential molecular mechanisms responsible for collagen accumulation in atrial myocardium have been elucidated (4,5).