Atrial amyloidosis and atrial fibrillation: a gender-dependent ?arrhythmogenic substrate??

This editorial refers to “Amyloid deposition as a cause of atrial remodelling in persistent valvular atrial fibrillation”1 by O. Leone et al. on page 1237 Atrial fibrillation (AF) is known to cause significant changes in atrial tissue architecture and electrophysiology.1,2 It has become clear over recent years that pre-existing alterations, such as autonomic dysbalance, degenerative tissue changes and fibrosis, can provide an electrophysiological and morphological substrate, which increases the likelihood of AF. In particular, alterations of the interstitial matrix in atrial tissue seem to be significant contributory factors.1 Increased amounts of fibrous tissue in fibrillating human atria were reported as early as 30 years ago3 and it is known to impair cell-to-cell coupling, thus causing heterogeneity in intra- and inter-atrial conduction. Initially, subsequent changes in atrial conduction may be subtle. However, isolated atrial amyloidosis (IAA) has recently been found to be of importance for the development of atrial conduction disturbances and AF.4 Amyloidosis represents a diverse group of diseases characterised by the presence of extracellular proteinaceous deposits showing characteristic structural and tinctorial properties. Amyloidoses are classified on the basis of the amyloid protein deposited and the clinical presentation5 and may affect the heart as part of a systemic disease, as in immunoglobulin-derived AL amyloidosis. In senile cardiovascular amyloidosis, the fibril protein consists of transthyretin (non-hereditary ATTR amyloidosis), and amyloid is observed in … *Correspondence to: A. Goette, Division of Cardiology, Otto-von-Guericke-University Hospital, Leipziger Str. 44, 39120 Magdeburg, Germany. E-mail address: andreas.goette{at}medizin.uni-magdeburg.de