Selective atrial profibrotic signalling in mice and man

Abstract

This editorial refers to ‘Molecular basis of selective atrial fibrosis due to overexpression of transforming growth factor-β1’ by D. Rahmutula et al. , pp. 769–779, this issue. Although oral anticoagulation can prevent the majority of strokes in patients with atrial fibrillation (AF) if used as recommended in treatment guidelines,1 patients with AF receiving optimal therapy still die prematurely, and are frequently hospitalized.2 Hence, we need a deeper understanding of the mechanisms behind AF in patients to develop better treatment. Most of the currently used treatments for AF were initially developed to treat ventricular heart disease, e.g. angiotensin-converting enzyme inhibitors, digitalis, beta-adrenoceptor blockers, spironolactone, and most antiarrhythmic drugs. Understanding electrophysiological differences between the atria and ventricles have allowed the recent development of atrial antiarrhythmic drugs (dronedarone, vernakalant), with others undergoing clinical development. Catheter ablation of AF also illustrates how the understanding of an atrial arrhythmia mechanism, i.e. focal firing in and around the pulmonary veins, helped develop a specific AF treatment. In this issue of Cardiovascular Research , Rahmutula et al. 3 characterize a molecular pathway leading to selective atrial fibrosis. By analysing human atrial and ventricular tissues, they identified an atrial preponderance of transforming growth factor-β (TGF-β) expression, and higher atrial TGF-β …