AF is associated with fibrotic processes both in atria and ventricles.
Despite common profibrotic pathways, signaling seems to differ in the ventricular and supraventricular parts of the heart.
Atrial fibrosis may precede development of AF, which in turn results in further progression of atrial remodeling. Structural heart disease appears to have a greater effect on both atrial and ventricular fibrosis than arrhythmia per se, but it allows persistent activation of profibrotic stimuli. Although the role of atrial fibrosis in AF is well documented, the implication of ventricular fibrosis in pathogenesis and the outcomes of conditions associated with AF clearly require further research.