This project characterises the time course of functional and structural remodelling in an atrial fibrillation model, exploring cardiomyocyte-non-myocyte properties and interactions to evaluate whether atrial fibrillation-induced atrial remodelling can be inhibited or reversed. The atrial fibrillation model is well established, and will be used in P16 to compare findings between atrial tissue of different species. Investigations will relate changes in cellular structure, function and tissue composition to the arrhythmogenic potential of the atrial myocardium. Atrial fibrosis will be tracked over time using in vivo PET / CT with fibroblast tracers (targeting fibroblast activation protein). Information about severity and type of atrial fibrosis will be linked to clinically relevant parameters to guide therapeutic decisions, including predicition of the likelihood of successful ablation therapy.