Targeting atrial cardiomyopathy and the pro-fibrillatory substrate, including risk factor modification and tissue fibrosis, promises to improve outcomes in atrial fibrillation management.
Targeting the underlying atrial cardiomyopathy and pro-fibrillatory substrate, rather than relying solely on pulmonary vein isolation, may be necessary to improve outcomes in atrial fibrillation management.
The identification of the pulmonary veins as a trigger source for atrial fibrillation (AF) has established pulmonary vein isolation (PVI) as a key target for AF ablation. However, PVI alone does not prevent recurrent AF in many patients, and numerous additional ablation strategies have failed to improve on PVI outcomes. This therapeutic limitation may be due, in part, to a failure to identify and intervene specifically on the pro-fibrillatory substrate within the atria and pulmonary veins. In this review paper, we highlight several emerging approaches with clinical potential that target atrial cardiomyopathy—the underlying anatomic, electrical, and/or autonomic disease affecting the atrium—in various stages of practice and investigation. In particular, we consider the evolving roles of risk factor modification, targeting of epicardial adipose tissue, tissue fibrosis, oxidative stress, and the inflammasome, along with aggressive early anti-AF therapy in AF management. Attention to combatting substrate development promises to improve outcomes in AF.
McCauley et al. (Wed,) conducted a review in Atrial fibrillation. Targeting atrial cardiomyopathy was evaluated. Targeting atrial cardiomyopathy and the pro-fibrillatory substrate, including risk factor modification and tissue fibrosis, promises to improve outcomes in atrial fibrillation management.
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