Why the study?
The role of endothelial dysfunction in AF was historically thought to be limited to mediating thromboembolism, but emerging evidence suggests it also promotes and maintains arrhythmic substrate and predicts adverse outcomes.
Endothelial dysfunction is increasingly recognized not just as a mediator of thromboembolism in atrial fibrillation, but as a key factor in promoting arrhythmic substrate and predicting recurrence after therapy.
May refine post-ablation recurrence risk stratification in AF; leaves open whether targeting endothelial dysfunction improves outcomes.
Endothelial dysfunction, a term used to describe both the physical damage and dysregulated physiology of this endothelial lining, is an increasingly recognized pathophysiological state shared by many cardiovascular diseases. Historically, the role of endothelial dysfunction in atrial fibrillation (AF) was thought to be limited to mediating atrial thromboembolism. However, there is emerging evidence that endothelial dysfunction both promotes and maintains atrial arrhythmic substrate, predicts adverse outcomes, and identifies patients at high risk of recurrence following cardioversion and ablation therapy. Treatments targeted at improving endothelial function also represent a promising new therapeutic paradigm in AF. This review summarizes the current understanding of endothelial function in AF.
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Black et al. (2021) studied this question.
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