Key result
Aging plays a critical role in the genesis of atrial fibrillation by creating atrial electrical and structural remodeling that leads to increased susceptibility to AF occurrence.
Aging plays a critical role in the pathophysiology of atrial fibrillation by modulating both the arrhythmogenic triggers and the atrial substrate through structural, electrophysiological, and metabolic remodeling.
May refine age-stratified AF risk assessment; leaves open targeted anti-remodeling trials.
Aging plays a critical role in the genesis of atrial fibrillation (AF) and also increases the risks of cardiac dysfunction and stroke in AF patients. AF is caused by increased AF triggering from abnormalities of the thoracic vein and/or modulated substrate (atrial) with enhancement of AF maintenance. Clinical and laboratory evidence indicates that aging is significant in the creation of atrial electrical and structural remodeling that leads to increased susceptibility to AF occurrence. Aging is commonly associated with cardiovascular comorbidities, oxidative stress, calcium dysregulation, atrial myopathy with apoptosis, and fibrosis, which all contribute to the genesis of AF. This review updates the current understanding of the effects of aging on the pathophysiology of AF.
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Lin et al. (2017) conducted a review in Atrial Fibrillation. Aging plays a critical role in the genesis of atrial fibrillation by creating atrial electrical and structural remodeling that leads to increased susceptibility to AF occurrence.
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