Action Potential Dynamics in Human Atrial Fibrillation

Zaman, Junaid; Narayan, Sanjiv M.; Franz, Michael R.

doi:10.1007/978-3-030-22672-5_20

Cited by 2 publications

(1 citation statement)

References 54 publications

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“…Late recurrence after catheter ablation (from 3 months to approximately one year after the procedure) in patients affected by paroxysmal AF without HF was independently associated with LA to total EAT volume ratio and greater sympathetic activity 54 . New specific mapping techniques, including those obtained by monophasic AP, have been shown to be useful in determining the AP characteristics of AF 89 . Owing to advances in imaging techniques, we should be able to define the clinical phenotypes adjusted for each patient with AF.…”

Section: Pathophysiological Mechanisms Of Af Related To Eatmentioning

confidence: 99%

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

et al. 2021

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Summary Obesity is a well‐known risk factor for atrial fibrillation (AF). Local epi‐myocardial or intra‐myocardial adiposity caused by aging, obesity, or cardiovascular disease (CVD) is considered to be a better predictor of the risk of AF than general adiposity. Some of the described mechanisms suggest that epicardial adipose tissue (EAT) participates in structural remodeling owing to its endocrine activity or its infiltration between cardiomyocytes. Epicardial fat also wraps up the ganglionated plexi that reach the myocardium. Although the increment of volume/thickness and activity of EAT might modify autonomic activity, autonomic system dysfunction might also change the endocrine activity of epicardial fat in a feedback response. As a result, new preventive therapeutic strategies are focused on reducing adiposity and weight loss before AF ablation or inhibiting autonomic neurotransmitter secretion on fat pads during open‐heart surgery to reduce the recurrence or postoperative risk of AF. In this manuscript, we review some of the novel findings regarding the pathophysiology and associated risk factors of AF, with special emphasis on the role of EAT in the electrical, structural, and molecular mechanisms of AF initiation and maintenance. In addition, we have included a brief note provided on epicardial fat preclinical models that could be useful for identifying new therapeutic targets.

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Section: Pathophysiological Mechanisms Of Af Related To Eatmentioning

confidence: 99%