Andrea David*
The description of atrial fibrillation (AF) as a functional electrical condition ignores the significant underlying structural abnormalities. The muscular sleeve of the atrium and the pulmonary vein (PV) undergo microstructural alterations, resulting in a weak foundation for AF maintenance. Current data indicate that this arrhythmia typically requires a trigger for start and a weak electrophysiological or anatomical substrate for maintenance, despite the lack of knowledge regarding the anatomical and functional foundations of AF. Whether the trigger mechanisms are focused improved automaticity, prompted activity, or micro re-entry from cardiac tissue is currently unknown. AF onset can be sped up by both sympathetic and parasympathetic stimuli, which appear to also play a role in AF maintenance. A mechanism that may involve cellular ageing, apoptosis, and subsequent atrial fibrosis and inflammation is linked to both new-onset and recurrent AF, according to growing clinical data.
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