Journal
LIFE-BASEL
Volume 13, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/life13061260
Keywords
atrial fibrillation; fibrosis; triggers; inflammation oxidative stress
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Atrial fibrillation (AF) is a common arrhythmia in older individuals. The mechanism of AF involves trigger activation and arrhythmia perpetuation, with the pulmonary veins as the most common triggers. Electrical isolation of the pulmonary veins through ablation is the key treatment for AF. Various factors and comorbidities lead to myocardial stretch and the formation of a fibrotic substrate, promoting AF perpetuation. Multiple mechanisms are employed in the clinical practice for the interventions and medical treatments of AF.
Atrial fibrillation (AF) is a very common arrhythmia that mainly affects older individuals. The mechanism of atrial fibrillation is complex and is related to the pathogenesis of trigger activation and the perpetuation of arrhythmia. The pulmonary veins in the left atrium arei confirm that onfirm the most common triggers due to their distinct anatomical and electrophysiological properties. As a result, their electrical isolation by ablation is the cornerstone of invasive AF treatment. Multiple factors and comorbidities affect the atrial tissue and lead to myocardial stretch. Several neurohormonal and structural changes occur, leading to inflammation and oxidative stress and, consequently, a fibrotic substrate created by myofibroblasts, which encourages AF perpetuation. Several mechanisms are implemented into daily clinical practice in both interventions in and the medical treatment of atrial fibrillation.
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