Key result
Pulmonary vein stretch promotes arrhythmogenesis via calcium overload, highlighting a mechanistic target for AF.
Why the study?
To review the laboratory and translational relevance of mechanoelectrical feedback in pulmonary vein arrhythmogenesis and its potential therapeutic opportunities in atrial fibrillation.
Understanding mechanoelectrical feedback in pulmonary vein arrhythmogenesis provides insights into the pathophysiology of atrial fibrillation and highlights potential therapeutic targets.
Answers are grounded in this paper and cite their sources.
Pulmonary vein mechanoelectrical feedback may offer an AF target; leaves open clinical translation pending prospective trials.
Mechanoelectrical feedback is an important factor in the pathophysiology of atrial fibrillation (AF). Ectopic electrical activity originating from pulmonary vein (PV) myocardial sleeves has been found to trigger and maintain paroxysmal AF. Dilated PVs by high stretching force may activate mechanoelectrical feedback, which induces calcium overload and produces afterdepolarization. These results, in turn, increase PV arrhythmogenesis and contribute to initiation of AF. Paracrine factors, effectors of the renin-angiotensin system, membranous channels, or cytoskeleton of PV myocytes may modulate PV arrhythmogenesis directly through mechanoelectrical feedback or indirectly through endocardial/myocardial cross-talk. The purpose of this review is to present laboratory and translational relevance of mechanoelectrical feedback in PV arrhythmogenesis. Targeting mechanoelectrical feedback in PV arrhythmogenesis may shed light on potential opportunities and clinical concerns of AF treatment.
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Lu et al. (2020) conducted a review in Atrial fibrillation. Mechanoelectrical feedback induced by pulmonary vein stretch increases arrhythmogenesis through calcium overload and altered electrophysiology, serving as a potential therapeutic target for atrial fibrillation.
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