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Gut Pathway 3, first reaction)
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Pathological expansion and dysfunction of EAT promote AF through paracrine and vasocrine secretion of pro-inflammatory and pro-fibrotic cytokines, release of extracellular vesicles carrying arrhythmogenic cargo, direct infiltration, and modulation of local electrophysiology and autonomic signaling, thereby creating a substrate for atrial cardiomyopathy, fibrosis, electrical remodeling, and AF initiation/persistence
The gastrointestinal effects typically emerge within the first few weeks of treatment and may evolve as the body adapts to the medication
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