## Mechanism of Atrial Fibrillation **Key Point:** Pulmonary vein (PV) myocytes are the primary source of ectopic activity in paroxysmal atrial fibrillation, particularly in patients without structural heart disease. ### Pathophysiology Atrial fibrillation arises from two main mechanisms: 1. **Automaticity** — Enhanced diastolic depolarization in PV myocytes (which have properties intermediate between atrial and ventricular tissue) 2. **Re-entry** — Multiple wavelets of re-entrant activity propagating through atrial tissue ### Role of Pulmonary Veins Pulmonary vein myocytes: - Express L-type calcium channels and automaticity properties - Generate ectopic beats that trigger AF, especially during sympathetic activation - Account for ~90% of ectopic foci in paroxysmal AF - Are the anatomical target for catheter ablation (pulmonary vein isolation) **High-Yield:** Pulmonary vein isolation (PVI) is the cornerstone of catheter ablation for AF precisely because PV myocytes are the primary source of triggering activity. ### Why Other Mechanisms Are Secondary | Mechanism | Role in AF | |-----------|------------| | AV nodal reentry | Causes AVNRT, not AF; AV node is a passive bystander in AF | | Atrial flutter with variable conduction | Flutter is organized; AF is disorganized; different arrhythmias | | Sinus node dysfunction | Causes bradycardia/pauses; not the primary AF mechanism | **Clinical Pearl:** The "focal trigger" model explains why a single ectopic beat from a PV can degenerate into AF, especially when atrial substrate is abnormal (fibrosis, inflammation, or electrical remodeling).
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