New concepts in atrial fibrillation: mechanism and remodeling

Abstract

Atrial fibrillation (AF) is a complex disease with many possible mechanisms. Studies indicate that the arrhythmogenic foci within the thoracic veins are AF initiators. Once initiated, AF alters atrial electrical and structural properties in a way that promotes its own maintenance and recurrences and may alter the response to antiarrhythmic drugs. The exact mechanisms by which the initiators trigger AF remain elusive, however. Evidence to date suggests that autonomic modulation does have an adjunctive role to play in catheter AF ablation, especially when applied selectively. Further mechanistic and clinical studies are warranted before a wider application can be recommended.

Figure 1

Patterns of activation during sustained AF in dog with chronic rapid atrial pacing. Panel A, snapshots of focal discharge and reentrant activation patterns within right super PV at baseline AF. Asterisk in the left upper corner indicates the anatomical location of focal discharge at the proximal right superior PV. Black horizontal dotted line indicates the PV-LA junction. The number below each snapshot represents the time in ms with the beginning of data acquisition as time zero. In snapshots, red color represents the wavefront; black arrows, the direction of wave propagation; black dotted line, line of block; arrow head, site of focal discharge. The color bar on the right shows the time scale (0 to 50 ms). Panel B, snapshots of focal discharge and reentrant activation patterns within right superior PV after 0.02 mg/kg ibutilide infusion. A rectangle towards the end of the ECG tracings shows the time period corresponding to the snapshots in Panels A and B. (permission from Chou et al. Am J Physiol Heart Circ Physiol 289: H2704, Figure 2)