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The myriad pathologies leading to and resulting from atrial fibrillation (AF) have led to many theories regarding how substrate should be defined and how to reconcile substrate ablation with trigger ablation. The identification of spatiotemporally stable areas of very low amplitude short cycle length CFAE in a sea of otherwise discrete normal amplitude and relatively longer cycle length electrograms led to ablate the complex fractionated atrial electrogram (CFAE) as a marker of abnormal substrate. This pure substrate-based ablation strategy has shown promising result of benefit in stroke and mortality reduction in high-risk patients. In this review which has been modified and abridged from the recent publication on this subject 1, we discuss the prevailing mechanisms underlying CFAE, how to map and ablate CFAE sites, correlation of CFAE areas to those of ganglionic plexi, clinical outcomes of the approach, and the controversy surrounding targeting CFAE as substrate sites for AF ablation.
K. Nademanee (Mon,) studied this question.