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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 CFAE as a marker of abnormal substrate.1 This pure substrate-based ablation strategy has resulted in remarkable success with great benefits, which include stroke and mortality reduction in high-risk patients with very long standing persistent AF. In this review, 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.
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