AIMS: Targeting of complex fractionated electrograms (CFEs) in the atria is not yet beneficial in treating drug-refractory atrial fibrillation (AF). In order to gain insight into potential anatomical hotspots of fractionated electrograms, a structured literature search was performed. METHODS AND RESULTS: PubMed was searched for studies describing fractionation during human atrial electrophysiological measurements (n = 565), of which 36 articles described the pre-ablation distribution of fractionated electrograms for the left atrium and/or right atrium in at least four regions. Fractionation was commonly found in high proportions within all regions of both atria, without clear preference for specific regions. Furthermore, no differences in the fractionation distribution between paroxysmal AF and persistent AF patients were observed. CONCLUSION: Whereas atrial inhomogeneous conduction is widely believed to play a key role in AF initiation and perpetuation, different electrophysiological causes for fractionation and the influence of measurement properties complicate identification of the arrhythmogenic substrate. Thereby, simply targeting all CFEs would be short-sighted. Further research is warranted on how to distinguish 'physiologic CFEs' from 'pathologic CFEs', with only the latter reflecting potential targets for ablative therapy of AF.
AIMS: Targeting of complex fractionated electrograms (CFEs) in the atria is not yet beneficial in treating drug-refractory atrial fibrillation (AF). In order to gain insight into potential anatomical hotspots of fractionated electrograms, a structured literature search was performed. METHODS AND RESULTS: PubMed was searched for studies describing fractionation during human atrial electrophysiological measurements (n = 565), of which 36 articles described the pre-ablation distribution of fractionated electrograms for the left atrium and/or right atrium in at least four regions. Fractionation was commonly found in high proportions within all regions of both atria, without clear preference for specific regions. Furthermore, no differences in the fractionation distribution between paroxysmal AF and persistent AF patients were observed. CONCLUSION: Whereas atrial inhomogeneous conduction is widely believed to play a key role in AF initiation and perpetuation, different electrophysiological causes for fractionation and the influence of measurement properties complicate identification of the arrhythmogenic substrate. Thereby, simply targeting all CFEs would be short-sighted. Further research is warranted on how to distinguish 'physiologic CFEs' from 'pathologic CFEs', with only the latter reflecting potential targets for ablative therapy of AF.