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Association of Complex Fractionated Electrograms with Atrial Myocardial Thickness and Fibrosis

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Background and Objectives: Although ablation of complex fractionated atrial electrograms (CFAE) in atrial fibrillation (AF) is one of the strategies for atrial substrate modification, the mechanism behind CFAE as an electrophysiological substrate remains unclear. We investigated structural differences between CFAE sites and their matched non-CFAE sites by comparing their histopathologic characteristics in canine AF models. Methods: Atrial electrograms of four dogs were obtained from the epicardial site. AF was induced through burst atrial pacing at 600 bpm for 30 min. CFAE sites were identified during AF according to patterns visualized on the electrograms, and their matched non-CFAE sites were selected in the adjacent region, within 5 mm of each CFAE site. Tissues were harvested from CFAE sites and their matched non-CFAE sites at various locations in both atria. Histopathologic differences were identified between CFAE and non-CFAE sites. Results: A total of 24 atrial tissues (12 with CFAE, 12 with non-CFAE) were evaluated. The atrial myocardium was significantly thicker at CFAE sites (1757.5±560.5 μm) than at non-CFAE sites (1279.5±337.2 μm) (p=0.036). At CFAE sites, it was filled with a significantly larger amount of fibrotic tissue than at non-CFAE sites (22.8±6.9% versus 7.2±4.7%, p<0.001). Results were consistent across various tissue locations. The distribution of autonomic nerve innervation was similar between CFAE and non-CFAE sites. Conclusion: This study provides a better understanding of histological characteristics of CFAE sites, namely a thicker wall and greater amount of fibrosis. These findings may be associated with the development of CFAE and its pathophysiological contribution to AF.

Abstract

Background and Objectives: Although ablation of complex fractionated atrial electrograms (CFAE) in atrial fibrillation (AF) is one of the strategies for atrial substrate modification, the mechanism behind CFAE as an electrophysiological substrate remains unclear. We investigated structural differences between CFAE sites and their matched non-CFAE sites by comparing their histopathologic characteristics in canine AF models. Methods: Atrial electrograms of four dogs were obtained from the epicardial site. AF was induced through burst atrial pacing at 600 bpm for 30 min. CFAE sites were identified during AF according to patterns visualized on the electrograms, and their matched non-CFAE sites were selected in the adjacent region, within 5 mm of each CFAE site. Tissues were harvested from CFAE sites and their matched non-CFAE sites at various locations in both atria. Histopathologic differences were identified between CFAE and non-CFAE sites. Results: A total of 24 atrial tissues (12 with CFAE, 12 with non-CFAE) were evaluated. The atrial myocardium was significantly thicker at CFAE sites (1757.5±560.5 μm) than at non-CFAE sites (1279.5±337.2 μm) (p=0.036). At CFAE sites, it was filled with a significantly larger amount of fibrotic tissue than at non-CFAE sites (22.8±6.9% versus 7.2±4.7%, p<0.001). Results were consistent across various tissue locations. The distribution of autonomic nerve innervation was similar between CFAE and non-CFAE sites. Conclusion: This study provides a better understanding of histological characteristics of CFAE sites, namely a thicker wall and greater amount of fibrosis. These findings may be associated with the development of CFAE and its pathophysiological contribution to AF.

참고문헌 (27)

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