INTRODUCTION: Descriptions for left atrial macroreentry tachycardia (LAMRT) in patients without obvious structural heart disease or previous surgery orcatheter radiofrequency (RF) ablation have been sparse. METHODS AND RESULTS: Ten of 226 patients (7 women, mean age 57 ± 14) with LAMRT underwent electroanatomic mapping and catheter ablation. None of the 10 patients had structural heart disease or history of previous surgery or catheter ablation. In all patients, the reentry circuits were located within a large low-voltage (bipolar voltage ≤ 0.5 mV) area in left atrium (LA), which contained 2.6 ± 1.2 electrically silent areas (ESAs) and/or lines of double potentials (LDPs). The tachycardia circuit propagated through a narrow isthmus (<5 mm width) bounded by ESAs/LDPs and adjacent anatomical barriers (e.g., mitral annulus). In these isthmus, low amplitude (0.21 ± 0.05 mV), long-duration (123 ± 14 milliseconds) fractionated electrograms were found in 8 tachycardias, accounting for 43 ± 5% of the tachycardia cycle length. In 2 other tachycardias without fractionated electrograms, the electrogram amplitude in the isthmus was extremely low (<0.1 mV). RF energy was delivered at the isthmuses and terminated all 10 tachycardias. After ablation, the original LAMRT was not inducible in all patients. During follow-up (mean 14 ± 10 months), 2 patients developed recurrence of ATs and were successfully ablated. CONCLUSION: Extensive scarring of the LA formed arrhythmogenic substrates of LAMRT in this group of patients. Ablation targeting these narrow, slow conduction zones eliminated atrial tachycardia in all patients.
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INTRODUCTION: Descriptions for left atrial macroreentry tachycardia (LAMRT) in patients without obvious structural heart disease or previous surgery or catheter radiofrequency (RF) ablation have been sparse. METHODS AND RESULTS: Ten of 226 patients (7 women, mean age 57 ± 14) with LAMRT underwent electroanatomic mapping and catheter ablation. None of the 10 patients had structural heart disease or history of previous surgery or catheter ablation. In all patients, the reentry circuits were located within a large low-voltage (bipolar voltage ≤ 0.5 mV) area in left atrium (LA), which contained 2.6 ± 1.2 electrically silent areas (ESAs) and/or lines of double potentials (LDPs). The tachycardia circuit propagated through a narrow isthmus (<5 mm width) bounded by ESAs/LDPs and adjacent anatomical barriers (e.g., mitral annulus). In these isthmus, low amplitude (0.21 ± 0.05 mV), long-duration (123 ± 14 milliseconds) fractionated electrograms were found in 8 tachycardias, accounting for 43 ± 5% of the tachycardia cycle length. In 2 other tachycardias without fractionated electrograms, the electrogram amplitude in the isthmus was extremely low (<0.1 mV). RF energy was delivered at the isthmuses and terminated all 10 tachycardias. After ablation, the original LAMRT was not inducible in all patients. During follow-up (mean 14 ± 10 months), 2 patients developed recurrence of ATs and were successfully ablated. CONCLUSION: Extensive scarring of the LA formed arrhythmogenic substrates of LAMRT in this group of patients. Ablation targeting these narrow, slow conduction zones eliminated atrial tachycardia in all patients.