BACKGROUND: Atrioventricular (AV) nodal reentrant tachycardias (AVNRT) with variable AV relationships are infrequently observed and might be misdiagnosed as atrial tachycardia. OBJECTIVE: This single-center, retrospective study was performed to elucidate the mechanism of AVNRT showing variable AV relationship. METHODS: This study included a total of 340 patients with all forms of AVNRT. The induced AVNRTs were classified into those with variations in the AV relationship (>or=30 ms) (irregular AVNRT) and those without (regular AVNRT). RESULTS: A total of 364 AVNRTs (typical and atypical form = 297 and 67) were induced in the 340 patients. Of the 364 AVNRTs, the variations in the AV relationship were observed in 8 atypical AVNRTs (2%) induced in 8 patients (2%). The patients with irregular atypical AVNRT were significantly younger than those with regular typical AVNRT and those with regular atypical AVNRT (35+/-15 vs 51+/-18 and 47+/-16 years, respectively). Irregular atypical AVNRTs showed atypical Wenckebach periodicity with simultaneous prolongation in the A-A intervals and Wenckebach block proximal to the His bundle. Irregular atypical AVNRTs showed a shorter tachycardia cycle length (TCL) (305+/-78 ms vs 381+/-95 ms; P<.05) and higher prevalence of eccentric coronary sinus (CS) activation than regular atypical AVNRTs (5 (63%) of 8 tachycardias vs 15 (25%) of 59 tachycardias; P<.05). An ablation applied to the earliest retrograde activation sites (CS and right inferoseptum = 5 and 3 cases, respectively) eliminated all irregular atypical AVNRTs. CONCLUSION: The variations in the AV relationship were observed exclusively during atypical AVNRT in 2% of all AVNRT cases. Irregular atypical AVNRT was characterized by younger age of the patients and shorter TCL, and it more frequently required an ablation inside the CS for success. We postulate that the noted irregularity was attributable to the short TCL that gave rise to the unstable conduction in the tachycardia circuit and Wenckebach block in the lower common pathway.
BACKGROUND:Atrioventricular (AV) nodal reentrant tachycardias (AVNRT) with variable AV relationships are infrequently observed and might be misdiagnosed as atrial tachycardia. OBJECTIVE: This single-center, retrospective study was performed to elucidate the mechanism of AVNRT showing variable AV relationship. METHODS: This study included a total of 340 patients with all forms of AVNRT. The induced AVNRTs were classified into those with variations in the AV relationship (>or=30 ms) (irregular AVNRT) and those without (regular AVNRT). RESULTS: A total of 364 AVNRTs (typical and atypical form = 297 and 67) were induced in the 340 patients. Of the 364 AVNRTs, the variations in the AV relationship were observed in 8 atypical AVNRTs (2%) induced in 8 patients (2%). The patients with irregular atypical AVNRT were significantly younger than those with regular typical AVNRT and those with regular atypical AVNRT (35+/-15 vs 51+/-18 and 47+/-16 years, respectively). Irregular atypical AVNRTs showed atypical Wenckebach periodicity with simultaneous prolongation in the A-A intervals and Wenckebach block proximal to the His bundle. Irregular atypical AVNRTs showed a shorter tachycardia cycle length (TCL) (305+/-78 ms vs 381+/-95 ms; P<.05) and higher prevalence of eccentric coronary sinus (CS) activation than regular atypical AVNRTs (5 (63%) of 8 tachycardias vs 15 (25%) of 59 tachycardias; P<.05). An ablation applied to the earliest retrograde activation sites (CS and right inferoseptum = 5 and 3 cases, respectively) eliminated all irregular atypical AVNRTs. CONCLUSION: The variations in the AV relationship were observed exclusively during atypical AVNRT in 2% of all AVNRT cases. Irregular atypical AVNRT was characterized by younger age of the patients and shorter TCL, and it more frequently required an ablation inside the CS for success. We postulate that the noted irregularity was attributable to the short TCL that gave rise to the unstable conduction in the tachycardia circuit and Wenckebach block in the lower common pathway.