OBJECTIVE: The occurrence of supernormal excitability and conduction in the atrium has been attributed to the internodal pathways in several animal experiments. However, little is known about the role of supernormal atrial conduction (SNC) in the genesis of arrhythmias. The specific aim of this study was to evaluate prospectively the relationship between SNC, atrial conduction defects and atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation. METHODS: Programmed atrial stimulation was performed in 38 control patients (group 1), and 21 patients with idiopathic paroxysmal atrial fibrillation (group 2) to assess some determinants of atrial conduction defects, SNC, and atrial fibrillation inducibility. RESULTS: The mean P-wave duration was 99 +/- 8 ms in group 1, and 110 +/- 12 ms in group 2; p < 0.001. The maximum interatrial conduction delay was 36 +/- 40 ms in group 1, and 56 +/- 21 ms in group 2; p < 0.005. Supernormal atrial conduction was observed in 27 (71 percent) patients of group 1, and in 5 (24 percent) of group 2; p < 0.0003. The SNC zone was 70 +/- 29 ms in group 1, and 16 +/- 31 ms in group 2; p < 0.0001. The maximum decrease in conduction time during the period of SNC was 12 +/- 4 ms in group 1 and 3 +/- 6 ms in group 2; p < 0.0005. The SNC zone showed a significant inverse correlation with the P-wave duration (r = -0.53; p < 0.0005), and with the maximum conduction delay (r = -0.38; p < 0.005). CONCLUSIONS: Patients with idiopathic paroxysmal atrial fibrillation have a significantly decreased incidence of SNC than controls. There is an inverse relation between the atrial conduction defects and the SNC. The association of the absence of SNC with defects in atrial conduction may play some role in the development of atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation.
OBJECTIVE: The occurrence of supernormal excitability and conduction in the atrium has been attributed to the internodal pathways in several animal experiments. However, little is known about the role of supernormal atrial conduction (SNC) in the genesis of arrhythmias. The specific aim of this study was to evaluate prospectively the relationship between SNC, atrial conduction defects and atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation. METHODS: Programmed atrial stimulation was performed in 38 control patients (group 1), and 21 patients with idiopathic paroxysmal atrial fibrillation (group 2) to assess some determinants of atrial conduction defects, SNC, and atrial fibrillation inducibility. RESULTS: The mean P-wave duration was 99 +/- 8 ms in group 1, and 110 +/- 12 ms in group 2; p < 0.001. The maximum interatrial conduction delay was 36 +/- 40 ms in group 1, and 56 +/- 21 ms in group 2; p < 0.005. Supernormal atrial conduction was observed in 27 (71 percent) patients of group 1, and in 5 (24 percent) of group 2; p < 0.0003. The SNC zone was 70 +/- 29 ms in group 1, and 16 +/- 31 ms in group 2; p < 0.0001. The maximum decrease in conduction time during the period of SNC was 12 +/- 4 ms in group 1 and 3 +/- 6 ms in group 2; p < 0.0005. The SNC zone showed a significant inverse correlation with the P-wave duration (r = -0.53; p < 0.0005), and with the maximum conduction delay (r = -0.38; p < 0.005). CONCLUSIONS:Patients with idiopathic paroxysmal atrial fibrillation have a significantly decreased incidence of SNC than controls. There is an inverse relation between the atrial conduction defects and the SNC. The association of the absence of SNC with defects in atrial conduction may play some role in the development of atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation.