Concealed Conduction and Dual Pathway Physiology of the Atrioventricular Node
Shaowen Liu, S. Bertil Olsson, Yanzong Yang, Eva Hertervig, Ole Kongstad, Shiwen Yuan
Abstract
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Shaowen Liu, S. Bertil Olsson, Yanzong Yang, Eva Hertervig, Ole Kongstad, Shiwen Yuan
Abstract
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INTRODUCTION: Both concealed conduction and dual pathway physiology are important electrophysiologic characteristics of the AV node. The interaction of AV nodal concealment and duality, however, is not clearly understood. METHODS AND RESULTS: The properties of AV conduction curves in the presence and absence of a conditioning blocked impulse were prospectively studied during premature atrial stimulation in 20 patients with AV nodal reentrant tachycardia before and after slow pathway ablation and in 14 control patients. AV nodal duality in the control conduction curve in the absence of a conditioning impulse was observed in 19 (95%) of 20 patients with AV nodal reentrant tachycardia. However, AV nodal duality in the modulated conduction curve in the presence of a blocked impulse was only identified in 2 (10%) of 20 patients (2/20 vs 19/20, P < 0.0001). The modulated curve was characterized by a significantly longer AV nodal effective and functional refractory periods compared to the control curve (P < 0.0001) in both patients with and without AV nodal reentry and in AV nodal reentry patients after successful slow pathway ablation. The maximum AH interval (AH(max)) of the modulated curve was significantly shorter than the control curve in both patients with (217 +/- 74 ms vs 347 +/- 55 ms, P < 0.0001) and without AV nodal reentry (178 +/- 50 ms vs 214 +/- 54 ms, P = 0.02). AH(max) of the control curve was significantly longer in AV nodal reentry patients than in controls (P < 0.0001). AH(max) of the modulated curve, however, was not significantly different between the two groups. After slow pathway ablation, AH(max) of the control curve was significantly reduced (347 +/- 55 ms vs 191 +/- 40 ms, P < 0.0001). Significant reduction in AH(max) of the modulated curve was not observed. CONCLUSION: An interaction of AV nodal concealed conduction and dual pathway physiology was demonstrated by our data. Slow pathway conduction of the AV node was prevented by the concealed beat in both patients with and without AV nodal reentry.
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INTRODUCTION: Both concealed conduction and dual pathway physiology are important electrophysiologic characteristics of the AV node. The interaction of AV nodal concealment and duality, however, is not clearly understood. METHODS AND RESULTS: The properties of AV conduction curves in the presence and absence of a conditioning blocked impulse were prospectively studied during premature atrial stimulation in 20 patients with AV nodal reentrant tachycardia before and after slow pathway ablation and in 14 control patients. AV nodal duality in the control conduction curve in the absence of a conditioning impulse was observed in 19 (95%) of 20 patients with AV nodal reentrant tachycardia. However, AV nodal duality in the modulated conduction curve in the presence of a blocked impulse was only identified in 2 (10%) of 20 patients (2/20 vs 19/20, P < 0.0001). The modulated curve was characterized by a significantly longer AV nodal effective and functional refractory periods compared to the control curve (P < 0.0001) in both patients with and without AV nodal reentry and in AV nodal reentry patients after successful slow pathway ablation. The maximum AH interval (AH(max)) of the modulated curve was significantly shorter than the control curve in both patients with (217 +/- 74 ms vs 347 +/- 55 ms, P < 0.0001) and without AV nodal reentry (178 +/- 50 ms vs 214 +/- 54 ms, P = 0.02). AH(max) of the control curve was significantly longer in AV nodal reentry patients than in controls (P < 0.0001). AH(max) of the modulated curve, however, was not significantly different between the two groups. After slow pathway ablation, AH(max) of the control curve was significantly reduced (347 +/- 55 ms vs 191 +/- 40 ms, P < 0.0001). Significant reduction in AH(max) of the modulated curve was not observed. CONCLUSION: An interaction of AV nodal concealed conduction and dual pathway physiology was demonstrated by our data. Slow pathway conduction of the AV node was prevented by the concealed beat in both patients with and without AV nodal reentry.
Key concepts: Reentry, NODAL, Medicine, Refractory period, Nodal signaling, Tachycardia, Ablation, Effective refractory period