OBJECTIVE: To examine the hypothesis that the anatomic equivalents of the fast and slow pathways identified in patients with atrioventricular (AV) nodal tachycardia may be universal and represent the principal sites of atrial input into the normal compact AV node. METHODS: 15 patients undergoing complete AV junction ablation for paroxysmal atrial fibrillation were studied. Radiofrequency energy was delivered first in the anterior "fast pathway" position so as to prolong the atrium to bundle of His (AH) interval by over 50% of baseline (protocol 1) and then to the "slow pathway" position using the anatomical technique (protocol 2). RESULTS: Ablation protocol 1 resulted in prolongation of AH interval in all patients. Subsequent lesions at the level of the coronary sinus produced complete heart block in four patients, and in five caused a further increase in AH interval above that produced by protocol 1. Four of these latter patients developed complete block after delivery of RF energy slightly anterior to the level of the coronary sinus os, as did three further patients in whom ablation at the level of the coronary sinus had no effect. In four patients complete heart block could not be achieved by protocol 2. CONCLUSIONS: A discrete anterior "fast" pathway and a posterior "slow" pathway or network of posterior pathways form the principal inputs to the compact AV node in most patients with atrial fibrillation. The absence of dual AV nodal physiology in the majority of these patients may be related to the functional properties of the individual components of this posterior network.
OBJECTIVE: To examine the hypothesis that the anatomic equivalents of the fast and slow pathways identified in patients with atrioventricular (AV) nodal tachycardia may be universal and represent the principal sites of atrial input into the normal compact AV node. METHODS: 15 patients undergoing complete AV junction ablation for paroxysmal atrial fibrillation were studied. Radiofrequency energy was delivered first in the anterior "fast pathway" position so as to prolong the atrium to bundle of His (AH) interval by over 50% of baseline (protocol 1) and then to the "slow pathway" position using the anatomical technique (protocol 2). RESULTS: Ablation protocol 1 resulted in prolongation of AH interval in all patients. Subsequent lesions at the level of the coronary sinus produced complete heart block in four patients, and in five caused a further increase in AH interval above that produced by protocol 1. Four of these latter patients developed complete block after delivery of RF energy slightly anterior to the level of the coronary sinus os, as did three further patients in whom ablation at the level of the coronary sinus had no effect. In four patients complete heart block could not be achieved by protocol 2. CONCLUSIONS: A discrete anterior "fast" pathway and a posterior "slow" pathway or network of posterior pathways form the principal inputs to the compact AV node in most patients with atrial fibrillation. The absence of dual AV nodal physiology in the majority of these patients may be related to the functional properties of the individual components of this posterior network.
Authors: M R Jazayeri; S L Hempe; J S Sra; A A Dhala; Z Blanck; S S Deshpande; B Avitall; D P Krum; C J Gilbert; M Akhtar Journal: Circulation Date: 1992-04 Impact factor: 29.690
Authors: W M Jackman; K J Beckman; J H McClelland; X Wang; K J Friday; C A Roman; K P Moulton; N Twidale; H A Hazlitt; M I Prior Journal: N Engl J Med Date: 1992-07-30 Impact factor: 91.245
Authors: J J Langberg; A Leon; M Borganelli; S J Kalbfleisch; R el-Atassi; H Calkins; F Morady Journal: Circulation Date: 1993-05 Impact factor: 29.690
Authors: M A Lee; F Morady; A Kadish; D J Schamp; M C Chin; M M Scheinman; J C Griffin; M D Lesh; D Pederson; J Goldberger Journal: Circulation Date: 1991-03 Impact factor: 29.690