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Time-dependent change in fast pathway refractoriness after slow pathway ablation in atrioventricular node reentrant tachycardia


, : Time-dependent change in fast pathway refractoriness after slow pathway ablation in atrioventricular node reentrant tachycardia. Canadian Journal of Cardiology 13(6): 583-588

OBJECTIVE: To determine the time course of change in fast pathway refractoriness after slow pathway ablation. BACKGROUND: Antegrade fast pathway refractoriness has been observed to shorten in patients undergoing slow pathway ablation for atrioventricular (AV) node reentrant tachycardia. The time course and mechanism of this observation have not been explained. METHODS: Twenty-eight patients with AV node reentrant tachycardia and dual AV node pathways undergoing slow pathway ablation had the fast pathway effective refractory period (ERP) assessed immediately before, and at 0, 15, 30 and 45 mins after slow AV node reentry and dual pathways involved in a multicenter protocol evaluating the Mansfield Polaris LE catheter underwent assessment of fast pathway refractoriness before and after slow pathway ablation, and at a routine three-month follow-up electron physiology study (Group 2). RESULTS: In Group 1, antegrade fast pathway ERP fell from 394 ms before ablation to 334 ms immediately after slow pathway ablation, increased to 348 ms within 15 mins and was 353 ms at 45 mins (ANOVA P lt 0.001). Retrograde fast pathway ERP fell from 325 ms before ablation to 294 ms at 45 mins (P=0.02). In Group 2, antegrade fast pathway ERP fell from 390 ms before ablation to 337 ms after ablation, and rose to 362 ms at three months (P=0.01). Retrograde fast pathway ERP also fell from 347 ms to 319 ms after ablation (P=0.01), and remained unchanged at three months. CONCLUSION: Slow pathway ablation results in an immediate and sustained change in antegrade and retrograde first pathway refractoriness. There are immediate reversible and long term nonreversible components to this phenomenon. The latter finding may be related to loss of electrotonic inhibition of the fast pathway by the slow pathway.

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