Key result
Sinus node dysfunction in patients with AVNRT was associated with prolonged anterograde fast pathway Wenckebach cycle lengths compared to controls (559 vs 361 msec; P<0.01).
Why the study?
What are the electrophysiologic characteristics and clinical presentation of AVNRT in patients with sinus node dysfunction compared to those without?
Case-Control (n=20)
What are the electrophysiologic characteristics and clinical presentation of AVNRT in patients with sinus node dysfunction compared to those without?
Patients with AVNRT and sinus node dysfunction exhibit characteristic electrophysiologic alterations resulting in more frequent tachycardia episodes, but slow pathway ablation remains safe and effective.
May explain more frequent AVNRT episodes with sinus node dysfunction; extends AV conduction observations but leaves practice unchanged.
INTRODUCTION: Sinus node dysfunction (SND) is frequently associated with impaired AV conduction. This study investigated the electrophysiologic properties of dual AV nodal pathways in patients suffering from both SND and AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Two groups of patients with slow-fast AVNRT underwent invasive electrophysiologic testing and catheter ablation of the slow pathway. Group A comprised 10 patients with SND (age 70 +/- 8 years). Group B included 10 age-matched patients without SND (age 69 +/- 7 years; P = NS) who served as controls. Patients of group A exhibited prolongation of the anterograde Wenckebach cycle lengths (WBCLs) of both the fast pathway (559 +/- 96 vs 361 +/- 38 msec; P < 0.01) and the slow pathway (409 +/- 57 vs 339 +/- 32 ms; P < 0.01). However, the delta between the WBCLs of the fast and the slow pathways was larger in patients of group A (150 +/- 80 vs 22 +/- 20 msec; P < 0.01). Retrograde fast pathway conduction was well preserved with no difference in WBCLs (356 +/- 42 vs 330 +/- 47 msec; P = NS). Cycle lengths of AVNRT were longer in group A (468 +/- 46 vs 363 +/- 37 msec; P < 0.01). Clinically, all patients of group A suffered from multiple episodes of AVNRT per week, which was not the case in any patient of group B (P < 0.01). Catheter ablation of the slow pathway eliminated AVNRT in all patients without complications. CONCLUSIONS: Patients with AVNRT and SND exhibit characteristic electrophysiologic alterations of both AV nodal pathways. Clinically, this results in significantly more frequent episodes of tachycardia. Slow pathway ablation appears to be safe and effective in these patients.
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Kreiner et al. (1998) conducted a case-control in Atrioventricular Nodal Reentry Tachycardia (AVNRT) and Sinus Node Dysfunction (SND) (n=20). Slow pathway ablation vs. Patients without sinus node dysfunction was evaluated on Anterograde Wenckebach cycle lengths (WBCLs) of the fast pathway (p=<0.01). Sinus node dysfunction in patients with AVNRT was associated with prolonged anterograde fast pathway Wenckebach cycle lengths compared to controls (559 vs 361 msec; P<0.01).
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