Background— The existence of an atypical fast-slow (F/S) atrioventricular nodal reentrant tachycardia (AVNRT) including a superior (sup) pathway with slow conductive properties and an atrial exit near the His bundle has not been confirmed. Methods and Results— We studied 6 women and 2 men (age, 74±7 years) with sup-F/S-AVNRT who underwent successful radiofrequency ablation near the His bundle. Programmed ventricular stimulation induced retrograde conduction over a superior SP with an earliest atrial activation near the His bundle, a mean shortest spike-atrial interval of 378±119 milliseconds, and decremental properties in all patients. sup-F/S-AVNRT was characterized by a long-RP interval; a retrograde atrial activation sequence during tachycardia identical to that over a sup-SP during ventricular pacing; ventriculoatrial dissociation during ventricular overdrive pacing of the tachycardia in 5 patients or atrioventricular block occurring during tachycardia in 3 patients, excluding atrioventricular reentrant tachycardia; termination of the tachycardia by ATP; and a V-A-V activation sequence immediately after ventricular induction or entrainment of the tachycardia, including dual atrial responses in 2 patients. Elimination or modification of retrograde conduction over the sup-SP by ablation near the right perinodal region or from the noncoronary cusp of Valsalva eliminated and confirmed the diagnosis of AVNRT in 4 patients each. Conclusions— sup-F/S-AVNRT is a distinct supraventricular tachycardia, incorporating an SP located above the Koch triangle as the retrograde limb, that can be eliminated by radiofrequency ablation.
The length of the slow pathway (SP-L) in atrioventricular (AV) nodal reentrant tachycardia (NRT) has never been measured clinically. We studied the relationship among (a) SP-L, i.e., the distance between the most proximal His bundle (H) recording and the most posterior site of radiofrequency (RF) delivery associated with a junctional rhythm, (b) the length of Koch’s triangle (Koch-L), (c) the conduction time over the slow pathway (SP-T), measured by the AH interval during AVNRT at baseline, and (d) the distance between H and the site of successful ablation (SucABL-L) in 26 women and 20 men (mean age 64.6 ± 11.6 years), using a stepwise approach and an electroanatomic mapping system (EAMS). SP-L (15.0 ± 5.8 mm) was correlated with Koch-L (18.6 ± 5.6 mm; R2 = 0.1665, P < 0.005), SP-T (415 ± 100 ms; R2 = 0.3425, P = 0.036), and SucABL-L (11.6 ± 4.7 mm; R2 = 0.5243, P < 0.0001). The site of successful ablation was located within 10 mm of the posterior end of the SP in 38 patients (82.6 %). EAMS-guided RF ablation, using a stepwise approach, revealed individual variations in SP-L related to the size of Koch’s triangle and AH interval during AVNRT. Since the site of successful ablation was also correlated with SP-L and was usually located near the posterior end of the SP, ablating anteriorly, away from the posterior end, is not a prerequisite for the success of ablation procedures.
Case PresentationA 72-year-old man with a history of multiple episodes of paroxysmal supraventricular tachycardia underwent electrophysiologic studies and a catheter ablation procedure. The 12-lead electrocardiogram during tachycardia showed long RP' tachycardia with negative P waves in leads II, III, and aVF. Ventriculoatrial (VA) conduction with a shortest 1:1 pacing cycle length of 780 ms and earliest atrial activation at the ostium of coronary sinus was observed during ventricular overdrive pacing. A narrow QRS tachycardia documented previously was reproducibly induced by programmed atrial, though not ventricular, stimulation. During tachycardia, the His-atrial (HA) and atrial-His (AH) intervals were 381 and 156 ms, respectively. The atrial activation sequence during tachycardia seemed identical to that during ventricular pacing. A 2-mg bolus injection of adenosine triphosphate reproducibly terminated the tachycardia after a last ventricular event, following progressive prolongation of the atrial cycle length. Overdrive ventricular pacing for >30 seconds during tachycardia, at a cycle length 10-30 ms shorter than the tachycardia cycle length, invariably caused VA dissociation without atrial capture or termination of the tachycardia (Fig. 1). What is the tachycardia mechanism? CommentSince (1) the earliest atrial activation was in the right posteroseptal atrium, and (2) the Disclosure: The authors have no conflict of interest to disclose.AH interval was shorter than the HA interval, the differential diagnosis includes (a) atrial tachycardia (AT) originating in the posterior septum, (b) atypical fast-slow atrioventricular nodal reentrant tachycardia (AVNRT), and (c) orthodromic atrioventricular reentrant tachycardia (AVRT) using a slowly conducting decremental posteroseptal accessory pathway. As shown in Figure 1, VA dissociation was observed during overdrive ventricular pacing, ruling out AVRT. Entrainment of the tachycardia by ventricular pacing at a slightly shorter cycle length usually provides key information to discriminate between AT and AVNRT. 1,2 This maneuver is useful when, before cessation of ventricular pacing, the atrial rate accelerates to the ventricular pacing rate. 1,2 In the present case, the tachycardia was not entrained, and burst pacing had no effect on the tachycardia. However, the reproducible termination of the tachycardia without atrial activation, with a single ventricular extrastimulus delivered during the tachycardia, was sufficient to confirm the diagnosis of AVNRT (Fig. 2). 3 Although failure of ventricular overdrive pacing to change the atrial rate and the atrial activation sequence during tachycardia is observed in the minority of AVNRT, it does not exclude this diagnosis. 2,4,5 This phenomenon suggests the existence of a lower common pathway, below the site of AV nodal reentry, where VA block occurs during overdrive pacing. 3 The diagnostic contribution of ventricular extrastimulation during tachycardia in such cases of AVNRT has not been previously discussed in the literature....
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