Case report
A 26-year old man underwent an electrophysiologic (EP) study and
catheter ablation because of recurrent palpitation. 12-lead surface
electrocardiogram (ECG) documented the alternating narrow and wide
complex tachycardia. The ECG during the sinus rhythm and the
echocardiography were normal.
The operation was performed under local anesthesia. Multipolar electrode
catheters were placed to the coronary sinus, His bundle region and right
ventricular apex of the patient respectively. The intracardiac
electrogram during sinus rhythm was recorded, with the HV interval of 52
ms. Wide complex tachycardia (cycle length 358ms) was induced by
ventricular S1S2 stimulation. The QRS
complex morphology presented as right bundle branch block pattern (rSR′)
in lead V1. The rate of the ventricle was higher than that of the
atrium. The His bundle potential preceded ventricular wave with a
shorter HV interval (16ms) than that (52ms) during sinus rhythm
(Figure1.A). Atrial burst pacing at a cycle length of 300ms had no
effect on QRS morphology and R-R interval. Based on these findings, the
wide QRS complex tachycardia could be identified as LFVT.
During the onset of tachycardia, the atrial rate speeded up and the V-A
relationship changed to 1:1, the morphology of the QRS complex changed
between narrow and fused, with inconstant AV and VA interval. (Figure
1.B).Besides that, the wide complex tachycardia could occur immediately
after the termination of the narrow complex tachycardia. The HV interval
(52ms) during narrow complex tachycardia was identical to that during
the sinus rhythm (Figure 1.C). The surface electrocardiogram showed that
the morphology of the QRS complex alternately transformed among wide,
narrow and fused. The cycle length of the tachycardia fluctuated between
341ms and 358ms (Figure 1.D). Based on these characteristics, the
supraventricular tachycardia (SVT) was ascertained.
LFVT was induced repeatedly by spontaneous premature ventricular beat
and ablated primarily. An irrigated Thermocool Navistar catheter
(Biosense Webster, Inc) was advanced in the left ventricle via the right
femoral artery. Ablation was applied at the site of the earliest
Purkinje potential during tachycardia and rendered LFVT non-inducible.
After that, atrial S1S2 stimulation revealed AV conduction jumping
phenomenon. The narrow complex tachycardia was still easily induced by
ventricular stimulation. During tachycardia, The RP’
interval(191ms)was longer than P’R interval (159ms) (Figure2.A). When
ventricular pacing (SS=330ms) was delivered at a rate faster than the
tachycardia, the ventricle was captured without changing the cycle
length of the AA interval (345ms), which ruled out atrioventricular
reentrant tachycardia. The earliest retrograde atrial activation
recorded at the ostium of the coronary sinus was same to that recorded
during the tachycardia, which implied the unlikely of atrial
tachycardia. (Figure2.B). It was also found that the tachycardia could
be terminated by ventricular stimulation (SS=320ms) without retrograde
ventricular-atrial conduction and so atrial tachycardia was excluded
(Figure2.C) [1]. Based on the above findings, slow-slow AVNRT was
diagnosed. Successful ablation was achieved near the CS ostium guided by
the fluoroscopy during tachycardia. Repeated EP study showed that there
was neither retrograde VA conduction during ventricular pacing
(Figure2.D) nor AV conduction jumping phenomenon during atrial
extra-stimulation. During one-year follow-up, no recurrence was found.