Case report
A 73-year-old woman with no history of heart disease developed symptoms
of palpitations during hospitalization after surgery for a cerebral
aneurysm. The twelve-lead electrocardiogram revealed a long-RP, narrow
QRS, regular tachycardia with a heart rate of 132 beats per minute
(Figure 1A). After written informed consent was obtained from the
patient, an electrophysiological study was performed. Multielectrode
catheters were placed at the high right atrium (HRA), His bundle,
coronary sinus (CS), and right ventricular apex (RVA). The absence of
ventriculoatrial (VA) conduction was inferred by ventricular pacing at
several cycle lengths without obtaining retrograde atrial capture
(Figure 1B). The supraventricular tachycardia (SVT) was easily induced
by burst atrial pacing. The earliest atrial activation was recorded at
the His-bundle electrodes (HBE) during the SVT. Ventricular burst pacing
during the SVT revealed ventriculoatrial (VA) dissociation. VA linking
was not observed during differential atrial overdrive pacing (Figure
1C)4 and the SVT was reproducibly terminated without
AV block by a 4-mg bolus injection of adenosine 5’-triphosphate (Figure
1D). Based on these findings, the SVT was diagnosed as an
adenosine-sensitive AT.
The activation map in the RA during the AT revealed a centrifugal
pattern. The EAS of the RA (EAS-RA) was located slightly toward the
septal portion of the site where the His potentials were recorded
(Figure 2A). A local atrial electrogram of the EAS-RA preceded that of
the CS proximal (CSp) electrode by 35 ms (Figure 2B). Considering the
risk of injuring the AV node by a radiofrequency (RF) application to the
EAS-RA, entrainment pacing during the AT with a pacing cycle length
(PCL) of 10–20 ms shorter than the tachycardia cycle length (TCL) was
performed at various sites in the RA (RA appendage [RAA], high
anterolateral RA, high posteroseptal RA, and cavotricuspid isthmus
[CTI]) and from the CS electrodes (1 o’clock and 3 o’clock on the
MA) to identify the entrance of the SCZ. However, manifest entrainment
could not be observed.
Subsequently, the ablation catheter was inserted into the noncoronary
aortic sinus (NCS) via a retrograde transaortic approach. Although
entrainment pacing from various sites of the NCS was also performed,
manifest entrainment could not be demonstrated. The EAS of the NCS
(EAS-NCS) with a local potential recorded 41 ms earlier than
that of the CSp electrode (Figure
2B) was located above and slightly posterior to the EAS-RA (Figure 2A).
An RF application (25–30 W, 40℃, 30 seconds) was delivered at the
EAS-NCS; however, the AT did not terminate. RF applications (20–25 W,
40℃) at the EAS-RA where a His potential could not be recorded were also
ineffective and were discontinued owing to transient AV block.
Thereafter, activation mapping in the LA performed via a transseptal
approach revealed the EAS of the LA (EAS-LA), which was 44ms earlier
than that of the CSp electrode (Figure 2B), and was on the opposite side
of the EAS-RA (Figure 2A). An RF application (25 W, 40℃) at the EAS-LA
terminated the AT, however, it was interrupted due to transient PR
interval prolongation and the AT was still easily inducible after that.
Considering the risk of AV block, we hesitated to deliver an additional
RF application around the EAS-LA. Thus, entrainment pacing from various
sites of the LA were performed considering the possibility that the SCZ
of the AT circuit was in the LA. Manifest entrainment could not be
observed from the anterior mitral annulus (MA) or base of the left
atrial appendage, but was demonstrated from the high anteroseptum
(Figure 2A). Entrainment pacing from site A was performed with a PCL of
440 ms during the AT with a TCL of 455 ms, and the atrial electrograms
recorded from the CS were captured antidromically, and those recorded
from the HRA and HBE were captured orthodromically with a long
conduction interval. Ventricular electrograms recorded from the CS, HBE,
and RVA were also orthodromically captured (Figure 3A). From this
finding, site A was considered to be proximal to the SCZ, and the
entrance of the SCZ was presumed to be located between this pacing site
and the EAS-LA (Figure 3B). When the ablation catheter came in contact
with Site B, which was 13 mm superoposterior from the EAS-LA (Figure
2A), and the local elctrogram appeared 8ms later than that of the
EAS-LA, the AT became an incessant form. An RF application (25–30 W,
40℃, 30 seconds) at site B terminated the AT in 3s without PR interval
prolongation. Thereafter, the AT could no longer be induced. The patient
had no recurrence of the tachycardia during a 10-month follow-up period
without any antiarrhythmic drugs.