CASE PRESENTATION:
A 70-year-old man with drug refractory symptomatic paroxysmal atrial
fibrillation (AF) was referred for pulmonary vein isolation (PVI). After
completing anatomical PV encirclement, interrogation of the PVs with a
circular mapping catheter (CMC) showed that left superior PV (LSPV)
remained electrically connected (entrance block into left inferior PV
was confirmed). Body surface ECG and intracardiac electrograms during
sinus rhythm [sinus cycle length (CL), 1000 ms] (figure 1-A) and
during pacing from distal coronary sinus (CS) at a CL of 600 ms are
shown (figure 1-B). When the pacing CL was lengthened to 750 ms, atrial
trigeminy appeared with a fixed coupling interval (figure 2). The
trigeminy vanished when pacing CL was 700, 800, and 900 ms (data not
shown), however, it was reproducibly induced only when pacing CL was 750
ms.
What is the mechanism of the atrial trigeminy induced only at the
specific pacing CL?
COMMENTARIES:
During sinus rhythm, the 2 distinct PV potentials (P1 and P2) were
recorded on the CMC placed within the LSPV ostium (figure 1-A). The
interval between P1 and P2 was 210 ms during sinus. When pacing at the
CL of 600 ms from the distal CS, however, the P2 disappeared (figure
1-B). When the pacing CL is increased up to 750 ms, not only the P2
appeared again, but also the P1-P2 interval presented a Wenckebach
periodicity increasing slightly from 235 to 245 ms (figure 3-A).
Moreover, the third PV potential (P3) appeared every third beat and was
conducted to the left atrium (LA), resulting in the atrial trigeminy.
The P1-P3 interval was constant (245+135 ms), which led to the fixed
coupling interval. The third pacing impulse did not capture the LA which
remained refractory (figures 2 and 3-A).
Then, what is the mechanism of the double or triple PV responses to a
single atrial impulse? The P1 and P3 were recorded on the all bipoles of
the CMC but they were different in activation sequence [note the site
of earliest PV spike of each PV potential (arrows in figure 3-A)].
Whereas, the P2 was recorded only on limited bipoles of the CMC,
suggesting far-field signals from the distal LSPV. These findings
indicated that the P3 was an “echo” from the distal LSPV. The
reproducible induction of the PV echo by atrial stimulation at the
specific pacing CL indirectly suggested reentry as its mechanism.
Proposed mechanism of the intra-PV reentry causing the echoes is
demonstrated in Figure 3-B. Two PV myocardial sleeves which meet the
following criteria are assumed: 1) each of the 2 sleeves remains
connected to the left atrium (LA); 2) one of the 2 sleeves has a slower
conduction velocity and a slightly longer refractory period than the
other (“faster” and “slower” sleeves); and 3) the 2 sleeves are
connected at the site distal to the slow conduction zone existing
between the proximal and distal PVs. When the pacing CL was 600-700 ms,
P2 (represents depolarization of distal PV sleeve) was not produced
since the slow conduction zone was refractory (figure 3-B1). When the
pacing CL was 750-1000 ms, the P2 was produced via the faster sleeve. P3
was not present since retrograde impulse from the faster sleeve was
blocked within the slower sleeve due to refractoriness or collision with
impulse via the slower sleeve (figure 3-B2). When the pacing CL was 750
ms, both the P2 and P3 appeared since unidirectional block occurred in
the slower sleeve, and the P3 was conducted to the LA (figure 3-B3).
Almost no difference in length of refractory period of the two PV
sleeves may have resulted in the very narrow echo zone.
After the radiofrequency application at the anterior carina of the LSPV,
which resulted in entrance block into the LSPV, the PV echo was no
longer inducible despite pacing within the PV or provocative
isoproterenol and adenosine. The patient is currently asymptomatic 1
year after the procedure, with no evidence of AF recurrence.
In the present case, an uncommon cause of atrial trigeminy; atrial
impulse-triggered PV echo associated with conduction gaps in PV
encircling lesions, has been described. Moreover, the PV echo was
induced only at the specific pacing CL. Atrial impulse-triggered PV echo
has not been reported at the present moment. Bun and colleagues observed
double PV response to a single PV stimulus within the electrically
isolated PV1. In our patient, however, PV echo was not
inducible after the LSPV was electrically isolated from the LA. Recently
we reported sinus impulse-triggered echoes within superior vena cava
(SVC) resulting in atrial bigeminy, although response of the SVC to
programed atrial stimulation was not evaluated2. In
conclusion, the atrial rate-specific repetitive PV response resulting in
atrial premature beat is a newly observed phenomenon that may provide
insights into the arrhythmogenesis of the incompletely ablated PV
muscular sleeves.