Discussion
Repetitive reentrant ventriculoatrial synchrony (RRVAS), also known as
pacemaker-mediated tachycardia (PMT) or endless loop tachycardia (ELT),
is the term to describe a repetitive process characterized by a
retrograde P-wave followed by atrial-tracked bi-ventricular pacing
(BVP), in which VA conduction works as the retrograde limb and
subsequent atrial-tracked BVP works as the antegrade limb. Any
conditions that cause AV dissociation in a patient with VA conduction
can trigger RRVAS, in which VA conduction plays a key
role.1 The rest types of PMA dependent on VA
conduction in initiating and sustaining include repetitive non-reentrant
ventriculoatrial synchrony (RNRVAS) and repetitive non-reentrant
ventriculoatrial 1:2 synchrony (RNRVA1:2S), both are characterized by
making the retrograde P-wave fall in post-ventricular atrial refractory
period (PVARP) and subsequent loss of capture or capture of atrial
pacing.2 In a bi-ventricular pacing system, a
relatively short AV interval is commonly programmed to obtain the best
left ventricular (LV) pump function by allowing complete activation of
ventricles from the bi-ventricular pacing sites, which also prevents the
appearance of VA conduction. And a higher maximum tracking rate, a
relatively short PVARP and turning off algorithms that extend PVARP are
recommended to avoid the loss of optimal AV synchrony (due to the loss
of atrial tracking) and subsequent ineffective CRT.3Therefore, RRVAS is rare due to its less predisposition to the
appearance of AV dissociation and subsequent VA conduction in a
bi-ventricular pacing system.
In Figure 1-A, one episode of RBBB pattern PMA was initiated by a
premature ventricular contraction (PVC) with a VA interval of 200 ms and
subsequent prolonged sensed AV interval (SAVI) of 280 ms, which was
characterized by a repetitive process characterized by a retrograde
P-wave followed by atrial-tracked BVP. All these findings accord with
RRVAS. VA interval in RRVAS measured from LV stimulus to the onset of
the retrograde P-wave was 320 ms. In addition, the third PVC, rather
than the second PVC, triggered RRVAS, both of which had the same VA
interval of 200 ms. “Intermittent atrial under-sensing” seemed to
explain this phenomenon. However, the pattern that always the third PVC
triggered RRVAS could be observed repetitively in the ambulatory ECG
monitoring. These findings accord with “Tracking Preference” that is
designed to avoid the loss of atrial tracking in a Boston Scientific CRT
device, so that the device can short PVARP to establish the subsequent
atrial-tracked BVP after two successive sequences of a sensed
ventricular event preceded by an atrial sensed event in the refractory
period. In some certain conditions, “Tracking Preference” may
facilitate the development of RRVAS due to the maximum tracking rate
limit.4 The RBBB pattern in RRVAS suggested a
tachycardia-dependent (TD) loss of capture (LOC) of right ventricular
(RV) lead, which meant the appearance of TD threshold changes on the
electrode-tissue interface in RV. Considering that TD threshold changes
are commonly voltage-dependent,5 adjusting the pacing
output may avoid the appearance of TD failure of RV capture.
To our surprise, in most episodes of RBBB pattern RRVAS, it was a PAC
followed by atrial-tracked BVP accompanied by the appearance of VA
conduction with no prolongation of AV delay, which seems to be
unconformable to the initiation of classic RRVAS/PMT. How did VA
conduction appear without any prolongation of AV delay? From a
mechanistic point of view, VA conduction time from the epicardial
ventricular pacing (VP) will be longer than that from the endocardial VP
due to the transmural conduction delay from the epicardium to the
endocardium, which can be verified by differences in VA conduction
between PVC and epicardial left VP (LVPepi) (Figure 2-B,
C). In a normally atrial-tracked bi-ventricular pacing sequence, there
is no appearance of the retrograde P-wave from VA conduction generated
by endocardial right VP (RVPendo), as the retrograde
pulse may fall in the refractory period of atrial myocardium
(RPmyo); the pulse from LVPepipropagates slowly than that from RVPendo due to the
transmural conduction delay, and may be blocked in some position of the
intrinsic conduction system due to the concealed conduction created by
the pulse from RVPendo (Figure 2-A). When
tachycardia-dependent LOC of RV lead occurs, the pulse from
LVPepi falls outside RPmyo and
retrogradely activates the atrium. Once the retrograde P-wave is formed,
the bi-ventricular pacing system has the potential to be involved in
initiating and sustaining pacemaker-mediated arrhythmias, with or
without AV dissociation (Figure 2-C). In Figure 2-A (upper panel), a PAC
with a relatively long P-P coupling interval was followed by normally
atrial-tracked BVP with no retrograde P-wave, which also verified that
the appearance of VA conduction might be due to tachycardia-dependent
LOC of RV lead. During some episode of RRVAS (Figure 3-A, B), some BVP
was followed by a PVC (true fusion beat) with a VA interval of about 240
ms, which may be due to the fact that LVPepi captured
partial ventricle myocardium and delayed VA conduction from PVC (Figure
2-D). In addition, every episode of RRVAS was self-terminated by a
short-coupling PVC accompanied by BVP within it, with no retrograde
P-wave. A short-coupling PVC blocked VA conduction by making the
retrograde pulse fall in RPmyo to terminate RRVAS
(Figure 3-B).
The main adverse effects associated with RRVAS include (1) pacemaker
syndrome due to the loss of optimal AV synchrony; (2) inappropriate
increase in VP ratio, which is associated with the development of atrial
fibrillation and heart failure.6,7 RRVAS in the
bi-ventricular system is rare due to its less predisposed to the
appearance of AV dissociation and subsequent VA conduction, but urgent
in its adverse impact on CRT (due to AV dissociation and rate-dependent
LOC on one ventricular lead), which may be associated with obvious
clinical symptoms and predispose to exacerbated heart
failure.8,9
Each device manufacturer has its proprietary algorithm ( “PMT
termination/intervention” ) to detect and terminate RRVAS, which
prolongs PVARP of the suspected episode of RRVAS for one cardiac cycle
to attempt to interrupt VA conduction. Whereas, it is possible for an
intrinsic atrial rate to meet the RRVAS detection criteria, which may
result in a periodic loss of atrial tracking due to the extended PVARP
by the algorithm. Considering a low incidence of RRVAS in CRT and the
potential risk of ineffective CRT due to the periodic loss of atrial
tracking, turning off PMT termination is recommended. Program PVARP to a
value longer than the VA interval in RRVAS of 400 ms, in our case, can
directly prevent RRVAS but may also increase the risk of loss of atrial
tracking and ineffective CRT.
A pacemaker interrogation showed a capture threshold on RV lead at 2.0
V/0.5 ms. When the pacing rate exceeded 120 bpm in DDD mode with a fixed
interval of 120 ms, LOC of RV lead accompanied by the appearance of VA
conduction time of 320 ms was observed. Considering the appearance of VA
conduction and subsequent initiating RRVAS are due to LOC of RV lead,
increasing the pacing output of RV lead is an effective measure without
increasing the risk of loss of atrial tracking. With outputs increasing
to 3.0 V/0.5 ms, a stable capture of RV lead was observed even at the
rate of 130 bpm. No episode of RRVAS was recorded in another ambulatory
monitoring before the patient’s discharge. At six months of follow-up,
the patient reported that he did not experience any episodes of
palpitation and corresponding symptoms of dyspnea and dizziness, and EF
increased from 31% to 43%.