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%.