Automatic switching between the AAI and the DDD algorithm can prevent repetitive non-reentrant ventriculoatrial synchrony

Abstract

A 67-year-old man with non-obstructive hypertrophic cardiomyopathy had received an implantable cardioverter-defibrillator (ICD) for an unstable, sustained ventricular tachycardia (VT) induced by programmed stimulation during an electrophysiological study 5 years earlier. An intracardiac electrogram recorded by the ICD revealed repetitive, non-reentrant ventriculoatrial synchrony (RNRVAS) associated with hypotension. Electrophysiologic and hemodynamic studies indicated that RNRVAS was induced and reproducibly termed by a single ventricular extrastimulus from the right ventricular apex. Following attainment of the elective replacement indicator, we replaced the ICD with another having managed ventricular pacing, which automatically switched AAI and DDD, thereby avoiding unnecessary ventricular pacing. Thus far, the patient has not experienced further RNRVAS. Thus, we believe that automatic switching between AAI and DDD can prevent RNRVAS.

1 Case Report

A 67-year-old man with non-obstructive hypertrophic cardiomyopathy had received a dual-chamber implantable cardioverter-defibrillator (ICD) (7278 Maximo^® DR, Medtronic, Minneapolis, MN, USA) 5 years earlier for an unstable, sustained ventricular tachycardia (VT) induced by programmed stimulation during an electrophysiological study (EPS). The ICD was programmed to provide atrial overdrive suppression for paroxysmal atrial fibrillation and to avoid unnecessary ventricular pacing. The electrophysiological study (EPS) record during ICD implantation revealed a maximum sinus node recovery time of 11,100 ms; moreover, the patient's 12-lead electrocardiogram (ECG) showed first-degree atrioventricular block (DDIR) with a lowered heart rate of 80 beats/min (bpm). The atrioventricular (AV) delay after atrial pacing was 350 ms. The postventricular atrial refractory period (PVARP) was maintained at 310 ms for containing retrograde ventriculoatrial (VA) conduction, with a VA conduction time of approximately 190 ms. In addition, we prescribed 160 mg/day sotalol to prevent ventricular tachycardia.

In our clinic, the intracardiac electrogram recorded by the ICD showed repetitive non-reentrant ventriculoatrial synchrony (RNRVAS), which was associated with hypotension and chest discomfort (Fig. 1). We suspected that the RNRVAS caused the hypotension; therefore, we performed electrophysiologic and hemodynamic studies. A 24-h ambulatory electrocardiograph also indicated RNRVAS that was initiated by either a premature ventricular or atrial beat. The EPS indicated that a single ventricular extrastimulus from the right ventricular apex reproducibly induced and termed the RNRVAS. Under the setting for DDIR, the heart rate was lowered to 70 bpm and 80 bpm, and RNRVAS was induced repetitively. The shortened AV delay caused heart failure due to increasing ventricular pacing. Other setting changes such as prolonging the lowered rate interval were not effective in preventing RNRVAS. During RNRVAS, the patient's systolic blood pressure decreased by approximately 20 mmHg (60–70 mmHg) compared to that during the atrial pacing ventricular sensing rhythm (80–90 mmHg, Fig. 2). During the atrial pacing ventricular pacing rhythm, his blood pressure also decreased compared to that during the ventricular sensing rhythm.

Fig. 1. Repetitive non-reentrant ventriculoatrial synchrony (RNRVAS) on the intracardiac electrogram recorded by the implantable cardioverter-defibrillator (ICD). Ventricular extrastimulus from the right ventricular apex lead caused retrograde VA conduction in the postventriculoatrial refractory period (PVARP). Ineffective atrial pacing noted as AV delay and lower rate interval occurred in the atrial refractory period (ARP). Thereafter, ventricular pacing occurred, leading to retrograde VA conduction; thus, RNRVAS was maintained. PVARP, postventriculoatrial refractory period; RNRVAS, repetitive non-reentrant ventriculoatrial synchrony.

Fig. 2. Hemodynamics during RNRVAS with the AAI mode. Blood pressure during RNRVAS decreased by 20mmHg compared to that during atrial pacing ventricular sensing rhythm. RNRVAS was termed by an atrial premature beat. RNRVAS, repetitive non-reentrant ventriculoatrial synchrony; APB, atrial premature beat.

In addition, the site of earliest retrograde atrial activation during RNRVAS was recorded on the electrograms of the His bundle (Fig. 3). Because this atrial activation involved only a single retrograde pathway with a decremental conduction property, we considered it to be retrograde VA conduction occurring via the fast AV nodal pathway. The elective replacement indicator was triggered in the ICD; therefore, we replaced the ICD with another device (7278 PROTECTA^®, Medtronic, Minneapolis, MN, USA), to manage the ventricular pacing mode and to provide functional AAI/R pacing that was equipped with a safe dual-chamber ventricular support that would allow automatic switching between AAI and DDD mode pacing. The parameters after replacement were as follows: MVP mode (AAI, 80 bpm and DDD, 80–120 bpm), paced AV delay 180 ms, and PVARP 320 ms. Cumulative percentages of pacing and sensing were atrial pacing (AP)–ventricular sensing (VS) 97.3%, AP 99.1%, and ventricular pacing 1.8%. Thus far, no report of RNRVAS following ICD replacement has been reported. After this replacement, the patient's hypotension improved.

Fig. 3. Intracardiac electrogram recording during RNRVAS. The site of earliest retrograde atrial activation during RNRVAS was recorded on the electrograms of the His bundle during RNRVAS. Because this atrial activation involved only a single retrograde pathway with a decremental conduction property, we considered it to be retrograde VA conduction occurring via the fast AV nodal pathway. RNRVAS, repetitive non-reentrant ventriculoatrial synchrony; VPC, ventricular premature complex; PVARP, postventriculoatrial refractory period; ARP, atrial refractory period; HRA, high right atrium; HBE, His bundle electrogram; CS, coronary sinus; RVA, right ventricular apex; d, distal; p, proximal.

2 Discussion

To the best of our knowledge, this is the first report describing the hemodynamic state and retrograde conduction in a patient with an ICD who showed RNRVAS on an intracardiac electrogram. We found that automatic mode switching between AAI and DDD could prevent RNRVAS.

RNRVAS is becoming a well-known pacemaker for arrhythmia, as DDD or DDI modes have often been selected in clinical situations [1–4]. This arrhythmia occurs in cases of intact retrograde VA conduction. Furthermore, the pacemaker must be programmed with a sufficiently long PVARP so that retrograde conduction does not induce endless loop tachycardia. One final prerequisite is a sufficiently high base rate to ensure a relatively short atrial escape interval and an even shorter interval from the retrograde atrial depolarization, thus rendering the atrial tissue physiologically refractory.

Functional undersensing occurs when the retrograde P wave is not sensed because it coincides with the PVARP. Because of the relatively high rate and the failure to reset the atrial timing cycle, atrial pacing is delivered while the atrial myocardium is physiologically refractory, resulting in functional atrial non-capture. Functional undersensing and non-capture play critical roles in maintaining RNRVAS. After the ineffective atrial pacing, the AV interval times out, and a ventricular paced event occurs, by which time, the AV node and atrial myocardium are fully recovered, facilitating retrograde conduction. Thus, RNRVAS is caused by the sequence of a combination of an AV paced rhythm with repeated functional atrial undersensing and non-capture [5].

In the present case, RNRVAS onset was recorded (Fig. 1). The pattern was consistent with ventricular pacing from the right ventricular ICD lead, which led to retrograde conduction in PVARP and produced an atrial refractory period in the atrium. Thus, programmed atrial pacing during the atrial refractory period caused a functional atrial non-capture. This repeated AV synchronous rhythm, RNRVAS has been described previously.

Clinical symptoms consist of the pacemaker syndrome, including palpitations and hemodynamic instability, as in our case. The definitive management of RNRVAS requires sufficient time for the atrial tissue to recover from the refractory period. Barold et al. reviewed several general modes that could prevent RNRVAS [1]. First, the atrial escape interval must be prolonged to allow the atrial myocardium to recover. Second, the lower base rate should be decreased or the lower rate increased. Third, the sensor-driven upper rate should also be decreased. Lastly, the AV delay must be shortened. In addition, a higher base rate is effective for suppressing atrial fibrillation. However, some of these management options are not clinically appropriate. Other algorithms to prevent RNRVAS have also been suggested; however, to our knowledge, automatic switching between AAI and DDD has not yet been reported. Furthermore, ablation of a retrograde pathway, which involves maintaining RNRVAS, may be a therapeutic option, provided that the retrograde pathway is not the AV nodal fast pathway, as determined from the EPS.

The mechanism by which RNRVAS is prevented via automatic mode switching between AAI and DDD involves the termination of the inappropriate synchronous atrial and ventricular pacing mode using an AV conduction check. The MVP mode (Medtronic, Minneapolis, MN, USA) [6,7] is one such switching mode. During a sequential atrial and ventricular pacing rhythm in the MVP mode, an AV conduction check is scheduled every 1, 2, 4, and 8 min for up to 16 h following a transition from AAI to DDD. The AV conduction check is temporary, consists of only 1 beat, and uses an AAI pacing mode to monitor for conducted ventricular sensing. In this case, during RNRVAS, the scheduled AV conduction check in the MVP mode allowed both atrial and ventricular sensing, which did not initiate retrograde VA conduction because the AV node had not recovered from the refractory period (Fig. 4). Hence, the RNRVAS was terminated. In addition, the MVP mode has other algorithms, including a dynamic atrial refractory period and postventricular premature beat option, which can prevent RNRVAS given that the atrial escape interval is prolonged after a non-conducted P wave or ventricular premature beat.

Fig. 4. RNRVAS termination through the managed ventricular pacing (MVP) mode. Scheduled AV conduction check in the MVP mode allowed atrial and ventricular sensing, which did not initiate retrograde VA conduction leading to RNRVAS. RNRVAS, repetitive non-reentrant ventriculoatrial synchrony; AP, atrial pacing; VP, ventricular pacing; AR, atrial sensing in atrial refractory period; AS, atrial sensing; VS, ventricular sensing; ARP, atrial refractory period; PVARP, postventriculoatrial refractory period.

To suppress atrial fibrillation, a higher rate of atrial pacing with a dual-chamber pacing mode and a long AV delay, a relatively fast lower rate, or both has recently been applied in clinical situations. Overdrive pacing over intrinsic atrial activity may reduce paroxysmal atrial fibrillation by affecting the pattern of atrial depolarization and suppressing premature atrial beats. However, an increase in the cumulative proportion of right apex ventricular pacing is associated with an increased risk of death and heart failure, most likely through ventricular desynchronization and hemodynamic deterioration [8]. It is difficult to prevent unnecessary right ventricular pacing in patients with a dual-chamber ICD with prolonged settings for the AV delay alone.

Thus, there are many possible clinical situations where RNRVAS might arise. In this case, atrial pacing prevented atrial fibrillation; hence, we maintained atrial pacing. However, AV-sequential and RNRVAS ventricular pacing led to hemodynamic instability and deterioration. To prevent unnecessary ventricular pacing, including RNRVAS with atrial pacing, the MVP mode was employed to provide the AAI or AAIR mode for monitoring AV conduction, and to provide an automatic switching to DDD or DDDR mode when the AV block persisted beyond a single dropped ventricular beat [4]. The MVP mode successfully addresses a high rate of atrial pacing and consequently prevents unnecessary ventricular pacing, including both RNRVAS and AV sequential pacing.

3 Conclusion

We believe that automatic switching between AAI and DDD can prevent RNRVAS and hemodynamic instability.

Conflict of interest

None.