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  • Changing the pacemaker mode to VDD is a good

    2019-04-23

    Changing the pacemaker mode to VDD is a good approach in cases of normal sinus node function and loss of atrial lead capture, especially if atrial sensing is stable. In this case, Short AV delay is a good way to reduce the risk of R on T phenomenon which is theoretically possible if a ventricular ectopy is sensed by the atrial lead before the ventricular lead, which may cause inappropriate ventricular spiking after programmed AV delay. But as an AV delay optimization improves hemodynamics and clinical parameters in patients treated with a dual-chamber-pacemaker, if this short AV delay causes atrioventricular dyssynchrony, with a stable P-wave sensation by atrial lead, a DDD mode with an active ventricular safety pacing may be a better option for this case. It should be noted that ventricular safety pacing is not an option when the device is operating with VDD mode.
    Case history An 82-year-old frail woman with a prior history of hypertension, complete heart block, and dual permanent pacemaker (Sensia DR SEDR01, Medtronic Inc., Minneapolis, MN) presented to pacemaker clinic with symptoms of shortness of breath (SOB), dizziness, and “low pulse rate”. Pacemaker interrogation showed underlying normal sinus rhythm, sinus rate of around 74beats/min with atrial sensed events, and ventricular paced rhythm with frequent symptomatic premature ventricular complexes (PVC). Pacemaker parameters were DDD, lower rate limit (LRL) of 60beats/min, and maximum tracking rate of 120beats/min, along with paced/sensed AV delay of 300/250ms. Also noted was high pacing threshold of 3.5V at 1ms in the atrial lead with normal sensing parameters. In view of these, the pacemaker mode was reprogrammed to VDD mode and the patient was given beta-blocker therapy for frequent PVCs. She presented to arrhythmia clinic a few weeks later because of worsening SOB, light-headedness, and transient ischemic attack-like symptoms. Electrocardiography (ECG) performed in the clinic showed ventricular paced rhythm with retrograde P waves (Fig. 1). What was the underlying arrhythmia mechanism? What treatment options are available?
    Discussion This case highlights the importance of understanding different modes of pacemaker modes and its role in different patient populations. In our patient, ECG revealed retrograde atrial depolarizations that were occurring in the post-ventricular atrial refractory (PVAR) period, and therefore were not tracked in the VDD mode. With no subsequent atrial pacing, tracking of the subsequent ventricular beat requires a sinus beat prior to timing out of ventricular escape SB 431542 length of 1000ms, which was suppressed by beta-blockers. Based on physiological and ECG findings, this condition is similar to repetitive non-reentrant ventricular atrial synchrony (RNRVAS), with both of these conditions leading to ventricular pacing at a LRL with retrograde p waves falling during PVAR period and therefore not tracked (functional undersensing) [1]. Both of these conditions can result in palpitations, typical pacemaker syndrome symptoms, congestive heart failure, light-headedness, and possibly syncope. RNRVAS is, however, observed in DDD mode with lack of atrial capture with subsequent atrial pacing due to refractoriness of atrial myocardium due to prior retrograde atrial depolarization (functional non-capture). As atrial sensed events during the PVAR period do not reset the atrial pacing interval and both atrial senses and atrial paced events are counted toward mode switching, these patients may have pseudo-mode switch episodes on pacemaker interrogation. Fig. 2 illustrates an example of RNRVAS in our patient in DDD mode that was triggered by lack of atrial capture (subthreshold output) with underlying high pacing thresholds. There are few options to resolve this pacemaker-induced arrhythmia in our patient. The most obvious would be right atrial lead revision and reprogramming the device back to the DDD mode. However, this may still result in RNRVAS triggered by PVC. In addition, in an elderly, frail woman with significant kyphosis and other comorbidities, surgical option was not favored. Shortening of the PVAR period is another consideration but would have led to pacemaker-mediated tachycardia. While stopping beta-blocker therapy may help, it would worsen the PVC. We changed the pacemaker mode to DDD, accepting high thresholds, but decreased the base rate to 50beats/min and shortened the AV delay to 150/180ms in the sensed/paced configuration. With lowering of the base rate, atrial pacing would be minimized to preserve battery life. Moreover, decreasing basal rate and shortening of the AV interval would provide longer time for atrial repolarization and would either allow return of sinus activity and/or ensure atrial capture with the subsequent atrial pacing. Finally, noncompetitive atrial pacing (NCAP) was turned on to prevent atrial pacing with atrial sensed events in refractory in order to prevent RNRVAS. A repeat ECG after these programmings revealed a normal sinus rhythm, with a sinus rate of 56beats/min and normal tracking of sinus beats. During follow-up, the patient had complete resolution of her symptoms without requiring lead revision.