Dual chamber pacing systems utilize different timing cycles to provide pacing support
and coordination of atrioventricular synchrony. At times, this can result in unexpected
pacing behavior. This case illustrates one such example.
A 64-year-old man with a history of nonischemic cardiomyopathy received a St. Jude
Medical (Sylmar, CA) dual-chamber implantable cardioverter-defibrillator (ICD) in
2011. He had sick sinus syndrome with intact atrioventricular (AV) conduction. He
was recently admitted to the hospital for treatment of pneumonia. His ICD was programmed
to DDI pacing at 90 beats per minute (bpm) with a paced AV interval of 350 milliseconds.
While on telemetry, the patient was noted to have nonsustained episodes of pacing-associated
tachycardia at a rate of approximately 150 bpm. His ICD was interrogated and found
to be functioning normally. Because a ventricular tachycardia monitor zone was programmed
to 130 bpm, data from the tachycardia episode were stored. Review of the data revealed
atrial pacing at a rate of approximately 150 bpm. What could be causing the device
to pace at a rate faster than what was programmed?
Dual-chamber pacing requires the coordination of timing cycles from both the atrium
and the ventricle. Hence, a given pacing mode (eg, DDD, DDI, managed ventricular pacing)
can operate predominantly based on atrial- or ventricular-based timing intervals.
Whereas managed ventricular pacing and DDD pacing modes rely on modified atrial-based
algorithms, DDI pacing mode uses ventricular-based timing cycles.
Hence, the cycle length between 2 atrial paced events is dictated not on the A-A interval
but on the V-A interval. This feature is illustrated in Figure 1. The device was programmed
to DDI 90 (approximately 662 milliseconds) with a programmed paced AV delay of 350
milliseconds. Hence, the calculated VA interval = 662 milliseconds −350 milliseconds,
or 312 milliseconds. Rather than an AP-AP interval of 662 milliseconds, an interval
of 609 milliseconds was observed, because the intrinsic conduction through the AV
node was 297 milliseconds. With a fixed V-A interval of 312 milliseconds, this resulted
in the next AP event to occur earlier, so that the AP-AP interval = 297 milliseconds
+312 milliseconds, or 609 milliseconds.
The nature of the ventricular-based timing cycle is also the reason for the episode
of pacing-induced tachycardia. At the initiation of the tachycardia in Figure 2A,
3 premature atrial complexes (PACs) are noted (red asterisks). The first PAC conducts
down the AV node after 230 milliseconds. The second PAC falls in the postventricular
atrial refractory period of the conducted ventricular sensed (VS) event (no AS marker)
and conducts down the AV node with more decrement. Because the second PAC fell in
the postventricular atrial refractory period, the device delivers an AP event (†)
312 milliseconds after the VS event resulting from the first PAC. Coincidentally,
this AP event (†) occurs 98 milliseconds prior to the VS event resulting from the
second PAC (which is outside of the device’s postatrial ventricular blanking [PAVB]
period of 65 milliseconds). Given the ventricular-based timing cycle, the device then
delivers the next AP event (‡) 312 milliseconds after the VS event resulting from
the second PAC. A third PAC then occurs, which also results in conduction down the
AV node. The VS event resulting from the third PAC occurs 78 milliseconds after the
AP event (‡) and triggers the next AP event (§) to occur 312 milliseconds afterward.
The AP event (‡) conducts down the AV node at a timing interval that allows for the
VS to occur just outside the PAVB and perpetuates the tachycardia as seen. Toward
the end of the tachycardia, there are greater degrees of decremental conduction through
the AV node such that the second-to-last AP event (red ↓) blocks in the AV node and
allows the device to return to pacing at slower rates. This phenomenon was also nicely
illustrated in the telemetry recordings obtained at the bedside (Figure 2B).
DDI is a ventricular-based pacing mode and the cycle length between 2 atrially paced
events is dictated by the V-A interval.
With greater emphasis on minimizing right ventricular pacing, the programmed paced
AV delay is often lengthened, thus resulting in a shorter V-A interval. When intrinsic
conduction times through the AV node are faster than the programmed paced AV delay,
the lower rate of pacing (ie, cycle length between 2 AP events) is necessarily faster
than what is programmed. In this example, the VS events resulting from the 3 fortuitously
timed PACs managed to occur just outside the PAVB of the preceding AP event, thus
resulting in a form of “pacemaker-mediated tachycardia”. Unlike traditional pacemaker-mediated
tachycardia (also known as “repetitive reentrant ventriculoatrial synchrony”
), where tachycardia is mediated by ventricular pacing in response to atrial sensed
events, the tachycardia in this example is mediated by atrial pacing in response to
VS events. Hence, we have termed this phenomenon “repetitive reentrant atrioventricular
synchrony”. In an effort to reduce the likelihood of this event, we reprogrammed the
device to an atrially based pacing mode (eg, DDD). Other possible solutions to reduce
the likelihood of repetitive reentrant atrioventricular synchrony include lengthening
the PAVB interval (not available in this device), reducing the lower pacing rate and
shortening the programmed paced AV interval.