Pacing Below the Programmed Rate

A 75-year-old male with a history of interstitial lung disease, chronic kidney disease, and hyperlipidemia presented with dyspnea, weakness, and hypotension. ECG demonstrated sinus rhythm with complete heart block and a ventricular escape rhythm at 40 bpm. He underwent placement of a permanent dual-chamber pacemaker with active fixation leads in the right atrium and right ventricular septum (Medtronic, Minneapolis, MN, USA). The device was programmed DDD 60–130 bpm, with sensed and paced AV intervals of 150 and 180 ms, respectively, and post-ventricular atrial refractory period (PVARP) of 320 ms. In the recovery unit, an ECG was obtained due to a low heart rate (Figure 1A). The ECG obtained immediately post procedure is also shown (Figure 1B). What is the diagnosis? What other findings do the ECGs demonstrate? Why was sinus rhythm suppressed on the first ECG? The first ECG (Figure 1A) demonstrates AV pacing at 44 bpm (1360 ms) except for the fifth complex which occurs early due to an appropriately sensed and tracked spontaneous P wave. With a lower rate of 60 bpm (1000 ms) and an AV interval of 180 ms, the VA interval is 820 ms (i.e., atrial-pacing should occur 820 ms following a sensed or paced ventricular complex if no intrinsic atrial activity is sensed). Tracing back 820 ms from an atrial paced event (Figure 2A), it becomes obvious that the T-wave is over-sensed by the ventricular lead, which resets the VA interval, thereby lengthening the effective pacing interval. The post-procedure ECG (Figure 1B) reveals P-wave synchronous ventricular pacing except for one AV-paced complex. Tracing back from this atrial-paced event, T-wave oversensing (TWOS) is evident here too (Figure 2B). However, the effect of TWOS (decrease in effective atrial pacing rate) is not manifested in the rest of this tracing because spontaneous atrial activity is sensed and tracked. Closer inspection of the first ECG reveals ectopic atrial activity throughout the tracing mostly at a cycle length of 1300 ms, at a varying coupling interval to atrial paced events, unaffected by atrial pacing (Figure 2A). One inter-ectopic interval is 2600 ms, twice the cycle length of the other ectopic beats. This is therefore an atrial parasystole. A parasystole is an ectopic focus that is protected from incoming impulses (entrance block) and therefore fires at its inherent rate. If the surrounding myocardium is refractory, some of these outgoing impulses might encounter exit block. Therefore, the inter-ectopic intervals are multiples of each other. Atrial parasytolic activity can also be observed in the second tracing, at a slightly longer cycle length of 1540 ms, with one inter-ectopic interval being three times this cycle length (Figure 2B). In the first tracing, most parasystolic activity falls within the extended PVARP. The PVARP is also reset by TWOS and is not tracked, which mandates atrial pacing when the VA interval times out. The combination of atrial pacing and fortuitously timed atrial parasytolic activity suppresses sinus rhythm except when atrial refractoriness prevents capture of the parasytolic focus, thereby allowing sinus rhythm to escape (Figure 2A). In the second tracing, most tracked P waves are sinus in origin, while others are from the parasystolic atrial focus or from fusion between the two. Sinus rhythm is suppressed only for one beat when the parasytolic activity falls within the PVARP (Figure 2B). Device electrograms confirmed TWOS and atrial parasytolic activity (Figure 3A). The ventricular sensitivity was decreased from 0.9 to 2.0 mV, which resolved TWOS. The final ECG reveals a combination of atrial pacing, sinus rhythm and atrial parasytole with no evidence of TWOS (Figure 3B). We present an unusual case of interaction between an atrial parasystole and the timing periods of a dual chamber pacemaker extended by TWOS, resulting in intermittent suppression of sinus rhythm. Parasystole is a rare phenomenon that is generally considered benign, but has recently renewed interest with possible links to progressive conduction system abnormalities including ventricular fibrillation [1, 2]. A high index of suspicion is required to diagnose parasystole, particularly when overdrive suppression is not occurring as expected. D.S.: concept/design, data analysis/interpretation, drafting article, critical revision, data collection. J.P.E.: concept/design, data analysis/interpretation, critical revision. V.P.: concept/design, data analysis/interpretation, critical revision, data collection. H.D.: concept/design, data analysis/interpretation, drafting article, critical revision, data collection. The authors have no relevant conflicts of interest or financial disclosures. Patient consent was obtained for publication of this manuscript. The data that support the findings of this study are available from the corresponding author upon reasonable request.

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Journal
Pacing and Clinical Electrophysiology
Published
2025-02-10
DOI
https://doi.org/10.1111/pace.15163
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Network Time Synchronization Technologies
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article

Pacing Below the Programmed Rate

Jacob Elrod, Vibhu Parcha, Danial Saleem, Harish Doppalapudi
Pacing and Clinical Electrophysiology
Network Time Synchronization Technologies
article

Pacing Below the Programmed Rate

Jacob Elrod, Vibhu Parcha, Danial Saleem, Harish Doppalapudi
article en

Abstract

A 75-year-old male with a history of interstitial lung disease, chronic kidney disease, and hyperlipidemia presented with dyspnea, weakness, and hypotension. ECG demonstrated sinus rhythm with complete heart block and a ventricular escape rhythm at 40 bpm. He underwent placement of a permanent dual-chamber pacemaker with active fixation leads in the right atrium and right ventricular septum (Medtronic, Minneapolis, MN, USA). The device was programmed DDD 60–130 bpm, with sensed and paced AV intervals of 150 and 180 ms, respectively, and post-ventricular atrial refractory period (PVARP) of 320 ms. In the recovery unit, an ECG was obtained due to a low heart rate (Figure 1A). The ECG obtained immediately post procedure is also shown (Figure 1B). What is the diagnosis? What other findings do the ECGs demonstrate? Why was sinus rhythm suppressed on the first ECG? The first ECG (Figure 1A) demonstrates AV pacing at 44 bpm (1360 ms) except for the fifth complex which occurs early due to an appropriately sensed and tracked spontaneous P wave. With a lower rate of 60 bpm (1000 ms) and an AV interval of 180 ms, the VA interval is 820 ms (i.e., atrial-pacing should occur 820 ms following a sensed or paced ventricular complex if no intrinsic atrial activity is sensed). Tracing back 820 ms from an atrial paced event (Figure 2A), it becomes obvious that the T-wave is over-sensed by the ventricular lead, which resets the VA interval, thereby lengthening the effective pacing interval. The post-procedure ECG (Figure 1B) reveals P-wave synchronous ventricular pacing except for one AV-paced complex. Tracing back from this atrial-paced event, T-wave oversensing (TWOS) is evident here too (Figure 2B). However, the effect of TWOS (decrease in effective atrial pacing rate) is not manifested in the rest of this tracing because spontaneous atrial activity is sensed and tracked. Closer inspection of the first ECG reveals ectopic atrial activity throughout the tracing mostly at a cycle length of 1300 ms, at a varying coupling interval to atrial paced events, unaffected by atrial pacing (Figure 2A). One inter-ectopic interval is 2600 ms, twice the cycle length of the other ectopic beats. This is therefore an atrial parasystole. A parasystole is an ectopic focus that is protected from incoming impulses (entrance block) and therefore fires at its inherent rate. If the surrounding myocardium is refractory, some of these outgoing impulses might encounter exit block. Therefore, the inter-ectopic intervals are multiples of each other. Atrial parasytolic activity can also be observed in the second tracing, at a slightly longer cycle length of 1540 ms, with one inter-ectopic interval being three times this cycle length (Figure 2B). In the first tracing, most parasystolic activity falls within the extended PVARP. The PVARP is also reset by TWOS and is not tracked, which mandates atrial pacing when the VA interval times out. The combination of atrial pacing and fortuitously timed atrial parasytolic activity suppresses sinus rhythm except when atrial refractoriness prevents capture of the parasytolic focus, thereby allowing sinus rhythm to escape (Figure 2A). In the second tracing, most tracked P waves are sinus in origin, while others are from the parasystolic atrial focus or from fusion between the two. Sinus rhythm is suppressed only for one beat when the parasytolic activity falls within the PVARP (Figure 2B). Device electrograms confirmed TWOS and atrial parasytolic activity (Figure 3A). The ventricular sensitivity was decreased from 0.9 to 2.0 mV, which resolved TWOS. The final ECG reveals a combination of atrial pacing, sinus rhythm and atrial parasytole with no evidence of TWOS (Figure 3B). We present an unusual case of interaction between an atrial parasystole and the timing periods of a dual chamber pacemaker extended by TWOS, resulting in intermittent suppression of sinus rhythm. Parasystole is a rare phenomenon that is generally considered benign, but has recently renewed interest with possible links to progressive conduction system abnormalities including ventricular fibrillation [1, 2]. A high index of suspicion is required to diagnose parasystole, particularly when overdrive suppression is not occurring as expected. D.S.: concept/design, data analysis/interpretation, drafting article, critical revision, data collection. J.P.E.: concept/design, data analysis/interpretation, critical revision. V.P.: concept/design, data analysis/interpretation, critical revision, data collection. H.D.: concept/design, data analysis/interpretation, drafting article, critical revision, data collection. The authors have no relevant conflicts of interest or financial disclosures. Patient consent was obtained for publication of this manuscript. The data that support the findings of this study are available from the corresponding author upon reasonable request.

Pacing and Clinical ElectrophysiologyVol. 48(3)
University of Alabama at Birmingham (US)
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