Pitfalls of Dual‐Chamber Pacemakers in Identifying Tachycardia: An Under‐Recognized Programming Peril

A sexagenarian man with symptomatic sick sinus syndrome received a dual-chamber pacemaker (St. Jude Medical Endurity Core device) 2 years ago. He has complained of recurrent palpitations for the past 2 months. Device interrogation showed no events, and his electrocardiogram (ECG) displayed an ApVs rhythm without significant abnormalities. Key pacemaker settings included a DDDR mode and a lower rate of 60 bpm, with normal threshold and impedance (Table 1). There were no clues to sustained tachycardia based on the heart rate histograms (e.g., high proportion of elevated ventricular rates) during prior interrogations. Despite these findings, the patient has had repeated hospital visits for brief episodes of palpitations for around 15–20 min each, but no tachycardia has been documented on an ECG or 24-hour ambulatory ECG monitoring (during which he was asymptomatic). The confirmation of tachycardia through the use of wearable devices (e.g., KardiaMobile, smartwatches) could have been pursued. Following the non-detection of the arrhythmia, the necessity of an electrophysiology study (EPS) was comprehensively discussed, and the patient ultimately elected to proceed with the invasive EPS for reasons of financial constraints and overall cost-effectiveness. What are the possible tachycardias which may be missed by pacemakers?. An interrogation of the patient's pacemaker revealed six episodes of pacemaker-mediated tachycardia (PMT) without stored electrograms just before the procedure (likely due to the buffer limit which allows 2 min for two channels as the maximum storage time for this specific device and prioritization to add more important events). Despite this finding, we proceeded with an EPS. The study showed AH and HV intervals of 84 and 42 ms, respectively, during atrial pacing at a cycle length of 800 ms. During catheter positioning, manipulating the catheter induced a narrow-complex, short-VA tachycardia via an atrial premature complex with a possible AH jump (Figure 1A, B). The patient's device had a programmed AV delay that could extend up to 325 ms (225 ms without VIP), which meant an AH jump might be missed due to precocious ventricular pacing by the device, thus the induction of tachycardia. To address this, the device was reprogrammed to AAI mode. Subsequently, during atrial extra-stimulus pacing, a narrow-complex tachycardia was induced with an AH jump. The tachycardia cycle length (TCL) was 345 ms (173 bpm) (Figure 2A) and was easily inducible with both atrial burst and refractory pacing protocols. Ventricular entrainment maneuvers produced a long post-pacing interval (PPI) (PPI-TCL 133 ms) and a long SA-VA interval (87 ms) (Figure 2B). A His-synchronous ventricular extra-stimulus did not affect the tachycardia, which further supported the involvement of the AV node in the re-entrant circuit. Based on the presence of dual AV nodal physiology, the entrainment findings, and the short-VA tachycardia, we diagnosed the patient with typical atrioventricular nodal re-entrant tachycardia (AVNRT). A successful slow pathway ablation was performed, which completely eliminated the ability to induce tachycardia, even under aggressive pacing protocols and an isoprenaline challenge. A post-procedure EPS showed normal AH and HV intervals and an AV Wenckebach cycle length of 380 ms. The patient is doing well on follow-up, with no recurrence of symptoms. The clinical tachycardia was most likely an easily inducible AVNRT, but it was neither detected nor stored by the device. PMT was not marked as the device detected only Vs events at a high rate. A prerequisite for confirming a PMT is an AsVp rhythm [1]. The event wasn't stored as a VHR event since it was below the detection limit. Maximum tracking rate (MTR) or automatic mode switch (AMS) did not come into play because there were no atrial events during the tachycardia. The reasons for only ventricular sensing despite existing atrial activity are summarized in Table 2 and Figure 3. Supraventricular tachycardia/rhythm with Short RP Atrioventricular nodal reentrant tachycardia (AVNRT) Atrioventricular reciprocating tachycardia (AVRT) Junctional Ectopic tachycardia with 1:1 VA relation (JET) Junctional rhythm (above the rate of sensor driven corresponding VA interval) Signal-related undersensing Atrial undersensing due to low atrial potential These events are characterized by Vs events below the VHR rate, with the P wave falling within the post-ventricular atrial blanking period (PVAB). This can be due to near-simultaneous atrial and ventricular activation or a long PR interval that pushes the P wave into the PVAB of the preceding V. The next V event occurs before the expiration of the VA interval in dual-chamber pacing, causing the device to assume it is a run of PVCs. A previous case of possible AT or AVNRT was documented in a biventricular pacing device, which led to a loss of the resynchronization effect [2]. An additional point worth mentioning is that the device's Non-Invasive Programmed Stimulation (NIPS) could have been used to induce tachycardia before the invasive EPS, but its utility was precluded by several pitfalls: (i) Atrial NIPS includes ventricular backup pacing in VOO/ VVI mode for safety, the final paced beat of which may interfere with the evaluation of the AH jump during induction; (ii) a very prolonged slow pathway conduction time might require programming an AV delay (in DDD mode) that is insufficient or necessitate VVI mode with a low base rate; and (iii) while ventricular NIPS can assess retrograde conduction, it cannot discern the activation pattern, which is crucial because a patient with dual AV nodal physiology might have a different clinical tachycardia (e.g., mediated by a right-sided accessory pathway making it a short VA tachycardia) that is missed. These technical limitations prevented NIPS from definitively diagnosing the clinical tachycardia mechanism in our case, especially since its use has been predominantly confined to terminating atrial/ ventricular arrhythmias and inducing ventricular arrhythmias, making its application for evaluating SVT mechanisms rare. Continuous monitoring by CIEDs is a valuable complement to, but cannot replace, ambulatory ECG monitoring in suspected cases of short RP tachycardias. It is crucial to be aware of “V-on-A” tachycardias, which can be easily missed by dual-chamber devices. If a patient experiences recurrent symptoms despite optimal device programming for PMT, an EPS is warranted. The absence of stored episodes does not mean the absence of arrhythmia. Prior to an EPS, the device should be programmed to ODO or AAI (as feasible) or VVI with a low base rate (e.g., 30–40 bpm) to ensure accurate interpretation. Before moving to an invasive electrophysiology study without a documented tachycardia in a patient with an implanted device, a stepwise outpatient approach should be followed (Table 3): Adjust device settings to improve arrhythmia detection. –Lower the VHR detection rate or add a monitor-only zone. –Modify PVAB/PVARP settings as clinically appropriate. –Lowering VHR increases sensitivity but reduces specificity, causing excess alerts and possibly unwarranted EPS. —Increasing PVAB/PVARP prevents PMT but may cause exertional dyspnoea due to lowering the 2:1 track rate. –Reducing PVAB/PVARP may unmask atrial waves but heightens PMT risk –Dependent on the availability and compatibility of remote monitoring. –Limited effectiveness if patient engagement or compliance is poor. –Potential patient cost burden. –Variable recording quality and user adherence issues. –Difficult interpretation of the AH jump –Exact mechanism evaluation of tachycardia is virtually impossible In conclusion, this case presents an extremely rare documentation of AVNRT in a patient with a dual-chamber pacemaker. It was undetected by the device, and its diagnostic and therapeutic nuances were confirmed in the EP lab. Sudipta Mondal: conceptualization (equal); formal analysis (lead); writing – original draft (lead); writing – review and editing (lead). Nadeem Afroz Muslim: conceptualization (equal); formal analysis (lead); writing – original draft (lead); writing – review and editing (lead). The authors have nothing to report. Obtained from the patient in line with COPE guidance. The authors declare no conflicts of interest. No new data were generated or analyzed in support of this research.

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Pacing and Clinical Electrophysiology
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2026-01-19
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https://doi.org/10.1111/pace.70128
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Cardiovascular Syncope and Autonomic Disorders
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article

Pitfalls of Dual‐Chamber Pacemakers in Identifying Tachycardia: An Under‐Recognized Programming Peril

Nadeem Afroz Muslim, Sudipta Mondal
Pacing and Clinical Electrophysiology
Cardiovascular Syncope and Autonomic Disorders
article

Pitfalls of Dual‐Chamber Pacemakers in Identifying Tachycardia: An Under‐Recognized Programming Peril

Nadeem Afroz Muslim, Sudipta Mondal
article en

Abstract

A sexagenarian man with symptomatic sick sinus syndrome received a dual-chamber pacemaker (St. Jude Medical Endurity Core device) 2 years ago. He has complained of recurrent palpitations for the past 2 months. Device interrogation showed no events, and his electrocardiogram (ECG) displayed an ApVs rhythm without significant abnormalities. Key pacemaker settings included a DDDR mode and a lower rate of 60 bpm, with normal threshold and impedance (Table 1). There were no clues to sustained tachycardia based on the heart rate histograms (e.g., high proportion of elevated ventricular rates) during prior interrogations. Despite these findings, the patient has had repeated hospital visits for brief episodes of palpitations for around 15–20 min each, but no tachycardia has been documented on an ECG or 24-hour ambulatory ECG monitoring (during which he was asymptomatic). The confirmation of tachycardia through the use of wearable devices (e.g., KardiaMobile, smartwatches) could have been pursued. Following the non-detection of the arrhythmia, the necessity of an electrophysiology study (EPS) was comprehensively discussed, and the patient ultimately elected to proceed with the invasive EPS for reasons of financial constraints and overall cost-effectiveness. What are the possible tachycardias which may be missed by pacemakers?. An interrogation of the patient's pacemaker revealed six episodes of pacemaker-mediated tachycardia (PMT) without stored electrograms just before the procedure (likely due to the buffer limit which allows 2 min for two channels as the maximum storage time for this specific device and prioritization to add more important events). Despite this finding, we proceeded with an EPS. The study showed AH and HV intervals of 84 and 42 ms, respectively, during atrial pacing at a cycle length of 800 ms. During catheter positioning, manipulating the catheter induced a narrow-complex, short-VA tachycardia via an atrial premature complex with a possible AH jump (Figure 1A, B). The patient's device had a programmed AV delay that could extend up to 325 ms (225 ms without VIP), which meant an AH jump might be missed due to precocious ventricular pacing by the device, thus the induction of tachycardia. To address this, the device was reprogrammed to AAI mode. Subsequently, during atrial extra-stimulus pacing, a narrow-complex tachycardia was induced with an AH jump. The tachycardia cycle length (TCL) was 345 ms (173 bpm) (Figure 2A) and was easily inducible with both atrial burst and refractory pacing protocols. Ventricular entrainment maneuvers produced a long post-pacing interval (PPI) (PPI-TCL 133 ms) and a long SA-VA interval (87 ms) (Figure 2B). A His-synchronous ventricular extra-stimulus did not affect the tachycardia, which further supported the involvement of the AV node in the re-entrant circuit. Based on the presence of dual AV nodal physiology, the entrainment findings, and the short-VA tachycardia, we diagnosed the patient with typical atrioventricular nodal re-entrant tachycardia (AVNRT). A successful slow pathway ablation was performed, which completely eliminated the ability to induce tachycardia, even under aggressive pacing protocols and an isoprenaline challenge. A post-procedure EPS showed normal AH and HV intervals and an AV Wenckebach cycle length of 380 ms. The patient is doing well on follow-up, with no recurrence of symptoms. The clinical tachycardia was most likely an easily inducible AVNRT, but it was neither detected nor stored by the device. PMT was not marked as the device detected only Vs events at a high rate. A prerequisite for confirming a PMT is an AsVp rhythm [1]. The event wasn't stored as a VHR event since it was below the detection limit. Maximum tracking rate (MTR) or automatic mode switch (AMS) did not come into play because there were no atrial events during the tachycardia. The reasons for only ventricular sensing despite existing atrial activity are summarized in Table 2 and Figure 3. Supraventricular tachycardia/rhythm with Short RP Atrioventricular nodal reentrant tachycardia (AVNRT) Atrioventricular reciprocating tachycardia (AVRT) Junctional Ectopic tachycardia with 1:1 VA relation (JET) Junctional rhythm (above the rate of sensor driven corresponding VA interval) Signal-related undersensing Atrial undersensing due to low atrial potential These events are characterized by Vs events below the VHR rate, with the P wave falling within the post-ventricular atrial blanking period (PVAB). This can be due to near-simultaneous atrial and ventricular activation or a long PR interval that pushes the P wave into the PVAB of the preceding V. The next V event occurs before the expiration of the VA interval in dual-chamber pacing, causing the device to assume it is a run of PVCs. A previous case of possible AT or AVNRT was documented in a biventricular pacing device, which led to a loss of the resynchronization effect [2]. An additional point worth mentioning is that the device's Non-Invasive Programmed Stimulation (NIPS) could have been used to induce tachycardia before the invasive EPS, but its utility was precluded by several pitfalls: (i) Atrial NIPS includes ventricular backup pacing in VOO/ VVI mode for safety, the final paced beat of which may interfere with the evaluation of the AH jump during induction; (ii) a very prolonged slow pathway conduction time might require programming an AV delay (in DDD mode) that is insufficient or necessitate VVI mode with a low base rate; and (iii) while ventricular NIPS can assess retrograde conduction, it cannot discern the activation pattern, which is crucial because a patient with dual AV nodal physiology might have a different clinical tachycardia (e.g., mediated by a right-sided accessory pathway making it a short VA tachycardia) that is missed. These technical limitations prevented NIPS from definitively diagnosing the clinical tachycardia mechanism in our case, especially since its use has been predominantly confined to terminating atrial/ ventricular arrhythmias and inducing ventricular arrhythmias, making its application for evaluating SVT mechanisms rare. Continuous monitoring by CIEDs is a valuable complement to, but cannot replace, ambulatory ECG monitoring in suspected cases of short RP tachycardias. It is crucial to be aware of “V-on-A” tachycardias, which can be easily missed by dual-chamber devices. If a patient experiences recurrent symptoms despite optimal device programming for PMT, an EPS is warranted. The absence of stored episodes does not mean the absence of arrhythmia. Prior to an EPS, the device should be programmed to ODO or AAI (as feasible) or VVI with a low base rate (e.g., 30–40 bpm) to ensure accurate interpretation. Before moving to an invasive electrophysiology study without a documented tachycardia in a patient with an implanted device, a stepwise outpatient approach should be followed (Table 3): Adjust device settings to improve arrhythmia detection. –Lower the VHR detection rate or add a monitor-only zone. –Modify PVAB/PVARP settings as clinically appropriate. –Lowering VHR increases sensitivity but reduces specificity, causing excess alerts and possibly unwarranted EPS. —Increasing PVAB/PVARP prevents PMT but may cause exertional dyspnoea due to lowering the 2:1 track rate. –Reducing PVAB/PVARP may unmask atrial waves but heightens PMT risk –Dependent on the availability and compatibility of remote monitoring. –Limited effectiveness if patient engagement or compliance is poor. –Potential patient cost burden. –Variable recording quality and user adherence issues. –Difficult interpretation of the AH jump –Exact mechanism evaluation of tachycardia is virtually impossible In conclusion, this case presents an extremely rare documentation of AVNRT in a patient with a dual-chamber pacemaker. It was undetected by the device, and its diagnostic and therapeutic nuances were confirmed in the EP lab. Sudipta Mondal: conceptualization (equal); formal analysis (lead); writing – original draft (lead); writing – review and editing (lead). Nadeem Afroz Muslim: conceptualization (equal); formal analysis (lead); writing – original draft (lead); writing – review and editing (lead). The authors have nothing to report. Obtained from the patient in line with COPE guidance. The authors declare no conflicts of interest. No new data were generated or analyzed in support of this research.

Pacing and Clinical ElectrophysiologyVol. 49(3)
Mission Hospital Durgapur (IN)
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Cardiovascular Syncope and Autonomic Disorders
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