Pacemaker Exit Block: An Unusual Cause of Ventricular Tachycardia

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EP LAB DIGEST. 2023;23(11):11,24-26.

Exit block occurs when an electrical impulse fails to depolarize nonrefractory adjacent myocardium and can occur in the context of myocardial pacemaker cells as well as implanted pacemakers.¹ In the context of implanted pacemaker or defibrillator leads, exit block can occur as a result of electrolyte abnormalities,² stereotactic radiation,³ or scar tissue at the myocardium-lead interface.

Ventricular tachycardia (VT) generally occurs because of abnormal automaticity, triggered activity, or reentry.⁴ While pacemaker-mediated VT has been documented in the setting of inappropriate timing of stimuli,⁵ there are no documented cases of pacemaker exit block-mediated VT through a triggered mechanism.

Herein we describe 2 patients with pacemaker exit block-mediated VT and subsequent management.

Case Presentation #1

A 77-year-old man with nonischemic cardiomyopathy (left ventricular [LVEF] ejection fraction of 36%-40%) and a cardiac resynchronization therapy-defibrillator (CRT-D) (Quadra Assura MP, Abbott, implanted in 2013 with a generator change in 2020) was referred for recurrent VT. Two weeks prior to referral, the patient was seen by his primary cardiologist, who noted increased LV lead capture threshold and subsequently increased the lead output (to 4.0V at 1 millisecond from electrode 1-2). LV lead sensing and impedance measurements were stable. Shortly thereafter, the patient began experiencing palpitations and lightheadedness. He sought hospital care, and device interrogation demonstrated dozens of episodes of monomorphic VT of approximately 150 beats per minute (bpm) each day. Echocardiography and coronary angiography demonstrated a reduced LVEF of 35% with no significant coronary artery disease. Amiodarone and mexiletine were administered, but his episodes of VT persisted (Figure 1).

At this point, the patient was transferred to our facility for consideration of electrophysiology (EP) study and ablation of VT. The patient was brought to the EP lab, and the authors elected to perform a combined epicardial/endocardial ablation due to the nonischemic etiology and delayed maximal deflection index of the clinical VT. The EnSite X mapping system (Abbott) was used. Since the patient was pacing dependent, the voltage maps were created during right ventricular (RV)-only pacing. Epicardial voltage mapping demonstrated overall healthy voltage in the epicardium, with a small area of low voltage posteriorly, and endocardial voltage mapping in the LV demonstrated overall healthy voltage. Intravenous isoproterenol infusion and standard provocative pacing maneuvers did not induce VT. However, with pacing from LV lead 1->2, his clinical VT was reproduced (Figure 2). Pacing from the LV lead 1->2 @ 4V for 1 millisecond induced the clinical VT (Figure 3). Endocardial and epicardial mapping of the clinical VT was then performed with the Advisor HD Grid Mapping Catheter, Sensor Enabled (Abbott). Activation mapping showed the earliest focal activation in the epicardial basal lateral left ventricle (Figure 4). This VT was not entrainable, suggesting a triggered mechanism. The corresponding epicardial voltage map during sinus rhythm showed relatively healthy voltage at 0.5 mV-1.5 mV in the location of the ablation lesions (Figure 5). The wave speed map shows a region of slower conduction velocity in the epicardial space (Figure 6). There are several regions of slow conduction on this map, suggesting that no one map can be interpreted in isolation—the data from one map needs to be correlated against the others to determine the appropriate lesion set. The electrogram of the earliest signal using the HD Grid was -44 ms pre-QRS (Figure 7). Epicardial VT usually has a broad slurring to the initial portion of the QRS, making annotation to the surface QRS challenging.

After pacing to ensure no phrenic stimulation and coronary angiography to confirm safe distance from the coronary arteries, a bidirectional TactiCath F-J SE catheter (Abbott) using half-normal saline as the irrigation solution was used to perform epicardial ablation in this region. Figure 8 shows an anterior-posterior fluoroscopy of the location of the ablation catheter at the earliest spot on the activation map in the epicardial space during an injection of the left main coronary artery, showing safe distance. The ablation catheter is between electrodes 1-2 of the LV lead in the middle cardiac vein. Maximum power was up to 40 watts and several consolidation lesions were performed. Following ablation, VT could not be induced despite provocative pacing maneuvers from the RV and LV leads with and without isoproterenol infusion. The patient’s LV lead was also reprogrammed from 1-2 to LV 4 to RV coil with a 45 ms LV first offset. The final paced electrocardiogram (ECG) morphology is shown in Figure 9.

He has had no further episodes of VT over the past 12 months despite being off antiarrhythmics.

Case Presentation #2

An 85-year-old man with apical hypertrophic cardiomyopathy (HCM) (LVEF 30%-35%), atrial fibrillation, and complete heart block, with prior dual-chamber pacemaker implantation in 2014 with a CRT-D upgrade in 2020 (Sprint Quattro ICD lead 6947, Medtronic, with prior RV pacing lead abandoned), was referred for recurrent episodes of monomorphic VT. Although device interrogation demonstrated normal capture thresholds and impedance, there were 37 episodes of VT requiring 1 shock and several rounds of anti-tachycardia pacing (all successful). The patient continued to have VT despite normal electrolytes and administration of amiodarone, so he was brought to the EP lab for potential ablation. LV and RV mapping demonstrated overall healthy bipolar voltage (Figure 10 and 11), and RV mapping demonstrated fractionated signals by the tip of the RV apex immediately adjacent to the prior RV pacing lead. A 12-lead ECG of the patient’s clinical VT is shown in Figure 12. An activation map of this VT showed earliest activation in the RV apex (Figure 13). Subsequent pace-mapping near the old pacing lead demonstrated an electrogram (EGM) that was 98% similar to his clinical VT (Figure 14). Pacing from this location also induced the patient’s clinical VT (Figure 15). Hence, endocardial RV ablation was performed with an irrigated bidirectional TactiCath F-J SE catheter. On intracardiac echocardiography, the ablation catheter was more apical to the septal insertion of the moderator band. Consolidation lesions were also placed across the septum from the LV apical septum (Figure 16). Pace-mapping and induction of VT with the electrogram of the earliest signal -56 ms pre-QRS from the His distal catheter positioned in the RV apex (Figure 17). This VT was not entrainable, suggesting a triggered mechanism.

At 2-month follow-up, the patient began experiencing further episodes of VT. At this point, his VT matched the morphology of QRS complexes when pacing from the LV lead only (Figure 18), but there were none from the RV apex. This suggested he was now having VT near the LV lead, but not from his RV apex.

Unfortunately, there was only one LV pacing vector that captured, and this was the same pacing vector (LV4-RV coil) that triggered VT. This extended bipolar pacing configuration may have contributed to stimulating a region of scar and triggering VT. LV pacing was then turned off (Figure 19) and the VT immediately resolved. He had an underlying narrow QRS but did not have good chronotropic competence, so was currently being RV-only paced. He has not had any recurrent VT over the past 10 months. Interestingly, this patient also had VT from his LV lead, suggesting that an abnormality with his myocardium predisposed him to having VT from pacing from 2 different leads.

Discussion

Pacemaker exit block is an increasingly rare but important complication of permanent pacing systems. It may present indolently and be heralded by slowly increasing threshold and changes in impedance, especially without antecedent trauma or lead fracture, and may ultimately result in the need for lead repositioning or replacement.⁶ This can be life-threatening if the patient is pacing dependent. Studies conducted with early lead design estimated the incidence at up to 7%,⁷ though the incidence is much lower with modern pacing leads.⁶ The mechanism of pacemaker exit block is generally due to scar tissue formation or calcium crystal deposition, and has been nearly eliminated with the use of steroid-eluting tips.⁷ In the cases described here, it is not clear what precipitated the exit block, although there is insufficient data in the literature on patient, operator technique, or lead-specific factors that may predict this complication. Indeed, prior work has suggested this complication to be rather unpredictable.⁷

In circumstances where exit block is precipitated by nonreversible circumstances, lead replacement is necessary if further pacing is required. To our knowledge, there are no studies reporting the initiation of tachycardia due to pacemaker exit block. In the first case, while the LV lead was fairly modern (2013), the subtle change in threshold suggested late scar tissue formation. As the output was increased to capture the surrounding myocardium, it is thought that abnormal tissue was captured and VT was initiated. After ablation, the patient was noninducible and we were able to make use of an alternate pacing vector, suggesting that initiation of the triggered VT was dependent not only on abnormal surrounding myocardium, but also a specific vector of impulse. In the second case, we surmise that abnormal myocardial architecture and fibrosis due to HCM as well as scar tissue from multiple closely spaced leads (in the setting of RV lead exit block, the initial VT) was substrate enough to lead to pacing-impulse-triggered exit block. If this is clinically suspected, one possible treatment may be to change the pacing vector to see if VT episodes are alleviated.

Conclusion

Pacemaker exit block is an unusual cause of VT and can be managed with optimization of device programming and ablation. 

Acknowledgment. The authors would like Kaitlin Kurth and the rest of the Abbott EnSite X mapping team for their crucial teamwork in performing these procedures and preparing several images for this publication.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Rao reports consulting fees from Medtronic, Abbott, and Biosense Webster.

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