Abstract
Background
Delayed lead perforation is a rare complication of cardiac implantable electronic device (CIED). Clinical presentations range from completely asymptomatic to pericardial tamponade. Surgical lead extraction is recommended and transvenous lead extraction (TLE) with surgical backup is an alternative method.
Case presentation
A male with paroxysmal atrial fibrillation and sick sinus syndrome implanted a dual-chamber pacemaker with two passive fixation lead. He was on oral anticoagulants and played golf for almost 1 h every day after implantation. However, he complained of thoracic stabbing in the sternal manubrium with abnormal findings on pacemaker interrogation. Imaging confirmed the perforated atrial electrode with lead tip protrusion from the pericardium adjacent to the inferior wall of the main right pulmonary artery, but without pericardial effusion. Lead removal by TLE with surgical support was suggested, but he refused. Given the stable conditions, conservative treatment was chosen in the absence of complications during a follow-up period of 14 years. Then ventricular lead failure and battery depletion appeared and a leadless pacemaker was implanted.
Conclusions
Chest pain in CIED with abnormal electrical parameters, especially ongoing treatment with anticoagulants and regular physical activity, should always raise suspicion of lead perforation. A conservative strategy may be appropriate and feasible for those in the absence of perforation-related complications. For patients with noninfectious abandoned leads and battery depletion after CIED, leadless pacemaker may be an alternative approach according to patient and provider preferences.
Keywords: Lead perforation, Leadless pacemaker, Conservative approach, Battery depletion, Case report
Background
Lead perforation is a rare complication of cardiac implantable electronic device (CIED) with a median prevalence of 0.4% [1], which is more often affected by right ventricular lead than atrial lead [2]. Delayed lead perforation, defined as longer than 30 days, is highly variable in presentation, ranging from completely asymptomatic to pericardial tamponade [3]. Management of lead perforation includes conservative or lead extraction based on the symptoms and life-threatening complications. Surgical lead extraction is recommended by expert consensus [4], and transvenous lead extraction (TLE) with surgical backup is an alternative method [5, 6]. Here we report on a male patient with atrial lead perforation that occurred 10 months after a dual-chamber implantation without severe complications. After battery depletion, he preferred conservative treatment and had a leadless pacemaker implanted, with the entire time span being 16 years.
Case presentation
A 59-year-old man complained of palpitations due to paroxysmal atrial fibrillation (PaAF) and underwent radiofrequency catheter ablation on Aug. 23, 2001. He was readmitted to hospital, presented with dizziness, syncope, and intermittent palpitations, and was diagnosed with sick sinus syndrome and PaAF on Oct. 21, 2007. Several episodes of syncope were reappeared while electrocardiographic monitoring showed sinus pauses (6.08 s). A temporary pacemaker was implanted in the right ventricular apex on the second day. Owing to PaAF, the patient was on oral anticoagulants (warfarin 3.125 mg once/day), which had been stopped 24 h before implantation. A dual-chamber pacemaker (a tined J-shaped atrial lead, St. Jude Medical, 1642T/52 cm; a tined ventricular lead, St. Jude Medical, 1646T/58 cm; generator, Verity ADx XL DR 5356; St. Jude Medical, Sylmar, America) was implanted in Oct. 30, 2007. Atrial lead was fixed passively in the anterolateral right atrial appendage (RAA), and ventricular lead was fixed in the apical right ventricle (RV) (Fig. 1A, Jan. 2, 2008). The pacemaker was assigned to pacing programmed to a base rate of 60 bpm and rate-adaptive pacing (DDDR-60), with both lead parameters within the normal range (Fig. 2A).
Fig. 1.
Imaging changes showing atrial lead perforation. (A and B) Chest x-ray 6 days and 10 months after the implant, showing no displacement of the leads. (C to F) Coronary computed tomography angiography showed atrial lead perforation; the broken circles indicate the lead tip protruding from the pericardium adjacent to the inferior wall of the main right pulmonary artery (pentagrams). (G and H) Fluoroscopic images of the lead and leadless pacemaker
Fig. 2.
Temporal changes in lead parameters. (A) Leads parameters. (B) Pacing ratio
Six months after implantation, the patient played golf for almost 1 h every day and swam occasionally. However, he suddenly complained of thoracic stabbing in the sternal manubrium. The measurements showed significant worsening of atrial lead impedance of more than 2,500 Ω (Fig. 2A) on Aug. 8, 2008, which was 10 months after implantation and 4 months after golf. Atrial pacing failure was also observed occasionally. Chest x-rays (CXR) indicated no obvious lead perforation or fracture (Fig. 1B). Then, atrial impedance gradually decreased to 780 Ω, but the threshold increased to 4.5 V/ 0.4 ms (Fig. 2A). Transthoracic echocardiography (TTE) ruled out pericardial effusion. In consideration of CXR excluding lead perforation and fracture, device interrogation excluding battery depletion, and impedance reducing to the normal range, the elevated threshold might be associated with atrial fibrosis at the insertion site because of PaAF. The pacemaker was programmed to a base rate of 45 bpm to reduce energy waste. The patient responded well to analgesic therapy. Relieved symptoms and normal pacing resulted in patient discharge. During follow-up from Sep. to Dec. 2008, the atrial lead threshold fluctuated between 2.75 V/0.4 ms and 3.75 V/0.4 ms (Fig. 2A), and percent atrial pacing between 7% and 22% (Fig. 2B).
However, he complained of recurrent chest pain on Jan. 6, 2009. Pericardial effusion was still absent and atrial lead threshold was still 3.75 V/0.4 ms. Owing to the long-term golf and symptom characteristics, lead perforation was suspected. Three-dimensional (3D) reconstruction of coronary computed tomography angiography (CCTA) confirmed the perforated atrial electrode with lead tip protrusion from the pericardium adjacent to the inferior wall of the main right pulmonary artery (MRPA), but without pericardial effusion and no contrast extravasation seen (Fig. 1C and F). He was hemodynamically stable, and chest pain was alleviated when the pacing mode changed to VVI with a base rate of 45 bpm. Lead removal by TLE with surgical support was suggested, but the patient refused. In view of his stable clinical status and the absence of any mechanical complications, we advised vigilant and close follow-up for anything. The patient was discharged with a plan for interval TEE to monitor pericardial effusion and device interrogations. During follow-up, PaAF became more frequent and evolved into persistent AF in April 2013. CCTA was repeated in Aug. 2013 and Aug. 2023, respectively, and there was no migration in the position of the lead tip.
Device interrogation found decreasing impedance (290–310 Ω) and increasing threshold (2.75 V/0.8 ms) of ventricular lead (Fig. 2) from Sep. 27, 2022 and battery depletion on Aug. 15, 2023. In consideration of ventricular lead dwell time more than 15 years, low ventricular pacing burden (12–16%), and the patient’s preferences, a leadless pacemaker (MC1AVR1, Medtronic, America) was implanted at the right ventricular septum on Sep. 14, 2023 (Fig. 1G and H). The pacing mode was programmed to a base rate of 50 bpm and VVI with a ventricular threshold of 0.25 V/0.24 ms, sensitivity of 11.3 mV, and impedance of 740 Ω. One month after the procedure, it showed a threshold of 0.13 V/ 0.24 ms, impedance of 830 Ω, and pacing burden of 11%. The patient was doing very well 3 months after the last hospital discharge. Figure 3 shows a timeline of the case.
Fig. 3.
Timeline of the case
Discussion
To the best of our knowledge, this is the first report of a very late occurrence of a passive atrial lead perforation managed by a conservative approach and followed up for 16 years without complications. A leadless pacemaker was implanted after battery depletion and ventricular lead aging.
Delayed lead perforation is defined as such when it occurs after 30 days and exhibits considerable variability in clinical presentation. Chest pain was the most frequent symptom for delayed perforation, which was typically pleuritic, localized, sharp, or electrical, sometimes with a pulsatile component, including positional or respiratory variability [7]. Additionally, significant lead parameter changes are associated with definite lead perforation [5, 8, 9]. The patient complained of chest pain, and abnormal electrical parameters should be treated with a high index of suspicion for perforation. However, TTE and CXR showed no abnormalities related to the CIED or pericardial effusion. Temporary improvement in symptoms and electrical parameters led to the ignorance of perforation. Therefore, further examinations, such as CT, were not performed on the patient.
Recent studies have established CT as the modality of choice for diagnosing lead perforation with good inter-observer agreement [5, 10] of 97% sensitivity [7]. A retrospective study showed the accuracies of CXR, TTE, and electrocardiography–gated contrast-enhanced cardiac CT imaging for the diagnosis of lead perforation were 73.1%, 82.7%, and 98.1%, respectively [10]. In this case, CT is useful for documenting lead position and assessing lead perforation, whereas the artifacts at the tip of the lesion could make assessment of surrounding tissues difficult. However, cardiac contrast CT provided 3D images and clearly showed the lead tip protrusion from pericardium adjacent to the inferior wall of MRPA in the absence of vascular injury, a tamponade, or hemothorax. Therefore, cardiac contrast CT is considered to be more accurate than CT in confirming lead perforation.
The patient had three major risk factors for lead perforation: a history of temporary pacing, anticoagulant use, and regular physical activity, but other risk factors (active fixation lead, female sex, older age, steroid therapy, body mass index of < 20 kg/m2, lead long procedure times, and infections) were absent [11, 12]. The main reason for perforation may be repeated golf swing, because the lead perforated four months after repeated identical swing action. The understanding of the specific mechanism of perforation remains unclear. The action resulted in the electrode being pulled repeatedly, increasing tension, which might have created a strong force per unit area [13] toward the atrial wall, leading to lead perforation.
The mechanisms responsible for delayed lead perforation have been proposed as a gradual process in which the combination of contracting myocardium, reactive fibrosis, and the lead itself are thought to “self-seal” the heart and the investing visceral pericardium, thereby limiting rapid fluid accumulation and the size of the resulting effusion [3, 11]. Our patient had markedly high impedance, an increase in capture threshold, and then impedance decreased to normal, with a higher threshold value compared to the early postoperative threshold. Impedance may vary depending on the tissue components around the lead tip, such as muscle, blood (decreased), and air (e.g., lung, pericardial space, and increased) [14]. The atrial lead tip gradually protruded from RAA to near the inferior wall of MRPA and still in the pericardium, and did not penetrate the artery. The tip was then adhered to thrombo-fibrotic lead encapsulations [15] and surrounding myocardium or tissues. Therefore, the process of perforation corresponded to changes in electrical parameters.
The management of lead perforation includes conservative, surgical, and TLE, depending on patient’s symptoms, hemodynamic status, and presence of any significant pericardial or pleural effusion, although lead extraction is usually mandated [16, 17]. Surgical removal is usually considered the preferred strategy [11], but removal by traction under fluoroscopic guidance has also shown to be safe and effective [6, 9]. However, a lack of conservative management in part relates to the criteria used for case identification and the definitions chosen for clinically significant cardiac perforation [7]. Cases where a conservative strategy may be appropriate include those in the absence of perforation-related pain, bleeding, malfunction, or in which perforation-related symptoms have resolved without significant pericardial effusion, or in which perforations were detected incidentally by CT [7, 17]. In most instances, it has been suggested that conservative treatment without removal of right atrial lead is a viable option for treatment, especially for microdislodgement. When planning a conservative strategy, patient preferences must be considered through an open discussion regarding the potential future risk of complications requiring re-intervention versus the upfront risks of lead revision [7]. Some studies reported that anticoagulation status was associated with pericardial tamponade [7, 18]. Although anticoagulant use of the patient, the lead tip did not penetrate into the artery without tamponade. Regarding the patient preference, chest pain diminished after the mode changed, ventricular pacing parameters were stable, and a conservative approach was finally administered. During a follow-up period of nearly 16 years, perforation-related symptoms or pericardial effusion were always absent.
Lead failure is increasingly common over time, with reported failure rates of 7–16% at 8 ∼ 10 years [19]. Lead dwell time more than 10 years with impedance and threshold changed, excluding microdislodgement, lead aging should be considered. It is challenging to quantify the risks and benefits of cap and abandon noninfectious leads versus extract noninfectious leads [20]. The benefits include removal of unnecessary hardware that might be harder to remove in the future for a mandatory extraction indication such as infection, chronic pain secondary to the lead insertion site, or facilitate access to magnetic resonance imaging [17]. Several small studies reported no difference in rates of complications between extracting versus abandoning leads [21, 22]. However, a large study found lead extraction was associated with lower adjusted 5-year infection rates compared with a cap and abandon strategy in noninfectious indications [20]. Lead dwell time is a strong predictor of procedural success and complications during TLE procedures [23, 24]. Recently, a study found TLE of very long dwell time (VLDT) (≥ 15 years) leads had a lower procedural and clinical success and a higher complication rate than TLE of leads with a shorter dwell time [25]. However, another larger study demonstrated that TLE with very old leads (≥ 10 years) was safe and feasible at experienced specialized centers [26]. In addition to atrial lead perforation, ventricular lead failure and battery depletion appeared after 16 years. Removing the old and reimplanting a new CIED maybe a feasible and conventional approach. Considering the two existed noninfectious leads, lead perforation, quantifying risks and benefits of TLE and patient preference, a leadless pacemaker was implanted ultimately.
Conclusions
Herein, we describe the first case of leadless pacemaker implantation after delayed atrial lead perforation, subsequently ventricular lead malfunction and battery depletion. In view of lead perforation, conservative treatment was chosen in the absence of complications during a follow-up period of 16 years. A conservative strategy may be appropriate and feasible for those in the absence of perforation-related complications. For patients with noninfectious abandoned leads and battery depletion after CIED, leadless pacemaker may be an alternative approach according to patient and provider preferences.
Acknowledgements
Not applicable.
Author contributions
Liu JQ and Chen FF interpreted the patient data and wrote the manscript. Zhao YC and Su LP collected and analyzed the clinic data. Wang H performed the imaging examination. Gao YC collated the pacemaker data and Luan C draw Fig. 2. All authors read and approved the final manuscript.
Funding
This work was supported by the National Natural Science Foundation of China (81700301), Scientific Research Foundation of Education Department of Liaoning Province (LZ2020058), Liaoning Revitalization Talents Program (XLYC2203195) and Scientific Research Project of Dalian Medical Key Specialty “Climbing Peak Plan” (2022DF016).
Data availability
No datasets were generated or analysed during the current study.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.
Competing interests
The authors declare no competing interests.
Clinical trial number
Not applicable.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Yichang Zhao and Liping Su are co-first authors.
Contributor Information
Jinqiu Liu, Email: 18098875755@163.com.
Feifei Chen, Email: sdaqchenfei@126.com.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
No datasets were generated or analysed during the current study.