ABSTRACT
Introduction
Leadless pacemakers are typically implanted in the mid‐septum of the right ventricle (RV) to mitigate the risk of perforation. However, reports on the precise location of these implants are limited. This study aimed to elucidate tine‐based leadless pacemaker position and presence of subclinical RV perforation through computed tomography (CT) imaging, along with the associated prognosis.
Methods
Patients who underwent heart, chest or abdomen CT after leadless pacemaker implantation were consecutively included. Two cardiologists and one radiologist reviewed the CT images to assess the position of tines and to detect RV perforation. The implantation position was categorized as the septum, RV free wall, junction of septum and RV free wall, moderator band, and RV apex. Subclinical perforation was defined as the tines of a leadless pacemaker beyond the outer myocardial contour without symptoms, pericardial effusion, hemodynamic instability, or pacemaker malfunction.
Results
A total of 88 patients (age, 72.9 ± 12.1 years; 42 males) were included. The interval between procedure and CT scanning was 8.6 ± 9.2 months. In 68 patients (77.3%), the leadless pacemaker was implanted at the junction of the septum and the RV free wall. Subclinical RV perforation occurred in 15 patients (17.0%). Among patients with RV perforation, the most common implantation site was the junction of the septum and the RV free wall. None of the patients with RV perforation experienced any adverse events for 12.4 ± 12.3 months.
Conclusions
The most common leadless pacemaker implantation site is the junction of the septum and the RV free wall. Subclinical RV perforation is not uncommon and not associated with overt adverse outcomes.
Keywords: artificial, pacemaker, pericardial effusion, tomography, X‐ray computed
1. Introduction
The leadless pacemaker has emerged as an alternative to conventional transvenous pacemakers. Since its approval by the US Food and Drug Administration (FDA) in 2016, the annual number of leadless pacemaker implantations has increased steadily [1, 2]. Compared with conventional transvenous pacemakers, leadless pacemakers present a lower risk of infection and eliminate complications related to pacemaker leads; however, the incidence of cardiac perforation is higher with leadless pacemakers than with conventional transvenous pacemakers [3, 4, 5]. While numerous cases of overt right ventricular (RV) perforation associated with leadless pacemakers have been documented, reports of subclinical RV perforation are limited. In the absence of acute symptoms or hemodynamic compromise, cardiac perforation may go unnoticed. In this context, there has been a confirmed case of subclinical perforation by the device cup of a leadless pacemaker identified through computed tomography (CT) [6]. Additionally, there was a case in which a previously implanted leadless pacemaker tine perforating the RV free wall, which was incidentally discovered during cardiac surgery [7].
To reduce the risk of cardiac perforation, it is recommended that a leadless pacemaker be implanted in the RV mid‐septum. Some evidence suggests that a left lateral fluoroscopic view may facilitate optimal implantation [8]. Despite ongoing efforts, implanting leadless pacemakers in the RV septum remains challenging. A study utilizing the FDA Manufacturer and User Facility Device Experience database reviewed 563 cases of RV perforation caused by the tine‐based leadless pacemaker (Micra, Medtronic), and found that 54 of these cases were associated with non‐septal deployment [9]. In a cohort of 358 patients who underwent leadless pacemaker implantation, device location was assessed using chest radiography, revealing apical septum placement in 109 cases (30.5%) [10]. Another study, in which device location was confirmed via CT, reported true septal implantation in less than half of the 67 cases (n = 28, 41.8%) [11]. This study aimed to assess the implantation site and the incidence of subclinical RV perforation in patients who underwent CT following leadless pacemaker (Micra, Medtronic, Minneapolis, Minnesota, USA) implantation, as well as to evaluate the prognosis of subclinical perforation.
2. Methods
2.1. Study Design and Participants
This retrospective cohort study was conducted across five university hospitals. The inclusion criteria were as follows: (1) age ≥18 years; (2) patients who underwent heart, chest, or abdomen CT after tine‐based leadless pacemaker (Micra, Medtronic, Minneapolis, Minnesota, USA) implantation for reasons unrelated to leadless pacemaker complications. The exclusion criteria were as follows: (1) patients with CT images of poor quality, such as severe metallic artifacts; (2) cases where images from abdominal CT alone did not visualize the leadless pacemaker. All patients received either the Micra VR or Micra AV leadless pacemaker, implanted using previously described technique [12]. After positioning the delivery sheath, contrast injection is performed to confirm the position and avoid the free wall before applying pressure to the tip of the delivery system.
Medical records were reviewed to collect demographic data, including age, sex, body mass index (BMI), and information on underlying conditions such as atrial fibrillation, hypertension, diabetes mellitus, coronary artery disease, chronic kidney disease, and ischemic stroke. Medication usage, including anticoagulants and antiplatelet agents, was also obtained. Indications for leadless pacemaker implantation were identified and categorized as either sinus node dysfunction or atrioventricular block. An electrocardiogram taken before and after the procedure provided the duration of both native and paced QRS complex. All patients underwent echocardiography before the leadless pacemaker implantation. Echocardiographic measurements included ejection fraction, left atrial diameter (LAD), and left atrial volume index (LAVI).
2.2. CT Analysis
CT scans of the heart, chest, or abdomen were independently analyzed by two cardiologists (Y.S. Lee and J.S. Uhm) and one radiologist (H.J. Lee) to ensure complete visualization of all leadless pacemaker components. Two cardiologists independently assessed the implantation site and presence of perforation, yielding a Cohen's kappa coefficient of 0.80 for implantation site classification and 0.86 for perforation detection. Any discrepancies between the cardiologists were resolved through discussion with the radiologist. To minimize metallic artifacts caused by the device, images reconstructed using an iterative algorithm were selected, and the observers reviewed them using a bone window setting (window level, 300–500 HU; window width, 1500–2000 HU). The implantation position was assessed by analyzing the placement of the four tines of the leadless pacemaker, which were categorized into five groups: (1) septum, (2) RV free wall, and (3) junction of septum and RV free wall defined as a location where at least one tine was embedded in the RV septum and at least one tine in the adjacent RV free wall. (4) Moderator band or (5) RV apex (Figure 1). Subclinical perforation was defined as the penetration of leadless pacemaker tine beyond the outer border of the myocardial contour without the presence of acute symptoms, pericardial effusion, hemodynamic compromise, or pacemaker malfunction.
FIGURE 1.
Classification of implantation position of leadless pacemaker. (A) RV septum; (B) RV free wall; (C) Junction of RV septum and free wall; (D) Moderator band; and (E) RV apex RV, right ventricular.
2.3. Outcome Ascertainment
The occurrence of complications, including pericardial effusion and vascular access‐related complications, was monitored throughout the follow‐up period. R wave amplitude, pacing threshold, and impedance were recorded immediately after leadless pacemaker implantation and at the last follow‐up visit. Adverse clinical outcomes were defined as any occurrence of pericardial effusion, cardiac tamponade, or device malfunction.
2.4. Ethical Statement
This retrospective study adhered to the ethical standards outlined in the 2013 Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of all participating hospitals (2024‐3488‐001, 2024‐12‐125, 2024‐12‐028). Given the retrospective nature of this study, the requirement for informed patient consent was waived by the Institutional Review Board.
2.5. Statistical Methods
Data are presented as mean ± standard deviation or median (interquartile range), depending on the result of the Shapiro–Wilk test for normality. Continuous variables are reported as medians (interquartile range) and were analyzed using the t‐test and Mann‐Whitney U test. Categorical variables are presented as numbers and percentages and were compared using χ 2 test or Fisher's exact test as appropriate. Statistical significance was defined as a two‐sided p value <0.05. All statistical analyses were performed using the R software (version 4.3.2; www.R‐project.org; R Foundation for Statistical Computing, Vienna, Austria).
3. Results
From February 2021 to April 2024, 88 patients (mean age, 72.9 ± 12.1 years; male, 47.7%) were included in this study. Patient demographics and test results, categorized by the presence of subclinical RV perforation, are presented in Table 1. The primary indications for leadless pacemaker implantation were sick sinus syndrome in 49 patients (55.7%) and atrioventricular block in 39 patients (44.3%). The average time from leadless pacemaker implantation to CT scanning was 8.6 ± 9.2 months. Twelve patients received heart CT, fifty‐seven received chest CT (49 with contrast and 8 without), and 19 received abdomen CT. The leadless pacemakers were implanted at the junction of septum and RV free wall in 68 patients (77.3%), the RV free wall in seven patients (8.0%), moderator band in five patients (5.7%), the RV apex in four patients (4.5%), and at septum in four patients (4.5%) (Figure 1). Subclinical RV perforation by the leadless pacemaker occurred in 15 of 88 patients (17.0%) (Figure 2).
TABLE 1.
Baseline characteristics and imaging findings between non‐RV perforation and RV perforation groups.
|
Non‐RV perforation group (N = 73) |
RV perforation group (N = 15) |
p value | |
|---|---|---|---|
| Age at implantation, years | 73.0 ± 11.9 | 72.1 ± 13.3 | 0.795 |
| Male | 33 (45.2) | 9 (60.0) | 0.447 |
| Height, cm | 159.7 ± 9.6 | 161.5 ± 8.9 | 0.501 |
| Weight, kg | 60.1 ± 13.1 | 62.0 ± 10.4 | 0.599 |
| BMI, kg/m2 | 23.5 ± 3.8 | 23.8 ± 3.3 | 0.761 |
| Comorbidities | |||
| Atrial fibrillation | 40 (54.8) | 7 (46.7) | 0.771 |
| Hypertension | 45 (61.6) | 8 (53.3) | 0.757 |
| Diabetes | 22 (30.1) | 3 (20.0) | 0.632 |
| Dyslipidemia | 12 (16.4) | 0 (0.0) | 0.202 |
| Coronary artery disease | 10 (13.7) | 1 (6.7) | 0.748 |
| Heart failure | 10 (13.7) | 3 (20.0) | 0.820 |
| Valvular heart disease | 11 (15.1) | 0 (0.0) | 0.239 |
| CKD | 16 (21.9) | 3 (20.0) | >0.999 |
| History of malignancy | 8 (11.0) | 2 (13.3) | >0.999 |
| Cerebrovascular accident | 6 (8.2) | 1 (6.7) | >0.999 |
| Medication history | |||
| Vitamin K antagonist | 9 (12.3) | 0 (0.0) | 0.333 |
| NOAC | 29 (39.7) | 6 (40.0) | >0.999 |
| Single antiplatelet agents | 14 (19.2) | 4 (26.7) | 0.762 |
| Antihypertensive agents | 52 (71.2) | 11 (73.3) | >0.999 |
| Diuretics | 14 (19.2) | 1 (6.7) | 0.426 |
| Statin | 31 (42.5) | 6 (40.0) | >0.999 |
| Laboratory values | 11.6 ± 2.5 | 12.5 ± 1.7 | 0.245 |
| Hemoglobin, g/dL | 11.8 ± 2.4 | 12.0 ± 2.1 | 0.752 |
| Albumin, g/L | 3.9 ± 0.6 | 3.9 ± 0.6 | 0.839 |
| eGFR, mL/min/1.73 m2 | 63.9 ± 30.3 | 68.4 ± 28.0 | 0.592 |
| Pacemaker indications | 0.207 | ||
| Sick sinus syndrome | |||
| Sinus bradycardia or sinus pause | 26 (35.6) | 3 (20.0) | |
| Tachycardia‐bradycardia syndrome | 16 (21.9) | 4 (26.7) | |
| Atrioventricular block | |||
| Complete | 20 (27.4) | 3 (20.0) | |
| Paroxysmal | 1 (1.4) | 2 (13.3) | |
| High‐degree | 5 (6.8) | 2 (13.3) | |
| Atrial fibrillation with SVR | 5 (6.8) | 1 (6.7) | |
| Computed tomography | 0.803 | ||
| Heart with contrast | 10 (13.7) | 2 (13.3) | |
| Chest with contrast | 40 (54.8) | 9 (60.0) | |
| Chest without contrast | 6 (8.2) | 2 (13.3) | |
| Abdomen with contrast | 17 (23.3) | 2 (13.3) |
Note: Values are presented as mean ± standard deviation and numbers (%).
Abbreviations: BMI, body mass index; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; LAD, left atrial diameter; LAVI, left atrial volume index; LV, left ventricular; NOAC, non‐vitamin K antagonist oral anticoagulant; RV, right ventricular; SVR, slow ventricular rate.
FIGURE 2.
CT images of subclinical RV perforation by leadless pacemaker. CT, computed tomography; RV, right ventricular. [Colour figure can be viewed at wileyonlinelibrary.com]
There were no significant differences in age, sex, physical measurements, comorbidities, medication history, or laboratory values between the two groups. There were no significant differences in the indications for leadless pacemaker and the type of CT between the two groups. The patients with subclinical RV perforation had a significantly shorter interval from leadless pacemaker implantation to CT scanning than the patients without subclinical RV perforation (9.5 ± 9.5 vs. 4.4 ± 5.8 months, p = 0.011).
The LAD and LAVI were significantly smaller in the RV perforation group, compared with the non‐RV perforation group (LAD, 43.8 ± 8.9 vs. 38.3 ± 9.6 mm, p = 0.033; LAVI, 53.1 ± 22.8 vs. 38.1 ± 17.1 mL/m2, p = 0.023, respectively). However, the position of the leadless pacemaker implantation did not differ significantly between the groups. In both groups, the junction of the septum and RV free wall was the most common implantation site [56 (76.7%) vs. 12 (80.0%), p = 0.609], though no RV perforations occurred when the leadless pacemaker was implanted at the septum. Immediately after implantation, no significant differences were noted in pacemaker parameters between the groups. There were no significant differences in change in impedance from baseline to the last follow‐up between the non‐RV perforation group and the RV perforation group (236.8 ± 174.2 vs. 373.1 ± 371.3 Ω, respectively; p = 0.217). The follow‐up duration was longer in the non‐RV perforation group than the RV perforation group (19.5 ± 12.3 vs. 12.4 ± 12.3 months, p = 0.047), and pericardial effusion was developed in two patients without RV perforation. In addition, among patients in the non‐RV perforation group, one developed pacemaker syndrome and another experienced moderator band rupture (Table 2).
TABLE 2.
Baseline pacemaker parameters and outcomes between non‐RV perforation and RV perforation groups.
|
Non‐RV perforation group (N = 73) |
RV perforation group (N = 15) |
p value | |
|---|---|---|---|
| Native QRS duration, ms | 103.3 ± 22.3 | 114.3 ± 27.7 | 0.100 |
| Paced QRS duration, ms | 160.6 ± 18.9 | 159.6 ± 7.3 | 0.795 |
| Echocardiographic parameters | |||
| LV ejection fraction, % | 65.1 ± 8.5 | 60.0 ± 9.7 | 0.043 |
| LAD, mm | 43.8 ± 8.9 | 38.3 ± 9.6 | 0.033 |
| LAVI, mL/m2 | 53.1 ± 22.8 | 38.1 ± 17.1 | 0.023 |
| Implantation position | 0.609 | ||
| Septum | 4 (5.5) | 0 (0.0) | |
| RV free wall | 5 (6.8) | 2 (13.3) | |
| Junction of the septum and the RV free wall | 56 (76.7) | 12 (80.0) | |
| Moderator band | 5 (6.8) | 0 (0.0) | |
| RV apex | 3 (4.1) | 1 (6.7) | |
| Pacemaker parameters at implantation | |||
| R wave amplitude, mV | 9.5 ± 3.8 | 9.2 ± 3.2 | 0.834 |
| Pacing threshold, mV × 0.24 ms | 0.7 ± 0.5 | 0.9 ± 1.2 | 0.569 |
| Impedance, Ω | 819.2 ± 217.7 | 997.3 ± 451.8 | 0.156 |
| Implantation to CT duration, months | 9.5 ± 9.5 | 4.4 ± 5.8 | 0.011 |
| Follow‐up duration, months | 19.5 ± 12.3 | 12.4 ± 12.3 | 0.047 |
| Pacemaker parameters at last follow‐up | |||
| R wave amplitude, mV | 12.2 ± 4.7 | 13.6 ± 5.0 | 0.344 |
| Pacing threshold, mV × 0.24 ms | 0.8 ± 0.7 | 0.8 ± 0.5 | 0.847 |
| Impedance, Ω | 578.0 ± 112.0 | 652.3 ± 154.7 | 0.042 |
| ΔImpedance, Ω | 236.8 ± 174.2 | 373.1 ± 371.3 | 0.217 |
| Pericardial effusion during follow‐up | 2 (2.7) | 0 (0.0) | >0.999 |
| Pacemaker syndrome | 1 (1.4) | 0 (0.0) | >0.999 |
| Moderator band rupture | 1 (1.4) | 0 (0.0) | >0.999 |
Note: Values are presented as mean ± standard deviation and numbers (%).
Abbreviations: BMI, body mass index; CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate; LAD, left atrial diameter; LAVI, left atrial volume index; LV, left ventricular; NOAC, non‐vitamin K antagonist oral anticoagulant; RV, right ventricular; SVR, slow ventricular rate.
4. Discussions
4.1. Main Findings
The main findings of the present study are as follows: (1) the most common leadless pacemaker implantation site was the junction of the septum and RV free wall; (2) subclinical RV perforation by leadless pacemaker was developed in 17.0%; and (3) no clinically significant complications were observed during follow‐up in patients with subclinical RV perforation confirmed by CT imaging.
4.2. Leadless Pacemaker Implantation Site
Arial et al. categorized leadless pacemaker implantation sites as either septal or non‐septal based on CT findings in a cohort of 67 patients [11]. In their study, cardiac injury occurred in four patients, all in the non‐septal group. However, the perforation rate in their study might be underestimated, as cardiac injury was identified through clinical signs such as apical hematoma or pericardial effusion rather than direct visualization of myocardial perforation by the tines of the leadless pacemaker. In addition, a study that analyzed lead location via CT after cardiac implantable electronic device implantation (excluding leadless pacemaker) reported 26 subclinical perforations among 463 leads [13]. Among the 258 RV leads, 19 (7.4%) were associated with subclinical RV perforation. In this study, although the distribution of implantation sites did not differ significantly between patients with and without subclinical RV perforation, no perforations occurred in cases with true septal implantation, and the proportion of free wall implantations was higher in the perforation group. The relatively high overall proportion of free wall implantations is consistent with previous reports describing the limitations of fluoroscopic guidance in accurately targeting the septum and the association between non‐septal deployment and an increased risk of perforation.
In our study, RV perforation and the frequency of implantation at sites other than the septum were higher compared with previous reports. That might be because we meticulously observed and tracked each of the four tines of leadless pacemakers from the CT images.
4.3. Characteristics of Patients With Subclinical RV Perforation
LAD and LAVI were significantly smaller in patients with subclinical RV perforation. It is reasonable to speculate that a smaller cardiac chamber size may increase the risk of perforation, potentially due to the increased difficulty of sheath manipulation in these patients. However, no study has identified cardiac chamber size as a predictor of pericardial effusion development following leadless pacemaker implantation. One study that assessed risk factors for pericardial effusion after leadless pacemaker implantation found that a low BMI (under 20 kg/m2) and female sex, both of which are associated with smaller cardiac chamber size, were identified as significant risk factors [14]. These factors have also been identified as predictors of pericardial effusion after transvenous pacemaker implantation [15, 16]. However, in this study, no differences were observed in sex distribution or BMI according to subclinical RV perforation. Moreover, RV size and myocardial thickness were not assessed via echocardiography, leaving these findings inconclusive.
Although not statistically significant, impedance immediately after implantation was higher in the RV perforation group, and the reduction in impedance from baseline to the last follow‐up tended to be greater in this group. It is hypothesized that RV perforation may cause a slightly larger decrease in impedance due to reduced pressure and contact between the tines and the myocardium [17]. Therefore, if impedance decreases relatively pronouncedly during follow‐up, echocardiography is recommended to assess for potential complications. In Arai's study, impedance was significantly lower in the leadless pacemaker of septal implantation, likely due to poor electrode contact [11]. Additionally, impedance may decrease over time post‐implantation, which could be influenced by the significantly different follow‐up durations between the groups.
4.4. Implications for Implantation Technique and Device Retrieval
Our findings may provide practical insights for improving leadless pacemaker implantation techniques. Despite the use of fluoroscopic guidance and contrast injection, true septal implantation remains challenging, with most devices positioned at the junction of the septum and RV free wall. This observation highlights the inherent limitations of fluoroscopic imaging in accurately identifying the interventricular septum. Greater attention to septal orientation and the use of contrast injection with multiple fluoroscopic projections, including left lateral view, may help improve the accuracy of septal targeting and potentially reduce the risk of free wall engagement and myocardial perforation.
Another potential implication of our findings relates to leadless pacemaker retrieval. Although device extraction is rarely required, it may become necessary in cases of infection, device malfunction, or battery depletion. Detailed knowledge of the tine position and the presence of subclinical myocardial perforation may provide useful anatomical information when planning retrieval procedures. In particular, CT imaging may help identify cases in which device tines extend beyond the myocardial contour, which could influence procedural strategy and risk assessment during device extraction.
4.5. Limitations
Our study focused exclusively on the tine‐based leadless pacemaker, which may limit the generalizability of the findings to other types of leadless pacemakers. Additionally, including only patients who underwent CT for reasons unrelated to device complications introduces selection bias toward clinically stable cases and may underestimate the true incidence of adverse events. RV size and wall thickness were not assessed, limiting the evaluation of RV‐specific risk factors. Moreover, all patients did not receive post‐procedural echocardiography, resulting in missed complications such as pacing‐induced cardiomyopathy. Methodologically, the use of non‐ECG‐gated chest or abdominal CT scans in some patients may have limited our ability to detect small perforations. Finally, the relatively small sample size of 88 patients may limit statistical power to detect differences between the groups.
5. Conclusions
The most common tine‐based leadless pacemaker implantation site is the junction of the septum and the RV free wall. Subclinical RV perforation is not uncommon and not associated with overt adverse outcomes. These findings may have important implications for procedural technique and for the management of leadless pacemakers in situations where device retrieval is required. While no perforations occurred with true septal placement, the small number of such cases precludes definitive conclusions. Further prospective studies are warranted to clarify whether septal targeting reduces perforation risk.
Author Contributions
All authors read and approved the final manuscript. Jae‐Sun Uhm, Seung‐Jung Park: conceptualization. In‐Soo Kim, Moon‐Hyun Kim: data curation. Young Shin Lee, Je‐Wook Park, Ye Chan Kim: formal analysis. Tae‐Hoon Kim, Jin‐Bae Kim, Jong‐Youn Kim: investigation. Hye‐Jeong Lee, Hanjin Park, Daehoon Kim, Hee Tae Yu: methodology. Boyoung Joung, Hui‐Nam Pak, Moon‐Hyoung Lee: validation. Jae‐Sun Uhm, Seung‐Jung Park: visualization. Young Shin Lee, Je‐Wook Park, Ye Chan Kim: writing – original draft. Young Shin Lee, Jae‐Sun Uhm, Seung‐Jung Park: writing – review and editing.
Ethics Statement
This retrospective study adhered to the ethical standards outlined in the 2013 Declaration of Helsinki and its subsequent amendments. The study was approved by the Institutional Review Board of all participating hospitals (2024‐3488‐001, 2024‐12‐125, 2024‐12‐028).
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
The authors have nothing to report.
Contributor Information
Jae‐Sun Uhm, Email: jason@yuhs.ac.
Seung‐Jung Park, Email: orthovics@gmail.com.
Data Availability Statement
The data are available to bona fide researchers through the corresponding author upon application. Analytic methods and study materials are available from the corresponding author upon reasonable request.
References
- 1. Meredith A., Naaraayan A., Nimkar A., Acharya P., and Aziz E. F., “The Rise of Leadless Pacemaker Utilization in United States,” American Journal of Cardiology 154 (2021): 127–128. [DOI] [PubMed] [Google Scholar]
- 2. Khan M. Z., Nassar S., Nguyen A., et al., “Contemporary Trends of Leadless Pacemaker Implantation in the United States,” Journal of Cardiovascular Electrophysiology 35, no. 7 (2024): 1351–1359. [DOI] [PubMed] [Google Scholar]
- 3. Piccini J. P., El‐Chami M., Wherry K., et al., “Contemporaneous Comparison of Outcomes Among Patients Implanted With a Leadless vs Transvenous Single‐Chamber Ventricular Pacemaker,” JAMA Cardiology 6, no. 10 (2021): 1187–1195. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Hauser R. G., Gornick C. C., Abdelhadi R. H., Tang C. Y., Casey S. A., and Sengupta J. D., “Major Adverse Clinical Events Associated With Implantation of a Leadless Intracardiac Pacemaker,” Heart Rhythm 18, no. 7 (2021): 1132–1139. [DOI] [PubMed] [Google Scholar]
- 5. El‐Chami M. F., Bockstedt L., Longacre C., et al., “Leadless vs. Transvenous Single‐Chamber Ventricular Pacing in the Micra CED Study: 2‐Year Follow‐Up,” European Heart Journal 43, no. 12 (2022): 1207–1215. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6. Togashi I., Sato T., Hoshida K., and Soejima K., “Subclinical Cardiac Perforation Caused by a Micra™ Leadless Pacemaker,” Journal of Arrhythmia 34, no. 3 (2018): 326–328. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Tan N. Y., Madhavan M., Greason K. L., and Cha Y. M., “The Subtle Tine: Asymptomatic Micra Perforation Incidentally Discovered During Cardiac Surgery,” Journal of Cardiovascular Electrophysiology 34, no. 1 (2023): 229–230. [DOI] [PubMed] [Google Scholar]
- 8. Hai J.‐J., Fang J., Tam C.‐C., et al., “Safety and Feasibility of a Midseptal Implantation Technique of a Leadless Pacemaker,” Heart Rhythm 16, no. 6 (2019): 896–902. [DOI] [PubMed] [Google Scholar]
- 9. Hauser R. G., Gornick C. C., Abdelhadi R. H., et al., “Leadless Pacemaker Perforations: Clinical Consequences and Related Device and User Problems,” Journal of Cardiovascular Electrophysiology 33, no. 2 (2022): 154–159. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Shantha G., Brock J., Singleton M., et al., “Anatomical Location of Leadless Pacemaker and the Risk of Pacing‐Induced Cardiomyopathy,” Journal of Cardiovascular Electrophysiology 34, no. 6 (2023): 1418–1426. [DOI] [PubMed] [Google Scholar]
- 11. Arai H., Mizukami A., Hanyu Y., et al., “Leadless Pacemaker Implantation Sites Confirmed by Computed Tomography and Their Parameters and Complication Rates,” Pacing and Clinical Electrophysiology 45, no. 2 (2022): 196–203. [DOI] [PubMed] [Google Scholar]
- 12. El‐Chami M. F., Roberts P. R., Kypta A., et al., “How to Implant a Leadless Pacemaker With a Tine‐Based Fixation,” Journal of Cardiovascular Electrophysiology 27, no. 12 (2016): 1495–1501. [DOI] [PubMed] [Google Scholar]
- 13. Lim Y.‐M., Uhm J.‐S., Kim M., et al., “Subclinical Cardiac Perforation by Cardiac Implantable Electronic Device Leads Detected by Cardiac Computed Tomography,” BMC Cardiovascular Disorders 21 (2021): 1–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14. Piccini J. P., Cunnane R., Steffel J., et al., “Development and Validation of a Risk Score for Predicting Pericardial Effusion in Patients Undergoing Leadless Pacemaker Implantation: Experience With the Micra Transcatheter Pacemaker,” EP Europace 24, no. 7 (2022): 1119–1126. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Mahapatra S., Bybee K. A., Bunch T. J., et al., “Incidence and Predictors of Cardiac Perforation After Permanent Pacemaker Placement,” Heart Rhythm 2, no. 9 (2005): 907–911. [DOI] [PubMed] [Google Scholar]
- 16. Cano O., Andres A., Alonso P., et al., “Incidence and Predictors of Clinically Relevant Cardiac Perforation Associated With Systematic Implantation of Active‐Fixation Pacing and Defibrillation Leads: A Single‐Centre Experience With Over 3800 Implanted Leads,” EP Europace 19, no. 1 (2017): 96–102. [DOI] [PubMed] [Google Scholar]
- 17. Tolosana J. M., Guasch E., San Antonio R., et al., “Very High Pacing Thresholds During Long‐Term Follow‐Up Predicted by a Combination of Implant Pacing Threshold and Impedance in Leadless Transcatheter Pacemakers,” Journal of Cardiovascular Electrophysiology 31, no. 4 (2020): 868–874. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data are available to bona fide researchers through the corresponding author upon application. Analytic methods and study materials are available from the corresponding author upon reasonable request.