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Address reprint requests and correspondence: Dr Mitsuru Takami, Kobe University Hospital, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe City, Hyogo Prefecture, Japan, 650-0017.
Very late lead perforation should be considered in the differential diagnosis of chest pain and pacing failure in a patient with an implanted pacemaker.
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Several factors are related to very late lead perforation.
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A combination treatment of a surgical approach and percutaneous lead extraction was an appropriate strategy in the present case.
Introduction
Lead perforation of cardiac implantable electronic devices is a rare but life-threatening complication. A recent study showed that the rate of perforation was 0.50%.
This complication usually occurs within 30 days of device placement. Delayed lead perforations (those diagnosed more than 30 days after implantation) are extremely rare. Here we report the case of very late perforation of a passive fixation lead into the thoracic cavity that occurred 8 years after pacemaker implantation. We discuss the mechanisms of very late perforation with passive fixation leads and the treatment strategy.
Case report
An 89-year-old man with a previously implanted pacemaker came to the emergency department complaining of chest pain and presyncopal episodes. He had suddenly felt chest pain while pruning in the garden 2 weeks earlier. The 12-lead electrocardiogram (ECG) showed severe bradycardia at 20–40 bpm with ventricular pacing failure (Figure 1A ). Pacemaker interrogation indicated significant worsening of the ventricular lead threshold to 4.25 V at 0.4 ms and lead impedance of 425 Ω. The intrinsic heart rate was so slow that R-wave sensing could not be measured. The patient eventually was transferred to our hospital.
Figure 1Examination of the patient. A: Electrocardiogram shows intermittent ventricular pacing failure (black arrows).B: Temporal changes of ventricular lead parameters. Pacing threshold (top), R-wave sensing (middle), and lead impedance (bottom) are shown. Red triangle indicates the time of hospital admission. C: Chest radiograph taken at the time of initial pacemaker implantation (8 years ago). Orange arrow indicates the ventricular lead tip. D: Chest radiograph on hospital admission shows that the ventricular lead tip had advanced to the distal end of the cardiac silhouette (red arrow).E: Echocardiography shows a lead perforation on the right RV wall (yellow arrow).F: Computed tomographic image (right anterior oblique view) shows that the lead had penetrated the pericardium and reached the thoracic cavity (blue arrow). LV = left ventricle; RV = right ventricle.
The patient had a medical history of hypertension and chronic obstructive pulmonary disease. At age 81 years, he had undergone implantation of a DDD pacemaker with dual passive fixation leads for sick sinus syndrome and atrioventricular block. The right ventricular (RV) lead (CapSure Sense MRI SureScan 4074-58, Medtronic, Minneapolis, MN) was implanted in the RV apex. He had undergone regular device checks every 6 months. Ventricular lead impedance had gradually decreased since December 2018, but no other significant changes in lead parameters were observed for 8 years before hospital admission (Figures 1B and 1C). He took antihypertensive drugs but did not take antithrombotic drugs or steroids.
Device-related factors (lead fractures, lead dislodgment or mispositioning, and battery abnormalities) and patient-related factors (fibrosis/inflammation, advanced cardiomyopathy, and electrolyte imbalances) were considered as different diagnoses of pacing failure.
Investigation
The patient’s blood pressure was 128/97 mm Hg, pulse rate 40 ppm, and SpO2 98% (room air). Chest radiograph revealed that the ventricular lead tip had advanced to the distal end of the cardiac silhouette (Figure 1D). Pacing failure frequently occurred during the patient`s inspirations. An echocardiogram revealed normal left ventricular wall motion and no pericardial effusion; however, the tip of the RV lead was speculated to have penetrated the RV wall (Figure 1E). Computed tomographic (CT) scan showed that the lead had perforated the myocardium and pericardium, then reached the thoracic cavity (Figure 1F). Neither a pneumothorax nor pleural effusion was observed. The patient was diagnosed as having a very late perforation of the RV lead into the thoracic cavity.
Management
Ventricular pacing output was increased to 6.0 V at 1.5 ms and the lower rate changed to 80 ppm from 60 ppm. These changes improved the pacing failure. Temporary pacing was not necessary. The heart team members consisted of interventional cardiologists, noninterventional cardiologists, cardiac surgeons, and radiologists who discussed the treatment strategy. We decided to perform a combination therapy consisting of a surgical approach with a small thoracotomy and percutaneous lead extraction. The surgery was performed while the patient was under general anesthesia and isolated lung ventilation. An 8-cm incision in the left lateral thoracic region was made, and the chest was opened through the left fifth intercostal space. The lead was seen to have penetrated the RV wall and pericardium, then reached the thoracic cavity close to the pulmonary ligament. The tip of the lead was covered with fatty tissue (Figure 2A ). The fatty tissue had not adhered to the lead. After the fatty tissue was removed, the lead tip became visible and was seen protruding 12 mm from the RV apex (Figure 2B). The myocardium around the perforation site was threaded so that the bleeding may be stopped at any time.
Figure 2Surgical findings. A: Small left lateral thoracotomy with perforated lead (black arrow). The tip of the lead is covered with fatty tissue (green arrows).B: After the fatty tissue was removed, the perforation site of the lead with tines is clearly seen.
Transvenous lead extraction was performed with a 9F Evolution Shortie RL sheath (Cook Medical LLC, Bloomington, IN) with an outer sheath. The subclavian vein puncture site was dissected. During traction, the tip of the ventricular lead was trailed into the cardiac cavity. The surgeons ligated the preplaced thread and sutured the perforation site, resulting in only a small amount of bleeding. The perforation hole of the myocardium was so small that no patch was needed to close the hole. Lead extraction then was performed successfully without any complications. A new RV lead with active fixation was implanted at a site 2–3 cm proximal to the RV apex without any excessive slack. The patient was discharged after 12 days. A device check at the outpatient clinic showed that the patient had normal lead parameters and that he had been free from any events during a 6-month follow-up period.
Discussion
Generally, lead perforations are more often associated with active fixation leads than with passive fixation leads.
reviewed the literature for late perforations of passive fixation leads in 8 cases and found that the time to presentation of lead perforation was between 1 month and 3 years. To our knowledge, this is the first case of a passive fixation lead perforation that became apparent 8 years after implantation.
Reported common risk factors for perforations include female sex, advanced age, infections, active fixation leads, corticosteroid use, and a history of temporary pacing.
Advanced age was the only risk factor for perforation in the present case. The assumed mechanisms of the perforation in the present case are as follows. (1) The RV lead was implanted in the thinnest part of the RV apex, which would have a localized vulnerability because of age-related factors. (2) Upon examination of the radiographic and CT images taken 1–2 years before the perforation, excessive slack on the RV lead was identified, which could have caused increased transmission of force to the RV apex (Figure 3A ). The lead tip might have gradually become buried in the myocardium over a period of months or years. In addition, upon careful examination of the trend of lead parameters (Figure 1B), lead impedance had gradually decreased since December 2018 (3 years before perforation), then suddenly increased at admission. Ahmed et al
reported a case of subacute lead perforation causing left-sided hemothorax and epicardial hematoma. Lead impedance usually decreases with lead perforation. However, if the lead migrates to an air-filled space, such as the lung, impedance would increase.
In the present case, we speculated that the existence of epicardial and pericardial fat worked as a plug and cushioned material between the lead and surrounding organs (Figure 3B), which would prevent injury to the surrounding organs.
Figure 3Before and after lead perforation. A: Before perforation. Top: Radiograph taken 2 years before the perforation. Middle: Computed tomographic image taken 1 year before the perforation. Both images show that the RV lead (yellow dots) was strongly slack (red arrows).Bottom: Schematic diagram of the heart. The excessive slack on the RV lead (red arrows) would cause strong pressure on the lead tip (black dotted arrow).B: After perforation. The lead tip reached the thoracic cavity (top). However, pericardial fatty tissue covered the lead tip (green arrows)(middle, bottom), which might protect the lungs from any injury from the lead.
retrospectively analyzed 54 patients with device lead perforations. The leads were removed or repositioned by a percutaneous approach, with no major complications and without surgical intervention in any of the patients. However, we chose a combination therapy with a surgical procedure and percutaneous lead extraction. The duration from implantation to perforation was extremely long in this case. We were concerned about the potential fragility of the myocardium and the lead adhesions with pericardial tissue. Furthermore, the lead was a passive fixation lead with tines; thus, there was a possibility of enlarging the site of the perforation due to the tines pulling on the lead, which would cause severe acute bleeding. In retrospect, the adhesion of the lead tip to the surrounding tissue was not strong, and the hole of the RV myocardium was small. Therefore, percutaneous lead extraction alone would have been safe as well. However, it was difficult to estimate the degree of tissue adhesion and the size of the hole on preoperative CT. Considering the risk of continuous bleeding from the RV hole, we thought a hybrid approach with a minimally invasive small thoracotomy and percutaneous lead extraction would be an appropriate strategy in the present case.
Conclusion
We report a unique case in which symptomatic lead perforation with a passive fixation lead occurred 8 years after pacemaker implantation. A combination treatment consisting of a surgical approach and percutaneous lead extraction was an appropriate strategy in the present case.
Acknowledgment
The authors would like to thank Mr John Martin for his linguistic assistance.
References
Waddingham P.H.
Elliott J.
Bates A.
et al.
Iatrogenic cardiac perforation due to pacemaker and defibrillator leads: a contemporary multicentre experience.
Funding Sources: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Disclosures: The Section of Arrhythmia (from the Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan) is supported by an endowment from Medtronic JAPAN, Abbott JAPAN and Boston Scientific JAPAN. Dr Hirata chairs the Section, and Drs Fukuzawa and Takami are members. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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