Delayed Right Ventricular Pacemaker Lead Perforation 9 Years After Implantation

Background

Cardiac perforation is a rare complication of cardiac implantable electronic devices (CIEDs), with a reported incidence ranging from 0.1% to 5.2% [1,2]. Delayed perforation, defined as perforation occurring more than 1 month after implantation, is more uncommon [3]. In this report, we present a case of cardiac perforation involving the right ventricle (RV) wall that occurred 9 years after pacemaker implantation.

Case Report

A 79-year-old woman presented with symptoms of dyspnea and was subsequently admitted to a hospital. She had undergone pacemaker implantation (a tined J-shaped atrial lead, Medtronic 4574-45 cm; a tined ventricular lead, Medtronic 4074-52 cm; generator, Medtronic Advisa MRI A3DR01; Medtronic, Minneapolis, MN) for a complete atrioventricular block 9 years prior to the presentation. Her past medical history included diabetes mellitus requiring insulin therapy, chronic subdural hematoma, and bronchial asthma.

An electrocardiogram revealed a heart rate of 32 bpm with a complete atrioventricular block, demonstrating right ventricular failure to capture despite increases of the pacemaker output or pulse width. Impedance remained unchanged from the previous check, and computed tomography (CT) imaging indicated no obvious lead perforation or pericardial effusion. A temporary pacing lead was inserted through the right jugular vein to the RV, and another permanent pacing lead insertion was scheduled. Three days later, the patient reported pinpoint chest pain in the left sixth intercostal space, and CT imaging revealed that the pre-existing RV lead had clearly protruded outside the heart, yet with no pericardial effusion. The patient was then transferred to our hospital for surgical intervention. She was afebrile; her vital signs were stable with a ventricularly paced rhythm, and chest pain was well-controlled with analgesia. Laboratory results were largely within the expected range, except for a slightly elevated C-reactive protein level of 5.44 mg/dL. A chest radiography revealed that the ventricular lead had advanced forward, when compared to its position 2 months prior (Figure 1). A CT scan performed at our hospital suggested that the RV pacing lead had penetrated the RV apex and reached the left sixth rib. No pericardial effusion was detected (Figure 2). Transthoracic echocardiography revealed normal cardiac function. As the patient had double-coronary vessel disease at the time of the first pacemaker implantation, we performed coronary angiography, which indicated the progression to triple-vessel disease. Device interrogation revealed a sudden increase followed by a gradual decrease in the RV pacing threshold over 2 months (Figure 3).

Differential diagnosis for the causative factors of delayed perforation of the RV pacemaker lead included the potential presence of infection, myocardial ischemia, cardiomyopathy, trauma, and an idiopathic origin.

On the third day after admission, surgery was performed for removal and implantation of the RV lead and coronary artery bypass grafting. A median sternotomy was performed to expose the heart, revealing a minimal serous, non-bloody effusion in the pericardial sac. The RV lead protruded approximately 3 cm from the RV apex (Figure 4). There were no findings of infection or adhesion in the pericardium or on the surface of the heart. We disconnected the RV lead from the generator and withdrew it, without any resistance, via the protruding portion of the RV. A biopsy sample of the myocardium at the RV perforation site was harvested, and the defect was closed using a 4-0 polypropylene thread with felt pledget. Off-pump coronary artery bypass grafting was subsequently performed to the left anterior descending artery with the left internal mammary artery and posterolateral artery and posterior descending artery with the great saphenous vein. An epicardial lead (Medtronic 4968-35 cm) was then placed on the RV diaphragmatic surface and connected to the newly replaced generator along with the original atrial lead. After confirming successful pacing, the procedure was completed. The patient was extubated 15 h later in the intensive care unit, and there were no postoperative complications.

Histopathological examination of the tissue from the perforated site of the RV confirmed slight inflammation without any specific findings such as ischemic changes or infiltrative damage. Although the length of hospital stay was prolonged due to non-clinical reasons, the patient was discharged 22 days after surgery. The patient was doing very well 6 months after hospital discharge.

Discussion

The incidence of cardiac perforation caused by the lead of a CIED ranges from 0.1% to 5.2% [1,2]. Typically, this occurs within 24 h after implantation. Delayed perforation is a rare phenomenon, with only few documented cases in the literature of instances occurring more than 5 years after implantation [4–6]. To the best of our knowledge, our case represents the most delayed instance of RV perforation caused by CIEDs.

The gradual decrease in the pacing threshold observed over the 2 months preceding perforation may have been indicative of the lead tip slowly advancing into the RV myocardium. It is worth noting this gradual decrease in the pacing threshold over the 2 months preceding perforation, as the RV pacing threshold usually increases over time [7]. Therefore, we must pay attention not only to an increasing but also to a decreasing pacing threshold during the daily CIED check via remote monitoring. Some resistance is noted during lead removal due to the formation of adhesive thrombo-fibrotic lead encapsulations and adhesions to the vein wall and endocardium [8]. However, in this case, there was almost no resistance present during removal, and no thrombus or fibrous tissue adherence to the lead was identified after its removal (Figure 5), which might have contributed to this delayed RV perforation by lead displacement.

Upon recognition of cardiac perforation, lead extraction is typically recommended to prevent further lead migration and extracardiac complications [3,5]. Rajkumar et al reported the efficacy of non-surgical transvenous lead extraction for this condition [9]. However, in our case, the presence of a triple-vessel disease necessitated a surgical extraction; if pericardial effusion had accumulated after transvenous lead extraction, the patient may have immediately become hemodynamically unstable.

In addition, we found no evidence of bloody effusion in the pericardial sac, which may have been due to the oblique penetration of the RV wall of the low-pressure system. Although the patient’s demographic as a thin, older woman was consistent with established risk factors mentioned in the literature, the etiology of the perforation remained uncertain [1,3]. No indications of infection were present, and there was no history of any improvement in cardiac enlargement following amelioration of congestive heart failure. Histological analysis of the tissue obtained from the perforated region failed to uncover any evidence of cardiomyopathy or infarction. The fact that the lead had not adhered to the vasculature may have been a contributing factor to the perforation.

Conclusions

In this study, we describe the case of a delayed RV pacemaker lead perforation that occurred 9 years post-implantation, which was managed via open surgical repair.