ICD-Electrode-Perforation of the Right Ventricle to the Pericardium with and without Pericardial Effusion

A B S T R A C T

Two cases are described of iatrogenic traumatic perforation of an ICD electrode through the myocardium in the right ventricle and to the pericardium. The diagnostic gold standard gated CT was not necessary in either case. In the first case the lead insertion was difficult, time-consuming, and complicated by the Post-Cardiac Injury Syndrome and a slowly accumulating hemorrhagic pericardial effusion causing cardiac tamponade, diagnosed by the clinical picture, elevated CRP, ECG with low voltage and electrical alternans, chest X-ray revealing enlarged cardiac silhouette and echocardiography a large effusion, treated with pericardiocentesis and drainage. In the other case there was painful pericardial irritation and extracardiac pacing and ICD failure with loss of capture, no diagnostic changes in ECG, chest X-ray, and echocardiography; diagnosed by fluoroscopy during replacement at the lead, which went without complications and without pericardial effusion.

Keywords

ICD-electrode, cardiac perforation, cardiac tamponade, loss of capture, echocardiography, gated CT

Introduction

About 1% of all pacemaker implantations are complicated by symptomatic perforation of the cardiac wall within one month after implantation. The perforation spans from insignificant with the cardiomyocytes contracting and closing the defect to perforation of the helix outside the heart injuring the pericardium, pleura, and organs. The symptoms span from discrete to lethal. Knowledge of this potentially fatal complication is important in order to diagnose and treat it in due time [1-6].

Case-1

A 64-year-old male had a VVI-Pacemaker (PM) implanted due to slow atrial fibrillation and syncope. CRP was <2,9 mg/L and BMI was 30. Two weeks later, he was diagnosed with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) and Ventricular Tachycardia (VT). He had the brady pacemaker explanted and a VVI-Implantable Cardioverter Defibrillator (ICD) implanted instead. Upon examination, the right cavities were found to be hugely dilated. On both occasions, the electrode was tested in several positions. The ICD electrode was finally secured on the septum with acceptable values which remained stable. He was discharged the following day.

Two weeks later, he started experiencing increasing dyspnea and growing edemas. CRP was elevated to 140 mg/L. Six weeks after the implantation procedure he was readmitted in a very poor state with severe respiratory difficulties, orthopnea, pulsus paradoxus, and anasarca corresponding to pericardial tamponade. CRP 30 mg/L. ECG (Figure 1), chest X-ray (Figure 2), and echocardiography (Figure 3) confirmed the diagnosis. Echocardiography revealed a large pericardial effusion measuring 4 cm around the swinging heart and compressing the cavities. Pericardiocentesis resulted in removal of three liters of sanguineous serous fluid. Afterwards the CRP was elevated to 100 mg/L for about a fortnight, when it started to fall and about a month after the pericardiocentesis CRP was <2,9 mg/L, where it has remained since. The ICD electrode was operating well. As the electrode was still located on the septum, it did not cause the pericardial perforation and for this reason, it was not replaced. A small pericardial effusion was seen for some weeks after the pericardiocentesis and then disappeared without any treatment and the patient recuperated.

Case-2

A 70-year-old male had a secondary prophylactic VVI-ICD implanted due to ischemic heart disease, VT, and syncope. The electrode was secured in the apex of the right ventricle. The surgeon reported no problems. BMI was 25. Two days after the surgical procedure he was readmitted due to severe back and chest pain worsening with respiration. Loss of capture and accentuation of the pain during pacing was observed. Based on the clinical picture and the pacemaker test it was concluded that the electrode had probably perforated the cardiac wall. ECG was unchanged. Chest X-ray not diagnostic (Figure 4). Fluoroscopy confirmed that the electrode had perforated several centimeters through the apex of the right ventricle to the pericardial sac between the base of the heart and the diaphragm. No pericardial effusion was found. The electrode was replaced without complications, still without pericardial effusion. No further problems were encountered.

Discussion

The risk of cardiac perforation is higher with insertion of an ICD electrode than with an ordinary pacemaker electrode [3-8]. The electrode should be fixed with caution. Other risk factors are female gender, BMI<20, age>80 years, corticosteroid treatment, anticoagulation, platelet therapy, restless patient, inexperienced surgeon, over screwing of the electrode, excessive pressure on the electrode during fixation, and excessive electrode loop [2-4, 8-11]. None of these risk factors was present in neither case 1, nor case 2.

Perforation is a risk when the electrode is secured in the free wall or in the apex which is relative thin walled, as in case 2. Instead, the surgeon should attempt to fix the electrode on the septum, as in case 1 [1, 3, 8]. In addition to this, there is an increased risk of perforation when one electrode is replaced by another (as in case 1) when repeated repositioning of the electrode is necessary (as in case 1) and in patients with a thin-walled dilated cardiomyopathy (as in case 1) or ischemic cardiomyopathy (as in case 2) [8].

In case 1, a perforation occurred while checking for a good lead position, not when the lead was positioned on the septum. Therefore, lead replacement was not necessary. Slow accumulation of pericardial fluid allowed the collection of a large effusion in weeks before a significant increase in the pericardial pressure caused symptoms and signs. After treatment of the tamponade by drainage of the pericardial effusion, there were no more significant events. Pericardial bleeding is a trigger for the immune-mediated inflammatory post-cardiac injury syndrome (PCIS), which is difficult to differentiate from simple mechanical consequences of surgery. PCIS is associated with elevated CRP, as in case 1 [2, 12].

In patient 2, the perforation happened at the typical site, in the apex of the right ventricle. This patient had no pericardial effusion but pericardial irritation with severe pain accentuated by respiratory movements and by pacing. The pacemaker had no capture in the heart but there was painful extracardiac pacing. Despite perforation, the pacemaker values may remain normal; otherwise, the typical finding is an increase in the threshold or loss of capture, as in this case, or inappropriate shock [2-8, 11].

The two cases illustrate typical symptoms and consequences of perforation. The diagnostic gold standard is gated CT, which has optimal demarcation of the interface between the myocardium, blood and fat, although star artefacts from the pacemaker wire sometimes make it difficult to precisely identify the tip of the lead. Fluoroscopy, chest radiography, and echocardiography are not as reliable to diagnose perforation of the heart, as in case 2 where perforation was diagnosed from the clinical picture and ICD-failure with loss of capture [2-5, 7, 11, 13-15]. In acute and subacute perforation, transvenous lead extraction is possible without any difficulties, as in case 2. However, extraction demands hemodynamic and echocardiographic monitoring and preparedness to perform pericardiocentesis and surgical extraction [3-9, 11].

Conflicts of Interest

None.

Funding

None.

Article Info

Article Type

Case Report

Publication history

Received: Sat 30, May 2020
Accepted: Fri 12, Jun 2020
Published: Fri 19, Jun 2020

Copyright

© 2023 Line Lisbeth Olesen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.RDI.2020.02.09

Author Info

Line Lisbeth Olesen

Corresponding Author

Line Lisbeth Olesen
Department of Cardiology, Zealand University Hospital, Roskilde, Denmark

Figures & Tables

Figure 1: Case 1, Atrial fibrillation and ventricular pacing. A) ECG during cardiac tamponade demonstrating relative low voltage (compared to B) and pulsus paradoxus with variation in amplitude/electrical alternans and swinging baseline. B) ECG after resolution of the pericardial effusion.

Figure 2: Case 1, X-ray of thorax after implantation of ICD. A) On the way of the implantation. B) 3 weeks later. C) 6 weeks later. Gradually enlarging heart shadow and increasing distance from the tip of the electrode to the rim of the cardiac silhouette, corresponding to expanding pericardial effusion.

Figure 3: Case 1, Echocardiography. Pericardial effusion of 4 cm surrounding the heart. Fibrinous coating of the wall of the right ventricle. The ICD electrode lies in the right ventricle and the tip is secured on the septum (red circle).

Figure 4: Case 2, A) The day the ICD was implanted. B) The following day: the electrode has straightened and moved- and perforated apex of the right ventricle to the pericardial sac.

References

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