
==== Front
Perm J
tpj
tpj
The Permanente Journal
1552-5767
1552-5775
The Permanente Press

38980767
10.7812/TPP/24.044
TPJ-24-044
Evidence-Based Case Report
A Rare Case of Acute Pericarditis With Cardiac Tamponade Secondary to Pacer Lead Perforation 8 Years After Placement
http://orcid.org/0000-0003-4082-2829
Nader Georgette MD 1
http://orcid.org/0009-0006-2291-7348
Watat Kevin DO 1
http://orcid.org/0000-0002-1748-4262
Wang Enhua MD 2
http://orcid.org/0000-0002-7352-6682
Sharma Akhil DO 3
http://orcid.org/0009-0006-9808-5218
Jandali Mhd Hussam Al MD 4
1 MSU Department of Medicine, Sparrow Hospital, Lansing, MI, USA
2 Department of Cardiology, Jefferson Einstein Medical Center, Philadelphia, PA, USA
3 Department of Pulmonary and Critical Care Medicine, Henry Ford Hospital, Detroit, MI, USA
4 Department of Critical Care Medicine, Sparrow Hospital, Lansing, MI, USA
Georgette Nader, MD nadergeo@msu.edu
2024
18 6 2024
28 3 185189
© 2024 The Authors.
2024
https://creativecommons.org/licenses/by-nc-nd/4.0/ Published by The Permanente Federation LLC under the terms of the CC BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.

Keywords:

pericarditises
cardiac tamponade
cardiothoracic surgery
catheterization
echocardiography
electrophysiology
intensive care
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pmcIntroduction

Cardiac perforation is defined as puncture or migration of a lead through myocardium.1 Cardiac perforation of the right ventricle is a rare and lethal complication that occurs in approximately 0.4% to 0.8% of pacemaker placements.2,3 Most common causes of perforation are through trauma secondary to catheter or lead manipulation and/or myocardial rupture secondary to injury or ablation.4 Timing differentiates cardiac perforation subtype. Acute perforation occurs within 24 hours of pacemaker placement, subacute perforation occurs within 1 month of placement, and delayed perforation occurs within 30 days of placement.5 Delayed or chronic perforations are extremely rare, occurring in 0.1% of all cases.6 In isolated case reports, management has commonly involved percutaneous extraction of lead under transesophageal echocardiography (TEE) observation, with surgical intervention on standby.7–9 The case presented pertained to a delayed pacemaker perforation occurring 8 years after implantation that was managed medically without surgical intervention.

Case Presentation

A 77-year-old man with past medical history remarkable for sick sinus syndrome (following a permanent Medtronic dual chamber pacemaker placed 8 years prior) and paroxysmal atrial fibrillation (AFib)—on Apixaban with hyperlipidemia, depression, and obstructive sleep apnea— presented to the emergency room with chief complaints of nausea, emesis, and sharp nonradiating pleuritic chest pain, 4/10 in severity. Patient initially attributed his symptoms to gastroenteritis after eating takeout food the night prior. On presentation, he was afebrile; hypotensive requiring levophed 0.1 mcg/kg/min IV infusion; and hypoxic and tachypneic requiring nonrebreather mask at 15 L. Physical examination showed an ill-appearing man in acute distress, with lungs clear to auscultation bilaterally, distant heart sounds with diminished pulses, cool lower extremities, and mild abdominal tenderness. Laboratory values were indicative of shock (Table 1).

Table 1: Initial vitals and laboratory workup upon admission

Investigation	Values	Reference range	
Blood pressure	80/40 mmHg	120/80 mmHg	
Respiration rate	27 bpm	12–20 bpm	
Initial troponin
Repeat troponin	< 2 ng/dL
21 ng/dL	0–18 ng/L	
Lactate	5.8 mmol/L	0.2–1.8 mmol/L	
Serum bicarbonate	10 mmol/L	20–32 mmol/L	
Anion GAP	11	2–16	
Aspartate aminotransferase	116 U/L	10–40 U/L	
Alanine transaminase	Alanine transaminase 174 U/L	2–45 U/L	
Lipase	5.8 U/L	22–51 U/L	
Blood urea nitrogen	Blood urea nitrogen 31 mg/dL	Blood urea nitrogen 6–23 mg/dL	
Creatinine	1.35 mg/dL	Patients baseline creatinine 0.5 mg/dL
Reference range creatinine 0.6–1.4 mg/dL	
White blood cell count	10.4 × 103/ U/L	4–12 × 103/ U/L	
Hemoglobin	14.4 g/dL	12.6–16.5 g/dL	
Platelet count	125 × 103/ U/L	150–400 × 103/ U/L	
bpm, Beats per minute; g/dL, Grams per deciliter; mg/dL, Milligrams per decliter; mmHg, Millimeters of mercury; mmol/L, Millimoles per liter; ng/dL, Nanograms per deciliter; U/L, Units per liter.

Initial electrocardiogram (EKG) revealed intermittently atrial-paced rhythm with diffuse ST elevations, which was concerning for acute pericarditis when compared to baseline EKG (Figure 1a and b). Echocardiogram (ECHO) showed a large pericardial effusion with early diastolic collapse and plethoric inferior vena cava. ECHO showed preserved left ventricular ejection fraction (LVEF) of 70% to 75% and large pericardial effusion with right ventricular diastolic collapse consistent with cardiac tamponade (Figure 2a). Subsequent contrast-enhanced ECHO with bubble study was without pericardium extravasation. Computer tomography (CT) of the chest demonstrated presence of large pericardial effusion, with right ventricular pacer lead appearing to extend beyond the apex of the myocardium into pericardial space (Figure 2b). Interrogation of the pacemaker showed atrial pacing of 95% with normal threshold sensing and impedance.

Figure 1: (A) Baseline EKG prior to presentation; (B) EKG on presentation; (C) EKG prior to hospital discharge. EKG = electrocardiogram.

Figure 2: (A) Parasternal long axis view showing large effusion surrounding the myocardium, evidence of a device lead noted in apical right heart chambers; (B) coronal CT scan depicting pacemaker lead tracking through the right ventricle myocardium into the pericardial space with surrounding pericardial effusion. CT = computer tomography.

Treatment Pathway

Given the fact that the patient was afebrile and had mild leukocytosis, diminished pulses, and cool extremities, he was thought to be in in cardiogenic shock secondary to cardiac tamponade from lead perforation. Thus, the patient was taken to cardiac catheterization laboratory for emergent pericardiocentesis, with drainage of 470 mL grossly bloody fluid and percutaneous drain placement. Post-pericardiocentesis labs showed improvement in perfusion with lactate, trending from 5.8 to 2.7. Anticoagulation was discontinued given nature of the effusion. The following day, the patient developed AFib with rapid ventricular response, which was controlled with IV amiodarone infusion of 1 mg/min. It was later transitioned to oral amiodarone of 400 mg daily. Electrophysiology, along with cardiovascular and thoracic surgery, were consulted. They recommended no acute intervention due to greater chance of harm coming from open-heart surgery or lead extraction in the patient, who was maintaining hemodynamic stability following pericardiocentesis. Percutaneous drain was removed 7 days after placement, and the patient was medically managed with colchicine of 1 mg q12 hours, followed by colchicine of 0.5 mg q12 for pericarditis.

Outcomes

Patient was subsequently discharged home with plans for outpatient Watchman device placement. EKG continued to show atrial-paced rhythm (Figure 1c). Repeat complete ECHO 7 days following discharge showed LVEF of 65% to 70%, pacemaker lead within the right ventricle, and no further evidence of pericardial effusion. Patient was contacted 1.5 years following hospital discharge and reported no recurrent episode of perforation or necessary extraction of the lead.

Discussion

Cardiac perforation is a rare phenomenon that can occur with any intracardiac lead. It tends to occur more commonly with implantable cardioverter-defibrillator (ICD) placements (0.6%–5.6%) than with pacemakers (0.1%–0.8%).10,11 Review of literature suggests that lead-induced cardiac perforation occurs more commonly in patients with temporary pacemakers, patients with pacemakers placed through active fixation, or patients with atrial stimulation. Meanwhile, ICD perforation occurs more commonly with double spiral leads, increased lead length, small tip surface/diameter, and apical positioning.12 Despite cardiac ventricles having greater wall thickness, right apical ventricular lead perforation tends to occur more commonly than atrial perforation.11,13 Additional studies have shown that thinner areas of the myocardium, dilated cardiac chambers with impaired systolic function, or recent myocardial infarction in the inferior wall or right ventricle can create a predisposition to lead perforation.13,14

Cardiac perforation induced by pacemaker lead places patients at an increased chance of pacemaker failure, hemopericardium, tamponade, pneumothorax, longer hospital stay, and chance of in-hospital death.1,15 Early detection and management of lead perfusion can help improve patient outcomes. The most common risk factors in patients creating a predisposition to lead perforation include steroid use prior to insertion, BMI of less than 20 kg/m2, older age (70.1 years ± 12.3 years), female sex, anticoagulation within 7 days of pacemaker implantation, worsening New York Heart Association heart failure class, and nonischemic cardiomyopathy. Conversely, patients with lower odds of perforation are those with history of AFib, diabetes mellitus, cardiac bypass surgery, or higher implanter procedural volume.1,15 On initial presentation, patients with pacemaker lead perforation often exhibit chest pain, syncope, hiccups, defibrillation, or inadequate shocks of their ICD.1,5,16 Typical presentation involves altered electrical lead parameters. Increase in capture threshold, reduction in sensing threshold, and inappropriate shocks have been documented.7,13 However, as this case has illustrated, not all pacemaker perforations present with altered electrical lead parameters. The authors hypothesize that the lead continued to have residual function, as it may have remained in contact with otherwise functional cardiac tissue. Thus, clinicians should not exclude perforation in the absence of altered parameters.

Clinical presentation and further diagnostic imaging are crucial, as patients with late pacemaker perforation often present with more varied symptoms than patients in the acute or subacute state and patients with varied lead positions.11,13 In this patient, imaging with chest x-rays (CXRs) and altered electrical parameters were nondiagnostic of pacemaker perforation. Transthoracic ECHO (TTE) imaging was suggestive of lead advancement into the myocardium. However, TTE was unable to locate the exact lead position and/or confirm perforation. CT was most beneficial in depicting lead advancement through the myocardium and into the pericardial space. Recent data have supported the use of CT imaging over CXR and TTE in the diagnosis of cardiac perforation. Comparison studies of non-EKG-gated multidetector CT to right ventriculography showed non-EKG-multidetector CT to have a specificity of 68.2% and right ventriculography to have a specificity of 94.8%.17 Meanwhile, EKG-gated contrast-enhanced cardiac CT compared with CXR and TTE was shown to have sensitivities of 100% and 85.7%, respectively.18 Additionally, several case reports have supported CT imaging’s ability to aid in detecting lead tip and surrounding damage, as well as to guide in future interventions.12,16

Management of pacemaker lead perforation varies based on the timing of onset (acute and subacute vs chronic) and complications of perforation. In this patient, pacemaker perforation resulted in pericarditis and tamponade, which required emergent pericardiocentesis. Generally, pacemaker perforation in the absence of tamponade requires percutaneous or simple extraction of the lead under TEE observation with surgery on standby in the operating room. The majority of case reports opted for surgical intervention due to hemodynamic compromise, chance of damage to neighboring organs, and the acute or subacute nature in relation to pacemaker placement.3,16,19 However, the team opted against surgical intervention to reposition or extract the lead due to increased risk of cardiac compromise in the setting of delayed pacemaker perforation 8 years after initial placement. There were growing concerns that electrode leads might have been adherent to the myocardium and extraction, or that repositioning might have predisposed the patient to escalated cardiac compromise and death. Given the fact that the patient remained hemodynamically stable with retained function of the pacemaker lead, the authors felt that extraction or repositioning would pose a greater chance of imminent harm than supposed benefit. Thus, medical management was deemed to be the safest option to reduce chance of death or reaccumulation of tamponade. Following pericardiocentesis, the patient became hemodynamically stable, the pacemaker function remained intact, and the patient was treated medically for pericarditis. The patient was subsequently discharged home with plans for outpatient Watchman placement. Repeat complete ECHO 7 days and 90 days following discharge showed LVEF of 65% to 70%, pacemaker lead within the right ventricle, and no further evidence of pericardial effusion. The patient was contacted 1.5 years following this encounter and reported no recurrent episode of perforation or necessary extraction of the lead.

Although the patient had no further episodes of cardiac tamponade or lead perforation, several factors supported conservative management in this patient. These factors included a long latency period between implantation and perforation, retained function of pacemaker lead, and—most importantly—normal ventricular wall thickness. It can be hypothesized that patients with evidence of ischemia, necrosis, or conditions that affect underlying ventricular wall structure would not benefit from such conservative measures, as the chance of recurrent perforation and tamponade would be great.

Conclusion/Take-Home Points

Contrary to previous literature, this case demonstrated the fact that not all delayed pacemaker perforations present with altered electrical lead parameters. Providers must therefore have high clinical suspicion for early detection. Additionally, this case contributed to practice change in the management of pacemaker lead perforation, as lead perforations have often been managed with lead extraction under TEE guidance with surgery on standby. However, in this particular case, given the long latency period between lead placement and perforation, medical management was felt to be the safest option for the patient. The patient’s continued hemodynamically stability—and lack of cardiac compromise necessitating lead extraction 1.5 years following discharge—has created support of medical management in some cases. This case also highlighted a team-based approach to patient care in the management of rare and complicated cases such as delayed lead perforation. The case does this by exemplifying the importance of multidisciplinary input including cardiac electrophysiologists, cardiovascular and thoracic surgeons, and intensive care physicians. To the knowledge of the authors, this case represented the longest duration of delayed pacemaker lead perforation: 8 years after placement.

Author Contributions: Georgette Nader, MD, participated in the data collection, drafting, review, and submission of the manuscript. Kevin Watat, DO, participated in the data collection and drafting of the manuscript. Enhua Wang, MD, participated in the data collection and review of the manuscript. Akhil Sharma, DO, participated in the data collection, review, and submission of the manuscript. Mhd Hussam Al Jandali, MD, participated in the review and submission of the manuscript.

Conflicts of Interest: None declared

Funding: None declared

Informed consent: Informed consent over phone and witnessed by additional provider.

Correction Notice: This is the corrected version of record. Please see corrigendum in this issue, which corrects the previously published Online First version of this article in which a figure was inadvertently duplicated.

Relevancy Statement: This case contributes to practice change in the management of pacemaker lead perforation as lead perforations are often managed with lead extraction under transesophageal echocardiography guidance with surgery on standby. Furthermore, this case highlighted a team-based approach to patient care in management of rare and complicated cases, such as delayed lead perforation, by exemplifying the importance of multidisciplinary input, including cardiac electrophysiologists, cardiovascular and thoracic surgeons, and intensive care physicians.
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