The Pandora’s Box of Cardiac Devices: A Case of Infective Endocarditis Postpatent Foramen Ovale Closure

Abstract

Patent foramen ovale (PFO) is a congenital cardiac defect present in approximately 30% of the general population. While often asymptomatic, it is associated with cryptogenic stroke and paradoxical embolism. Percutaneous closure using atrial septal defect occluder is an effective preventive strategy, but these devices carry a risk of rare complications, including infective endocarditis. Device-associated infective endocarditis is often linked to transient bacteremia following invasive procedures, highlighting the importance of antibiotic prophylaxis. However, the clinical presentation can be variable, requiring a high index of suspicion and advanced imaging for the diagnosis. We describe the case of a 55-year-old woman with hypertension, obesity, and a history of PFO closure with an Amplatzer occluder, who developed infective endocarditis weeks after a dental procedure. She presented with fever, vomiting, and confusion, initially misdiagnosed with encephalitis. Transesophageal echocardiography revealed large filamentous vegetation on the Amplatzer occluder, causing functional mitral regurgitation. Blood cultures identified Staphylococcus aureus and Streptococcus pneumoniae, confirming a mixed bacterial infection. The patient underwent surgical removal of the infected device and mitral valve repair. Postoperatively, she improved significantly and was discharged with a complete course of antibiotics. This case underscores the need for vigilance in patients with intracardiac devices, particularly following bacteremia-inducing procedures. Early diagnosis using echocardiography and prompt surgical intervention are essential to managing device-related infective endocarditis. While antibiotic prophylaxis may reduce the risk of bacteremia-related infections, the lack of high-quality evidence necessitates further research to guide preventive strategies. Multidisciplinary care and strict adherence to diagnostic and therapeutic protocols remain pivotal to improving patient outcomes.

INTRODUCTION

Patent foramen ovale (PFO) is a congenital cardiac defect, characterized by a small, persistent opening between the left and right atria, present in approximately 25%–30% of the general population.[1] While often asymptomatic, PFO is implicated in paradoxical embolism and cryptogenic stroke, particularly in younger patients.[2] In these cases, percutaneous closure using intracardiac devices, such as the Amplatzer PFO occluder, has proven to be an effective preventive measure.[3] Despite the success of such interventions, these devices carry a risk of complications, including infective endocarditis, a rare but potentially life-threatening condition.[4]

Infective endocarditis associated with intracardiac devices is often linked to transient bacteremia, which can result from the invasive procedures, such as dental treatments. Patients with intracardiac devices are at heightened risk for bacteremia-related infections, making antibiotic prophylaxis a critical component of care during high-risk procedures.[5] Nonadherence to prophylactic protocols elevates the risk of bacterial seeding on device surfaces, leading to severe complications.

The clinical presentation of device-related infective endocarditis can be variable, ranging from the systemic signs of infection, such as fever and malaise, to more specific neurological symptoms caused by embolic phenomena. As these symptoms often overlap with other conditions, timely diagnosis requires a high index of suspicion, particularly in patients with a history of intracardiac device placement. Imaging modalities, including transthoracic and transesophageal echocardiography, are indispensable in identifying vegetations and assessing valve function.[6]

We present a case that underscores the importance of recognizing the potential for infective endocarditis in patients with PFO closure devices, especially following procedures associated with transient bacteremia. It also highlights the need for stringent antibiotic prophylaxis, comprehensive diagnostic evaluation, and prompt management to improve the outcomes in this vulnerable population.

CASE REPORT

The patient, a 55-year-old woman, was brought to the emergency department due to disorientation, accompanied by vomiting and fever. The symptoms reportedly began approximately 3 weeks earlier, 4 days after a dental procedure, with a progressive worsening over the past 48 h. Upon evaluation, she denied chest pain and presented as drowsy but arousable, with tachypnea. Her body temperature was 38.5°C, she was tachycardic with a heart rate of 105 beats per min, and had hypotension with a blood pressure of 105/60 mmHg. Her oxygen saturation was 93% on room air.

The patient had a history of hypertension and obesity and had undergone percutaneous PFO closure with an Amplatzer device 10 years earlier following a transient ischemic attack.

Initially considered diagnoses included encephalitis, meningitis, systemic bacterial infection, pneumonia, and infective endocarditis. The patient’s neurological symptoms guided the initial differential diagnosis process, raising the suspicion of encephalitis.

On physical examination, a holosystolic murmur was noted in the mitral area, along with decreased breath sounds in the bilateral basal lung fields. A 12-lead electrocardiogram revealed sinus tachycardia with normal atrioventricular conduction and right axis deviation. Laboratory results revealed an elevated white blood cell count of 19,000 cells/mm³, indicating an infectious response. Inflammatory markers were significantly raised, with a C-reactive protein level of 27 mg/L and an erythrocyte sedimentation rate of 53 mm/h, both suggestive of acute infection. The comprehensive metabolic panel showed mildly elevated liver enzymes, with AST and ALT levels slightly above normal (57 U/L and 61 U/L, respectively), while renal function remained within the normal limits (0.9 mg/dL). Cerebrospinal fluid analysis showed elevated protein levels (96.8 mg/dL) and a high white blood cell count (389 cells/mm³), suggesting an inflammatory or infectious process, although the normal glucose level (53 mg/dL) did not support typical bacterial or viral meningitis. Electroencephalogram indicated diffuse cerebral abnormalities. Brain computed tomography (CT) scan was unremarkable for hemorrhage, while chest CT scan showed bilateral pneumonia [Figure 1]. Cardiac evaluation with transthoracic echocardiogram (TTE) showed normal left ventricular function but noted left atrial enlargement and mitral valve regurgitation [Figure 2]. Transesophageal echocardiography (TEE) identified a large filamentous vegetation on the Amplatzer PFO occluder [Figure 3 and Video 1], which was not visible on TTE, indicating infective endocarditis. The mass was large enough to interfere with mitral valve coaptation, leading to significant functional mitral regurgitation [Video 2]. Brain magnetic resonance imaging (MRI) confirmed multiple embolic phenomena [Figure 4]. Blood cultures were positive for Staphylococcus aureus, and urinary antigen testing identified Streptococcus pneumoniae, confirming a diagnosis of mixed bacterial infection. No peripheral stigmata of infective endocarditis was observed during the examination.

Figure 1.

Chest computed tomography scan showing bilateral lower lobes pneumonia and bilateral pleural effusion

Figure 2.

Transthoracic continuous wave Doppler echocardiography showing mitral regurgitation

Figure 3.

Transesophageal echocardiography showing a large filamentous vegetation originating from the patent foramen ovale occluder (a) and extending to involve the mitral valve (b and c), causing significant valve regurgitation (d)

Figure 4.

Magnetic resonance imaging of the brain showing subacute ischemia

The patient initially received empirical treatment with ampicillin/sulbactam and acyclovir. Upon identification of Staphylococcus aureus and S. pneumoniae, the antibiotic regimen was adjusted to vancomycin. Urgent surgical intervention included the removal of the infected PFO occluder [Figure 5] and mitral valve repair. The mechanism of mitral insufficiency was functional rather than stenotic, as the mass primarily interfered with valve coaptation rather than diastolic inflow obstruction. Although removing the vegetation was expected to improve regurgitation, intraoperative assessment revealed persistent dysfunction of the mitral valve apparatus. Likely contributing factors included chronic annular dilation and prolonged leaflet malcoaptation due to altered hemodynamics. Consequently, mitral valve repair was performed to ensure optimal valve function and prevent residual regurgitation.

Figure 5.

Surgical stages of the removal of the patent foramen ovale occlude

Postoperatively, intravenous antibiotics were continued, leading to clinical improvement and eventual discharge.

The patient’s postoperative recovery was uneventful, with significant clinical improvement, resolution of fever, and stabilization of respiratory status. She was discharged with a complete course of antibiotics.

DISCUSSION

PFO is a common finding among the general population and, even if it is often asymptomatic, it can contribute to paradoxical embolism and cryptogenic stroke, making closure necessary in certain cases.[7] Devices such as the Amplatzer PFO occluder have been widely adopted for this purpose, offering significant protective benefits against embolic events. Infective endocarditis associated with PFO and atrial septal defect (ASD) occluder devices occurs at an estimated incidence rate of 0.3%–1.3% per patient-year following device implantation.[8] Statistical evaluations indicated a notable increase in the average duration from the procedure to the onset of IE over the past 5 years, likely linked to modifications in antiplatelet treatment protocols following ASD closure. The pathogenesis of device-associated infective endocarditis is often linked to transient bacteremia, frequently arising from the invasive procedures such as dental work, as in this case. The absence of documented antibiotic prophylaxis underscores the critical need for preventive measures during high-risk procedures. However, it is important to note that the lack of high-quality clinical trials limits definitive conclusions about the effectiveness of antimicrobial prophylaxis to support its routine use.[9,10] This gap in evidence highlights the need for further research to establish definitive recommendations for prophylaxis in patients with intracardiac devices.

The diagnostic challenge of device-associated infective endocarditis lies in its often ambiguous presentation.[11] In this case, the patient’s initial symptoms, characterized by fever and confusion, were misinterpreted as encephalitis. Only through comprehensive investigations, including TTE and ultimately TEE, were vegetations on the PFO occluder identified. The utility of TEE in detecting device-related infections was evident, particularly as vegetations were missed on TTE.[12] Further, brain MRI confirmed embolic phenomena, linking the infection to the patient’s neurological manifestations.

Regarding the mechanism of mitral regurgitation, the large vegetation on the occluder functionally impaired mitral valve coaptation rather than causing direct leaflet damage. While some cases of large atrial vegetations can lead to mitral stenosis, the specific position and mobility of the vegetation in this case resulted in regurgitation instead. Despite removing the infected occluder, persistent functional mitral regurgitation required surgical valve repair, likely due to annular dilation and leaflet malcoaptation from prolonged hemodynamic stress.

Effective management of device-associated infective endocarditis relies on the timely diagnosis and prompt intervention. In this case, early surgical removal of the infected device, coupled with mitral valve repair and targeted antibiotic therapy, resulted in favorable outcomes.[13] The transition from empirical antibiotic therapy to pathogen-specific treatment also underscores the importance of rapid microbiological diagnosis in guiding therapy.

CONCLUSIONS

While PFO closure devices effectively prevent paradoxical emboli, they can occasionally lead to severe complications such as infective endocarditis. This case not only emphasizes the importance of early recognition and multidisciplinary management but also provides a critical reminder of the potential importance of antibiotic prophylaxis in patients with intracardiac devices. Although the effectiveness of antimicrobial prophylaxis is uncertain, adherence to prevention, diagnosis, and treatment protocols remain essential to reducing the risk of severe complications like infective endocarditis. Further clinical studies are urgently needed to refine prophylactic strategies and optimize care for this vulnerable population.

Clinicians should maintain a high index of suspicion for device-related infections, especially in patients presenting with systemic or neurological symptoms. Early diagnosis through echocardiography and timely surgical intervention are essential for improving the patient outcomes.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.