Non-infectious inflammation in atrial septum after GORE® CARDIOFORM septal occluder implantation

Abstract

Figures

(A and B): (A) Mid-oesophageal aortic valve short-axis view, (B) mid-oesophageal bicaval view. The first transoesophageal echocardiography shows marked thickening of the atrial septal wall at the site of GORE CARDIOFORM septal occluder (GSO) implantation (arrow). (C) An 18F-fluorodeoxyglucose (FDG) positron emission tomography shows a high level of 18F-fluorodeoxyglucose accumulation at the site of the GORE CARDIOFORM septal occluder implanted in the atrial septum (arrow). (D) Mid-oesophageal bicaval view. The second transoesophageal echocardiography shows a remission of the atrial septal wall thickening at the site of the GORE CARDIOFORM septal occluder implantation (arrow). Ao, aorta; LA, left atrium; RA, right atrium; SVC, superior vena cava.

Full text

Case description

A 56-year-old female patient was admitted to our institution with fever 5 days after uncomplicated implantation of a 25-mm GSO device for patent foramen ovale which caused paradoxical cerebral infarction. Although the laboratory test showed a high level of inflammatory reaction (C-reactive protein: 9.45 mg/dL), repeated blood cultures and procalcitonin were all negative. Transoesophageal echocardiography demonstrated marked wall thickening of the atrial septum at and around the site of the GSO implantation (Figure 1A and B), though no other abnormal findings such as vegetation, intracardiac thrombus, pericardial effusion, or erosion were detected. An ^18^F-fluorodeoxyglucose positron emission tomography (FDG-PET) revealed a high level of FDG accumulation at the site of the GSO implanted in the atrial septum (Figure 1C). A patch testing for components of GSO [nickel, titanium, and expanded polytetrafluoroethylene (ePTFE)] was all negative. Her fever gradually subsided within 7 days of admission, and the laboratory test showed that her inflammatory response was decreasing day by day. The second TEE, 1 week after the first, demonstrated a spontaneous remission of the atrial septal wall thickening (Figure 1D). She was discharged after careful observation and had no recurrence of symptoms at her 1-month follow-up. Based on the results of each examination, the origin of the fever was considered to be a non-infectious, non-allergic inflammation caused by excessive healing process of the atrial septum. Patent foramen ovale closure using a percutaneous occluder is a well-established procedure, and complications requiring surgical explantation of a device due to infection, erosion, and allergy are rarely reported.^1,2^ However, the development of fever and inflammation after the procedure is sometimes observed, which resolves spontaneously.^3^ The present case suggests that close observation should be sought first instead of hasty explantation after exclusion of device infection, erosion, thrombosis, and allergic reaction.

(A and B): (A) Mid-oesophageal aortic valve short-axis view, (B) mid-oesophageal bicaval view. The first transoesophageal echocardiography shows marked thickening of the atrial septal wall at the site of GORE CARDIOFORM septal occluder (GSO) implantation (arrow). (C) An 18F-fluorodeoxyglucose (FDG) positron emission tomography shows a high level of 18F-fluorodeoxyglucose accumulation at the site of the GORE CARDIOFORM septal occluder implanted in the atrial septum (arrow). (D) Mid-oesophageal bicaval view. The second transoesophageal echocardiography shows a remission of the atrial septal wall thickening at the site of the GORE CARDIOFORM septal occluder implantation (arrow). Ao, aorta; LA, left atrium; RA, right atrium; SVC, superior vena cava.

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Funding: None declared.