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European Heart Journal Advance Access originally published online on September 14, 2006
European Heart Journal 2007 28(6):684; doi:10.1093/eurheartj/ehl245
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Pathology of explanted ASD occluder

Gerhard Bauriedel1,2,*, Dirk Skowasch2 and Matthias Peuster3

1 Department of Internal Medicine I/Cardiology, Klinikum Meiningen, Meiningen, Germany
2 Department of Internal Medicine II/Cardiology, University of Bonn, Bonn, Germany
3 Department of Pediatric Cardiology and Pediatric Intensive Care Medicince, University of Rostock, Rostock, Germany

* Corresponding author. E-mail address: g.bauriedel.med1{at}klinikum-meiningen.de

A 45-year-old woman with previous apoplexia due to paradoxical embolism via atrial septal defect (ASD) received a 28 mm Amplatzer ASD occluder (AGA Medical Corp., USA). The device was explanted by surgery 15 months later when transoesophageal echocardiography documented that a small residual interatrial shunt post-intervention increased continuously.

Macroscopic inspection of the explanted occluder showed large surface areas covered by white glistening tissue of variable thickness and some patches with bare metal nitinol struts (Panel A). In contrast, tissue localized between the occluder discs appeared hyperaemic and prevented complete disc separation (Panel B). Although no wire fraction was observed, detailed electron microscopy gave ample evidence for pit corrosion (Panel C). Immunohistochemistry demonstrated most device areas covered by an endothelial monolayer and collagen-rich fibroelastic tissue that continuously merged into broad fibrous endocardium. This ‘pseudointima’ showed numerous alpha-smooth muscle actin+ cells and signalling of heat shock protein 47 indicative of ongoing collagen synthesis. Cell-rich, vascularized granulation tissue between the wire mesh discs comprised monocyte infiltrates composed of CD68+ macrophages as well as single cells expressing CD34 as haematopoietic progenitor cell marker. Presence of dendritic cells indicated by S100 (Panel D) and fascin was found close to the metal struts, whereas CD3 lymphocyte immunolabelling was sparse throughout all tissue areas. No vegetations or histopathological evidence of acute infection were detected within the specimen.

The explanted Amplatzer ASD occluder demonstrated (i) a partly incomplete endothelial covering, (ii) pit corrosion, and (iii) ongoing inflammation and granulation adjacent to fibroelastic scarring even 15 months after device implantation.

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