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Eur J Cardiothorac Surg 2006;30:4-9
© 2006 Elsevier Science NL

Is device closure for direct access valved stent implantation safe?

Malgorzata Pawelec-Wojtalik a , * , Jerzy Nozynski b , Michal Wojtalik c , Maciej Piaszczynski c , Rafal Surmacz a , Dorota Bukowska d , Wojciech Mrówczynski c

a Department of Pediatric Radiology, University of Medical Sciences, Poznan, Poland
b Department of Histology and Embriology, Silesian Medical University, Zabrze, Poland and Department of Histopathology, Silesian Centre for Heart Diseases, Zabrze, Poland
c Department of Pediatric Cardiac Surgery, University of Medical Sciences, Poznan, Poland
d Department of Veterinary Medicine, University of Agriculture, Poznan, Poland

Received 17 October 2005; received in revised form 30 March 2006; accepted 31 March 2006.

* Corresponding author. Tel.: +48 61 8491 480; fax: +48 61 8669 130. (Email: mpwojt{at}poczta.onet.pl).

Objective: Despite the progress made in the development of valved stents for trans-apical valve replacement, a reliable closure of the access orifice remains a major issue. The present study was designed to evaluate if device closure of the ventricular wall is safe. Materials and methods: Transventricular access for pulmonary valve replacement was simulated with a 26F sheath and the resulting orifice was closed with an Amplatzer Muscular VSD Occluder (AMuscVSDO) in chronic sheep experiments (body weight 45–48 kg). Mean procedure time, blood loss, and standard hemo-dynamics were recorded. The animals were sacrificed electively and the histopathological changes in and around AMuscVSDO in the right ventricular wall were systematically studied by semi-quantitative analysis of collagenisation, inflammatory response and ‘resorptive’ process. Results: Mean procedure time was 31 ± 10.7 min, blood loss was 22.5 ± 8.7 ml, heart rate was 123 ± 22.6 bits/min before and 128 ± 28.7 bits/min after, mean arterial blood pressure was 88 ± 16.7 mmHg before and 82.6 ± 18.3 mmHg after the procedure. Mean survival was 5.3 weeks. The collagen and scar formation studies revealed three different periods: (1) initial fibrosis (0–3 weeks); (2) so-called ‘capsulation’ (3–9 weeks after the implantation of the Occluder); and (3) final remodelling and differentiation (9 weeks). The fabric inside the Occluder played the role of a collagenisation promoter, active from the 3rd week till it vanishes. Inflammation plays a role as a temporary reaction (0–3 weeks) during the healing process, with no signs of any active, focal or circumscribed, myocardial damage. Conclusions: (1) The closure of the free ventricular wall perforation with AMuscVSDO is safe due to the scar tissue resulting from the healing process around and in the device. (2) The myocardial healing around and inside an implanted AMuscVSDO represents two processes: extensive fibrosis ensues around metallic wires with the progression towards the inside of the myocardium, whereas inside AMuscVSDO the loose connective tissue fills the myocardial lesion. During cicatrisation, the fabric elements of AMuscVSDO act as the ground for collagen formation and fibroblast proliferation. (3) The cicatrisation processes after ventricular AMuscVSDO implantation show remodelling, with rearrangement of collagen fibres architecture and distribution.

Key Words: Valved stents • Closure device • Amplatzer device • Pathology • Hybrid procedures




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