Is device closure for direct access valved stent implantation safe?

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 watt 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 hemodynamics were recorded. The animals were sacrificed electively and the histopathotogical changes in and around AMuscVSDO in the right ventricular watt 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 mm Hg 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 rote of a collagenisation promoter, active from the 3rd week till it vanishes. Inflammation plays a rote as a temporary reaction (0-3 weeks) during the heating process, with no signs of any active, focal or circumscribed, myocardial damage. Conclusions: (1) The closure of the free ventricular watt perforation with AMuscVSDO is safe due to the scar tissue resulting from the heating process around and in the device. (2) The myocardial heating 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. (c) 2006 Elsevier B.V. All rights reserved.