HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Stock, U.A. Articles by Lutter, G. Search for Related Content PubMed PubMed Citation Articles by Stock, U.A. Articles by Lutter, G. Related Collections Valve disease

J Thorac Cardiovasc Surg 2006;131:1323-1330
© 2006 The American Association for Thoracic Surgery

Evolving Technology

Prevention of device-related tissue damage during percutaneous deployment of tissue-engineered heart valves

^a Department of Cardiothoracic and Vascular Surgery, Friedrich-Schiller-University, Jena, Germany
^b Department of Medical Physics and Biophysics, Charité University, Berlin, Germany
^c Department of Cardiovascular Surgery, Heart Center Brandenburg, Bernau/Berlin, Germany
^d Department of Cardiovascular Surgery, Christian-Albrechts-University, Kiel, Germany
^f Department of Medical Statistics, Christian-Albrechts-University, Kiel, Germany
^e Cardiovascular Research Laboratories, David Geffen School of Medicine, UCLA, Los Angeles, Calif.

Received for publication October 31, 2005; revisions received January 15, 2006; accepted for publication January 24, 2006.

^_* Address for reprints: Ulrich A. Stock, MD, Department of Medical Physics and Biophysics, University Hospital Charité, Invalidenstrasse 42, 10098 Berlin, Germany. (Email: ulrich.stock{at}charite.de).

BACKGROUND: Endovascular application of pulmonary heart valves has been recently introduced clinically. A tissue-engineering approach was pursued to overcome the current limitations of bovine jugular vein valves (degeneration and limited longevity). However, deployment of the delicate tissue-engineered valves resulted in severe tissue damage. Therefore the objective of this study was to prevent tissue damage during the folding and deployment maneuver.

MATERIAL AND METHODS: Porcine pulmonary heart valves, small intestinal submucosa, and ovine carotid arteries were obtained from a slaughterhouse. After dissection and antimicrobial incubation, the valves were trimmed (removal of sinus and most of the muscular ring) to fit into the deployment catheter. The inside (in-stent group, n = 6) or outside (out-stent group, n = 6) of a nitinol stent was covered by an acellular small intestinal submucosa, and the valves were sutured into the stent. The valves were folded, tested for placement in the deployment catheter, and decellularized enzymatically. Myofibroblasts were obtained from carotid artery segments and seeded onto the scaffolds. The seeded constructs were placed in a dynamic bioreactor system and cultured for 16 consecutive days. After endothelial cell seeding, the constructs were folded, deployed, and processed for histology and surface electron microscopy.

RESULTS: The valves opened and closed competently throughout the entire dynamic culture. Surface electron microscopy revealed an almost completely preserved tissue in the in-stent group. Stents covered with small intestinal submucosa on the outside, however, showed severe damage.

CONCLUSION: This study demonstrates that small intestinal submucosa covering of the inside of a pulmonary valved stent can prevent stent strut–related tissue damage.