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J Thorac Cardiovasc Surg 2008;135:1406-1407
© 2008 The American Association for Thoracic Surgery
Letter to the Editor |
Department of Cardiological, Thoracic and Vascular Sciences, Division of Cardiac Surgery, Padua University Medical School, Padua, Italy
To the Editor:
In their article focusing on in vivo autologous recellularization of a tissue-engineered heart valve, Vincentelli and colleagues1
raise 2 main questions: (1) Which are the best candidates for scaffold repopulation? (2) Does direct injection of cells into the scaffold guarantee adequate cellular recolonization?
According to the cell type chosen for scaffold seeding, the adoption of nonselected bone marrow–derived mononuclear cells was associated with early degeneration with thickening and retraction of the cusps, growth of fibrotic pannus along the suture lines, and thickening and calcification of the wall conduits. Histologically, a marked inflammatory response with extracellular matrix disarray and macrophage infiltration both in the adventitia and the media layers were observed, along with a loss of the proper collagen allocation between the ventricularis, spongiosa, and fibrosa of the leaflets. Additionally, a significant increase of both transvalvular and distal gradients were recorded at 4-month follow-up echocardiographic analysis. On the contrary, scaffolds repopulated with mesenchymal stem cells did not evidence either degenerative notes or inflammatory reactions.
These findings might suggest "the onset of a structural deterioration of the scaffold in the [bone marrow–derived mononuclear cell] group and a protective effect of the injections of [mesenchymal stem cells]."1 We are concerned that such conclusions seem audacious because the study suffers from a main limitation represented by the cell-seeding modality. In fact, the authors, looking for an answer to question number 2, choose to inject the cells directly into the decellularized scaffold (onto the conduit walls and valve annulus, excluding the leaflets), instead of adopting a biomimetic environment.
The adoption of this alternative technique, which has been derived from the myocardial setting,2 represents an innovative concept for the valvular field and therefore requires a careful validation. Fluorescent cell tracking, which was performed on 4 of 14 animals in the first postoperative week, evidenced, on day 1, the cell persistence onto the injection site and, on day 7, a few scattered cells into the matrix, the arterial wall, and the leaflets. Moreover, nonlabeled cells of host origin were found.
Is this enough to say that "in situ injection of bone marrow cells into a porcine decellularized scaffold before implantation enhanced the in vivo recolonization and induced full re-endothelization"?1 First, endothelialization and scaffold repopulation do not coincide. Even bioprostheses undergo an endothelialization process of the inert components once implanted. Second, the process of repopulation implies an architectural and hierarchic cell-specific distribution along the leaflet's ventricularis, spongiosa, and fibrosa,3 which was not observed in this experience.
In the article's "Discussion" section, the authors themselves affirm that they had no direct evidence that cells would grow inside the matrix. According to the hypothesis that injected cells might enhance autologous recellularization, further evidence is needed to draw definite conclusions, and the provided results do not concretely support the initial hypothesis.
References
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