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

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal 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 Malm, T. Articles by Bowald, S. Search for Related Content PubMed Articles by Malm, T. Articles by Bowald, S.

J Thorac Cardiovasc Surg 1994;107:628-0629
© 1994 Mosby, Inc.

Letters to the Editor

Antiadhesive membranes for cardiac reoperations

Department of Thoracic and Cardiovascular Surgery^a
Department of Surgery^b
University Hospital
S-751 85 Uppsala, Sweden

Reply to the Editor

Tomizawa and Moon have commented on our article titled "Prevention of Postoperative Pericardial Adhesions by Closure of the Pericardium With Absorbable Polymer Patches" (J THORAC CARDIOVASC SURG 1992;104:600-7). We would to reply to their comments.

A possible theoretical explanation for the absence of adhesions after implantation of absorbable patches was given in an article published in the Scandinavian Journal of Thoracic and Cardiovascular Surgery. ¹ Absorbability per se is not the most important issue in preventing adhesions. The most important factor is the environment created by the patch—a scaffold for mesothelial cell regeneration. Furthermore, the foreign body reaction is completely dominated by macrophages, which are known to produce growth factors for mesothelial growth. ² Mesothelial cells possess fibrinolytic and anticoagulatory properties, and they produce substances such as prostacyclin, heparansulphatprotoglycane, and thrombomodulin, ^1,3,4 which might be of importance for prevention of adhesion formation.

We agree that a surface that is covered by heparinlike molecules might be important in the prevention of adhesions. A patch that serves as a scaffold for regeneration of mesothelial cells with biochemical activity in effect produces such substances ¹ and thus might be equivalent to a coated patch shortly after implantation.

A sign of biocompatibility of the patch is the development of a mesothelial surface on the side facing the epicardium and of a collagen layer similar to that found in native pericardium. We also believe that it is important to have a foreign body reaction that consists only of a macrophage reaction without lymphocytes, because macrophages are known to produce growth factors for endothelium (and probably also mesothelium). The regeneration occurs on the surface of the patch. Separated from the regenerated tissue, the patch is invaded by macrophages, degraded, and absorbed. The macrophage invasion is the body's normal stimulus to the repair of an injury. We interpret the total absence of lymphocytes, granulocytes, and monocytes, which are the defense against harmful substances, as a sign of biocompatibility. One should be aware that total biocompatibility of implants does not exist. However, if an implant does not produce harmful tissue reactions, in the sense mentioned earlier, and does not inhibit normal cell proliferation, it should be considered biocompatible.

The interpretation of the histologic findings concerning the encapsulation of the polyhydroxybutyrate (PHB) patch is as follows. On the epicardial side of the regenerate, a dense collagen layer, similar to that in native pericardium, is found, but on the pleural side the connective tissue is thin and lacks the organized pattern. Pericardial regeneration occurs without cell growth inhibition from the PHB patch. The surrounding connective tissue disappears along with the macrophages when the patch is absorbed but the regenerated pericardial tissue remains.

The suspicion that our animal model was unable to produce significant adhesions is refuted by the findings in the control group.

Figs. 2, C and 3, C should be looked at together. The electron micrograph proves that no mesothelial cells exist on the adhesive surface in the control group.

In the study we tried to manipulate the heart as in cardiac surgery except for cardiopulmonary bypass. We did not prove the absence of mesothelial cells after the injury. The blood injected into the pericardial cavity was not drained and could not escape from the cavity in the study group because the cavity was completely closed by the patch. The operation was relatively short, so that drying out of the tissue was minimized.

In the test group the heart did not have any contact with surrounding pleural tissue, because the pericardial sac was completely closed with the patch, which was inserted with a running suture line. However, in the control group the pericardium was left open so that the heart was in contact with pleura or lung, and adhesions were encountered in all animals in the control group, despite the "completely biocompatible surface" of the surrounding tissue.

In another study, when the PHB patch was inserted after cardiopulmonary bypass a reduction of pericardial adhesions was also seen (unpublished data).

In a randomized study, including 100 patients, 50 received the PHB patch. Twenty-five patients from each group were followed up 6 months after the operation with a computed tomographic scan, revealing a significant pericardial space in the patients who had patch implantation (unpublished data).

We agree that the most important factors in prevention of pericardial adhesions are good drainage of the pericardial cavity after cardiac surgery and an atraumatic approach to the heart, trying, in particular, to prevent mesothelial injury by not letting the epicardium dry out and by minimizing handling of the heart. In addition, closure of the pericardial cavity either with the native pericardium or with a biocompatible patch is necessary to minimize adhesion formation. In our studies, the absorbable PHB patch offered a way to reduce adhesions.

References

1. Malm T, Bowald S, Saldeen T, Bylock A, Busch C. Regeneration of pericardial tissue on absorbable polymer patches implanted into the pericardial sac. Scand J Thorac Cardiovasc Surg 1992;26:15-21.[Medline]
   
2. Martin BM, Gimbrone MA, Unanue ER, Cotran RS. Stimulation of nonlymphoid mesenchymal cell proliferation by a macrophage-derived growth factor. J Immunol 1981;126:1510-15.[Abstract]
   
3. Boffa M-C, Burke B, Haudenschild CC. Preservation of thrombomodulin antigen on vascular and extravascular surfaces. J Histochem Cytochem 1987;35:1267-76.[Abstract]
   
4. Bourin M-C. Thrombomodulin: a novel proteoglycan. Dissertation from the Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden, 1990.
   

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal 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 Malm, T. Articles by Bowald, S. Search for Related Content PubMed Articles by Malm, T. Articles by Bowald, S.