Ann Thorac Surg 2001;71:1279-1280
© 2001 The Society of Thoracic Surgeons
Invited commentary
Bartley P. Griffith, MDa,
William R. Wagner, PhDa
a Division of Cardiothoracic Surgery, University of Pittsburgh School of Medicine, Presbyterian University Hospital, Pittsburgh, PA 15213, USA
e-mail: griffithbp{at}msx.upmc.edu
It has been a privilege to review and comment on this innovative article as it is scholarly and improves on what is known of intimal hyperplasia at the site of coronary artery bypass (CAB) anastomoses. This work, because it is bench oriented, provides a scaffold for others to follow and for this group of talented researchers to build on. There are some concerns about the results and interpretation of the data achieved. Generally speaking, we had some concern about the lack of change in overall cell numbers for any of the manipulations attempted. Given the variability in cell number means and given the relatively small number of cells expressing proliferating cell nuclear antigen (PCNA) (indicating proliferation), it would seem that any hyperplastic effect might have been buried in the noise of the cell number measurement. In other words, as the percentage of cells that were proliferating were so small compared to the deviation and the measurement of cell number the researchers might have had difficulty in detecting any change in cell numbers as a result of proliferation. We have several questions for this group of talented researchers that we believe is relevant to the commentary.
- How much does this proliferative effect contribute to the in vivo situation where platelets and leukocytes are intimately involved in the healing process and locally release growth factors and proteases? Of note, serum will mimic somewhat the growth factors environment, but the local concentrations and local delivery are not consistent. Have they tried in other culture setups to more clearly mimic human serum?
- How does the vein response vary from the artery (a radial artery was used in the study for the bypass graft)? Do they believe that the human vein from an elderly atherosclerotic patient may be different than the porcine artery from the healthy nondiseased pig?
- We have learned a great deal in tissue engineering of the benefit of mechanically stressing tissue that is designed ultimately to perform a specific purpose. Do they believe that cyclic stressing of the suture sites and perhaps a new environment of twisting and stretching lead to any changes in their outcomes? Would we see a more likely trigger for pronounced proliferative response under these circumstances? Might such mechanical forces on the suture injuries be an explanation for the observed anastomotic hyperplasia between synthetic grafts and native tissue, particularly adding the phenomena of compliance mismatch?
- Finally, for the future, do they believe that advances in vascular sealants offer a path that avoids or reduces the hyperplastic trigger of suture-related trauma? Might it be possible to provide antiproliferative pharmaceutical coatings for the sutures that are released locally at the hot spots of proliferation? Could this be controlled so as not to have a detrimental effect on the overall need to heal the graft and local tissue at the anastomoses?
We salute these researchers for stimulating us to think in a basic sense on what is happening so as to provide us with the scaffold on which we can test further an evermore physiologic hypothesis.
Related Article
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A novel organ culture method to study intimal hyperplasia at the site of a coronary artery bypass anastomosis
- Dario F. Del Rizzo, Michael C. Moon, Jeffrey P. Werner, and Peter Zahradka
Ann. Thorac. Surg. 2001 71: 1273-1279.
[Abstract]
[Full Text]
[PDF]
