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Ann Thorac Surg 1998;66:12-18
© 1998 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, McGill University, Montreal, Canada
b Department of Pathology, McGill University, Montreal, Canada
c Division of Plastic Surgery, McGill University, Montreal, Canada
Address reprint requests to Dr Chiu, Montreal General Hospital, Room C9.169, 1650 Pine Ave, Montreal, Quebec, H3G 1A4, Canada
e-mail: (mdiu{at}musica.mcgill.ca)
The Thoracic Surgery Directors Association (TSDA) Resident Research Award, sponsored by Medtronic, Inc, was established in 1990 to encourage resident research in cardiothoracic surgery. Abstracts submitted to The Society of Thoracic Surgeons (STS) Program Committee representing research performed by residents were forwarded to the TSDA to be considered for this award. The abstracts were reviewed by the TSDA Executive Committee, consisting of Mark B. Orringer, President, Gordon N. Olinger, President-Elect, Edward D. Verrier, Secretary/Treasurer, and Frederick L. Grover and D. Glenn Pennington, Executive Committeemen. The eighth TSDA Resident Research Award was given to Marc P. Pelletier, MD, a cardiac surgery resident in the Department of Surgery, McGill University, Montreal, Quebec, Canada, who completed a Thoracic Surgery Research Fellowship in the Department of Surgery in June 1997. He received a monetary award of $2,500 and an engraved desktop award. The TSDA, with support by Medtronic, Inc, makes this award annually, using the above selection procedure. The resident author of the selected study is recognized at the STS meeting.
Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.
Background. The mechanism by which transmyocardial revascularization (TMR) exerts a beneficial effect remains unknown. We hypothesize that the myocardial punctures of TMR cause a myocardial injury, leading to an angiogenic response mediated by a number of growth factors.
Methods. Fifty-three rats underwent ligation of the left coronary artery. Group I (n = 25) served as controls, whereas group II (n = 28) underwent concomitant TMR by the creation of six transmural channels with a 25-gauge needle in the ischemic zone. Surviving animals in both groups were sacrificed at intervals of 1, 2, 4, and 8 weeks (n = 5 in each subgroup). Immunohistochemistry in the infarct areas was performed for factor VIII to assess vascular density. Immunohistochemistry using specific antibodies was also performed for transforming growth factor-ß, basic-fibroblast growth factor, and vasoendothelial growth factor. Growth factor expression was quantitated by comparing areas of staining (in mm2) with computerized morphometric analysis.
Results. Mortality was similar in both groups (5/25 versus 8/28; not significant). Group II had significantly greater vascular density than group I (5.65 versus 4.06 vessels/high-power field; p < 0.001), with a peak at 1 week postoperatively (9.12 versus 5.56 vessels/high-power field; p < 0.0001) in both groups. Overall, levels of both transforming growth factor-ß and basic-fibroblast growth factor were significantly higher in the TMR group compared with the control group (0.207 versus 0.141 mm2/mm2, p < 0.05; and 0.125 versus 0.099 mm2/mm2, p < 0.05).
Conclusions. This model of TMR is associated with a significant angiogenic response, which appears to be mediated by the release of certain angiogenic growth factors such as transforming growth factor-ß and basic-fibroblast growth factor. With the long-term patency of laser-created myocardial channels in clinical TMR increasingly in doubt, its mechanism of myocardial revascularization may be similar to that observed in our model.
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