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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.
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Abstract |
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 Top Abstract Introduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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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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Introduction of Dr Pelletier by TSDA President Mark B. Orringer |
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TopAbstractIntroduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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The idea for this award originated in 1987 with Mr Earl Bakken, founder of Medtronic, Inc, again demonstrating the long-standing association between our organizations and the support of this company for our educational efforts, and the concept was developed in subsequent discussion with Ben Wilcox. The intent of the award was to encourage research in cardiothoracic surgery. The award was first presented in 1991 at the TSDA meeting that preceded the STS meeting. Medtronic has provided monetary sponsorship of the Award, which includes a check in the amount of $2,500 to the resident, and oak and black granite desk awards to both the resident and his or her program director/mentor, which are presented both at the TSDA meeting, which precedes this meeting, and at this plenary session of the STS.
As president of TSDA this year, I am pleased to present this year’s Resident Research Award to Dr Marc Pelletier of McGill University in Montreal for his abstract entitled "Angiogenesis and Growth Factor Expression in a Model of Transmyocardial Revascularization." This is an outstanding example of basic research at the resident level and is a real tribute to a fine thoracic surgery research laboratory, which has been directed by Dr Ray Chiu for a number of years. My congratulations to you both.
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Response to Dr Orringer by Dr Pelletier |
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TopAbstractIntroduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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Transmyocardial revascularization (TMR) is a surgical technique currently undergoing investigation for the treatment of refractory angina. In brief, TMR consists of creating transmural channels through ischemic tissue of the left ventricle, from the epicardial to the endocardial surface [1–5]. This is achieved via the use of high-powered CO2 lasers, yttrium-aluminum garnet lasers, or hypodermic needles [6]. Reports of early phase I trials recently have suggested that TMR may be highly effective in relieving the angina of Canadian Cardiovascular Society class IV patients who have exhausted all other medical and surgical therapies. However, the mechanism by which TMR leads to these apparent benefits is unknown. Although some believe that transmural channels remain patent, thus supplying the myocardium with intraventricular blood [7, 8], others have demonstrated that TMR channels are obliterated at histologic examination in a variety of different models [9–12].
In a search for other possible mechanisms, it has been proposed that the injury caused by TMR could lead to neovascularization in the areas of laser or needle injury [9]. Angiogenesis is known to be promoted by certain molecules termed angiogenic growth factors. Of these molecules, transforming growth factor-ß (TGFß) is a polypeptide that has been shown to have angiogenic actions in vivo [13]. It promotes the proliferation of endothelial cells engaged in angiogenesis in vitro [14] and induces the formation of capillarylike tubes of bovine microvascular endothelial cells [15]. Two others, vasoendothelial growth factor (VEGF) and basic-fibroblast growth factor (bFGF), also elicit angiogenesis and remodeling of the vasculature via their own endothelial receptors [13]. Therefore, the expression and release of these three growth factors, among others, could theoretically result in a process involving myocardial angiogenesis.
With this in mind, a study was designed to determine if TMR is associated with either angiogenesis or growth factor expression of TGFß, bFGF, or VEGF. An ischemic rat myocardial model was designed with needle-made channels as the injury-causing stimulus for inflammation and possible angiogenesis. Supporting the use of needle channels was a report suggesting that they are superior to laser channels in preserving rat myocardium subjected to left coronary ligation [5]. Rats were chosen as the animal model because of their minimal myocardial collaterals.
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Material and methods |
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TopAbstractIntroduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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Operation
In both groups, anesthesia was induced and maintained with enflurane 2% to 4% at 1 to 2 L/min. Rats were intubated with a 14-gauge intravenous catheter and ventilated at a tidal volume of 2.5 mL and a respiratory rate of 90/min. A left thoracotomy was created in the fourth intercostal space and the lung was retracted posteriorly. After the pericardium was incised, the LCA was identified in its course between the left atrium and pulmonary artery. In both groups, the LCA was ligated with one suture of 5-0 silk. In group I, the chest was then closed in three layers of 4-0 Vicryl (Ethicon, Somerville, NJ), whereas in group II, transmyocardial punctures were performed with a 25-gauge needle. Six transmural channels were created in the distribution of the LCA, with caution to avoid puncturing any large coronary veins. Hemostasis was achieved with slight pressure in all cases. Chest closure was identical to that in the control group. Both groups were allowed to recover, and postoperative pain was controlled with subcutaneous injections of buprinorphine (0.1 to 0.5 mg/kg). Each group was then divided into four subgroups, which were sacrificed at periods of 1, 2, 4, and 8 weeks postoperatively.
Harvest
After the predetermined period of 1 to 8 weeks, animals were again anesthetized, intubated, and ventilated as before. The sternum was removed, followed by isolation and cannulation of the aortic root with a 20-gauge intravenous cannula. Beating hearts were arrested and fixed in diastole with 4% paraformaldehyde, then stored at 4°C. After 24 hours, the hearts were washed and stored in phosphate-buffered saline solution containing 15% sucrose, again at 4°C.
Immunohistochemistry
Cryostat sections of tissue were immunostained with antisera to TGFß, bFGF, and VEGF ligands (Santa Cruz Biotechnology, Inc, Santa Cruz, CA) with a modification of the avidin biotin-peroxidase method [16]. Hearts were cut into 3- to 5-mm cross-sectional slices, and 10-µm sections were mounted on slides. Tissue sections were made permeable with Triton X-100, incubated in hydrogen peroxide to block endogenous peroxidase activity, and incubated first with normal serum for 30 minutes and then with the primary antibody for 16 hours at 4°C. Sections were then incubated with biotinylated immunoglobulin G and stained with an immunoperoxidase technique according to the manufacturer’s instructions (Vectastain ABC Elite Kit; Vector Laboratories, Burlingame, CA). Antiserum to factor VIII (the endothelial-cell marker von Willebrand factor) was also used. Extra sections also were stained with hematoxylin and eosin.
Image analysis
Angiogenesis was assessed by counting the number of vessels per high-power field (HPF, x250). Vessels were defined as round structures with a central lumen that is lined by cells staining positively to factor VIII. Sampling was performed by the accepted method of "systematic sampling with a random start" [17], and was performed in the infarcted area, which was defined by the following criteria: (1) thinning of ventricular wall, (2) loss of normal myocyte appearance and homogeneity, (3) presence of inflammatory cells and fibroblasts, and (4) presence of granulation tissue.
For TGFß expression, quantification was performed with digital morphometric image analysis. With use of the same sampling method as mentioned for factor VIII, the outlines of positively stained cells in each HPF (x400) were highlighted in both the infarcted and noninfarcted myocardium, using ten sampling sites per infarct zone. For VEGF and bFGF, expression was measured in the infarcted zone only. Results were quantitated as square millimeters per square millimeter of myocardial tissue.
Statistics
Data were analyzed with parametric (Student’s t test) and nonparametric (Mann-Whitney test) methods, using InStat (GraphPad Software, San Diego, CA) for Macintosh. A p value less than 0.05 was considered significant.
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Results |
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TopAbstractIntroduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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Comment |
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TopAbstractIntroduction of Dr Pelletier...Response to Dr Orringer...Material and methodsResultsCommentReferences |
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Despite clinically promising results, the mechanisms by which TMR reduces angina remain unknown. After original controversies surrounding channel patency, an increasing number of investigators currently believe that channels become obliterated, and are therefore unable to directly provide blood to the ischemic myocardium. One hypothesis to explain the effect of TMR is that this procedure may promote an angiogenic response, which would provide collateral blood flow to an otherwise underperfused area of the heart [9]. Our analysis of angiogenesis data by comparing vascular density yielded two main findings that appear to support this hypothesis. First, in all group II animals combined, the mean vascular density was significantly greater than that of the control group. Second, vascular density appeared to have maximized at 1 week before decreasing over the next 8 weeks. These results suggest that some component of the TMR procedure leads to angiogenesis, perhaps by the well-known mechanism of injury and wound healing response. If TMR is viewed as a form of mechanical trauma that creates a controlled injury to myocardium, certain comparisons can be made to other human tissues. In skin and muscle, for example, hypoxic or mechanical trauma will initiate a cascade of coagulation, inflammation, and granulation tissue formation. This is followed by fibroblast proliferation and wound remodeling [19]. Altogether, this inflammatory process is capable of inducing the formation of new vessels by secreting soluble angiogenic molecules [13]. In our model, both groups underwent ligation of the left coronary artery, creating severe hypoxia to the myocardium, in itself a potent inducer of angiogenesis. However, addition of the mechanical injury of TMR in group II is likely to have caused the observed additional increase in vascular density. Our second observation, that of decreasing vascular density over time, may be explained by the known process of wound healing. With time, the inflammatory process may lead to increased scar tissue formation via fibroblast proliferation and collagen deposition. Dense scar tissue may allow fewer vessels to survive. Another explanation may be a deficiency in our model, whereby the creation of an infarct failed to provide immature blood vessels with enough proteins and nutrients to stimulate their growth. Perhaps this observation of decreased vascular density over time would be different in a model of chronic ischemia, similar to that of the clinical TMR patients, which can provide a continued stimulus for angiogenic growth factor release.
These growth factors are a group of hormonelike polypeptides that have been shown to play a central role in different phases of wound healing. The repair of injury begins with the release of peptide growth factors from both inflammatory cells and injured cells as soon as tissue damage occurs [20]. They include bFGF, VEGF, TGFß, and platelet-derived growth factor. Our second major goal in this study was to examine the expression of angiogenic growth factors in our model of TMR. Of the three growth factors studied, the overall concentrations of TGFß and bFGF over 8 weeks were increased in the TMR group over the control group, although this was not observed with VEGF. For all three growth factors, however, maximal expression occurred at 1 week and decreased over the ensuing 8 weeks, as it had for vascular density. To understand this pattern of growth factor expression, it is helpful to identify which cells are capable of producing them. Transforming growth factor-ß, for example, when implicated in wound repair mechanisms, functions partly through its role as a potent chemoattractant for monocytes and fibroblasts [21, 22]. In other words, TGFß induces angiogenesis indirectly via other cells. These cells can then secrete angiogenic molecules, such as VEGF and bFGF, which act directly on endothelial cells. In addition to monocytes and fibroblasts, many other cells such as cardiocytes, macrophages, smooth muscle cells, and endothelial cells, among others, are capable of synthesizing VEGF and bFGF [13]. Unlike TGFß, they are direct-acting angiogenic molecules because they elicit angiogenesis and remodeling of the vasculature via their own receptors on endothelial cells [23]. In our experiment, the creation of a myocardial infarct led to a marked inflammatory and wound-remodeling response, mainly via its hypoxic effect. In the TMR group, increased levels of TGFß and bFGF suggest an increase in their progenitor cells as a possible explanation. Given a concomitant increase in vascular density, the increased presence of endothelial cells may itself be responsible for elevated levels of TGFß and bFGF. However, the injury to myocardium caused by TMR may conceivably cause a higher fibroblastic response, which in itself may increase growth factor expression. This issue needs further evaluation. A clear explanation is also lacking for the discrepancy between VEGF and bFGF results. Because both are mostly secreted by the same cell types, one would have expected similar results. However, our model appears to favor synthesis of bFGF, a molecule that has been shown to be induced rapidly and in time to yield beneficial effects in myocardial infarcts [24, 25]. We have not identified any model-related factors to explain this discrepency.
The observed decrease in vascular density and growth factor expression with time in our model may be explained by considering angiogenesis as occurring in two phases [23]. The first phase, activation, includes cell migration and extracellular matrix invasion, along with endothelial cell proliferation. This phase will introduce many cells that are known to stain for factor VIII (endothelial cells) and to produce TGFß, bFGF, and VEGF (macrophages, fibroblasts). The second phase, resolution, encompasses termination of angiogenesis and vessel maturation via steps such as inhibition of endothelial cell proliferation and cessation of cell migration. Our observations of declining vascular density may thus be a natural process of angiogenesis from the activation to resolution phases.
Finally, we also observed similar TGFß levels in the noninfarcted (control area) myocardia of groups I and II. The ability of myocytes to secrete TGFß explains their presence in these areas. Because no intervention was performed in these areas, one would have expected to find similar levels of growth factors.
Our future studies will focus on addressing the two main limitations of this study, namely (1) to observe the response to ischemia rather than infarction, and (2) to compare laser- versus needle-induced inflammation. Answers to these issues may help to elucidate the underlying mechanism of clinical TMR.
In conclusion, our data appear to support the hypothesis that angiogenesis may play a role in TMR. With the long-term patency of laser-created myocardial channels in clinical TMR increasingly in doubt, its mechanism may be similar to that observed in our model. If such a speculation can be confirmed, the efficacy of TMR using needle punctures, which is less expensive than using lasers, may deserve to be reevaluated clinically.
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weeks. Ann Thorac Surg 1996;61:1532-1535.This article has been cited by other articles:
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O. Rimoldi, S. M. Burns, S. D. Rosen, T. E. Wistow, P. M. Schofield, G. Taylor, and P. G. Camici Measurement of Myocardial Blood Flow With Positron Emission Tomography Before and After Transmyocardial Laser Revascularization Circulation, November 9, 1999; 100 (2009): II-134 - II-138. [Abstract] [Full Text] [PDF]
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V. Chu, J.-q. Kuang, A. McGinn, A. Giaid, S. Korkola, and R. C. -J. Chiu ANGIOGENIC RESPONSE INDUCED BY MECHANICAL TRANSMYOCARDIAL REVASCULARIZATION J. Thorac. Cardiovasc. Surg., November 1, 1999; 118(5): 849 - 856. [Abstract] [Full Text] [PDF]
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V. F. Chu, A. Giaid, J.-q. Kuang, A. N. McGinn, C. M. Li, M. P. Pelletier, and R. C.-J. Chiu Angiogenesis in transmyocardial revascularization: comparison of laser versus mechanical punctures Ann. Thorac. Surg., August 1, 1999; 68(2): 301 - 307. [Abstract] [Full Text] [PDF]
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X. M. Mueller, H. T. Tevaearai, C.-Y. Genton, P. Chaubert, and L. K. von Segesser Are there vascular density gradients along myocardial laser channels? Ann. Thorac. Surg., July 1, 1999; 68(1): 125 - 129. [Abstract] [Full Text] [PDF]
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