| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Ann Thorac Surg 1999;68:295-296
© 1999 The Society of Thoracic Surgeons
a Division of Cardiovascular and Thoracic Surgery, Duke University Medical Center, Box 3857, Durham, NC 27710, USA
To the Editor
We appreciate Dr Beranek’s interest in our recent study demonstrating neovascularization 6 months after transmyocardial laser revascularization (TMR) in hibernating myocardium [1]. Definitive proof that the observed neovessels are not lymphatics comes from collaborative work we have done with Dr Kari Alitalo, one of the senior authors on the manuscript Dr Beranek references regarding endothelial cell markers and lymphatics [2]. In this collaboration, the TMR-treated myocardium was stained with a number of vascular markers, including Flt4. The latter is a transmembrane receptor tyrosine kinase, which interacts with vascular endothelial growth factor C. Flt4 is a unique marker of lymphatic endothelial cells and, within the mature endothelium, is exclusively expressed by lymphatic vessels [3]. Staining of the TMR channels reveals that all of the vessels with a visualized lumen, which includes all of the vessels to which Dr Beranek refers, do not stain for Flt4. Consequently, none of these vessels are lymphatics. There is some Flt4 staining within the channels, but these vessels are small and thin walled with no visible lumen. Further proof that the identified neovessels are vascular in origin is the fact that these vessels have been seen in association with improved myocardial perfusion and function 6 months after TMR in our model of hibernating myocardium [4]. The vessels were seen only in the TMR-treated animals, suggesting they were responsible for the improved perfusion.
Finally, the vascular density analysis presented in the manuscript does not represent a true capillary density per se. As stated in the Methods section [1], "because vascular endothelial cells can be heterogeneous for the expression of endothelial cell markers [5], the results from endogenous endothelial alkaline phosphatase staining were compared with results obtained by immunohistochemical analysis." This entailed staining with anti-tie 2 (TEK), as well as anti-von Willebrand factor (vWF) and anti-smooth muscle actin (HHF-35), among others [1]. Consequently, the vessels counted in the lased and nonlased myocardium represent vessels that stained not only with endogenous endothelial alkaline phosphatase but also with the immunohistochemical markers. Our findings are very similar to those obtained by Burkhoff and colleagues in prior studies [6, 7]. Consequently, we stand by our methodology and results, and feel that this study supports the theory that myocardial angiogenesis is present long term after TMR.
References
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
