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Ann Thorac Surg 1998;66:1872
© 1998 The Society of Thoracic Surgeons

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Correspondence

Angiogenesis induced by transmyocardial laser revascularization

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To the Editor

In their article about the vascular growth induced by transmyocardial laser revascularization, Kohmoto and colleagues [1] have described newly formed arterylike vessels located in laser channel remnants and in adjacent myocardium. These vessels differ from normal intramyocardial coronary arteries in two aspects: their smooth muscle cells multiply and their "diameter to wall thickness ratio" is much lower than the normal one (which may attain 15:1).

The vessels described by Kohmoto and coworkers [1] remind me of the vessels that I observed in venous leg ulcers [2]. Initially, I also considered them to be muscular vessels (Fig. 8.5 [2]) but, when I carried out the immunostaining for factor VIII-related antigen, I realized that their walls were composed of several layers of endothelial cells (Fig. 8.8 [2]). That is why I called them "hyperplastic capillaries." They develop from hyperplastic capillary sprouts [Fig. 8.6 [2]] and may give rise either to capillaries and perivascular fibroblastic cells of endothelial origin [3, Fig. 4] or to muscular vessels. I am persuaded that the vessels described by Kohmoto and colleagues [1] are of the same kind as the vessels I observed in venous ulcers. In their Fig. 5, the immunoreactivity for factor VIII-related antigen is present not only in the luminal endothelium of the vessel situated in the lower right quadrant but also in the smooth muscle cells. Even though their immunopositivity is weak, it is still perceptible so clearly that the endothelial origin of these transdifferentiated cells is not in doubt.

The vessels with more than one layer of endothelial cells are products of angiogenesis associated with healing reaction and, possibly, with fibrosis [4]. The potentiality of fibrosis obliges one to ask the following questions: When does the healing of laser channels ends and will angiogenesis disappear when laser channels are replaced by scarcely vascularized scars? It is most plausible that the healing reaction will never end because there will always be friction and, consequently, and injury alongside of interface between the noncompliant scar and the surrounding contractile tissue. This may sound good to someone who believes that angiogenesis increases blood flow and contributes to clinical benefits after transmyocardial laser revascularization. The negative aspect of this situation is that unending injury leads to permanent inflammation, healing, and fibrosis at the end [5]. Cardiomyocytes neighboring healing channels will undoubtedly suffer and may die either by apoptosis or accidental cell death (usually called necrosis). This may alleviate hunger for oxygen but will aggravate the hemodynamic situation.

These complications may be avoided if one produces laser channels that do not heal and remain patent [6]. Even though these channels are connected neither with intramyocardial vessels nor with the ventricular cavity, they are part of the interstitial space and filled with interstitial fluid. As such, they may facilitate its movements between more and less oxygenated parts of myocardium, contributing thereby to a more efficient supply and washout of cardiac metabolites.

References

1. Kohmoto T., DeRosa C.M., Yamamoto N., et al. Evidence of vascular growth associated with laser treatment of normal canine myocardium. Ann Thorac Sug 1998;65:1360-1367.
2. Beranek J.T., Faulk W.P., Ortonne J.P., Hsi B.L. Clinical and immunobiological studies of human extra-embryonic membranes in wound healing. In: Hunt T.K., Heppenstall R.B., Pines E., Rovee D., eds. Soft and hard tissue repair. New York: Praeger, 1984:173-189.
3. Beranek J.T., Hsi B.L., Ortonne J.P. Occurrence of factor VIII-related antigen positive cells in perivascular infiltrates of venous stasis dermatitis. Br J Dermatol 1985;113(Suppl 28):128-132.
4. Beranek J.T., Masseyeff R., Desmet V.J. Hyperplastic capillaries and their possible involvement in the pathogenesis of fibrosis. Histopathology 1986;10:543-551.[Medline]
5. Beranek J.T. Unattainable homeostasis in healing leads to interstitial and vascular intimal fibroses: a unified hypothesis of their pathogenesis. Med Hypoth 1991;36:103-105.[Medline]
6. Beranek J.T. Why do channels remain patent after transmyocardial laser revascularization?. Ann Thorac Surg 1998;65:1200.[Free Full Text]

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				J. T. Beranek Emerging new concepts of myocardial laser revascularization J. Thorac. Cardiovasc. Surg., November 1, 1999; 118(5): 977 - 977. [Full Text] [PDF]

				J. T. Beranek Lymphatic angiogenesis induced by transmyocardial laser revascularization Ann. Thorac. Surg., July 1, 1999; 68(1): 295 - 295. [Full Text] [PDF]

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