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Ann Thorac Surg 1999;68:295
© 1999 The Society of Thoracic Surgeons
a 4101 S Wappel Dr, Columbia, MO 65203, USA
To the Editor
I agree with Hughes and colleagues [1] that blood angiogenesis is a long-standing sequela of transmyocardial laser revascularization (TLR) [2], but I cannot overlook several of their findings. They have identified blood vessels by endogenous alkaline phosphatase and by the antibodies to factor VIII-related antigen, to endothelial cell specific receptors tie 2, to smooth muscle, and to collagen IV. They did not mention, however, that all these activities also identify lymphatic vessels [3, 4].
It is known that successful wound healing reaction depends, inter alia, on the regeneration of lymphatics in newly formed granulation tissue. When the granulation tissue matures and transforms into a scar, the majority of regenerated lymphatic vessels disappear and remaining ones become more or less constricted by contracting fibrotic tissue. As a result, they often become dilated, tortuous, and varicose [5]. The alleged blood vessels presented by Hughes and colleagues [1] manifest the characteristics of such lymphatic vessels. For example, the ectatic vessels in Figures 2A, 3A, and 3B have practically the same appearance as the lymphangiectasias in Figure 8 [5]. The numerous thin-walled ectatic vessels at 3 o’clock in Figure 4A [1] are very similar to the lymphatic channels producing a "string of pearls" appearance in Figures 2 and 3 [6], and in the upper right corner in Figure 8 [5]. Note also that none of these ectatic vessels contains red cells even if the heart was not fixed by perfusion. All of the above facts suggest that the authors [1] have not distinguished blood vessels from lymphatics and that, consequently, their conclusions concern both vasculatures and not blood vessels alone.
Six months after the transmyocardial laser revascularization, Hughes and colleagues [1] quantified the vascular density in the lased ischemic myocardium (in the scarred laser channels and a narrow rim of the adjacent myocardium) and compared it with the vascular density in the remaining nonlased ischemic region. They counted vessels in 144 different random high-power (200x) microscopic fields. The vessels were identified by endogenous alkaline phosphatase activity on unfixed frozen sections. Their analysis revealed a mean of 29.2 ± 3.6 vessels/field in the lased myocardium and 4.0 ± 0.3 vessels/field in the rest of the ischemic region.
The number of vessels in the nonlased region is so low that one would like to know how many cardiomyocytes depended on them for their survival. In other words, there is a question as to how many cardiomyocytes were present in one high-power field (200x) when the original authors counted the vessels. They do not give these data but their Figure 4D is magnified 200x and visualizes cardiomyocytes. It is possible, therefore, to approximate the number of cardiomyocytes/high-power field (200x) from Figure 4D. My estimate is that there were at least 100 cardiomyocytes/field. This would be 0.04 capillary/cardiomyocyte at the most. No myocardium would be able to survive, much less function, at such a low density of vascularization, suggesting that these results suffer from methodological errors and must be considered with caution.
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