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Ann Thorac Surg 1997;63:597-598
© 1997 The Society of Thoracic Surgeons
4101 S. Wappel Dr, Columbia, Mo 65203
To the Editor:
As a contributor to the problem of transmyocardial laser revascularization [1, 2], I have read with great interest the case report by Burkhoff and associates [3] and the invited commentary by Frazier and Kadipasaoglu [4] about the functionality and persistence of the laser channels produced during this procedure. Because any scientific problem can be solved only if all related facts are taken into consideration, it is necessary to include myocardial "pseudovascular tubes" [2, 5] in the discussion concerning this subject. They are structures appearing as coronary arteries, veins, or capillaries at first sight, but displaying some features incompatible with genuine vessels when carefully studied [5, 6].
By way of example, I would like to mention two instances in which pseudovascular tubes induced by transmyocardial revascularization were interpreted as newly formed functional vessels. The first case [7] concerns the procedure in which one end of a polyethylene tube was inserted through the wall into the left ventricular cavity while the other end remained embedded in the myocardium. After 30 days, the polyethylene tubes were removed and the new "collagen vessels" formed around them were studied, as shown in Figures 2, 3, and 5 of Benjamin's article [7]. Their walls were formed by one layer of smooth muscle-like tissue which, curiously, manifested practically the same morphologic and tinctorial characteristics as the surrounding myocardium (Fig 2, the upper left corner; Fig 3, the bottom; Fig 5, the lower right corner). This unexpected fact finds its explanation in another article dealing with the same subject and written by the same author [8]. In Figure 4 of that article, the cardiomyocytes surrounding the "collagen vessel" transform gradually into its smooth muscle-like cells, betraying its myocardial derivation. Note, however, that numerous cells in the wall still manifest the longitudinal striation proper to cardiomyocytes (Figs 3 and 4 in reference 8].
In Figures 1, 2, 3, and 5 of reference 7, Benjamin presents "the specimens injected with contrasting material ...showing the wide distribution of new capillaries emanating from the main collagen coronary vessel." We do see, however, that the contrasting material is never present in the main tubes and fills only the small vessels in their vicinity (which have developed undoubtedly in reaction to the procedural injury) and the tears present in the tissue (caused most probably by the traumatic removal of polyethylene tubes). In summary, the newly formed tubes do not manifest the inner structure of genuine vessels and have not contributed to myocardial blood circulation. They correspond to the definition of myocardial pseudovascular tubes [5].
The second case concerns the transmyocardial laser revascularization of the experimental myocardial infarction in sheep after an ischemic interval lasting 1 hour [9]. Horvath and associates have found that in the experiments lasting 4 hours, the percent area of necrosis in the area of risk was 6% for the laser group and 39% for the control group, and in the experiments lasting 30 days, the average contractility of the ischemic area was 43% of that in the nonischemic area in the laser group whereas no significant contractility of the ischemic area was present in the control group. They explain these fascinating results by the formation of patent laser channels allowing the immediate and sustained revascularization of the ischemic tissue. They document their conclusion by colored photographs of the laser channels remaining patent 30 days after the revascularization. In their Figure 4D, they present a laser channel filled with dense red material, allegedly nonthrombosed blood. Numerous sinuous cross-sectioning fissures divide the red material into small "islands." These are so similar to each other that one cannot help but ask the question what mechanism has separated the nonthrombosed blood into such uniform entities. The answer becomes obvious when one realizes that, at the periphery of the channel, the fissures communicate with the interstitial spaces in the surrounding myocardium. Consequently, the fissures must be the remnants of the interstitium destroyed by laser and the red "islands" are the bundles of damaged hyalinized cardiomyocytes on the verge of fragmenting into "eosinophilic droplets" [1]. In Horvath and associates' Figure 4A, 4B, 4C, and E, a majority of cardiomyocytes have already disintegrated into eosinophilic droplets, which have invaded the interstitial space, creating the misleading impression of massive presence of blood in the channels.
The presence of damaged cardiomyocytes 30 days after the laser therapy falsifies Horvath and associates' [9] conclusion that this intervention has created patent transmyocardial channels leading to immediate revascularization. What is then the explanation of these extraordinary results? In acute total ischemia, the myocardium is dependent on the reserves of high-energy phosphates and on anaerobic glycolysis. The reserves of phosphates being quickly exhausted, anaerobic glycolysis, the only source of newly formed high-energy phosphates, becomes vital for the survival of myocardium. Its rate diminishes, however, as fast as lactate, the product of glycolysis, accumulates [10]. If lactate had been drained away or metabolized and if enough glucose had been available, anaerobic glycolysis would not stop and would allow the survival of the ischemic myocardium. This hypothesis may apply to the experiments of Horvath and associates [9]. The laser channels, even though obstructed by damaged cardiomyocytes and impermeable to red cells, might have been permeable to interstitial fluid and permitted the washout of lactate and the supply of glucose so that anaerobic glycolysis did not stop and prevented the necrosis of myocardium. This hypothesis accepts that a limited amount of blood might have penetrated into the channel as a consequence of the injury caused by the laser therapy and that a free passage for blood through the channel may be possible after the fragmentation of hyalinized cardiomyocytes.
References
weeks. Ann Thorac Surg 1996;61:1532–5.
weeks. Invited Commentary. Ann Thorac Surg 1996;61:1534–5.
This article has been cited by other articles:
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  J. T. Beranek Why Do Channels Remain Patent After Transmyocardial Laser Revascularization? Ann. Thorac. Surg., April 1, 1998; 65(4): 1200 - 1200. [Full Text] [PDF]
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