Ann Thorac Surg 1995;60:1831-1835
© 1995 The Society of Thoracic Surgeons
Our Surgical Heritage
The Phantom of ``Myocardial Sinusoids'': A Historical Reappraisal
John C.-C. Tsang, MD,
Ray C.-J. Chiu, MD, PhD
Division of Cardiovascular and Thoracic Surgery, McGill University, Montreal, Quebec, Canada
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Abstract
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The concept of myocardial sinusoids has been described in the literature during the past 60 years. They have been the basis of several revascularization procedures, such as the ``Vineberg'' procedure and more recently transmural laser revascularization. This article will review the historical evolution as well as the validity of the concept of ``myocardial sinusoid.''
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Introduction
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What are ``myocardial sinusoids''? They were the anatomic basis of the Vineberg procedure, in which a bleeding internal mammary artery (IMA) was implanted into an ischemic myocardium. The presumed flow into this ``sponge-like'' myocardium with its extensive network of ``sinusoids'' providing an excellent run-off for the implanted artery was the rationale for the development of this operation. More recently, they are being touted as the channels by which the new technique of transmural laser revascularization can improve the vascularity of an ischemic myocardium [1]. The sinusoids are thought to play a role in retrograde cardioplegia as well [2]. But, what exactly are these sinusoids? Vascular sinusoids are, by definition, endothelium-lined lakes and spaces with a discontinuous basement membrane. Sinusoids are known to exist in the liver, spleen, bone marrow, and certain endocrine organs. However, no major modern textbooks of histology describe the presence of sinusoids in the myocardium [3]. Instead, they illustrate in detail the architecture of the myocardial vasculature as blood flowing from the coronary arteries, to arterioles and capillaries through venules to veins, which then return to the cardiac cavities either via the coronary venous system or the thebesian system. Our present histologic knowledge of the myocardial microvasculature is complete to the point that we know that the myofiber-to-capillary ratio is about 1:1 [4]. It is indeed curious that despite the availability of sophisticated light microscopy, transmission and scanning electron microscopy, and all manners of special stains, the supposedly all-pervasive ``myocardial sinusoids'' seem to have evaded the inquisitive eyes of modern histologists. Yet, in the surgical literature, many authors continue to refer to myocardial sinusoids as an integral part of the functional anatomy of the heart. How did this paradox come about? Do surgeons simply have better histologic knowledge, or is this just a part of surgical lore that has been passed down through the years?
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Development of ``Sinusoid'' Concept of the Heart
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Reference to myocardial sinusoids has been frequent in the surgical literature during the past 60 years, since its initial description by Wearn and associates [5] in 1933 in a widely quoted article published in the American Heart Journal. The sinusoids were depicted as a run-off for coronary vessels that ``gradually loses its arterial character ...,'' breaks up into ``channels whose lumina are very irregular'' with thin walls ``made up of endothelium only or endothelium reinforced by a minimal amount of subendothelial connective tissue.'' The sinusoids were thought to be closely associated with muscle fiber bundles as well as the individual muscle fibers. This was the landmark article that gave rise to the notion of the myocardial sinusoids. Wearn and associates' description of these sinusoids was in part based on injection of a nonphysiologic substance at supranormal perfusion pressures into postmortem hearts. The histologic specimens were prepared for microscopic examination using methods available then, producing sections of lesser quality than those available today. Their results were, however, never disputed, and the notion persisted over the years in the literature.
In 1952, Truex and Angulo [6] tried to make a distinction between myocardial sinusoids and sinusoids of the liver and spleen, recognizing they were not structurally identical. Using techniques similar to those of Wearn and associates, they also confirmed the existence of such spaces. They called the ``sinusoids'' myocardial sinuses, recognizing their venous nature and continuity with the venous network. However, these were considered as a separate entity from the thebesian system, a vascular cavitary venous connection that could most easily be mistaken for Wearn and associates' sinusoids. Thus, this article served to reinforce the concept of the presence of myocardial sinusoids.
The notion of myocardial sinusoids was further perpetuated by Hammond and colleagues in two separate articles. First, by looking at the coronary arterial drainage patterns and assessing the level of saturation of the effluent in various cardiac chambers of an isolated heart model, they concluded that the only means by which partially desaturated drainage could enter the left ventricle was via the ``myocardial sinusoids'' [7]. Second, these investigators noted that as coronary arterial pressure was raised or lowered, blood would either directly enter the left ventricular cavity or flow from the cavity back into the coronary arterial system, through the ``myocardial sinusoids'' [8]. The major misconception that these findings were based on was the assumption that there were no thebesian vessels in the left ventricle, such that any direct vascular-cavitary flow had to be via the myocardial sinusoids. Yet today we know that there are indeed thebesian veins in all chambers of the heart [9]. Thus, these studies based on incomplete knowledge of the myocardial vasculature further sustained the belief in the existence of the myocardial sinusoids.
How did the concept of a vast network of intramyocardial ``lakes'' with direct communications to various chambers of the heart come about? It most likely was inspired by a phylogenetic extrapolation from more primitive vertebrate hearts. The myocardium is unlike other muscle tissue in that it did not always have a discrete vascular supply [10]. The single-chambered hearts of hagfish and lampreys, for example, show a complete lack of coronary vessels and are supplied directly by blood from the ventricular cavity [11]. Similarly, the single-ventricle reptile hearts such as those of the snakes have small external coronary vessels, and are also primarily supplied by luminal blood [12]. The blood flows in and out of the myocardial sinusoids, bathing the muscle fibers with oxygenated blood. However, with evolution, the increasing size and complexity of multichambered hearts led to the compaction of this ``sponge-like'' network. The direct nourishment of the myocardium by cavitary blood became neither efficient nor adequate. Thus, to adapt, the coronary veins, which developed before the coronary arteries, formed communications with this sponge-like network. Subsequently, a capillary network developed that finally anastomosed to the new coronary arterial system. This progressive substitution by a more highly developed and efficient vasculature can be seen in evolutionarily more advanced animals such as birds and mammals. Residual elements of the sinusoid system can occasionally be identified in various species such as cats, rats, dogs, and rabbits. However, the ``rare and irregular distribution of sinusoids ...calls their physiological relevance into question'' [13]. Further remnants of our phylogenetic history is preserved during the embryologic development of the human heart. The primordium of the heart shows invagination of large endothelium-lined spaces through which the primitive circulation could freely flow, providing direct nutrition. However, as the heart develops, these spaces are obliterated and extramyocardial blood supply via the coronary arteries takes on the main role of delivering oxygenated blood [14]. The persistence of the primitive state whereby the myocardial sinusoids continue to play a role in myocardial vasculature can be seen in certain abnormally developed hearts [15]. Often in hearts with elevated intracavitary pressure caused by obstructing lesions, such as pulmonary atresia with intact ventricular septum, the presence of the embryologic sinusoidal channels can be demonstrated histologically as well as angiographically. Their presence tends to be detrimental as they adversely affect the normal coronary flow. The blood from the abnormal communications results in retrograde flow into the coronary arteries, which may impede normal diastolic coronary perfusion and thereby cause myocardial ischemia and dysfunction.
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``Sinusoids'' as the Rationale for Myocardial Revascularization
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From the 1940s to the early 1960s, pioneering surgeons and investigators in cardiac surgery began to conceptualize new methods to revascularize ischemic myocardium by taking advantage of this putative ``sponge-like'' network of myocardial sinusoids. Several investigators attempted to divert cavitary blood by inserting conduits that would allow blood to flow into these ``wide open spaces'' [16, 17]. Others simply attempted to create holes by acupuncture to gain direct flow into this sinusoidal network [12]. The transmyocardial acupuncture procedure was nicknamed the ``snake heart'' operation. The concept was in essence to de-evolve the human heart back to that of a primitive reptilian poikliotherm whose lower metabolic demands allow for the direct luminal sinusoidal blood supply. All of these attempts met with minimal success.
In 1946, Vineberg [18] came up with a unique approach to myocardial revascularization. He freed the IMA from its bed, left the free end as well as side branches open, and implanted it directly into the wall of the left ventricle in experimental animals with occluded coronary arteries. These experimental animals seemed to show clinical improvement. Subsequently, the animals were sacrificed and polyvinyl acetate was injected through the IMA implant to obtain a digestion cast. In such a preparation, the heart was immersed in a strong alkaline solution to dissolve the cardiac tissue, leaving the polyvinyl acetate cast to delineate the vascular space. Vineberg noted that the implant formed anastomoses with a large myocardial sinusoid meshwork (Fig 1
) [19]. He was convinced that the availability of this large vascular network served as an excellent run-off, allowing the formation of anastomoses with the proximally occluded coronary arteries. The ``Vineberg procedure'' was remarkable as it was one of the first successful attempts at myocardial revascularization. Nevertheless, considerable skepticism persisted regarding the validity and efficacy of this procedure for many years. Not until the first human angiographic evidence of implant patency and communication with the coronary arteriolar system by Effler and associates [20] in 1963 was Vineberg's belief vindicated. Yet, as more investigators attempted the procedure in experimental animals as well as in clinical trials, the results were often conflicting [21, 22]. The need for a randomized, controlled clinical trial became evident. This was begun in 1968 by the Veteran's Administration hospitals. Shortly after the start of this trial, however, the IMA implant procedure became obsolete due to the advent and success of the new direct coronary artery bypass grafting. The study was abandoned and no conclusions were ever reached, as the Vineberg procedure was largely relegated to history as part of our surgical heritage. Nonetheless, it has been thought that implicit in the long-term angiographic evidence of the patency and run-off of the IMA implants (Fig 2) [23] was the validity of Vineberg's original concept based on the existence and importance of the myocardial sinusoids [24].
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Fig 1. . (A) Digestion cast produced by injection of polyvinyl plastic through a catheter implanted into the anterior wall of the right ventricle of a dog. This preparation was used by Vineberg as evidence of the existence of myocardial sinusoids in both ventricles. (cs = coronary sinus; R cor = right coronary artery.) (B) Diagram depicting Vineberg's concept of the ``myocardial sinusoids'' in nondiseased microcirculation. (Reprinted from Can Med Assoc J 1972;106:763–9, with permission from the publisher.)
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Fig 2. . Angiogram of a patient 20 years after double internal mammary artery implantation for coronary occlusive disease. This view demonstrates a patent left intenal mammary artery with extensive collaterals prior to reconstituting the distal anterior descending artery (Reprinted by permission of The Society of Thoracic Surgeons [Ann Thorac Surg 1991;51:1002–3].)
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One of the studies that cast doubt on the role of the myocardial sinusoid as the basis for the success of the Vineberg procedure was reported by Chiu and Scott [25]. Nucleated red blood cells from avian blood were instilled at physiologic pressures into a myocardial implant of a dog in a procedure similar to the Vineberg operation. Histologically and by electron microscopy, it was demonstrated that these nucleated red blood cells, which could be easily distinguished from the anucleated red blood cells of the dog, were in fact not found within any endothelium-lined sinusoids, but rather were found in the interstitial space (Fig 3). The ``lakes of sinusoidal space'' demonstrated by the digestion casts were in fact casts of the interstitial space! The earlier investigators using digestion cast technique could not tell whether such space was lined by endothelium or not, because the endothelial cells were digested away by the strong alkaline solution used to prepare the cast. The irregular spaces seen in the histologic specimens of Wearn and others were probably distorted coronary veins, which may be distinguished by the presence of a rudimentary tunica intima, media, and adventitia.
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Fig 3. . Electron microscopic view demonstrating that the nucleated avian erythrocytes infused through the myocardial implant are directly adjacent to the sarcolemma of the muscle fiber without intervening endothelium (A); whereas the anucleated canine erythrocytes from the coronary circulation are found within the endothelium-lined capillary (B). (Reprinted from Chiu RC-J, Scott HJ. The nature of early run-off in myocardial arterial implants. J Thorac Cardiovasc Surg 1973;65:773, with permission.)
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How then could one explain the long-term patency of the implanted vessel as well as the reported successes of this procedure? It has been suggested that the implanted IMA does not occlude even though it has virtually no run-off when measured with flow probes, because of the squeezing action of the muscle. This causes to-and-fro motion of the blood within the IMA, resulting in defibrination, thus preventing thrombosis [26]. Furthermore, more recently it has been proposed that the high patency rate of the IMA coronary bypass grafts may be due to certain unique properties of this vessel [27]. It may be hypothesized that these same inherent properties of the IMA also served in preventing the thrombosis of the IMA implants. Ischemic myocardium is now known to liberate factors for the development of collaterals [28]. When this is supplemented by blood-borne angiogenic factors, the process is amplified [29]. Recently, it has been shown that an IMA implant will indeed collateralize to a nearby left anterior descending artery when stimulated by platelet-derived growth factor. These anastomoses are able to maintain myocardial vascularity when the left anterior descending artery is subsequently ligated [30]. Presumably, this gradual development of collaterals could be the reason why it was often noted that there was a delay before the therapeutic benefits of the implant procedure became evident [31].
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``Sinusoids'' and Transmural Laser Revascularization
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By the early 1970s, as direct coronary artery bypass grafting became established, the efforts toward using the myocardial sinusoids as a conduit for revascularization waned. Yet, in the 1980s and the 1990s, as the success of coronary artery bypass grafting plateaued, people began to look for alternative solutions for diffuse coronary artery diseases. One such approach is transmural laser revascularization. The procedure is basically a reworking of the acupuncture revascularization of ischemic myocardium developed in the 1960s by Sen and associates. In 1982, Mirhoseini and co-workers [32] attempted to create similar transmyocardial channels using the new laser technology. Extensive research including clinical trials is being conducted on this procedure, with the outcome still uncertain [33, 34]. Once again, the ``myocardial sinusoids'' return to the forefront as the basis for myocardial revascularization. In a number of recent articles, Wearn and associates' initial descriptions of the sinusoids are still being quoted and accepted as fact. If transmural laser revascularization eventually turns out to be effective, it may be so not because of the presence of myocardial sinusoids, but perhaps in spite of their absence. Transmural laser punctures may establish coronary vessel-to-cavitary channels, which would be physiologically similar to the thebesian venous system. However, in the latter, the blood normally flows from the myocardium into the ventricular cavity, whereas laser channels created within an ischemic and dyskinetic myocardial zone may allow a reversal of flow from the cavity into the muscle. This could be due to the low myocardial tension in this area and diminished opposing coronary inflow pressure. Persistence of flow within the channels may keep them open, even allow them to endothelialize, and serve as the source for neo-angiogenesis in a scenario similar to that described above for the Vineberg procedure. Further studies are needed to verify such a hypothesis. In any event, it is time that we cardiac surgeons give up the idea that the heart is a giant sponge!
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Footnotes
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Address reprint requests to Dr Chiu, The Montreal General Hospital, 1650 Cedar Ave, Rm C9.169, Montreal, Que, Canada H3G 1A4.
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Abstract
Introduction
