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Eur J Cardiothorac Surg 2006;29:643-644
© 2006 Elsevier Science NL
Editorial |
Stanford University Medical Center, Stanford, CA 94305-5407, USA
* Corresponding author. Tel.: +1 650 7242925; fax: +1 650 7253846. (Email: fhanley{at}stanford.edu).
In this edition of the journal, Norgaard et al. [1] make their case that the major aorto-pulmonary collateral arteries (MAPCAs) found in patients with pulmonary atresia with ventricular septal defect are in fact nothing more than dilated bronchial arteries. The authors are to be commended both for tackling the difficult subject of the origin of these unusual vessels, and for taking a very creative approach in their study design and analysis. Their findings, although far from conclusive, suggest some similarities between the ‘road maps’ of the large number MAPCAs that they evaluated, and those of normal bronchial arteries, with respect to site of origin, total number of arteries per patient, course and branching patterns, and destination within the lungs. These observations alone make this an interesting study.
It is a far cry, however, to say that just because these two categories of arteries have some, or even significant, similarities, that they are the same entity, or as specifically stated by the authors, MAPCAs are dilated and hypertrophied bronchial arteries. The story is much more complex than that.
MAPCAs and bronchial arteries are vessels that we find in fully developed individuals, and like all fully differentiated tissues, each arose developmentally from primordial tissue in the early embryo. It may well be that the one valid finding in the Norgaard study is that MAPCAs and bronchial arteries share a common primordial vascular origin, but I am getting ahead of myself. Let us for a moment assume that MAPCAs and bronchials are derived from the same primordial vascular origins. That nascent vascular tissue is not a bronchial, at least not yet, and it is not a MAPCA, at least not yet. One must consider that the path of development that this multipotential vascular tissue takes will be profoundly influenced by the local environment that exists as development proceeds. In the case of the normally developed heart with forward pulmonary blood flow from the heart and a patent ductus arteriosus, the local environment allows normal pulmonary artery development, and the primordial vascular tissue that is destined to become a typical bronchial artery, does just that. In the case of one type of abnormal heart in which the specific combination of the absence of forward flow from the heart to the pulmonary arteries and also the absence of a ductus arteriosus occurs, a very different local environment is present. There is no stimulation for central pulmonary artery growth. In this setting the primordial vascular tissue that would have, in the normal heart, possibly (I would emphasize possibly) developed into a bronchial, might very well develop into a MAPCA. But does that make bronchial arteries and MAPCAs the same end differentiated tissue? I doubt it. That inference is no more valid than saying that a brain cell and a myocyte are the same because they originated from the same fertilized egg. The MAPCA and bronchial may share some common features, but they were exposed to very different environments over most of their developmental histories, and as with most other similar situations, each has likely developed quite a number of unique characteristics.
The situation at hand brings to mind an analogous exercise in logic in a somewhat different discipline. Anyone with even a cursory understanding of natural history and human evolution understands that man is not descended from the monkey, but rather man and monkey are two separate differentiated species with a common ancestor. That ancestor was neither man nor monkey, it was what it was, although it shares some features with both of its descendents, and both descendants also share some features. That is not to say that man and monkey are the same entity, not by a long shot. To argue, as Norgaard et al. do, that a MAPCA is nothing more than a jazzed up bronchial artery is the equivalent of saying a human is just a monkey on steroids. Most would agree that no amount of pharmacotherapy, or tutoring for that matter, could ever make a monkey write like Keats, compose like Wagner, or tell jokes like Seinfeld.
Enough for theory, and now to the practical. The authors attempt to make some practical points based on their interpretation of the findings in this study. They cite their own previous work, to support the argument that MAPCAs, being dilated bronchials, thus behave badly when used in surgical reconstruction of the pulmonary artery system in procedures such as unifocalization. There are many reasons in addition to those intrinsic to the vascular tissue itself, that can explain why a MAPCA would not grow and develop well after unifocalization, including technically poor reconstruction, late timing of unifocalization, and failure to address existing degenerated (stenotic) segments in MAPCAs at the time of unifocalization.
Although MAPCAs can unquestionably be difficult vessels to deal with, my belief is that much of that difficulty is related to ‘environmental’ conditions rather than intrinsic problems of the MAPCAs themselves. Thus, the idea arises of the MAPCA as the innocent bystander, finding itself in a hostile physiologic environment following birth. Not in all, but in many cases, MAPCAs are smooth walled uniform caliber vessels at birth. Obviously they have grown and developed that way thoughout most of gestation. Following birth, these vessels often become irregular, kinked, stenotic, and thickened in quite dramatic and accelerated fashion. One intriguing hypothesis is that the physiologic change that occurs in the pulmonary vascular bed after birth promotes increased velocity of flow and abnormal shear force in these vessels as the PVR drops and flow dramatically increases, leading to rapid degeneration of the vessel. Based on this hypothesis, our approach to these vessels is to remove them from the systemic circulation as soon as possible, place them in as normal a pulmonary circulation as possible, address any stenotic points which already exist, create the most accurate anastomoses that avoid torsion, kinking, rotation, and stenosis, and extend these anastamoses as far distal (i.e. into the lung tissue) as possible. Using this approach in over 1100 MAPCAs has convinced me that these vessels commonly have excellent growth potential. I will not go through the litany of evidence from our experience now in over 340 patients (most of which was recently peer reviewed and presented at the 2005 Scientific Sessions of the American Heart Association in Dallas, Texas) that support this position, other than to make one compelling point. About 20% of our patients (over 60 patients) have completely absent intrapericardial pulmonary arteries. The lungs in these patients are perfused by MAPCAs only. Using our techniques of complete unifocalization at about 3–4 months of age, and with follow up as long as 14 years in some cases, certainly enough time for the growth issue to be tested, these patients behave early and late just as well as those patients with MAPCAs and coexisting central pulmonary arteries, i.e. the pulmonary artery pressure has remained below half systemic pressure levels in the great majority even after years of follow-up. Thus, it is unequivocal that MAPCAs grow and grow well when managed appropriately.
Unless Norgaard et al. believe that mankind is descended from monkeys, I would urge them to reconsider their position on the relationship between MAPCAs and bronchial arteries, and the implications of that position.
References
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