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Ann Thorac Surg 2007;83:1053-1054
© 2007 The Society of Thoracic Surgeons
Division of Cardiovascular Surgery, The Mayo Clinic, 200 First St, SW, Rochester, MN 55905
(Email: sundt.thoralf{at}mayo.edu).
A few years ago Francis Robicsek [1] asked "is it dead or alive?" regarding size reduction ascending aortoplasty. This article [2] is evidence that it is indeed alive, although debate continues as to whether or not it should be so. This argument has carried on for more than 3 decades. The obvious question is why?
I will begin by confessing my personal opinion, so that the reader can be wary of bias that may underlie my comments. I am opposed to it. I would argue that there is more to the risk of mechanical failure of the aorta than the Law of LaPlace (ie, the strength of the wall is as important an issue as wall tension) and reduction aortoplasty addresses only the latter. Laboratory investigations performed by ourselves and others have raised concerns regarding the composition, molecular biology, and material properties of the dilated aorta. My aversion for reduction aortoplasty is consonant with the majority view today, although this does not mean it is correct. There remains discussion within my own institution and among my colleagues regarding this matter, with some strong proponents of the technique.
Why does the debate continue? Arguments regarding the comparative risk of aortoplasty vis-a-vis graft replacement of the ascending aorta have quieted in recent years with the introduction of low-porosity grafts and recognition that simple tube-graft replacement of the ascending aorta can be accomplished at very low risk. However there remains the difficult group of patients with only mild dilatation of the ascending aorta (most often associated with the bicuspid aortic valve) in whom one is hard pressed to make an evidence-based argument for extirpation of the aorta. What of the 3.9-cm or 4.2-cm diameter aorta with only mild dilatation of the greater curve? Do we really have the data to support graft replacement of such an aorta? Is it rational to replace the latter and not the former? Does 3 mm really make the difference? Or is it more appropriate to apply an intermediate procedure such as aortoplasty to the case with only intermediate enlargement?
In this study the authors revisit the technique of reduction aortoplasty, but they do so with several important provisos. They have excluded patients with Marfan syndrome as well as those with bicuspid aortic valve (BAV). There is no argument over the former, and the logic for excluding BAV patients on the basis of studies demonstrating inherent abnormality of the wall will be familiar to most. Unfortunately, of course, this is the very group with whom we are most often faced with this difficult choice.
Indeed I am surprised the authors found so many patients with mild to moderate dilatation exclusive of BAV patients. Furthermore, by excluding BAV patients, it is likely that they have severely limited the applicability of their technique. Nonetheless they have defined a clean study in this regard, and the data stand on their own. The authors have wisely excluded those patients with aortic diameters greater than 5 cm in whom today few would argue against simple graft replacement. The results demonstrate relative stability of the aorta for the intermediate term with enlargement of only 0.17 cm during a median follow-up just less than 3 years (ie, 32 months).
The authors have gone a step further as well in constructing an argument in favor of the procedure by examining a physiologic measurement. They argue an advantage to the unsupported aortoplasty beyond matters of perioperative risk by virtue of the elasticity or "Windkessel-function" of the retained native aortic wall. The authors argue reduction in the afterload of the left ventricle by expansion of the ascending aorta in systole complemented in diastole with elastic recoil augmenting coronary perfusion as well as that of other small vessel beds. This is a more sophisticated view of the aorta and its physiologic role beyond a purely anatomic one.
Despite the creativity evident in the work presented, we must remain circumspect in the interpretation of the data. Although the procedure was performed in 97 patients, preoperative diameter measurements are available in only 87, postoperative in only 46, and paired data in only 45. Of 94 hospital survivors, 5 are known to have died and another 12 were lost to follow-up. Only 82% of the patients are known to be alive. Another 23 patients declined to participate in follow-up, which leaves 54 patients on whom to base any estimates of late durability of the repair and only 45 in whom both early and late imaging studies can be compared.
Finally, I would take exception to the author’s method of aortic measurement using the mean diameter rather than minimal diameter in any given image. Despite these limitations, the data are intriguing and add to the literature.
Where then does size-reduction ascending aortoplasty stand in our armamentarium? We are still in need of data. Surgeons are notoriously anecdotal as we live constantly in the numerator seeing only those who come (back) for surgery. Few of us, including these authors who have meaningful follow-up in less than 50% of the original patient group, effectively follow our patients’ for the long term.
In addition, should the burden of proof of long-term success or failure of reduction aortoplasty be on the proponents or the detractors? I would argue that this remains an unproven procedure, and accordingly there is a burden of responsibility on advocates of aortoplasty to commit to long-term follow-up of any patient in whom they perform this procedure, just as both Robicsek and colleagues [1] and Sievers and colleagues [3] argued in 2004. This recommendation is consistent with an expanded view of the surgeon’s role in today’s healthcare environment, from responsibility solely for performance of the technical procedure to longitudinal involvement in disease management.
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