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John Eidt (Little Rock, AR): The authors have presented admirable results in a consecutive series of 105 patients scheduled for endovascular repair of abdominal aneurysms with the AneuRx endograft. They had a 2% 30-day mortality and an average 2-day hospitalization, and they were plagued, as all endograft centers have been, with the need for numerous secondary procedures to achieve moderately good clinical success. I have to admit that these definitions of success are a little bit confusing, as what is continuing success and secondary success. We have just finished the first decade of the endograft experiment and some authors have already declared the experiment a failure, citing the frequent problems such as endoleak and graft limb occlusion, requiring secondary interventions. I would caution that the initial phases of technological development are often fraught with unforeseen obstacles and I have no doubt that endovascular surgical techniques will play an important role in the management of vascular disease in the future. It is important to remember that the ultimate goal of aneurysm treatment is prevention of rupture and endografts have been generally successful in achieving this goal with reported long-term rupture rate of less than 3% in most reports. And as I think I understand your report today, there was one rupture in today’s report. I think it’s worthwhile to be able to offer an older, sicker patient, the potential for a very high assurance of rupture prevention with a less morbid procedure. Results with endografts are device-specific. The AneuRx graft is a modular graft with a nytenol skeleton covered by polyester fabric. It does not have fixation hooks but relies on friction, stent incorporation, and so-called column strength or longitudinal stiffness for fixation. Friction generated by a self-expanding nytenol stent is really quite low. Fibrous incorporation is unpredictable and column strength works poorly in tortuous vessels. At the summer vascular meetings last year, a group from Italy reported migration of greater than 10 mm in over 25% of their cases. Migration may result in the development of a proximal attachment site type 1 endoleak. Type 1 endoleaks are the most dangerous and the most likely to lead to rupture. You’ve described 9 patients with type 1 endoleak, which is nearly 10% of the total group. This is a slightly higher proportion of type 1 endoleaks that most other reports. So my first question relates to the cause for these type 1 endoleaks. What was the etiology of these type 1 endoleaks? Was it inappropriate patient and graft selection preoperatively or do you think it was due to some type of intraoperative technical error. For example, do you think you were too aggressive in trying to use endografts in every patient even though some may have had inappropriate anatomy? Did you undersize the grafts or do you think that these endograft endoleaks represent technical errors for not placing the graft close to the renal arteries? So the question is patient selection or technical error? Britt Tonnessen: I think the answer to that question is patient selection. The majority of the first half of these patients were done during phase 2 clinical trials before the graft was widely available on the market, and so the group was definitely more aggressive. Other studies that we’ve done have shown that angulation is an issue that we didn’t recognize early on and that migration certainly plays a role as far as contributing to type 1 endoleaks. In the presentation, we divided the patients into the first half and the last half. There were six type 1 endoleaks in the first half and only three in the latter half. This reflects our learning curve. John Eidt: You said that these patients were high risk or higher risk than your open repairs. How does that really compare with your open repair patients? You said 95% of your endograft repairs were in either class 3 or 4 ASA class. How does the open repair group compare to that? Britt Tonnessen: We haven’t yet broken down the open repair group into ASA class. What I can say is that a significant number of the patients who underwent endovascular repair had COPD and wouldn’t have been considered candidates for open repair. John Eidt: My last question is really sort of an extension of that. You had 11 people that died during the first year. Do you think you should be more selective in refusing endograft repair for some of these very old, very sick patients with limited life expectancy? I mean, are we really doing them any favors by repairing a moderate-sized aneurysm that may not really effect their life expectancy? Britt Tonnessen: I think that thus far the data’s borne out that perhaps the very old, very sick patients may be some of the best candidates for endovascular repair. Of the 10% mortality rate at one year, it was very diffuse as far as the various causes of death. A couple died from their pre-existing coronary disease, from CHF, pneumonia, renal failure, lung cancer, so it was very unpredictable as far as which patients died from what. There were four patients that had renal insufficiency, two of those died and both of those had some procedure-related complications as far as acute renal failure. So perhaps renal insufficiency is one factor to seriously look into prior to endovascular repair.</P> http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The American Journal of Surgery Elsevier
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