Wolfgang Ritter: We know that all devices have problems; for example, the VanGuard or the AneuRx® (Medtonic, Inc., Sunnyvale, California) can incur some disintegration 4 to 5 years postimplantation. With the Zenith device, the problem of late occlusion of the renal artery arises due to migration, and wiith the EBT device, hooks and ruptures occur. Our endoleakage results show that the unibody devices have only about 10% endoleak rates. Unfortunately, however, Ancure is no longer available on the market, so the only unibody design left now is the Endologic, which I don’t think is available in the U.S. We have only a 7% leakage rate, perhaps because of Endologic’s unibody design and the length of its body. The new devices now on the market have short bodies, so I think that manufacturers should consider making devices with long bodies for these protheses in order to prevent leakages. Ernst Schneider: This first slide shows an image of a 67-year-old patient who received an endograft prothesis in 2001. After six months, there was no evidence of leakage, but no reduction of the aneurysmal sac either. At one year, the sac size increased from 7 cm to 8.5 cm, and the patient was still asymptomatic and had no evidence of endoleak. At two years, the patient was symptomatic, with lower back pain and a very sensible aorta at palpation. At this time, the sac measured 11.5 cm; there was still no evidence of endoleak and no sign of thrombus in the long neck, as well as no sign of an inflammatory aortic aneurysm and no halo. In terms of pathogenesis, the surgeons intraoperatively evaluated this patient and found no thrombus at the upper end of the prothesis. Is it due to continuous degeneration of the arterial wall? Is it due to pressures other than hemodynamic, such as the colloid osmotic pressure in the sac? Because there must be a gradient when the other is enlarged. And what is the clinical significance of this? This patient was asymptomatic postimplantation, but is now symptomatic. Is there danger of rupture? Should we intervene or just treat the patient’s symptoms? This next patient underwent surgery. This image shows the open sac with fluid inside. Before opening the sac, the surgeon measured the pressure and found it at 65 mmHg. The upper part of the prosthesis showed no thrombus; a small opening was made at the inferior and posterior parts of the sac and the sac was then closed. The patient was immediately asymptomatic, and at six months, there was no evicence whatsoever of aneurysmal overgrowth. Thus, there was no leakage and no thrombus, because if the upper part of the prosthesis had shown thrombus, the sac would perhaps have grown again due to endotension caused by thrombus. So what is the explanation for this phenomenon? And I wonder if this phenomenon may just be brand-related? Klemens Barth: Does anyone want to tackle these questions? Michael Marin: So far, most of the data have been anecdotal. The trend of thought seems to be that PTFE grafts are perhaps a thinner form of the material which develops into the seroma. We recently treated a patient similar to that one involving the thoracic area. At a conference I recently attended, there were several anecdotes of this sort. None of the doctors have any radiographic proof of a leak. In our patient, there was a thoracic aneurysm that had reached 11 cm; the patient was too ill for surgery, so we percutaneously accessed the aneurysm, and got back the same serous fluid which re-accumulated within 48 hours. Although we don’t have numbers to back it up, we currently think that unless there’s actual shrinkage, there is pressure at a certain gradient, but whether it’s enough to make the aneurysm grow or maintain its size over time, and whether mortality will result due to potential growth and rupture, is not yet clear. We are hoping to correlate some of these data with the characterization of the thrombus as well as the pressures so that we can answer this question once and for all. Fortunately, what we do know is that the rupture rate, or freedom from rupture according to the mid-term (> 5 years) results, is approximately 97–98% overall. Thus, the chance of the aneurysm rupturing exists, but it’s difficult to predict at this point. Klemens Barth: We can perform ultrasound, use contrast media, delayed imaging, and also multi-slice CT scanning in phases — early phase, late phase, and so on — which allow the detection of some of the endoleaks that were previously undetectable. It’s a challenge, because we need to obtain a lot of quality images in the follow-up phase before we can conclude that there’s endotension. Andrew, you’ve been very involved in this, would you like to comment? Ernst Schneider: The surgeon who opened the aneurysm did not see any bleeding inside the aneurysmal sac, so he just closed it; the patient was asymptomatic and did not return. Michael Lawrence-Brown: The presentation we heard on pressure measurement with a device represents another “brick in the wall” that we’ve been waiting for. I commend those who worked on this technology. We must not forget that infection is still a possibility and that abcesses grow. A number of patients have developed infections, so we must be very wary of any aneurysm that is expanding. We have operated on a number of aneurysms where back-bleeding occurred, either leaving a hole or rupturing the sac. Thus, there is potential danger of missing a vessel and causing pressure to rise. Because of this, we do operate on aneurysms that are found to be expanding. Richard Heuser: If an aneurysm is enlarging, we become very concerned because we’re really not certain how to proceed. I admire your response, Mike, regarding the fact that an open operation should be performed. The group from Mount Sinai is pioneering the use of the measuring device, employing it in other applications as well, such as left atrial monitoring. This device, I believe, shows a great deal of promise, as it provides the operator with valuable information. Also, IVUS may be useful to determine if there are any leaks we’re missing, even though these leaks will usually be detected via other imaging methods. IVUS may be an application for virtual histology, which may allow the operator to see through the wall and determine what exactly that fluid is — seroma, thrombus, blood? Christopher Cates: In cases where just clear serous fluid has been percutaneously found, has there been any thought given to injecting fibrin glue or a thrombus enhancer, or a thrombin-fibrin amalgam into the lesion to try to seal it? Andrew Cragg: It has been done, anecdotally. My colleague form Vancouver, Lindsey McCann, and I have some limited experience with this type of approach. We have gone into the aneurysmal sac and injected a liquid polymer. It struck me as a rather rudimentary technique to inject a polymer around the lumbar arteries, hoping that it would stop the problem. We haven’t gained anough experience with this yet to know if we were doing it too much in that situation. I would like to discuss the devices as they currently exist and some of the patient issues we struggle with. We have discussed here and at many other meetings the topic of how rapidly technologies advance, but it sometimes strikes me as the just the opposite — things move slowly in this area. As a medical student, I worked on metal-fabric combinations in Kurt Amplatz’s lab over twenty years ago, yet we still have the same basic constructs today. I never really liked the idea of a metal-fabric construct because of the materials mismatch. We have all seen many devices fail. Biomaterials don’t work very well with any sort of movement when there’s a big difference in the compliance mismatch. That’s what this particular construct faces — where a tube is being placed in a vessel that’s pulsing. We need to move beyond these first-generation tubes that are put into the artery. There are, I believe, other concepts worth pursuing that might be able to treat aneurysms in other ways. If nothing else, we need to develop constructs that are not multi-material in terms of compliance. In that regard, what we see clinically are some rather perplexing things. I have patients who do fine for three years, and then all of a sudden, a graft starts moving. A well-known surgical tenet is that things don’t heal well — they do in animals, but not in humans. These tubes are basically just sitting in the aorta, for the most part, but I’ve had several patients whose grafts in their neck began to move after several years. As for patient issues, it is quite difficult to select among the patients I see. It is very seductive to put in an endograft, and it’s a very easy “sell” to convince a patient that this is the best treatment option. But one of the most difficult challenges we face as clinicians is to guide our patients appropriately toward the best course of treatment. Even though I have been doing this for a long time, I still have a fairly narrow indication for patient selection and a relatively lower bar than others may have for referring these patients for surgery. It is easy to put these endografts in patients, but it’s hell to follow them when things don’t go well. Thus, I would like to see the indications for this procedure narrowed rather than broadened. And when an endograft has been placed, I would agree with the other comments made here regarding endotension. We don’t know what the heck to do when an aneurysm starts creeping up in size after two, three, or four years. Currently, we are following these patients, but if I begin to feel ill at ease about things, I send the patient for surgery. Perhaps our contribution will ultimately be more than the endograft; but also the ability to determine how to treat aneurysms in general and how to survey them with monitoring techniques such as endosac measurements, or perhaps along the lines that Barry mentioned, noninvasive means could be developed to actually measure sac tension so that we could better determine, with small aneurysms, which patients are at greater risk, not just patient selection by aneurysm size. Klemens Barth: I would like to poll the panel here about which patients they think should receive endografts and which should undergo surgery. I would like to remind you about the recent publication by the FDA regarding the aneurysm trial ANEURX-ENDOGRAFT with three-year follow-up. This trial showed a tendancy toward a rise in mortality in aneurysmal-related deaths in the endograft group versus the open surgery group. The surgery group had an initial high of 5% moratlity, but after three years, there were no aneurysmal-related deaths, whereas the endograft group’s mortality rate increased at three years and beyond (a crossover point). Philip Walker: Did the Mount Sinai group have the opportunity to use your pressure transducer on open aortic grafts, perhaps sticking the transducer on Dacron grafts and PTFE grafts to see what the pressures were? Michael Marin: We initially plan on studying 20 patients, but when the study is completed, we will branch off into areas such as open repairs, placing the transducers in different locations — one, maybe right on the graft and one on the wall. In terms of the different thrombus characterizations, we are trying to accumulate data based on magnetic resonance imaging and place the transducers in different areas where we expect there to be different characterisitics in terms of stent graft repair. For example, from what I understand, the device is able to distinguish between six different transducers placed at one time. So, perhaps placing one by the proximal neck, one distally, one in an area by the lumbars where we would anticipate a potential type-2 leak, we hope to acquire better data both on the open repairs, as you mentioned, and on the character of the clot and whether endoleaks exist there. In in vitro and some animal studies, researchers have found that clot characteristics do potentially make a difference. Barry George: I like the idea of aneurysmal monitoring and I can imagine that this might be like pacemakers, where the pressure is called in a t one month, three months, six months, and yearly thereafter. If the patient experiences back pain, he would call in with the pressure data. Those of us who have placed a lot of endografts know that the easy part is placing the device, and the difficult part is following these patients and making the tough calls about whether the thing is a seroma. But there always seems to be this mysterious phenomenon in one or two patients — and the “what to do” with them question has still not been worked out. It makes sense to me that if a tiny Tracker-type catheter is placed on the outside after deploying the graft, and things are fairly well sealed, an assortment of collagen glues can be used interoperatively. We treated a patient who qualified as a “compassionate use” case. The patient had undergone a previous surgery, had terrible pre-existing general medical conditions, and no other alternatives. The patient developed left leg paralysis after placement of the graft. Later, when I analyzed one of the collagen glues, I found that it contained low-dose formaldehyde. Thus, I would recommend caution when using some of these products which may, on the surface, appear very enticing. It may not be much different than the repair of pseudoaneurysms using thrombin injections, with the notion that if something is very slowly trickled in, avoiding opposite flow into the lumbars, it would provide an advantage and perhaps eliminate many of the problems that arise six months or more down the road with type-2 endoleaks. Michael Lawrence-Brown: Some have tried glue, such as Onyx. The danger is not only the lumbar supply to the spinal cord, but the supply to the gut as well. There have been a few cases where the thrombin goes in and cuts off the blood supply to the gut, which is a terrible situation to find yourself in. We have seen the technology evolve over the years. I think you can make judgements too early on the success of a procedure. I foresee things changing from hybrid materials to plastic grafts in the next ten to fifteen years. The FDA has determined that it will be efficacious to place an endograft in 90% of the cases, and in 10% of the cases, another treatment will be needed. As soon a problem such as an expanding aneurysm occurs, a salvage strategy is needed going in; you may not need to take the graft out. When I perform the operation with endotension, I place a large balloon up inside a stiff wire, dilate the balloon, and open the sac so that I will have control. If there is no leakage around the graft, then I will deal with it in various ways. With salvage strategies, a flow chart is needed to guide the operator in what to do in various situations. If open surgeries are reduced form 100% to 10%, then good progress has been made. Barry George: There is some very intriguing eraly research under way involving magnetic materials, with a magnetic field being created in and around the aneurysm. Feromagnetic material — a gel-like substance — is injected, much like concrete being poured into a form. Research is being done to combine the sterile Taxus stent with feromagnetic gel-like materials that establish a magnetic field. Like a concrete form, the gel is injected and the magnetic field is left in place until the gel “sets” like concrete would, then the magnetic field is removed. This research is also being done for neurological applications and may be worth watching for in the future. Michael Lawrence-Brown: That is very interesting. It brings up the issue of compliance. The way gel material sets should be to the same compliance as the arterial wall, otherwise there will be rigid movement against a compliant structure. If the gel material can have the same compliance as the arterial wall once it sets, it would be great.