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Aortic Intervention
April 3rd, 2015

Does a clear final angiography mean long-term success for an EVAR?


TM Mastracci MD

Royal Free London NHS Foundation Trust

Assessing the predictive value of a completion angiogram on the long-term durability of EVAR is a task that has only recently been requested of endovascular providers. Now that the endovascular community has proven that endovascular aneurysm repair is safe and effective in the short term1- 3 we have set our sights on proving its utility for the lifetime of the patient. To rephrase the question above, I would ask the reader:

Can we rest when the intraoperative images are perfect, or is there anything that might indicate that a patient is headed toward late failure of a well-placed endograft?

The question of long term efficacy of endovascular repair was first called into question by the original trials that proved its worth: the DREAM and EVAR trial long term results show a departure from freedom from mortality after longer-term follow up in patients undergoing EVAR compared with open aneurysm repair.4, 5 Although both of these trials demonstrated effective repair in the perioperative period with decreased aneurysm related mortality, the test of time proved differently.6 Other data is beginning to converge on this finding as well: reports of experience with explant of infrarenal endografts has shown that reintervention and ultimate explantation is needed approximately 41 months after the first EVAR.7 Imaging studies looking at long term follow up of aneurysms show a steady rate of aneurysm growth in a significant portion of patients, especially those who have had treatments outside of the “instructions for use” [IFU].8  Furthermore, there is growing evidence that this is not a phenomenon limited to endovascular repair: a report of fenestrated reintervention after failed open infrarenal surgery found that a patient who developed proximal degeneration after open repair of infrarenal aneurysm will need it within 10.8 years after the index procedure.9

Although most aortic experts will admit that late failure is a phenomenon that can be observed in any modality of aneurysm repair, and that the lack of crossectional imaging follow up for most patients undergoing open aneurysm repair strongly biases the finding against EVAR, the apparent accelerated observation of failure in endovascular repair compared with the open experience is a topic of much debate. Mechanically, earlier failure in endografts is logical because endografts rely on a stable sealing zone for the integrity of repair – if proximal aorta degenerates in open surgery, it takes many years for it to grow to reach operative threshold, but in endovascular repair, only a few millimeters of growth will lead to re-pressurization of the sac. Numerous explanations have been proffered for the high incidence seen in the first randomized trials: early generation devices, limited early experience, poor understanding of the need for intervention in the case of persistent type II endoleaks.

But in all cases, vascular surgeons are left with limited gold-standard evidence-based guidance on how to prevent late failure.

In my opinion, sorting out the cause of late failure requires a step back to take a broader view of aortic disease in general. Although we have conventionally treated aortic disease as segmental disease, and there are some cellular differences between the vessel wall composition of proximal and distal aortic segments, the transition between these segments has never been as crisp and clear-cut as we have treated it. Thus, the continuous sheet of smooth muscle cells that extend from the aortic valve to the aortic bifurcation vary in composition slightly between all individuals, and aortic disease is best approached as progressive and contiguous, rather than focal, limited or segmental. Although this may be a very technical and subtle distinction, I believe it will change our approach to repair.

A search of published literature does reveal histologic data to support this theory. A study by Diehm et al in Journal of Vascular Surgery (2008) shows that normal caliber aorta in the neck of an infrarenal aneurysm – aortic which would be called ‘healthy’ based on cross sectional imaging, actually demonstrates histological evidence of medial degeneration.10 The appearance of the media in this normal caliber aorta adjacent to aneurysm is far more reminiscent of aneurysmal tissue than it is of normal tissue.  This has huge implications in the endovascular treatment of disease: if we land an endograft in this marginal or ‘vulnerable’ aorta, it stands to reason that it is only a matter of time before it fails. And that would be true regardless of the sealing or fixation techniques used to hold the endograft in place. Thus, independent of current device engineering, sealing in vulnerable aorta may be a short term victory, but will lead to failure if a patient lives long enough.

So what, if anything, should we do with this new knowledge? I believe the answer is twofold.

First and foremost, we need to investigate changing the natural history of aortic disease. The potential of mechanical and pharmacologic/biologic solutions in this arena are great, and far outside of the scope of this blog. However, it is clear that research efforts are sorely needed.

Second, and more likely, vascular surgeons may need to approach aneurysm disease as a lifelong condition. This means setting the patient up for a lifelong surveillance programme, and explaining that the first repair may not be the last repair if all his or her associated comorbidities are well managed. This may also have an effect on device design –infrarenal aneurysm repair design should be undertaken with a plan to extend proximally in the future: incorporating long body designs that provide good distal landing zones, and limiting cross renal coverage so that future fenestration or branching is easier.

Now, thankfully, it is true that not every patient will need a second repair – in fact, the majority of patients present with cardiac and respiratory comorbidities and their chances of dying of non-aneurysm related causes is greater than aneurysm related causes. But for those who do find themselves in the OR for a second or third repair, it would be ideal not to be cursed with a more challenging task, but rather create a situation that is “modular-by-design” from the outset.  What we as vascular surgeons should be asking for from device companies is a suite of devices that fit together easily, and can be staged with the expected pace and presentation of disease.

So my advice when looking at a well performed EVAR intraoperative angiogram: toast the short term win – but celebrate every subsequent anniversary with a contrast CT scan, a discussion, and a plan.

Reference List