The Mystery of Aneurysm Sac Shrinkage
What are the variables that affect sac shrinkage, and are they predictable?
Although significant differences exist between traditional and endovascular repair, the goals of each course of action are the same: to prevent aneurysm rupture.1 Obviously, the procedure’s success in preventing rupture cannot ultimately be determined until either the patient suffers a rupture or dies from other causes. Consequently, a proxy must be used to determine the success of the repair. One of the best proxies is whether the aneurysm sac grows, shrinks, or remains the same size.
As with any procedure, when deciding upon the most appropriate means of treating the aneurysm, the interventionalist must first weigh the risk of the procedure against the risk of the patient’s living with the aneurysm untreated. The risk involved with the procedure includes not only the initial challenges associated with its execution, but also the potential for problems that could emerge down the road. Therefore, it would be beneficial to know prior to the repair if there are any observable factors that may influence the recommendation for endovascular repair, open repair, or observation. Unfortunately, there are few published data available that elucidate the risks of sac shrinkage or gauge its predictors preoperatively. There is, however, a growing recognition among aneurysm repair experts about what some of these factors may be and why.
Because aneurysm sac shrinkage is commonly used as a surrogate for success, once an endovascular repair has been performed, it would also be helpful to know the potential danger of the sac’s failure to shrink. Clearly, sac growth is a worrisome outcome, and lack of shrinkage may also be troubling, especially if the aneurysm is quite large. Little is understood about aneurysm sacs that are stable and neither shrink nor expand.
Physicians need to understand the factors that contribute to postendograft aneurysm sac changes. For example, if a patient’s aneurysm sac does not shrink, the operating physician would know to look for a potential problem that might otherwise have gone undetected (Figures 1,2). Some of these factors are modifiable, whereas others are not. For example, if an aneurysm sac is not shrinking and the patient has an endoleak, perhaps the endoleak should be treated.
As previously mentioned, the literature on factors affecting sac shrinkage is relatively sparse. The following is an admittedly incomplete list (with little data to support it) of preoperative and intraoperative issues that some physicians believe could have varying impacts on just how an aneurysm will respond to endovascular stent graft placement. We encourage you to compare these factors to your own experiences and discuss your ideas about them with your colleagues in the hopes of building a collective understanding of their ability to be of assistance in performing an endovascular aneurysm repair.
The presence or absence of endoleaks often affects the growth or shrinkage of an aneurysm. Endovascular specialists know that endoleaks transmit systemic pressure into the aneurysm sac regardless of their type,2 and because the goal of endovascular repair is to eliminate the systemic pressure within the sac, the presence of an endoleak could potentially prevent aneurysm sac shrinkage.3 There are reports that patients having aneurysm sacs with endoleaks are less likely to experience sac shrinkage than patients without them.4
It is beginning to appear as if the type of stent graft used has a significant impact on aneurysm sac shrinkage after endovascular repair. Factors such as the type of material, for instance whether it is made of PTFE or Dacron, could possibly make a huge difference. The thickness of the material may also be a factor. Although grafts are picked based on the patient’s anatomy and graft availability, there are definite differences in the sac shrinkage rates between the different manufacturers.5
Initial Aneurysm Size
The size of the aneurysm sac prior to stent grafting will likely determine how fast it shrinks or whether it does at all. Some believe that larger aneurysm sacs tend to shrink more.5
Wall calcification may have an impact on how well the stent graft seals at the attachment sites. It may also affect the overall rigidity of the wall. One would expect a more heavily calcified aneurysm to be less likely to shrink to a great degree because the wall starts out rather rigid.6
The amount of pre-existing thrombus in the aneurysm sac may also affect sac shrinkage. If the aneurysm sac already contains a significant amount of thrombus, a more rapid and more complete thrombosis of the sac after repair is likely. Patients with more thrombus in the sac prior to aneurysm repair also tend to have more sidebranches, such as the lumbar arteries and the inferior mesenteric artery, already occluded prior to repair.7
Number of Branch Vessels
There is at least speculation that the presence or absence of a patent inferior mesenteric artery may affect the likelihood of spontaneous thrombosis. It has been suggested that if the inferior mesenteric artery is patent, the size of the inferior mesenteric artery was a factor in whether the type II endoleak closed spontaneously. Also, it is possible that a patent inferior mesenteric artery factors into whether a type II endoleak will cause growth.8
Infection can cause an aneurysm in and of itself. Endovascular repair of a mycotic aneurysm should always be avoided, as infection is known to be a problem in degeneration of an aneurysm wall. It can cause an aneurysm in a normal aorta, not to mention expansion in an already aneurysmal aorta.
Some grafts are known to be more prone to requiring revisions due to endoleak and aneurysm growth or lack of shrinkage. Aorto-uni-iliac devices require an occlusion device in the contralateral common iliac. The effectiveness and pressure transmission of that device can have a huge impact on potential pressure transmission into the aneurysm sac, and therefore the rate of shrinkage.
The data show that current smoking, not previous smoking history, is the risk factor for aneurysm expansion and aneurysm rupture in unrepaired aneurysms.9 We do not have data on how it affects the rate of aneurysm shrinkage after endovascular repair, but it is intuitive that if it has an effect on the unrepaired aneurysm, it would also impact the repaired aneurysm that may or may not be pressurized.
Hypertension and Pulse Pressure
Because an endoleak is to some extent pressure transmitted into the sac, the higher the lumen pressure is, the higher the patient’s overall systemic pressure will be, and the higher the sac pressure will be with an endoleak.10,11 Pulse pressure, the difference between systolic and diastolic pressure, indicates a factor that leads to aneurysm formation, but could also have an effect after stent-graft placement.12,13
Anticoagulation affects sac and endoleak thrombosis, and as a result could affect sac shrinkage rates.14
IS PLAN ADJUSTMENT NECESSARY?
A graft is not placed because it is believed that there will be more or less sac shrinkage; it is chosen because it fits the anatomy. Because there are now many different types of grafts available, surgeons are noticing definite variances in sac shrinkage rates among the different manufacturers and grafts. This occurrence is something few had anticipated, but that interests us all and should be discussed and explored in the future.
Although the endovascular repair of aneurysms has been performed for more than a decade, there are still a number of factors that affect its efficacy, about which our current understanding is incomplete. Understanding the physiology that occurs within the aneurysm sac after the stent graft is placed could provide clues to the long-term performance of these devices. Developing a stronger, data-supported knowledge base regarding the issues could decisively improve the care available to these patients.
Richard A. Baum, MD, of Brigham & Women’s Hospital, Boston, Massachusetts, and Mark F. Fillinger, MD, of Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, each contributed to this article.
1. Carpenter JP, Baum RA, Barker CF, et al. Durability of benefits of endovascular versus conventional abdominal aortic aneurysm repair. J Vasc Surg. 2002;35:222-228.
2. Baum RA, Carpenter JP, Cope C, et al. Aneurysm sac pressure measurements after endovascular repair of abdominal aortic aneurysms. J Vasc Surg. 2001;33:32-41.
3. Schunn CD, Krauss M, Heilberger P, et al. Aortic aneurysm size and graft behavior after endovascular stent-grafting: clinical experiences and observations over 3 years. J Endovasc Ther. 2000;7:167-176.
4. Farner MC, Carpenter JP, Baum RA, et al. Early changes in abdominal aortic aneurysm diameter after endovascular repair. J Vasc Intervent Radiol. 2003;14:205-210.
5. Bertges DJ, Chow K, Wyers MC, et al. Abdominal aortic aneurysm size regression after endovascular repair is endograft dependent. J Vasc Surg. 2003;37:716-723.
6. Flora HS, Talei-Faz B, Ansdell L, et al. Aneurysm wall stress and tendency to rupture are features of physical wall properties: an experimental study. J Endovasc Ther. 2002;9:665-675.
7. Armon MP, Yusuf SW, Whitaker SC, et al. Thrombus distribution and changes in aneurysm size following endovascular aortic aneurysm repair. Eur J Vasc Endovasc Surg. 1998;16:472-476.
8. Fan CM, Rafferty EA, Geller SC, et al. Endovascular stent-graft in abdominal aortic aneurysms: the relationship between patent vessels that arise from the aneurysmal sac and early endoleak. Radiology. 2001;218:176-182.
9. Smoking, lung function and the prognosis of abdominal aortic aneurysm. The UK Small Aneurysm Trial Participants. Eur J Vasc Endovasc Surg. 2000;19:636-642.
10. Schurink GW, Aarts NJ, Van Baalen JM, et al. Experimental study of the influence of endoleak size on pressure in the aneurysm sac and the consequences of thrombosis. Br J Surg. 2000;87:71-78.
11. Schurink GW, Aarts NJ, Malina M, et al. Pulsatile wall motion and blood pressure in aneurysms with open and thrombosed endoleaks—comparison of a wall track system and M-mode ultrasound scanning: an in vitro and animal study. J Vasc Surg. 2000;32:795-803.
12. Chuter T, Ivancev K, Malina M, et al. Aneurysm pressure following endovascular exclusion. Eur J Vasc Endovasc Surg. 1997;13:85-87.
13. Pitton MB, Duber C, Neufang A, et al. Pressure load of the aneurysm sac after endovascular treatment of aortic aneurysm. Rofo Fortschritte. 2000;172:189-194.
14. Fairman RM, Carpenter JP, Baum RA, et al. Potential impact of therapeutic warfarin treatment on type II endoleaks and sac shrinkage rates on midterm follow-up examination. J Vasc Surg. 2002;35:679-685.