DÄ internationalArchive8/2013The Place of Endovascular Treatment in Abdominal Aortic Aneurysm

Review article

The Place of Endovascular Treatment in Abdominal Aortic Aneurysm

Dtsch Arztebl Int 2013; 110(8): 119-25. DOI: 10.3238/arztebl.2013.0119

Greiner, A; Grommes, J; Jacobs, M J

Background: The endovascular treatment of abdominal aortic aneurysms has become more common. A careful comparison of this technique with the established treatment by open surgery is needed before it can be more widely adopted.

Methods: We selectively searched the Medline database for articles on the endovascular treatment of abdominal aortic aneurysms, with special attention to prospective, randomized trials comparing it to open aortic surgery (keywords: “endovascular abdominal aortic repair” and “prospective randomized trial”).

Results: Data on 30-day mortality and long-term survival are now available from four randomized multicenter trials. In three of these trials, endovascular treatment was found to lower 30-day mortality by two-thirds (endovascular: 0.2% to 1.7%, open repair: 0.7% to 4.7%), but this difference in survival was no longer present at two years. Compared to open open aortic surgery, endovascular treatment has a higher long-term complication rate. Endoleakage (perigraft leakage) accounted for more than 30% of complications and was the commonest reason for reintervention and unsuccessful intervention; in nearly all cases, it was successfully treated by the endovascular route. The rate of secondary aortic rupture was 0.8%, and migration of the prosthesis occurred in 5% of cases. Follow-up checks of the stent graft are now recommended at 3, 6 and 12 months after implantation, and annually thereafter.

Conclusion: Prospective randomized trials have shown that the endovascular technique lowers perioperative mortality. In the long term, however, it has a higher complication rate than open aortic surgery and leads to more frequent reintervention.

LNSLNS

The incidence of large-vessel aneurysms is 40 per 100 000 population. An aneurysm is an increase in the diameter of the aorta to more than 3 cm (1, 2). The abdominal aorta is affected in 60% of all patients. While 95% of these aneurysms begin below the renal arteries, the renal arteries are involved in only 3% of cases, and the visceral segment in only 2%. Men suffer large-vessel aneurysms six times more frequently than women (2, 3).

Aneurysms can rupture. The risk of rupture depends on the axial diameter of the aneurysm. The risk is approximately 3% for diameters of 4.0 to 4.9 cm, 10% for diameters of 5.0 to 5.9 cm, 15% for diameters of 6.0 to 6.9 cm, and 60% for diameters of more than 7 cm (4, 5). A further risk factor is the aneurysm’s growth rate. If growth over six months is more than 0.5 cm, the risk of rupture must be considered high. Asymptomatic aneurysms that grow by more than 0.5 cm over six months or are more than 5.5 cm in diameter should therefore be electively treated. Symptomatic aneurysms should be treated within 24 hours, and ruptured aneurysms require emergency treatment (3, 6).

Stent prostheses allow minimally invasive treatment of abdominal aortic aneurysms (AAAs) (Figure 1). Patients who are ineligible for open surgery as a result of a comorbidity or their age can now be treated with endovascular aneurysm repair (EVAR) with less risk. In particular, this includes patients with ASA (American Society of Anesthesiologists) classification III or IV, concomitant chronic obstructive pulmonary disease (COPD), or heart failure. Open aortic surgery requires cross-clamping while the aorta is reconstructed. Cross-clamping increases cardiac afterload and is the main cause of cardiac ischemia or cardiac decompensation during surgery or in the immediate post-operative period. EVAR avoids this cardiac afterload.

Endovascular aneurysm repair (EVAR)
Figure 1
Endovascular aneurysm repair (EVAR)

Endovascular treatment has also further reduced the perioperative mortality rate of open surgery (79). The introduction of stent prostheses also seems to reduce the risk of death caused by aneurysm rupture (10).

However, the endovascular method must be measured against the established but invasive procedures of open surgery. Further developments since the introduction of endovascular treatment and the use of modern, third-generation prostheses that have resulted from it allow increasingly widespread use of endovascular treatment. As a result, increasingly frequently physicians have to decide which procedure to recommend to a patient. For a patient with a low surgery risk profile whose aortic aneurysm meets the morphological requirements for EVAR (Figure 2), EVAR and open surgery are competing treatment options (11). What data can be used as the basis for a treatment decision, and what problems may arise after the implantation of a stent prosthesis in the abdominal aorta or after open surgery?

Endoprosthesis measurement and selection
Figure 2
Endoprosthesis measurement and selection

The principle of endovascular treatment for abdominal aortic aneurysms

Endovascular aneurysm removal is based on the principle of excluding an aneurysm using a stent prosthesis. Modular bifurcated prosthesis systems are usually used. This reduces the pressure in the aneurysm sac and prevents aneurysm rupture. In order for the procedure to be performed, it must be possible to anchor the endoprosthesis securely outside the aneurysm, proximally and distally. The main body consists of a Y-shaped bifurcated prosthesis with one long and one short leg. The short contralateral leg is lengthened using a contralateral tube graft. The individual components are inserted along the femoral arteries using an unloading system, under x-ray surveillance, and then released. Because of the morphology of aneurysms, this technique is not suitable for all cases. The neck of the aneurysm must have a length of at least 15 mm to act as the anchoring zone, and the diameter of the neck must not exceed 30 to 34 mm. In addition, this zone must present a normal aortic wall with no significant thrombotic plaque formation and moderate kinking. The distal landing zone must have a diameter of no more than 20 mm and should be at least 30 mm long. The stent prosthesis begins directly at the outlet of the renal arteries and ends before the iliac bifurcation. Its total length is therefore approximately 15 to 20 cm (Figure 1).

Outcomes following stent implantation in the abdominal aorta

Outcomes following EVAR from four prospective, randomized multicenter trials have been published to date. Long-term data are provided by the UK Endovascular Aneurysm Repair trial (EVAR 1) (9) and the Dutch Randomized Endovascular Aneurysm Management trial (DREAM) (12). In addition, medium-term outcomes are available from the Open versus Endovascular Aneurysm Repair trial (OVER, USA) (13) and the Anévrisme de l'aorte abdominale: Chirurgie versus Endoprothèse trial (ACE, France) (14). The general characteristics of these four trials are summarized in Table 1.

Characteristics, 30-day mortality rate, and cumulative survival rates in four randomized trials
Table 1
Characteristics, 30-day mortality rate, and cumulative survival rates in four randomized trials

30-day mortality and long-term survival

The overall 30-day mortality rate is shown in Table 1. This shows that endovascular aneurysm removal was the superior treatment in the DREAM (EVAR 1.2% versus OAR 4.6%) (12), EVAR 1 (1.7% versus 4.7%) (9), and OVER (0.2% versus 2.3%) (13) trials, with a significant reduction in the risk of death within 30 days. In the French ACE trial, endovascular treatment (1.3%) could not surpass the excellent outcomes of open AAA removal, which yielded a 30-day mortality rate of 0.9%. The difference between the two groups was not statistically significant, however (14). Comparison of the 30-day mortality rates in all four studies yields an approximately threefold risk reduction (according to the odds ratio) for EVAR (Table 1).

As stated above, in the DREAM, EVAR 1 and OVER trials there was an initial survival advantage for endovascular AAA treatment as a result of its lower 30-day mortality rate. In both EVAR 1 and DREAM, this advantage had been lost by the end of the trial (EVAR 1: 8 years; DREAM: 7 years). The authors of EVAR 1 attribute the EVAR group’s cumulative long-term survival rate in part to fatal endograft ruptures (9). Of a total of 25 patients who suffered ruptures following EVAR (3.9% of all patients randomized in EVAR 1), 18 died. No long-term outcomes for the other two trials (OVER and ACE) are yet available. Unlike the EVAR 1 and DREAM trials, in the OVER trial the Kaplan–Meier curves are parallel to each other: In other words, the EVAR group’s initial advantage of its significantly better 30-day mortality rate is not lost over the following 24 months. However, after two years the difference in the cumulative survival rate is no longer significant (13). Three-year outcomes for the ACE study are available. Unlike in the other three trials, in the ACE trial open surgery begins with the advantage of a lower 30-day mortality rate (though the difference is not significant). After a median follow-up period of three years, there was no difference between the cumulative survival rates of the two groups of patients (14).

The data from all four trials show that the original perioperative difference in survival between the two treatment methods is no longer detectable after approximately two years. This is caused by endoprostheses’ comparatively high long-term complication rate and the problems that result. However, the trials did not record long-term consequences of open aneurysm surgery, such as fistulas between the prosthesis and the intestine, erectile dysfunction, incisional hernias, abdominal adhesions, and surgery required as a result, making open surgery appear better in the long term.

Follow-up treatment and complications following EVAR

Endoleaks

The most common cause of repeat interventions and treatment failure following EVAR is an endoleak (Table 2). An endoleak is a persistent flow of blood in the aneurysm sac, outside the endoprosthesis (16). The incidence of endoleaks as stated in the literature varies greatly, but it may be above 30% (15). Endoleaks are divided into five types according to etiology. All five are described in detail in Figure 3. This classification can be used to assess the risk of secondary rupture and indicate treatment or monitoring.

Endoleaks
Figure 3
Endoleaks
Frequencies of complications following EVAR and OAR
Table 2
Frequencies of complications following EVAR and OAR

Type I endoleaks have a frequency of up to 10%. They may occur either immediately after implantation or subsequently (15). Because type I endoleaks pose a high risk of rupture, treatment is recommended in all cases. In almost all cases, these endoleaks can also be corrected endovascularly. If endovascular treatment proves unsuccessful, open surgery to remove the aneurysm and explant the endoprosthesis must be performed.

Type II endoleaks occur perioperatively in between 15% and 20% of cases. After one year, the type II endoleak rate spontaneously drops to 5% to 10% (15). “Indirect” endoleaks of this kind are usually fed via lumbar segment arteries or the inferior mesenteric artery. Type II endoleaks are treated conservatively provided the aneurysm sac does not grow, or even shrinks, during treatment. An increase in the size of the aneurysm sac represents treatment failure and must be treated if there is evidence of a persistent type II endoleak. Treatment is recommended if the diameter of the aortic aneurysm increases by more than 10 mm (17). In almost all cases, this can successfully be performed using various minimally invasive embolization methods. The inferior mesenteric artery, which is often the cause of a type II endoleak, can be coiled angiographically through the Riolan arc via the superior mesenteric artery. Similarly, under CT guidance the aneurysm sac can be punctured and the endoleak can be embolized using HistoacrylTM glue (1820). An alternative to this is laparoscopic retroperitoneal clipping of the lumbar arteries that feed the endoleak (21). Type III and IV endoleaks are now rare, thanks to the use of the latest generation of stent prostheses; they can usually be treated endovascularly.

An aneurysm sac that is under pressure even after EVAR and has no detectable endoleak is called an endotension. Endotensions are classified as type V endoleaks (22). The details of their underlying mechanism are not yet clear. One suspected cause is transmission of pressure via the thrombus or an endoleak that cannot be visualized (22, 23). Where no cause can be detected, treatment takes the form of open conversion if the aneurysm diameter increases (24).

Aneurysm expansion following endovascular aneurysm repair

If an aneurysm has been removed using a stent prosthesis, a reduction in the aneurysm diameter can be observed during follow-up. If an expansion of the aneurysm can be observed after a stent prosthesis has been inserted, there is a potential risk of rupture (25). This is usually caused by an endoleak (Figure 3), and treatment must be considered to have failed. A multicenter data analysis (10 228 patients) showed that five years after EVAR an increase in aneurysm size could be observed in 41% of patients (26). Interestingly, expansion did not begin until three years after EVAR in 30% of patients. Clearly, this is a problem that can occur in the long term. The trial also showed that patients treated between 2004 and 2008 presented aneurysm expansion significantly more frequently than patients treated between 1999 and 2003. The trial authors attribute this fact to a growing tendency to use stent prostheses off-label.

Off-label use of endoprostheses

Unlike open surgery, in order to be treated safely with EVAR aneurysms must meet certain morphological requirements—these include suitable iliac access routes, proximal and distal landing zones, wall structure, thrombus load, and aortic shaft angle—in order to guarantee secure implantation of commercially available standard prostheses. The various types of commercially available prostheses have different configurations, so the user can select the most suitable prosthesis for the patient according to anatomical requirements. Manufacturers provide usage restrictions and limitations for their stent prostheses. These instructions are based on preclinical tests and simulations and are derived from the engineering-related development of prostheses. The clinical trials that must be conducted as part of the authorization procedure for stent prostheses involve strict patient selection according to these instructions for use. Off-label use of stent prostheses occurs in everyday clinical practice in both Europe and the USA. It has been shown that only 42% of EVAR patients meet the recommended morphological requirements according to the industry’s instructions for use. Such off-label use of prostheses has been identified as one of the significant independent risk factors for aneurysm sac expansion following EVAR (26).

Rupture following endovascular aneurysm repair

Analysis of the data of UK EVAR trials 1 and 2 showed that in 27 of 848 patients who received elective EVAR treatment as part of these prospective trials, aneurysm rupture occurred after an average of 4.8 years (25). In five of these patients, rupture occurred within 30 days of EVAR. A total of 18 (67%) of the 27 patients died as result of the rupture. Type I endoleaks, type II endoleaks with sac expansion, and type III endoleaks with stent migration or kink formation were identified as independent, extremely significant (p<0.0001) risk factors (hazard ratio 8.83). In three patients, rupture occurred despite optimum aftercare and no identifiable cause. In all other patients, there were either identifiable causes for the rupture (endoleaks, sac expansion, etc.) or CT monitoring was incomplete. The authors therefore deduce that it is better to treat direct endoleaks aggressively. Regular monitoring is essential after EVAR to identify such complications early.

Recommendations for aftercare following endovascular aneurysm repair

The mortality rate for post-EVAR rupture is high (above 60%). However, the complications after EVAR that lead to secondary aneurysm rupture can be identified using appropriate imaging procedures, with only a very few exceptions (25). Checkups must assess the following:

  • Aneurysm sac dynamics (shrinking, expansion)
  • Endoleaks (presence, type)
  • Position of individual stent graft components (migration, dislocation).

The current gold standard for the follow-up examination is CT angiography (17). In addition to its advantage of being a very quick procedure, this method also provides detailed information on all the points listed above (27, 28). Two-phase CT angiography, with an arterial phase and a second, delayed phase, makes it possible to identify and classify almost all endoleaks. The disadvantage of this method is the radiation burden that accumulates over time and the iodinated, nephrotoxic contrast agent (29, 30). In order to reduce the burden of CT angiography on EVAR patients, annual contrast ultrasound checkups can be performed, in order to determine aneurysm sac size and to evaluate endoleaks. It seems possible that this may allow endoleaks to be identified with the same sensitivity (31). However, conventional two-plane abdominal x-ray must be performed in addition to ultrasound examination, in order to monitor the location of stent graft components (32). Another option, to reduce the cumulative dose of radiation following EVAR, is magnetic resonance angiography (MRA) (33).

Conclusion

The introduction of endovascular treatment of aortic aneurysms has led to a reduction in perioperative mortality and morbidity and is possible even in cases in which open surgery is not suitable as a result of concomitant illnesses. Although in randomized trials comparing it to open surgery the difference in survival rate can no longer be identified after two years, its high levels of acceptance by patients and physicians are leading to increasing use of endovascular treatment. In the long term, however, endovascular aortic prostheses are associated with a higher rate of complications, whereas open aortic surgery seems to cause fewer complications. Regular checkups are therefore currently recommended following EVAR, in order to identify complications early.

Conflict of interest statement
Dr. Grommes has received reimbursement of conference fees and travel expenses from Cook Medical. Prof. Greiner and Prof. Jacobs declare that no conflict of interest exists.

Manuscript received on 14 August 2012, revised version accepted on 3 December 2012.

Corresponding author:
Prof. Dr. med. Michael J. Jacobs

Aachen–Maastricht European Vascular Center
Vascular Surgery Facility, University Hospital of Rhine–Westphalia Institute of Technology, Aachen
Pauwelsstr. 30, 52074 Aachen, Germany
mjacobs@ukaachen.de

1.
Debus ES, Kölbel T, Böckler D, Eckstein HH: abdominale Aortenaneurysmen. Die Gefäßchirurgie 2010; 15: 154–68. CrossRef
2.
Lederle FA, Johnson GR, Wilson SE, et al.: Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med 1997;126: 441–9.
3.
DGG: Leitlinien zum Bauchaortenaneurysma und Beckenarterienaneurysma. 2008. www.gefaesschirurgie.de/fileadmin/websites/dgg/download/LL_Aneurysmen_Bauch_Becken_2011.pdf;
last accessed on 15 January 2013.
4.
Sakalihasan N, Limet R, Defawe OD: Abdominal aortic aneurysm. Lancet 2005; 365: 1577–89. CrossRef MEDLINE
5.
Nordon IM, Hinchliffe RJ, Loftus IM, Thompson MM: Pathophysiology and epidemiology of abdominal aortic aneurysms. Nature reviews cardiology 2011; 8: 92–102. MEDLINE
6.
Hirsch AT, Haskal ZJ, Hertzer NR, et al.: ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report. Circulation 2006; 113: e463–654. CrossRef MEDLINE
7.
Blankensteijn JD, de Jong SE, Prinssen M, et al.: Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med 2005; 352: 2398–2405. CrossRef MEDLINE
8.
Greenberg RK, Chuter TA, Cambria RP, et al.: Zenith abdominal aortic aneurysm endovascular graft. J Vasc Surg 2008; 48: 1–9. CrossRef MEDLINE
9.
Greenhalgh RM, Brown LC, Powell JT, et al.: Endovascular versus open repair of abdominal aortic aneurysm. N Engl J Med 2010; 362: 1863–71. CrossRef MEDLINE
10.
Giles KA, Pomposelli F, Hamdan A, et al.: Decrease in total aneurysm-related deaths in the era of endovascular aneurysm repair. J Vasc Surg 2009; 49: 543–50. CrossRef MEDLINE PubMed Central
11.
Rooke TW, Hirsch AT, Misra S, et al.: 2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (Updating the 2005 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology 2011; 58: 2020–45. CrossRef MEDLINE
12.
De Bruin JL, Baas AF, Buth J, et al.: Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med 2010; 362: 1881–9. CrossRef MEDLINE
13.
Lederle FA, Freischlag JA, Kyriakides TC, et al.: Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA 2009; 302: 1535–42. CrossRef MEDLINE
14.
Becquemin JP, Pillet JC, Lescalie F, et al.: A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg 2011; 53: 1167–73. CrossRef MEDLINE
15.
Veith FJ, Baum RA, Ohki T, et al.: Nature and significance of endoleaks and endotension: summary of opinions expressed at an international conference. J Vasc Surg 2002; 35: 1029–35. CrossRef CrossRef
16.
White GH, Yu W, May J, Chaufour X, Stephen MS: Endoleak as a complication of endoluminal grafting of abdominal aortic aneurysms: classification, incidence, diagnosis, and management. J Endovasc Surg 1997; 4: 152–68. CrossRef MEDLINE
17.
Moll FL, Powell JT, Fraedrich G, et al.: Management of abdominal aortic aneurysms clinical practice guidelines of the European society for vascular surgery. Eur J Vasc Endovasc Surg 2011; 41 Suppl 1: 1–58. CrossRef MEDLINE
18.
Binkert CA, Alencar H, Singh J, Baum RA: Translumbar type II endoleak repair using angiographic CT. J Vasc Interv Radiol 2006; 17: 1349–53. CrossRef MEDLINE
19.
Sarac TP, Gibbons C, Vargas L, et al.: Long-term follow-up of type II endoleak embolization reveals the need for close surveillance. J Vasc Surg 2012; 55: 33–40. CrossRef MEDLINE
20.
Baum RA, Carpenter JP, Golden MA, et al.: Treatment of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms: comparison of transarterial and translumbar techniques. J Vasc Surg 2002; 35: 23–9. MEDLINE
21.
Kolvenbach R, Pinter L, Raghunandan M, et al.: Laparoscopic remodeling of abdominal aortic aneurysms after endovascular exclusion: a technical description. J Vasc Surg 2002; 36: 1267–70. CrossRef MEDLINE
22.
Gilling-Smith G, Brennan J, Harris P, et al.: Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 1999; 6: 305–7. CrossRef MEDLINE
23.
White GH, May J, Petrasek P, et al.: Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 1999; 6: 308–15. CrossRef MEDLINE
24.
Koole D, Moll FL, Buth J, et al.: Annual rupture risk of abdominal aortic aneurysm enlargement without detectable endoleak after endovascular abdominal aortic repair. J Vasc Surg 2011; 54: 1614–22. CrossRef MEDLINE
25.
Wyss TR, Brown LC, Powell JT, Greenhalgh RM: Rate and predictability of graft rupture after endovascular and open abdominal aortic aneurysm repair: data from the EVAR Trials. Ann Surg 2010; 252: 805–12. CrossRef MEDLINE
26.
Schanzer A, Greenberg RK, Hevelone N, et al.. Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair. Circulation 2011; 123: 2848–55. CrossRef MEDLINE
27.
McWilliams RG, Martin J, White D, et al.: Use of contrast-enhanced ultrasound in follow-up after endovascular aortic aneurysm repair. J Vasc Interv Radiol 1999; 10: 1107–14. CrossRef MEDLINE
28.
Sato DT, Goff CD, Gregory RT, et al.: Endoleak after aortic stent graft repair: diagnosis by color duplex ultrasound scan versus computed tomography scan. J Vasc Surg 1998; 28: 657–63. CrossRef MEDLINE
29.
Brenner DJ, Hall EJ: Computed tomography—an increasing source of radiation exposure. N Engl J Med 2007; 357: 2277–84. CrossRef MEDLINE
30.
Walsh SR, Tang TY, Boyle JR: Renal consequences of endovascular abdominal aortic aneurysm repair. J Endovasc Ther 2008; 15: 73–82. CrossRef MEDLINE
31.
Mirza TA, Karthikesalingam A, Jackson D, et al.: Duplex ultrasound and contrast-enhanced ultrasound versus computed tomography for the detection of endoleak after EVAR: systematic review and bivariate meta-analysis. Eur J Vasc Endovasc Surg 2010; 39: 418–28. CrossRef MEDLINE
32.
Fearn S, Lawrence-Brown MM, Semmens JB, Hartley D: Follow-up after endovascular aortic aneurysm repair: the plain radiograph has an essential role in surveillance. J Endovasc Ther 2003; 10: 894–901. CrossRef MEDLINE
33.
Ayuso JR, de Caralt TM, Pages M, et al.: MRA is useful as a follow-up technique after endovascular repair of aortic aneurysms with nitinol endoprostheses. J Magn ResonImaging 2004; 20: 803–10. CrossRef MEDLINE
European Vascular Center Aachen-Maastricht, Department of Vascular Surgery, Aachen University Hospital:
PD Dr. med. Greiner, Dr. med. Grommes, Prof. Dr. med. Jacobs
University Hospital Maastricht: Prof. Dr. med. Jacobs
Endovascular aneurysm repair (EVAR)
Figure 1
Endovascular aneurysm repair (EVAR)
Endoprosthesis measurement and selection
Figure 2
Endoprosthesis measurement and selection
Endoleaks
Figure 3
Endoleaks
Key messages
Characteristics, 30-day mortality rate, and cumulative survival rates in four randomized trials
Table 1
Characteristics, 30-day mortality rate, and cumulative survival rates in four randomized trials
Frequencies of complications following EVAR and OAR
Table 2
Frequencies of complications following EVAR and OAR
1.Debus ES, Kölbel T, Böckler D, Eckstein HH: abdominale Aortenaneurysmen. Die Gefäßchirurgie 2010; 15: 154–68. CrossRef
2.Lederle FA, Johnson GR, Wilson SE, et al.: Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med 1997;126: 441–9.
3.DGG: Leitlinien zum Bauchaortenaneurysma und Beckenarterienaneurysma. 2008. www.gefaesschirurgie.de/fileadmin/websites/dgg/download/LL_Aneurysmen_Bauch_Becken_2011.pdf;
last accessed on 15 January 2013.
4.Sakalihasan N, Limet R, Defawe OD: Abdominal aortic aneurysm. Lancet 2005; 365: 1577–89. CrossRef MEDLINE
5.Nordon IM, Hinchliffe RJ, Loftus IM, Thompson MM: Pathophysiology and epidemiology of abdominal aortic aneurysms. Nature reviews cardiology 2011; 8: 92–102. MEDLINE
6.Hirsch AT, Haskal ZJ, Hertzer NR, et al.: ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report. Circulation 2006; 113: e463–654. CrossRef MEDLINE
7.Blankensteijn JD, de Jong SE, Prinssen M, et al.: Two-year outcomes after conventional or endovascular repair of abdominal aortic aneurysms. N Engl J Med 2005; 352: 2398–2405. CrossRef MEDLINE
8.Greenberg RK, Chuter TA, Cambria RP, et al.: Zenith abdominal aortic aneurysm endovascular graft. J Vasc Surg 2008; 48: 1–9. CrossRef MEDLINE
9.Greenhalgh RM, Brown LC, Powell JT, et al.: Endovascular versus open repair of abdominal aortic aneurysm. N Engl J Med 2010; 362: 1863–71. CrossRef MEDLINE
10.Giles KA, Pomposelli F, Hamdan A, et al.: Decrease in total aneurysm-related deaths in the era of endovascular aneurysm repair. J Vasc Surg 2009; 49: 543–50. CrossRef MEDLINE PubMed Central
11.Rooke TW, Hirsch AT, Misra S, et al.: 2011 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Peripheral Artery Disease (Updating the 2005 Guideline): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology 2011; 58: 2020–45. CrossRef MEDLINE
12.De Bruin JL, Baas AF, Buth J, et al.: Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med 2010; 362: 1881–9. CrossRef MEDLINE
13.Lederle FA, Freischlag JA, Kyriakides TC, et al.: Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA 2009; 302: 1535–42. CrossRef MEDLINE
14.Becquemin JP, Pillet JC, Lescalie F, et al.: A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg 2011; 53: 1167–73. CrossRef MEDLINE
15.Veith FJ, Baum RA, Ohki T, et al.: Nature and significance of endoleaks and endotension: summary of opinions expressed at an international conference. J Vasc Surg 2002; 35: 1029–35. CrossRef CrossRef
16.White GH, Yu W, May J, Chaufour X, Stephen MS: Endoleak as a complication of endoluminal grafting of abdominal aortic aneurysms: classification, incidence, diagnosis, and management. J Endovasc Surg 1997; 4: 152–68. CrossRef MEDLINE
17.Moll FL, Powell JT, Fraedrich G, et al.: Management of abdominal aortic aneurysms clinical practice guidelines of the European society for vascular surgery. Eur J Vasc Endovasc Surg 2011; 41 Suppl 1: 1–58. CrossRef MEDLINE
18.Binkert CA, Alencar H, Singh J, Baum RA: Translumbar type II endoleak repair using angiographic CT. J Vasc Interv Radiol 2006; 17: 1349–53. CrossRef MEDLINE
19.Sarac TP, Gibbons C, Vargas L, et al.: Long-term follow-up of type II endoleak embolization reveals the need for close surveillance. J Vasc Surg 2012; 55: 33–40. CrossRef MEDLINE
20.Baum RA, Carpenter JP, Golden MA, et al.: Treatment of type 2 endoleaks after endovascular repair of abdominal aortic aneurysms: comparison of transarterial and translumbar techniques. J Vasc Surg 2002; 35: 23–9. MEDLINE
21.Kolvenbach R, Pinter L, Raghunandan M, et al.: Laparoscopic remodeling of abdominal aortic aneurysms after endovascular exclusion: a technical description. J Vasc Surg 2002; 36: 1267–70. CrossRef MEDLINE
22.Gilling-Smith G, Brennan J, Harris P, et al.: Endotension after endovascular aneurysm repair: definition, classification, and strategies for surveillance and intervention. J Endovasc Surg 1999; 6: 305–7. CrossRef MEDLINE
23.White GH, May J, Petrasek P, et al.: Endotension: an explanation for continued AAA growth after successful endoluminal repair. J Endovasc Surg 1999; 6: 308–15. CrossRef MEDLINE
24.Koole D, Moll FL, Buth J, et al.: Annual rupture risk of abdominal aortic aneurysm enlargement without detectable endoleak after endovascular abdominal aortic repair. J Vasc Surg 2011; 54: 1614–22. CrossRef MEDLINE
25.Wyss TR, Brown LC, Powell JT, Greenhalgh RM: Rate and predictability of graft rupture after endovascular and open abdominal aortic aneurysm repair: data from the EVAR Trials. Ann Surg 2010; 252: 805–12. CrossRef MEDLINE
26.Schanzer A, Greenberg RK, Hevelone N, et al.. Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair. Circulation 2011; 123: 2848–55. CrossRef MEDLINE
27.McWilliams RG, Martin J, White D, et al.: Use of contrast-enhanced ultrasound in follow-up after endovascular aortic aneurysm repair. J Vasc Interv Radiol 1999; 10: 1107–14. CrossRef MEDLINE
28.Sato DT, Goff CD, Gregory RT, et al.: Endoleak after aortic stent graft repair: diagnosis by color duplex ultrasound scan versus computed tomography scan. J Vasc Surg 1998; 28: 657–63. CrossRef MEDLINE
29.Brenner DJ, Hall EJ: Computed tomography—an increasing source of radiation exposure. N Engl J Med 2007; 357: 2277–84. CrossRef MEDLINE
30.Walsh SR, Tang TY, Boyle JR: Renal consequences of endovascular abdominal aortic aneurysm repair. J Endovasc Ther 2008; 15: 73–82. CrossRef MEDLINE
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