Article

Indications for Endovascular Abdominal Aortic Aneurysms Treatment

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An aneurysm of the abdominal aorta (AAA) can be defined as an enlargement of the infra-renal aorta to a diameter of more than 29mm or 1.5 times the diameter of the aorta at the level of the renal arteries. Based on population studies, the prevalence of AAA in men older than 65 years is estimated 5-8%.1-5 In nearly 50% of these cases the aneurysm is > 40mm in diameter. In women in the same age category the prevalence is less (approximately 2%). The majority of AAAs are asymptomatic, and as such most patients are unaware of its presence. Most AAAs grow, although the speed of growth is different in every case.6 With growth the risk for rupture increases. The reported risk for rupture of asymptomatic AAAs <50mm is 0-2.5% per annum, but for AAAs >50mm, the risk for rupture is higher; 5-9%.7-12

In recent years the interest in minimally invasive surgery has been growing and the same trend can be observed in vascular surgery and interventional radiology.

In the early 1990s, Volodos and Parodi introduced endovascular treatment of AAA (EVAR) with a device composed of a Dacron graft and a Palmaz stent. Since the first use of a stent-graft for the endovascular exclusion of an AAA, endovascular treatment of AAAs has assumed large proportions. EVAR was expected to be a more effective alternative to open surgical repair if it can produce a substantial decrease in mortality and morbidity rates.

The standard treatment for an AAA is a trans-abdominal open surgical approach and replacement of the aneurysmatic part of the aorta by prosthesis. A full median laparotomy is usually required to clamp the aorta above the aneurysm. The circulation to the pelvis and legs is temporarily interrupted during this procedure. After implantation of the prosthesis the circulation to the pelvis and legs can be restored. In particular, de-clamping of the aorta at the level of the renal arteries after successful aneurysm repair is a considerable burden to the heart. Besides that, this operation is usually associated with a considerable blood loss. The cardiac risk factors are especially responsible for the peri-operative mortality and morbidity.

With EVAR a laparotomy is not required. The endovascular graft can be implanted from a remote access site in the groin with considerably fewer anaesthetic requirements. Once in position the graft is deployed immediately distal from the renal arteries. The aorta is not clamped and the blood loss will be considerably less than with open surgery. Not all patients with an AAA are suitable for endovascular repair. Pre-procedural assessment must reject unsuitable patients, identify potential difficulties and allow selection of an appropriate stent graft. The main criteria for patient selection apply to anatomical details of the vascular tree between the renal arteries and the external iliac artery. Endovascular repair of the aorta brings many new challenges for pre-operative imaging. Evidence from registries and randomised trials is currently available to guide the management of patients with AAAs.

During the last nine years two large-scale multicentre registries (European Collaborators Registry on Stent-graft Techniques for AAA repair (EUROSTAR) and Registry for Endovascular Treatment of Aneurysms (RETA) and two randomised trials (Endovascular Aneurysm Repair (EVAR-1) and Dutch Randomised Endovascular Aneurysm Management Trial (DREAM)) have been conducted.13-17 Almost 8,000 patients are included In the EUROSTAR Registry. The 30-day mortality rate after endovascular AAA repair is approximately 3% and 25-40% of the patients have complications that require an additional intervention or open surgical conversion. The long-term data from the registries have underlined the necessity of long-term surveillance after EVAR.

In 1999 the DREAM trial and the UK EVAR-1 trial started recruiting patients, both following an almost similar protocol. Initial and intermediate follow-up results from these trials are now available.

The DREAM trial randomised 345 patients. The operative mortality in the open-repair group was 4.6% versus 1.2% in the endovascular group. The EVAR-1 trial randomised 1,082 patients and showed almost similar results with 4.7% mortality in the open repair group and 1.7% (p=0.009). Both studies showed a significant reduction in duration of surgery, intra-operative blood transfusions, intensive care unit (ICU) and monitored care unit (MCU) stay, duration of postoperative mechanical ventilation and length of hospital stay.

Despite these initial optimistic results major concerns remained with regard to the durability of the devices and the need for re-interventions. In the EVAR-1 trial, the overall mortality at four years did not differ between endovascular patients and the open repair group. On the other hand, the aneurysm-related mortality was significantly different: 4% for the EVAR group compared with 7% for the open group. In the DREAM trial the cumulative survival rates were 89.6% for open repair and 89.7% for endovascular repair.

Re-interventions were more common in patients treated with endovascular repair during the four-year follow-up in EVAR-1 trial (20% in the endovascular group compared with 6% in the open surgery group). The potential benefits of EVAR include increased patient acceptance, less resource utilisation and, hopefully, cost saving. The cost-effectiveness of this technology is critically dependent on the potential to reduce mortality and morbidity rates as compared with conventional open surgery. EVAR is expensive due to the high cost of the devices and the need for close post-intervention surveillance and secondary interventions. The main possibility for cost saving is reduced requirements for blood transfusion, shorter ICU and hospital stay, a lower 30-day mortality and a lower systemic/remote complication rate.

Both the DREAM and EVAR-1 trials have performed cost analysis. However, only a brief report of the cost analysis of the EVAR-1 trial has been published.

Results from the EVAR-1 trial showed that there was already a difference in cost considering the primary hospital admission. During follow-up, differences became larger and total cost including four-year follow-up were £13,258 for endovascular treatment compared with £9,945 for open surgery. Also, the quality of life (QOL) analysis from both randomised trials was not able to show the supremacy of endovascular treatment. The DREAM trial reported deterioration in QOL in the first three weeks after intervention in both treatment arms. The decrease was most prominent in the open surgery group, reflecting the more invasive nature of the procedure. After three months both groups had returned to their pre-operative levels, and after one year, the QOL in the open surgery group was significantly better than in the endovascular group. This is somewhat in contrast with the results of EVAR-1 trial, which found no difference between the two groups at three, 12 and 24 months.

Mortality in patients with a ruptured AAA treated with open surgery remains high. Since 1994, endovascular aneurysm repair in patients with a ruptured AAA has proven to be feasible. Recently, this technique has become routine practice in Europe, and it is increasingly performed in the US. Several studies demonstrated a reduction in mortality and morbidity rates of endovascular repair compared with conventional open surgery in patients with ruptured AAAs. It should be acknowledged that most of these studies included haemodynamically unstable patients in the open surgery group, whereas in the endovascular group mostly haemodynamically stable patients were included.

In contradiction to the cost analysis in elective AAA, repair cost analysis of endovascular treatment of ruptured AAA showed a significant reduction in hospital costs in comparison with open surgical repair.18 After the one-year follow-up, cost for endovascular repair versus open surgical repair was Ôé¼23,588 and Ôé¼36,488, respectively.

In elective repair, mid-term results for all-cause mortality and aneurysm-related mortality, together with post-operative complications and re-interventions, QOL analysis and hospital cost, start to provide information on which clinical and political guidelines can be based. All-cause mortality did not differ between patients randomised to endovascular repair and those randomised to open repair of AAA, despite the initial advantage of endovascular repair. However, there was a significant difference in aneurysm related mortality.

In the treatment of ruptured AAA the situation is different. Most likely there is an advantage of endovascular repair compared with open surgery with respect to clinical outcome and cost analysis. Maybe ruptured AAA is the best indication for endovascular repair.

References

  1. Scott RA, Wilson NM, Ashton HA, et al., Lancet (1993);342: pp. 1395-1396.
    Crossref | PubMed
  2. Smith FCT, Grimshaw GM, Paterson IS, et al., Br J Surg (1993);80: pp. 1406-1409.
    Crossref | PubMed
  3. Lucarotti M, Shaw E, Poskitt K, et al., Eur J Vasc Surg (1993);7: pp. 397-401.
    Crossref | PubMed
  4. Collin J, Araujo L, Walton J, et al., Lancet (1988);2: pp. 613-615.
    Crossref | PubMed
  5. Pleumeekers HJ, Hoes AW, van der Does E, et al., Eur J Vasc Surg (1994);8: pp. 119-128.
    Crossref | PubMed
  6. Cronenwett JL, Sargent SK, Wall MH, et al., J Vasc Surg (1990);11: pp. 260-269.
    Crossref | PubMed
  7. Limet R, Sakalihassan N, Albert A, et al., J Vasc Surg (1991);14: pp. 540-548.
    Crossref | PubMed
  8. Cronenwett JL, Murphy TF, Zelenock GB, et al., Surgery (1985);98: pp. 472-483.
    PubMed
  9. Nevitt MP, Ballard DJ, Hallett JWJ, et al., N Engl J Med (1989);321: pp. 1009-1014.
    Crossref | PubMed
  10. Johansson G, Nydahl S, Olofsson P, et al., Eur J Vasc Surg (1990);4: pp. 497-502.
    Crossref | PubMed
  11. Glimåker H, Holmberg L, Elvin A, et al., Eur J Vasc Surg (1991);5: pp.125-130.
    Crossref | PubMed
  12. Johnston KW, J Vasc Surg (1989);9: pp. 437-447.
    Crossref | PubMed
  13. Liapsis CD, Kakisis JD, Eur J Vasc Endovasc Surg (2005);30: pp. 341-342.
    Crossref | PubMed
  14. Prinssen M, Verhoeven EL, Buth J, et al., N Engl J Med (2004);351: pp.1607-1618.
    Crossref | PubMed
  15. The EVAR Trial Participants, Lancet (2004);364: pp.843-848.
    Crossref | PubMed
  16. Blankensteijn JD, de Jong SE, Prinssen M, et al., N Engl J Med (2005);352: pp.2398-2405.
    Crossref | PubMed
  17. The EVAR Trial Participants, Lancet (2005);365: pp.2179-2186.
    Crossref | PubMed
  18. Visser JJ, van Sambeek MRHM, Hunink MGM, et al., Radiology (2006);240: pp. 681-689.
    Crossref | PubMed