**3. Treatment**

172 Aneurysm

(CRP)

Biomarker Number of

Sympt 52 Ruptured 62

35 AAA patients 35 controls

834 cases with AAA and 6971 controls for fibrinogen 264 cases with AAA and 403 controls for Ddimer.

110 patients with AAA 110- controls

growth, and provide a tool for monitoring this inhibition.[26]

C-reactive Protein

Serum highly sensitive CRP

CRP, alpha 1 antitripsin

D-dimer, fibrinogen/fibrin

Insulin-like Growth Factor 1

rupture of AAA

(IGF-I)

patients Summary of findings Author, year

symptoms or rupture of an AAA.

545 CRP levels are elevated in larger aneurysms

151 CRP did not correlate with size or expansion

39 Serum hsCRP is associated with aneurysmal

36 The largest diameter of AAA is correlated

Plasma fibrinogen and D-dimer

plasma fibrinogen and D-dimer

expansion.

rate of AAA

AAA growth.

presence of AAA.

115 small AAAs Serum IGF-I, but not IGF-II, correlated

**Table 1.** Summary of published studies reporting the role of circulating biomarkers in the growth and

Active investigations continue to identify markers other than size that would predict a risk of rupture. Circulating biomarkers could also indicate optimal intervals between the surveillance intervals. Finally, the identification of biomarkers also may identify potential pathogenic pathways, and thus may open possibilities for pharmacological inhibition of

for the natural history of AAA.

size.

FDP

No correlation. A significant elevation of CRP could be found in patients who presented

but do not appear to be associated with rapid

A positive correlation was found between CRP and AAA diameter and alpha 1 antitripsin and AAA growth. Alpha 1 antitripsin may be a promising biomarker of

with the preoperative levels of D-dimer and

concentrations are likely to be higher in cases with AAA than control subjects. Higher

concentrations may be associated with the

Fibrinogen was positively correlated with AAA size (r =0.323; p<0.01) and the percentage of intra-luminal thrombus occupying the lumen (r =0.358; p<0.05).

positively with AAA size and AAA growth. IGF-I levels may serve as a novel biomarker

Domanivits H et al.2002

Norman P et al. 2004

Lindholt J et al 2001

Vainas T et al.

M. Vega de Ceniga et al.2009 [23]

Yamazuni K et al.1998

Takagi H. Et al. 2009 [12]

Al-Barjas et al. 2006 [24]

J.S. Lindholt et al. 2011 [25]

2003

Surgical repair was first reported in 1962 and still remains the treatment with the best longterm results. The surgical technique is illustrated in **Figure 1**. It is a major surgical procedure done under general anaesthesia, usually consisting of a midline laparotomy and cross clamping of the aorta and iliac vessels.

**Figure 1.** Open surgery technique for AAA

The mortality of elective surgery is between 3 and 7%. These rates increase significantly in patients with comorbidities, particularly with coronary artery disease and carotid artery disease. Surgical results are impaired by chronic renal failure and COPD.

Increasing age is an important adverse determinant of mortality in both ruptured and intact aneurysms.

In the USA statistics indicate that more than 15000 deaths/year are caused by aneurysm rupture.

This is the reason why there are screening studies among the target population in order to save lives and decrease health costs. The great interest is to detect and treat the AAA before rupture but the problem is that most of them are asymptomatic.

Because open surgery has non-negligible mortality and postoperative complications associated with a long hospital stay (10.8 days average) scientists tried to develop alternative methods to treat this disease addressing those cases with surgical high risk.

Minimally invasive techniques were developed in order to exclude the aneurysm from the circulation and to provide a new circulator channel towards the legs. Potential applications of endovascular grafts have been found in all areas of vascular surgery but their use for aortic aneurysms was the first to be explored. Endovascular aneurysm repair (EVAR) is an alternative to open surgery in the management of AAA. Juan Parodi and colleagues performed the first endovascular aneurysm repair in Argentina in 1991 [27,28]. Two decades after, the technique has evolved immensely and new devices developed allowing to a greater number of patients to be treated with EVAR. Repair of aortic abdominal aneurysm (AAA) is performed to prevent progressive expansion and rupture. [27, 29 30]

EVAR is progressively replacing open surgery and now accounts for more than half AAA repairs [31] as for example endovascular repair of AAA in Kaiser Hawaii Hospital (USA) was 50% in 2004 of the surgical activity.

A study published in November 2011 identifies the rate of endovascular treatment for AAA in different countries during 2005-2009 (**Figure 2**), whose prospective data were included in

**Figure 2.** Rate of EVAR in the management of AAA in different countries

the VASCUNET database [32]. The study shows a rapid and extensive implementation of the endovascular treatment, with the advent of studies with favourable results in this direction.

EVAR in addition to the advantage of being a minimally invasive method and as such preferred by the patients, has many proven benefits compared with traditional open surgery: low rate of peri- and postoperative mortality and morbidity, shorter hospital stay, significantly reduced intraoperative blood loss and faster recovery. [33, 34, 35] One drawback is the significantly higher reintervention rate compared to open repair.
