By current reporting standards, an aneurysm is defined as a permanent dilation of the vessel diameter to 1.5 times the norm. The mean transverse diameter of the healthy infrarenal aorta is about 1.93 cm in men and about 1.67 cm in women [1]. According to international consensus, a diameter of 3.0 cm or more is considered an abdominal aortic aneurysm (AAA).
Epidemiology and aetiology
Accounting for 40–60% of cases, the most common location of aortic aneurysms is the abdominal aortic segment, with the renal artery origins involved in 5% of cases.
Population-based studies demonstrated an AAA prevalence of 4–7.6% in men over 50 years of age and about 1.3% in women of the same age [2, 3]. Hence, men are affected much more frequently, in a ratio of 6:1. According to major international registry studies, perioperative all-cause mortality ranges from 1.6% for intact AAA (iAAA) to 31.6% for ruptured AAA (rAAA) [4]. With a mortality rate of up to 90%, the prognosis of rAAA is particularly poor, so that effective strategies for elective treatment in the non-ruptured stage are required [5].
The key risk factors in the development of AAA are smoking, a positive family history, age and atherosclerosis. With an odds ratio of 5.07, nicotine consumption constitutes the most significant risk factor [3].
Diagnostic work-up
AAA is often diagnosed as an incidental finding during routine examinations or screening, and it is not uncommon for it to remain clinically silent until rupture. In the presence of a 3 cm AAA, clinical examination provides indications of an AAA in only 29% of cases [6]. The gold standard in the diagnostic work-up and treatment planning of AAA is contrast-enhanced spiral computed tomography (sensitivity 93–100%, specificity up to 96%). Considering the high radiation dose delivered by CT (27.4 mSV in three phases, as compared with about 2 mSv for plain abdominal radiography), MRI is an equivalent alternative, especially in postoperative follow-up, with a sensitivity of 96% and specificity of up to 100% [7, 8]. For initial and screening studies of the abdominal aorta, colour-coded duplex ultrasonography may be considered, which, depending on the experience of the operator, has a sensitivity and specificity of up to 100% [9].
Management
In addition to conservative and pharmacological treatment for optimising risk factors, invasive management of AAA comprises open aortic repair (OAR) and the endovascular aortic repair (EVAR) procedure. The approach should be selected individually and take into account the patient's individual circumstances (underlying diseases, life expectancy, patient preference).
Indication is fundamentally based on the present risk of rupture. For an AAA with a diameter of 4.4 cm, this is less than 1% per year and increases markedly from 5 cm onwards. For an AAA diameter of more than 5 cm, the annual risk of rupture is around 11% [10, 11]. In the elective treatment of an AAA, the individual risk of rupture must be weighed against a 30-day mortality of approximately 1.8% for EVAR and 4.3% for OAR [12]. However, the "early EVAR benefit" is offset over the long term, so that both procedures offer an equivalent long-term outcome [13]. It follows that the elective surgical risk in AAA <5 cm is higher than the annual rupture risk, which is why an indication for aneurysm exclusion only applies from 5–5.5 cm onwards. Small aneurysms <5 cm show an average annual growth rate of about 0.21 cm, which is why follow-up by duplex ultrasonography should be performed at 6- or 12-month intervals [11, 14]. Symptoms attributable to an AAA, as well as rapid progression in size beyond 0.5 cm within 6 months, are associated with a significantly increased risk of rupture and therefore represent an absolute indication for treatment.
For a long time, open surgical aortic repair according to Creech constituted the standard treatment of AAA [15], for which straight and Y-grafts made of Dacron or PTFE — some of them coated — are available. Three major randomised trials reported 30-day mortality as 3.0% (OVER, USA), 4.3% (EVAR-1, UK), and 4.6% (DREAM, Netherlands). Mortality, revision rate, and lethality are significantly lower when the procedure is performed in specialised vascular surgery centres: perioperative mortality is about 2.2% for vascular surgeons, 4.0% for cardiac surgeons, and 5.5% for general surgeons [16, 17]. Of particular importance for perioperative mortality are cardiopulmonary complications, renal insufficiency, bleeding complications, and infections.
After the initial description of the procedure in 1988 by Nikolay Volodos [18], a steady worldwide rise in EVAR procedures began. In 2010, the EVAR share was 74% in the United States [19], and in 2012 it was about 73% in Germany [20]. Whether EVAR can be performed depends, among other factors, on the anatomical conditions and morphology of the AAA as well as the access vessels. For complex anatomical situations, so-called "custom-made" endografts with fenestrations and cut-outs, e.g., for the origins of the visceral arteries, are now available. Their use should be reserved for specialised centres, as the mortality rate correlates significantly with the number of cases treated [17, 21].