By definition, a permanent dilation of the vessel diameter to 1.5 times the norm is termed an aneurysm. 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, males 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, 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 discovered as an incidental finding during routine examinations or as part of screening programmes, and it not uncommonly remains clinically silent until rupture. In the presence of a 3 cm AAA, clinical examination provides indications of the presence of an AAA in only 29% of cases [6]. The gold standard in diagnostics and treatment planning of AAA is contrast-enhanced spiral computed tomography (sensitivity 93–100%, specificity up to 96%). Considering the high radiation dose of CT (27.4 mSV for three phases; plain abdominal radiography for comparison: about 2 mSv), MRI is an equivalent alternative, particularly in postoperative follow-up, with a sensitivity of 96% and specificity of up to 100% [7, 8]. For initial and screening examinations 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 includes open aortic repair (OAR) and endovascular aortic repair (EVAR). 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. This is less than 1% per year for an AAA with a diameter of 4.4 cm and increases significantly at 5 cm and above. For an AAA diameter of more than 5 cm, the annual risk of rupture is around 11% [10, 11]. In elective treatment of an AAA, the individual risk of rupture must be weighed against a 30-day mortality of about 1.8% for EVAR and 4.3% for OAR [12]. However, the "early EVAR benefit" is offset over the long-term course, 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 have 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 in 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 replacement according to Creech constituted the standard treatment of AAA [15], for which straight and Y-grafts made of Dacron or PTFE — partially coated — are available. Three major randomized 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 specialized 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]. Cardiopulmonary complications, renal insufficiency, bleeding complications, and infections are of particular importance for perioperative mortality.
After the initial description of the procedure in 1988 by Nikolay Volodos [18], EVAR procedures saw a continuous rise worldwide. In 2010, the EVAR share was 74% in the United States [19] and about 73% in Germany in 2012 [20]. Whether EVAR can be performed depends, among other factors, on the anatomical circumstances and morphology of the AAA as well as the access vessels. For complex anatomical situations, so-called "custom-made" endografts with fenestrations and scallops, e.g., for the origins of the visceral arteries, are now available. Their use should be reserved for specialized centres, as the mortality rate correlates significantly with the number of cases treated [17, 21].