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Abdominal aortic aneurysm: should we loosen the threshold for repair?

An abdominal aortic aneurysm (AAA) will progressively grow until rupture if a repair is not performed in time, either by open surgery or endovascular techniques. Although the risk of AAA rupture increases with its diameter, there is still a lack of any accurate marker to predict the AAA growth rate or the rupture risk. However, early repair might not be a good approach as the morbidity and mortality associated with both techniques remain non-negligible. A looser and simple threshold of 50 mm diameter could replace the traditional 55 mm threshold for AAA repair, especially in a vulnerable population.

Diseases of the Aorta


Abdominal aortic aneurysm (AAA), a localised dilatation of the infrarenal aorta to a diameter of more than 30 mm or 1.5 times larger than the “expected normal” suprarenal aorta diameter, is not an uncommon vascular problem in an ageing population, especially in men aged over 65 years, who have ever smoked, have hypertension, or have a family history of AAA [1-4].

Why does AAA need to be repaired?

Theoretically, besides a high risk of future cardiovascular (CV) disease events (about 3.0% CV mortality per year in small AAA [5]), an untreated AAA will grow gradually until rupture, resulting in almost 100% mortality. In AAAs with a diameter of 39-49 mm with there is an annual growth rate of about 2.5 mm, faster in larger AAAs; this becomes 20-25% faster in current smokers and 25% slower in metformin-treated diabetic patients [1-4]. So far, no treatment has demonstrated effectiveness in reducing AAA growth, including beta-blockers, ACE inhibitors, statins, exercise, etc., except for smoking cessation.

The risk of AAA rupture can be minimised either by replacing the aneurysmal sac with a vascular synthetic graft (by open surgery repair [OSR]) or by excluding the AAA from the systemic circulation with a stent graft (by endovascular repair [EVAR]). The benefits of AAA repair (either OSR or EVAR) must be balanced with both aneurysm-related risk and procedure-related risk in the short and long term, with cost-effectiveness considerations, after taking into account life expectancy, quality of life, preference of patients, and reimbursement system. OSR itself is considered a high-risk procedure (cardiac risk of 5% or more in 30 days) while EVAR is considered an intermediate-risk procedure (cardiac risk between 1 and 5%) [6]. Notably, the morbidity and mortality associated with both techniques remain non-negligible (Table 1) [1-4].

In a recent individual-level meta-analysis, 30-day all-cause mortality was lower in elective EVAR, but the advantage was lost at follow-up and there was no early survival advantage from EVAR in patients with chronic kidney disease or coronary artery disease [7]. There was also no difference between elective EVAR and OSR in aneurysm-related mortality after 30 days; however, after 3 years, EVAR had a higher number of deaths.

Comparing elective EVAR with no intervention in patients unfit for OSR, data from the EVAR-2 trial showed that EVAR could reduce aneurysm-related mortality rather than overall death [8]. Although EVAR is the treatment preferred by patients, taking into account that the average survival after elective AAA is about 9 years [2,9], OSR should be the first strategy in younger, fitter patients with long life expectancy (more than 10-15 years); elective EVAR should not be recommended in patients with limited life expectancy of about 2-3 years [2-4]. On the other hand, data from the IMPROVE trial suggested that, as the EVAR approach for suspected rupture of AAA was associated with a survival advantage, better quality-adjusted life-years, a similar rate of reintervention, and lower costs, and was ultimately more cost-effective compared with OSR, then EVAR should be the first choice for a suspected rupture of AAA [1-4].


Table 1. Common complications of open surgical repair (OSR) and endovascular aortic repair (EVAR) of AAA during 5-year follow-up [1-4].

Open surgical repair (OSR) Endovascular aortic repair (EVAR)

Incisional hernia: 5-10%

Para-anastomotic aneurysm: up to 3%

Graft infection: 0.2-1.3%

Secondary aorto-enteric fistula: <1%

Graft limb occlusion: up to 2%

Sexual dysfunction: up to 70%

Access-site problems: 9-15%

Endoleak (all types): 20-50%

Stent graft infection: <1%

Stent graft migration: 8%

Graft limb occlusion: 4-8%

Sac expansion/secondary rupture: 10%


Why AAA repairs can fail in the long term

Late complications can happen after AAA repair in both OSR and EVAR. Although some complications are similar in both approaches after 5 years, such as graft infection (0.2-1%), limb occlusion (1-5%), secondary aorto-enteric fistula (0.3-0.5%) etc., others are unique to each technique, such as endoleak after EVAR or hernias after OSR [Table 1].

Both EVAR and OSR eliminate the mechanical stress of blood flow on the AAA wall, facilitate the healing process of thrombosis in the AAC sac, and hypothetically would minimise aneurysm-related complications even though not directly impacting on the progressive changes in the AAA wall resulting from the multifactorial response to genetic and environmental factors. However, aortic complications and reinterventions still happen in the long term, more so after EVAR than OSR, including many types of endoleak, device migration and even late AAA rupture [1-4].

The ongoing expansion of the AAA sac outside the graft and the cumulative flow from collaterals might explain an endoleak, device movements or aneurysm enlargements in the long term. The chimney technique or fenestrated/branched grafts have been used to elongate the effective proximal landing zone of EVAR, thus avoiding type IA endoleak and providing some support to reduce late device movement.

Supplementary devices such as an extra cup or an aortic plain stent (without graft but higher radial force) or a Heli-FX™ EndoAnchor™ system (Medtronic, Minneapolis, MN, USA) for transmural fixation have been developed to secure the proximal end of the EVAR graft, and reduce late stent migration, especially in anatomically difficult scenarios such as conical or angulated neck [1,2]. To avoid continued enlarging forces from an oversized stent graft, which might play an important role in triggering late neck expansion, an alternative concept, endovascular aneurysm sealing (EVAS), was also developed to fix the stent by a Bioring (Bioring SA, Lonay, Switzerland) and heal the AAA sac by BioGlue (CryoLife Inc., Kennesaw, GA, USA); however, their effectiveness and long-term durability are still under investigation [10].

When we need to repair the AAA

Quite a number of AAAs are asymptomatic and only detected incidentally when they have a significantly large diameter, are distorted and too difficult to be repaired (either OSR or EVAR might increase long-term complications). Smaller AAAs would be easier to repair and should have a slower progression of the AAA sac in the future, meaning that the “repair threshold” could be lower for better treatment modalities (such as better devices, i.e., smaller devices to reduce short-term complications, smarter concept to reduce long-term complications). However, AAA repair at the moment still has certain periprocedural risks, post-repair complications remain non-negligible, and a lower threshold for AAA diagnosis and treatment could be potentially harmful and have a less favourable benefit-harm balance due to substantial increases in overdiagnosis and overtreatment [11].

Until now, an AAA definitely required a repair if there were any symptoms related to the AAA. The decision for asymptomatic AAA repair should be based on the initial AAA diameter, the annual growth rate and the estimated risk of rupture. Previous data showed that the annual rupture risks were negligible for AAAs <40 mm, became 1.0 per 100 person-​years for AAAs of 40–54 mm, then rose sharply to nearly 10 per 100 person-years for AAAs 55–69 mm, and surpassed 30 per 100 person-​years for AAAs >70 mm [1,2,12]. It was presumed that 55 mm was the “danger threshold”. At present, asymptomatic AAA would be repaired if the maximum diameter was above 55 mm or if the growth rate exceeded 10 mm per year for an AAA of 40-55 mm [1-4].

Theoretically, 55 mm might be too high for populations having small aorta such as women or Asian people. The AAA rupture rate for women with a 45 mm AAA was nearly the same as a 55 mm, suggesting a lower threshold for repair in women, likely closer to 50 mm, but not too low, given that the operative mortality in women is higher than in men [13,14]. The ratio of aortic diameter and body surface area (ASI) could predict aortic rupture in women better than aortic diameter and might become a more appropriate marker: an ASI threshold of 25 mm/m2 could have avoided 80% of ruptures, while a threshold of 30 mm/m2 could have avoided 40% of ruptures in women having an AAA with a diameter <55 mm [15,16].

The rupture risk is also influenced by AAA morphology (the mycotic or saccular form has higher risks), and by histological/molecular characteristics (inflammation or multilayer of intraluminal thrombus weakening the AAA wall). Until now, ASI or complicated biomechanical indices derived from computational analysis (such as peak wall stress, peak wall shear stress, wall strain, peak wall rupture index, wall stiffness and so on), have been controversial, while fused functional imaging only showed conflicting results in terms of predicting the AAA growth rate or rupture risk [17,18]. Perhaps inflammation and biomechanical attributes only represented different features and needed to be comprehensively combined with other traditional demographic, geometric, genetic or patient-specific features to predict the future progression and rupture risk of an AAA, ideally with machine learning algorithms.

Conflicting results also reflected the heterogeneity in AAA diameter measurement protocols (vascular ultrasound or multislice computer tomography), the diversity in patient populations, the complexity of multifactorial interaction in pathology, as well as the inaccuracy (low sensitivity) to predict future AAA progression.

Consequently, 50 mm can be considered as a “simple and practical” clinical threshold to decide the time for repair in vulnerable populations such as women, Asians, saccular or mycotic AAA, etc., following the surveillance protocol (Table 2) proposed by Sakalihasan et al [1]. Other imaging modalities or indices could be used for further risk stratification if both doctors and patients hesitate on the time for AAA repair.


Table 2. Surveillance protocol for asymptomatic AAA patients.

Asymptomatic AAA AAA size (mm)
  30 - <40 mm 40 - <45 mm 45 - <50 mm 50 - <55 mm 55+ mm
Men with fusiform AAA Follow-up every 2-3 years Follow-up every 6-12 months Follow-up every 6 months Follow-up every 3-6 months Consider AAA repair

Saccular or mycotic AAA
Women with AAA
Asian patients

Follow-up every 3-6 months

Other imaging modalities/indices
Consider early repair



Despite of a lot of improvements and advanced techniques or devices in both OSR and EVAR approaches, there are still non-negligible complications after AAA repair, which make early AAA repair (or a low threshold for repair) inappropriate. However, a high threshold for repair could not reduce the fatal rupture risk and might theoretically create more complications in the future. While many promising sophisticated algorithms to predict AAA progression and future rupture are under investigation, a looser and simple threshold of 50 mm diameter of aneurysm could be easier to apply in daily practice, especially in vulnerable AAA patients. In a grey zone of 50-55 mm, other imaging modalities or biomechanical indices would further stratify the risk.  


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Notes to editor


Quang Ngoc Nguyen1,2, MD, PhD

  1. Department of Cardiology, Hanoi Medical University, Hanoi, Vietnam;
  2. Vietnam National Heart Institute, Bach Mai Hospital, Hanoi, Vietnam


Address for correspondence:

Associate Professor Dr. Quang Ngoc NGUYEN, Department of Cardiology, Hanoi Medical University, Vietnam National Heart Institute, Bach Mai Hospital, 78 Giai Phong Avenue, Dong Da District, Hanoi, Vietnam

E-mail: /


Author disclosures:

The author has no conflicts of interest to declare.


The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.