Abdominal Aortic Aneurysm

Table of Contents

  1. Overview
  2. Epidemiology
  3. Pathogenesis
  4. Risk Factors
  5. Clinical Presentation
  6. Screening and Surveillance
  7. Diagnosis and Imaging
  8. Size-Based Management
  9. Endovascular Repair (EVAR)
  10. Open Surgical Repair
  11. Medical Management
  12. Research Papers
  13. Connections
  14. Featured Videos

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1. Overview

An abdominal aortic aneurysm (AAA) is a permanent, localized widening of the abdominal aorta. The USPSTF notes that an AAA is typically defined as an aortic diameter of 3.0 cm or larger (USPSTF 2019). The 2022 ACC/AHA aortic disease guideline gives the conventional definition of an arterial aneurysm as an artery dilated to at least 1.5 times its expected normal diameter, a definition it says applies well to the abdominal aorta (Isselbacher 2022). A disease-primer review describes AAA as a localized dilatation of the infrarenal aorta, the segment below the renal arteries (Sakalihasan 2018).

Most AAAs are asymptomatic until they rupture (USPSTF 2019). The guideline estimates the mortality of ruptured AAA at 80% to 90%, with most patients never reaching the hospital; for those who do, the historical mortality of open repair was about 50%, and one observational series reported mortality after repair as low as 18.5% after adopting an endovascular-repair-first strategy (Isselbacher 2022). The USPSTF gives a risk of death with rupture as high as 81% (USPSTF 2019). Planned (elective) repair carries far lower risk in trials: 30-day mortality in EVAR trial 1 was 1.7% after endovascular repair and 4.7% after open repair (Greenhalgh 2004), and total operative mortality was 2.7% in the immediate-repair group of the ADAM trial (Lederle 2002, ADAM). The guideline describes the goal of targeted ultrasound screening as preventing rupture and the deaths it causes (Isselbacher 2022).

The guideline explains why diameter is the main criterion for elective repair: per Laplace's law, wall stress increases in proportion to the aortic radius and inversely with wall thickness (Isselbacher 2022). A review describes rupture as occurring when the mechanical stress of blood pressure on the wall exceeds the strength of the wall, and notes that AAAs of any size can rupture, although the risk rises with diameter (Sakalihasan 2018).

AAA shares risk factors with atherosclerosis, but the guideline describes it as histopathologically distinct, characterized by degeneration of the aortic media (Isselbacher 2022). Smoking, male sex and a family history are the most important risk factors, and AAA is most common in men over 65 (Sakalihasan 2018). Diabetes shows an inverse association with both AAA prevalence and growth (Xiong 2016), covered under Risk Factors below.

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2. Epidemiology

The USPSTF reports that the prevalence of AAA has declined over the past two decades among screened men 65 or older in several European countries, and that current US prevalence is unclear because few people are screened (USPSTF 2019). A US trial report describes AAA as affecting more than 3% of older adults in the United States (Baxter 2020). The 2022 guideline gives a lifetime risk of AAA of 8.2% in men and 10.5% in current smokers (Isselbacher 2022). In a cross-sectional study of 1.5 million women and 0.8 million men without known vascular disease who were screened in the United Kingdom or United States from 2008 to 2013, ultrasound detected 12,729 new AAAs (0.6%) (Carter 2020). A US cohort of 3.1 million people screened by ultrasound produced a risk model that, applied to national risk-factor statistics, estimated 1.1 million AAAs in the United States, about 569,000 of them in women, nonsmokers and people under 65; the authors estimated that about half of people with AAA are not eligible for screening under the criteria then in use (Kent 2010).

Sex. Male sex is a strong, independent risk factor for AAA; the guideline notes that female sex has not been proven an independent risk factor and that prevalence is lower in women (Isselbacher 2022). Once an aneurysm is present, outcomes differ. In an individual-patient meta-analysis of 15,475 people with small AAAs, rupture rates were almost fourfold higher in women than in men, while the mean growth rate (2.21 mm per year) did not depend on sex or age (Sweeting 2012). In the UK Small Aneurysm Trial, rupture caused 12 of the 85 deaths among women (14%) and 19 of the 411 deaths among men (5%) (UKSAT 2002), and the mean aneurysm diameter at rupture was 5.0 cm in women and 6.0 cm in men (Isselbacher 2022). In the UK/US screening study, the prevalence of AAA in female smokers was greater than in male never-smokers in every age group (Carter 2020).

Family history and race. At least 10% to 25% of patients with AAA have a family member with the condition. Small cohort studies of ultrasound screening in relatives have found new AAA in 10% to 20%, with the highest prevalence (25%) among brothers, and the lifetime prevalence of AAA is estimated at 32% in brothers of people with AAA (Isselbacher 2022). The guideline lists White race among the additional risk factors for AAA (Isselbacher 2022). In the 3.1-million-person screening cohort, Black, Hispanic and Asian participants had a lower risk of AAA than White and Native American participants (Kent 2010).

Age. Older age is one of the strong risk factors for AAA (Isselbacher 2022). In a UK population-based study cited by the guideline, two-thirds of acute AAA events occurred in people aged 75 or older, and in a US National Inpatient Sample study, 24% of patients with ruptured AAA (10,603 of 25,777) were under 65, below the usual screening age (Isselbacher 2022). Inherited vascular connective tissue disorders are among the guideline's additional risk factors, and AAA may occur together with thoracic aortic aneurysm, especially in some genetic aortopathies (Isselbacher 2022).

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3. Pathogenesis

The aortic wall has three layers: a thin inner intima of endothelial cells within connective tissue; a thicker media of smooth muscle cells, elastic fibers, collagen and polysaccharides arranged in more than 50 elastic lamellae; and a thin outer adventitia of connective tissue, fibroblasts, nerves and the vasa vasorum. The media provides the strength and distensibility of the aorta (Isselbacher 2022).

Medial Degeneration and Matrix Breakdown

The guideline characterizes AAA by medial degeneration of the aortic wall (Isselbacher 2022). A disease-primer review describes AAA as resulting from changes in wall structure, including thinning of the media and adventitia caused by the loss of vascular smooth muscle cells and degradation of the extracellular matrix (Sakalihasan 2018). Aberrant matrix turnover is believed to play a key role, and matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of metalloproteinases, TIMPs) are important enzymes in controlling extracellular matrix remodelling (Morris 2014).

Genetic Findings Involving MMPs

A meta-analysis of 13 case-control studies covering 58 variants in 10 MMP and TIMP genes found an association between AAA and a common variant in the MMP3 promoter region (odds ratio 1.48), but no association for the variants studied in MMP1, MMP9, MMP10, MMP12, MMP13, TIMP1 or TIMP3 (Morris 2014). A 2017 meta-analysis of genome-wide association studies (10,204 cases and 107,766 controls) identified four new AAA risk loci, one of them near PCIF1/MMP9/ZNF335; network analyses identified ERG, IL6R and LDLR as modifiers of MMP9, and the lead variants were not associated with coronary artery disease, blood pressure, lipids or diabetes (Jones 2017).

Intraluminal Thrombus and Inflammation

Most AAAs develop an intraluminal thrombus, which the guideline describes as contributing to ongoing wall degradation through oxidative stress, smooth muscle cell apoptosis, proteolysis of the extracellular matrix and adventitial inflammation (Isselbacher 2022). The guideline describes the thrombus as a complex matrix of platelets, inflammatory cells and fibrin that contributes to growth and progression, which is why antithrombotic therapy has been hypothesized, though not shown, to help (Isselbacher 2022). Inflammatory aortitis is a rare cause of AAA (Isselbacher 2022).

Diameter, Growth and Wall Stress

Wall stress rises with aortic radius under Laplace's law (Isselbacher 2022), and AAA growth is nonlinear (Isselbacher 2022). In the RESCAN individual-patient meta-analysis of 15,471 patients, each 0.5-cm increase in diameter raised the growth rate by an average of 0.59 mm per year and the rupture rate by a factor of 1.91 (Bown 2013).

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4. Risk Factors

The 2022 ACC/AHA guideline lists as strong risk factors for AAA a smoking history, older age, male sex, a family history of AAA and atherosclerotic cardiovascular disease, and as additional risk factors hypertension, hyperlipidemia, White race and inherited vascular connective tissue disorders (Isselbacher 2022). Diabetes is not on that list and is inversely associated with AAA (Xiong 2016).

Tobacco Smoking (Largest Modifiable Risk Factor)

The guideline calls cigarette smoking the largest modifiable risk factor for AAA. A smoking history is defined as lifetime use of 100 or more cigarettes, and risk is lowest in people with fewer pack-years (Isselbacher 2022). In the UK/US screening study, current smoking compared with never smoking was associated with 15 times the risk of AAA in women (risk ratio 15.0) and 7 times in men (7.3); in women under 75 the risk ratio was 26.4 (Carter 2020). In the 3.1-million-person US cohort, risk rose with years of smoking and cigarettes smoked and was lower after smoking cessation (Kent 2010). Among people with small AAAs, growth was 0.35 mm per year faster in smokers and rupture rates were double in current smokers (Sweeting 2012). The guideline adds that smoking may have a greater effect on growth in women than in men (Isselbacher 2022).

Male Sex

Male sex is a strong, independent risk factor for developing AAA, and prevalence is lower in women (Isselbacher 2022). Women who do have an AAA face higher rupture rates (Sweeting 2012) and, in registry data reviewed for the USPSTF, higher surgical complications and postoperative mortality after repair (Guirguis-Blake 2019). The guideline sets a lower repair threshold for women (5.0 cm, against 5.5 cm for men) because rupture occurs at smaller diameters in women (Isselbacher 2022).

Age

Older age is an independent, strong risk factor for AAA (Isselbacher 2022). In the individual-patient meta-analysis, the mean growth rate of small AAAs was independent of age (Sweeting 2012).

Family History

A first-degree relative with AAA is a well-established risk factor; at least 10% to 25% of patients with AAA have an affected family member, and the estimated lifetime prevalence in brothers of people with AAA is 32%. The guideline also states that growth may accelerate in the setting of a family history, and it recommends ultrasound screening for men and women aged 65 or older who are first-degree relatives of patients with AAA (Isselbacher 2022).

Hypertension

Hypertension is one of the guideline's additional risk factors, and uncontrolled hypertension is described as a known risk factor for aortic rupture and dissection (Isselbacher 2022). Among people with small AAAs, rupture rates increased with higher blood pressure, while mean arterial pressure had no effect on growth (Sweeting 2012). In the UK/US screening study, usual systolic blood pressure showed a positive log-linear association with AAA in both women and men (Carter 2020).

Hyperlipidemia and Atherosclerosis

Atherosclerotic cardiovascular disease is a strong risk factor and hyperlipidemia an additional one (Isselbacher 2022). The guideline considers AAA of atherosclerotic cause a coronary artery disease equivalent, with a greater than 20% risk of a cardiovascular event within 10 years (Isselbacher 2022). Usual LDL cholesterol and triglycerides showed positive log-linear associations with AAA (Carter 2020). The four genetic risk loci identified in 2017 were not associated with coronary disease or lipids, and the authors suggested that traditional cardiovascular risk-factor management may have only limited value in preventing the progression of aneurysmal disease (Jones 2017).

Diabetes: An Inverse Association

A 2016 meta-analysis of 49 prevalence studies and 13 growth studies found a strongly negative association between diabetes and AAA prevalence in population-based screening studies (adjusted odds ratio 0.66) and in prospective studies (0.52), but not a significant one in case-control studies (0.48, confidence interval crossing 1); the association held in North American and European studies and across periods of data collection, and diabetes was associated with slower aneurysm growth (mean −0.60 mm per year) (Xiong 2016). The 15,475-patient individual-data meta-analysis likewise found growth reduced by 0.51 mm per year in patients with diabetes (Sweeting 2012). These studies report the association; their abstracts do not establish its mechanism. The guideline's surveillance text nonetheless mentions diabetes, together with smoking, as a reason shorter scan intervals are often used (Isselbacher 2022).

Factors Associated With Lower Risk

In the 3.1-million-person screening cohort, smoking cessation, exercise and the consumption of nuts, vegetables and fruits were associated with a lower risk of AAA, and excess weight with a higher risk (Kent 2010). Usual body mass index and height also showed positive associations with AAA in the UK/US study (Carter 2020). These are associations from observational screening data, not trial results.

Fluoroquinolone Antibiotics

In a Swedish nationwide cohort of 360,088 propensity-matched treatment episodes, oral fluoroquinolone use was associated with a higher 60-day risk of aortic aneurysm or dissection than amoxicillin use (hazard ratio 1.66; an estimated 82 extra cases per million treatment episodes); the association was driven mainly by aortic aneurysm (hazard ratio 1.90) rather than dissection (0.93) (Pasternak 2018).

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5. Clinical Presentation

Most AAAs are asymptomatic until they rupture (USPSTF 2019). The guideline separates aneurysms that cause symptoms without rupturing from those that have ruptured (Isselbacher 2022).

Asymptomatic AAA (Most Common)

Intact AAAs are typically asymptomatic, and in settings without ultrasound screening programmes most cases are diagnosed incidentally (Sakalihasan 2018).

Symptomatic (Unruptured) AAA

About 6% to 22% of treated aneurysms are symptomatic but unruptured. The guideline describes pain in the back, abdomen or flank attributable to the AAA, sometimes radiating to the groin, as high risk for impending rupture; for patients presenting this way it describes admission to intensive care for arterial blood pressure monitoring, tight blood pressure control and medical optimization, with repair ideally within 24 to 48 hours. Tenderness over the aneurysm in the abdomen, back or flank, embolism (for example, blue toe syndrome) and compressive symptoms (for example, obstructive uropathy) are described as warranting expedited, though not necessarily urgent, repair. Observational studies show higher mortality and morbidity in patients treated for symptomatic aneurysms than in those treated electively (Isselbacher 2022).

Ruptured AAA

The guideline estimates the mortality of ruptured AAA at 80% to 90%, with most patients never reaching the hospital. Patients who do arrive often maintain adequate blood pressure, in part because of catecholamine responses, and can suffer circulatory collapse once general anesthesia removes that response (Isselbacher 2022). For hemodynamically stable patients, the guideline recommends CT imaging to judge whether the aneurysm is suitable for endovascular repair, and it recommends endovascular over open repair when the anatomy is suitable. It considers local rather than general anesthesia preferable for endovascular repair of rupture, and permissive hypotension (typically a systolic pressure of 60 to 90 mm Hg that maintains mentation) potentially beneficial to slow bleeding. In the IMPROVE trial, survival between 90 days and 3 years was better after endovascular than open repair of rupture (hazard ratio 0.57) (Isselbacher 2022).

Embolic, Compressive, Inflammatory and Infectious Presentations

Other presentations described in the guideline include embolism from the aneurysm (blue toe syndrome), compression of neighbouring structures (obstructive uropathy), inflammatory aortitis, which is a rare cause of AAA, and infectious aortitis, in which open surgical repair is recommended for an associated aneurysm and the presence of fistulae is one factor in choosing the operation; the guideline notes that endovascular intervention may improve survival in patients with an aorto-enteric fistula when used as a bridge to definitive therapy (Isselbacher 2022).

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6. Screening and Surveillance

The United States Preventive Services Task Force (USPSTF) updated its 2014 AAA screening recommendation in 2019 (USPSTF 2019):

The USPSTF recommends 1-time screening for AAA with ultrasonography in men aged 65 to 75 years who have ever smoked. (B recommendation)

The Task Force reached this with moderate certainty of moderate net benefit. It recommends that clinicians selectively offer screening to men aged 65 to 75 who have never smoked rather than routinely screening all of them (C recommendation, moderate certainty of small net benefit); recommends against routine screening in women who have never smoked and have no family history of AAA (D recommendation); and finds the evidence insufficient for women aged 65 to 75 who have ever smoked or have a family history (I statement) (USPSTF 2019).

Who Is and Is Not Covered

The 2022 ACC/AHA guideline recommends ultrasound screening for men 65 or older who have ever smoked and for men or women 65 or older who are first-degree relatives of patients with AAA; considers screening reasonable for women 65 or older who have ever smoked; says it may be considered under 65 in people with multiple risk factors or a first-degree relative with AAA; and does not recommend repeat screening in asymptomatic people over 75 who had a negative first scan. It notes that randomized trials and large observational studies of screening in women are lacking (Isselbacher 2022). The authors of the UK/US screening study, who found AAA more common in female smokers than in male never-smokers, called a policy of screening male never-smokers but not female smokers questionable (Carter 2020).

What the Screening Trials Found

In the evidence review for the USPSTF, a meta-analysis of four population-based randomized trials found that a screening invitation to men 65 or older was associated with lower AAA-related mortality (odds ratio 0.65) and fewer ruptures (0.62) over 12 to 15 years, and fewer emergency operations (0.57), but not with lower all-cause mortality (relative risk 0.99). Screening led to more elective operations (odds ratio 1.44) without long-term differences in quality of life (Guirguis-Blake 2019). On repeat screening, the guideline states that cohort data, though limited, suggest long-term AAA-related mortality is low among people with a negative first scan who later have an AAA detected after age 75 (Isselbacher 2022).

Surveillance Intervals After Diagnosis

The 2022 ACC/AHA guideline recommends these surveillance ultrasound intervals for AAAs below the repair threshold (Isselbacher 2022):

The guideline adds that even shorter intervals are often used in people who smoke, have diabetes, or both (Isselbacher 2022). The 2018 Society for Vascular Surgery guideline likewise recommends imaging at 12-month intervals for AAAs of 4.0 to 4.9 cm (Chaikof 2018). The RESCAN meta-analysis of 15,471 patients concluded that intervals of several years may be acceptable for most small AAAs: keeping the risk of rupture below 1% in men required intervals of about 8.5 years for a 3.0-cm aneurysm and 17 months for a 5.0-cm aneurysm (Bown 2013).

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7. Diagnosis and Imaging

The guideline recommends that aortic diameters be measured at reproducible anatomic landmarks perpendicular to the axis of blood flow, reporting the longest diameter and its perpendicular when the contour is oval or asymmetric, and that radiation doses be kept as low as feasible (Isselbacher 2022).

Abdominal Ultrasound (Screening and Surveillance)

The guideline describes vascular ultrasound as the recommended tool for AAA screening and surveillance. Its criterion for AAA is a diameter greater than 3.0 cm, measured mainly outer edge to outer edge in the anterior-posterior or transverse view. Its sensitivity for detecting an aneurysm approaches 100%, although interobserver variability exists and imaging can be limited by obesity and bowel gas. Ultrasound can also show plaque, mural thrombus, dissection, pseudoaneurysm, contained rupture and other findings that may prompt CT or MRI, and it is used after endovascular repair to detect sac expansion (Isselbacher 2022).

CT Angiography (Surgical Planning and Suspected Rupture)

CT gives superior visualization of the abdominal aorta and its branches, is the alternative when ultrasound is inadequate, and is generally preferred once an AAA reaches the repair threshold, both to confirm diameters and to detail anatomy for planning (Isselbacher 2022). In ruptured AAA, CT is recommended for hemodynamically stable patients to judge suitability for endovascular repair; the guideline notes that a CT already obtained may be enough, since a further dedicated scan can delay care (Isselbacher 2022).

Magnetic Resonance Imaging

MRI or MR angiography is a reasonable alternative to CT, for example when CT is contraindicated or to lower cumulative radiation, and non-contrast MRI techniques have also been useful in defining AAAs (Isselbacher 2022). The guideline lists MRI's limitations as higher cost, longer acquisition times, lower resolution and limited visualization of metallic stent-graft components (Isselbacher 2022).

Plain Abdominal Radiography

In the guideline, plain abdominal radiography appears as a companion to MRI after endovascular repair: because MRI cannot accurately show metallic stent struts, it is paired with a plain radiograph to check for stent fracture (Isselbacher 2022).

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8. Size-Based Management

The guideline states that thresholds for AAA repair must balance the expected risk of rupture against the risk of the operation, and that maximum diameter is one of the most significant risk factors for continued growth and rupture (Isselbacher 2022).

Rupture Risk by Diameter

The guideline cites these historical estimates of rupture risk by maximum diameter (Isselbacher 2022):

In 198 veterans with AAAs of at least 5.5 cm who did not have elective repair because of medical contraindication or refusal, the 1-year incidence of probable rupture was 9.4% at 5.5–5.9 cm, 10.2% at 6.0–6.9 cm (19.1% for 6.5–6.9 cm) and 32.5% at 7.0 cm or more; once an aneurysm reached 8.0 cm, 25.7% ruptured within 6 months (Lederle 2002, VA cohort). In the ADAM trial's surveillance group (aneurysms of 4.0–5.4 cm at entry), the rupture rate was 0.6% per year (Lederle 2002, ADAM). Rupture risk also differs between people with the same diameter: rates were almost fourfold higher in women, double in current smokers, and higher with higher blood pressure (Sweeting 2012).

Indications for Repair

The 2022 ACC/AHA guideline (Isselbacher 2022):

Management of Small AAA (3.0–5.4 cm)

Trials from the late 1990s and early 2000s (UKSAT and ADAM for early open repair; CAESAR and PIVOTAL for early endovascular repair) found no survival benefit from repairing aneurysms of 4.0 to 5.4 cm (Isselbacher 2022). In ADAM (569 patients assigned to immediate repair, 567 to surveillance), death from any cause did not differ between immediate repair and surveillance (relative risk 1.21) despite a low operative mortality, and AAA-related hospitalization was 39% lower with surveillance (Lederle 2002, ADAM). In UKSAT (1,090 patients), mean survival did not differ (6.7 versus 6.5 years); total mortality was lower in the early-surgery group after 8 years, which the authors attributed partly to more smoking cessation in that group (UKSAT 2002). The USPSTF evidence review found no significant difference in AAA-related or all-cause mortality across four early-surgery trials (3,314 patients), with substantially more procedures in the early-surgery groups (Guirguis-Blake 2019).

Mean growth of small AAAs was 2.21 mm per year in the individual-patient meta-analysis (Sweeting 2012); the guideline cites a mean of 2.6 mm per year for AAAs under 5.0 cm, and pooled surveillance data of 1.5–2 mm per year at 3.0–3.9 cm and 3.3–5.7 mm per year at 4.0–5.9 cm (Isselbacher 2022). Surveillance intervals are listed in Section 6.

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9. Endovascular Repair (EVAR)

Endovascular repair uses non-aneurysmal aortic or iliac segments to anchor a stent-graft that excludes blood flow from the aneurysm sac (Isselbacher 2022). Most infrarenal AAA repairs in the United States are performed by endovascular methods (Schanzer 2011). For patients with suitable common femoral artery anatomy, the guideline recommends ultrasound-guided percutaneous access and closure over open cutdown, citing shorter operative time, less blood loss, shorter stay, faster wound healing and less pain (Isselbacher 2022).

Anatomical Requirements

The guideline lists neck diameter, length and angulation, iliac seal diameter and length, and vessel access as anatomic factors, and recommends adherence to the manufacturer's instructions for use: observational studies link treatment outside them to more sac enlargement, graft-related events and higher mortality (Isselbacher 2022). In an imaging database of 10,228 EVAR patients (1999–2008), only 42% met the most conservative instructions-for-use definition and 69% the most liberal; 59% had a maximum diameter below 5.5 cm; the 5-year rate of sac enlargement was 41%; and independent predictors of sac enlargement included endoleak, age 80 or older, aortic neck diameter of 28 mm or more, neck angle over 60° and common iliac diameter over 20 mm (Schanzer 2011).

Short-Term Outcomes

In EVAR trial 1 (1,082 patients with aneurysms of 5.5 cm or more), 30-day mortality was 1.7% with EVAR versus 4.7% with open repair (odds ratio 0.35), and secondary interventions were more common after EVAR (9.8% versus 5.8%) (Greenhalgh 2004). In the full 1,252-patient trial, 30-day operative mortality was 1.8% versus 4.3% (UK EVAR Trial Investigators 2010). In pooled data from 7 randomized trials, perioperative mortality was much lower with EVAR (odds ratio 0.36) (Isselbacher 2022). In the ACE trial of 299 analysed low- to intermediate-risk patients, in-hospital mortality did not differ significantly (0.6% open versus 1.3% EVAR) (Becquemin 2011). The guideline considers EVAR reasonable for patients at high perioperative risk, and in a Medicare comparison it cites, myocardial infarction, pneumonia, acute renal failure and dialysis were all less likely after infrarenal EVAR than after open repair (Isselbacher 2022).

Long-Term Surveillance and Re-Intervention

An endoleak is persistent blood flow outside the graft and inside the aneurysm sac, and the guideline states that patients with endografts need lifelong surveillance imaging. Its classification has five types (Isselbacher 2022):

The Society for Vascular Surgery recommends treating type I and III endoleaks and type II endoleaks with aneurysm expansion, and continued surveillance of type II endoleaks without expansion (Chaikof 2018). Endoleaks are present after 10% to 17% of EVARs at 30 days; late aortic rupture after EVAR exceeds 5% through 8 years, with endoleak plus sac enlargement as significant risk factors; and stent-graft fracture and migration occur in 3% to 4% of patients by 4 years (Isselbacher 2022). The guideline's surveillance schedule is CT at 1 month and, if there is no endoleak or sac enlargement, duplex ultrasound at 12 months and yearly after that, with CT or MRI every 5 years considered reasonable (Isselbacher 2022).

Long-term trial results differ. In EVAR trial 1 (mean follow-up 12.7 years), overall mortality did not differ significantly (adjusted hazard ratio 1.11); EVAR had lower mortality in the first 6 months, but beyond 8 years open repair had significantly lower total and aneurysm-related mortality, the latter mainly from secondary sac rupture (13 deaths after EVAR versus 2 after open repair) (Patel 2016). In DREAM (351 patients), 6-year survival was 69.9% after open repair and 68.9% after EVAR, and freedom from secondary interventions was 81.9% versus 70.4% (De Bruin 2010). In ACE, reinterventions were more frequent after EVAR (16% versus 2.4%) (Becquemin 2011). In the US OVER trial (881 patients, up to 14 years), deaths were 68.0% after EVAR and 70.0% after open repair (hazard ratio 0.96), with no significant trend in any period, more secondary procedures after EVAR, and rupture in 7 EVAR patients (1.6%) (Lederle 2019). In the pooled trials, after 8 years EVAR carried higher risks of aneurysm-related death, secondary intervention and rupture (Isselbacher 2022).

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10. Open Surgical Repair

The guideline describes the goal of open surgery as replacing the aneurysmal aortic segment with a prosthetic graft sewn to non-aneurysmal aortic tissue while preserving critical branch vessels (Isselbacher 2022). For patients at low to moderate operative risk whose anatomy suits either method, it recommends a shared decision-making process weighing the risks and benefits of open and endovascular repair (Isselbacher 2022).

Durability and Follow-Up

Operative Risk

Operative mortality after elective open repair was 4.7% at 30 days in EVAR trial 1 (Greenhalgh 2004), 5.5% at 30 days in the UKSAT early-surgery group (UKSAT 2002) and 2.7% (total operative mortality) in ADAM's immediate-repair group (Lederle 2002, ADAM). In the Medicare comparison cited by the guideline, myocardial infarction, pneumonia, acute renal failure and dialysis were more frequent after open repair than after infrarenal EVAR (Isselbacher 2022). The guideline describes risk calculators from US vascular quality registries as helpful for discussing repair options (Isselbacher 2022). The Society for Vascular Surgery suggests limiting elective open repair to hospitals with a documented mortality of 5% or less that perform at least 10 open aortic operations a year, and elective EVAR to hospitals with mortality and conversion rates of 2% or less that perform at least 10 EVARs a year (Chaikof 2018).

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11. Medical Management

The guideline lists the goals of medical therapy in aneurysmal disease as reducing growth, aortic-related death and the need for repair, and, secondarily, reducing non-aortic cardiovascular events, given the risk factors aneurysmal and atherosclerotic disease share. It notes that trial data on medical therapy for aortic aneurysms are limited (Isselbacher 2022).

Smoking Cessation

The guideline recommends smoking cessation efforts for patients with AAA who smoke. No randomized trial has tested the effect of quitting on AAA outcomes; the recommendation rests on cigarette smoking being the largest modifiable risk factor for AAA and on its link with growth, complications and perioperative risk. Options it lists include the “5 A’s” approach (Ask, Advise, Assess, Assist, Arrange), dedicated multidisciplinary programs, app-based tools and pharmacotherapy with nicotine replacement, bupropion or varenicline; it notes that the efficacy and safety of e-cigarettes in patients with AAA have not been shown (Isselbacher 2022). Growth of small AAAs was 0.35 mm per year faster in smokers (Sweeting 2012).

Beta-Blockers

In a randomized, double-blind trial of patients with AAAs of 3.0 to 5.0 cm (276 given propranolol, 272 placebo) followed for a mean of 2.5 years, propranolol did not significantly slow growth (0.22 versus 0.26 cm per year with placebo); patients tolerated it poorly, more stopped taking it (42.4% versus 26.8%), and quality-of-life scores were worse in several domains (Propranolol Aneurysm Trial 2002). The guideline states that the strongest evidence for antihypertensive therapy in AAA concerns beta blockers and renin-angiotensin agents, but that in prospective human trials no specific agent has been proven to inhibit AAA growth (Isselbacher 2022).

Statins

The guideline recommends moderate- or high-intensity statin therapy for patients with AAA and evidence of aortic atherosclerosis, and says it may be considered without such evidence. A meta-analysis it cites associated statin therapy with slower growth, fewer ruptures and lower 30-day mortality after repair, though it could not separate patients with and without atherosclerosis, while one prospective cohort found no slowing of growth (Isselbacher 2022). In a Danish case-control study it cites, current statin use was associated with lower 30-day mortality after rupture (46.1% versus 59.3%) (Isselbacher 2022).

Antihypertensive Therapy

The guideline recommends antihypertensive medication for patients with AAA whose average systolic pressure is 130 mm Hg or higher or diastolic pressure 80 mm Hg or higher, to reduce cardiovascular events (Isselbacher 2022). In the AARDVARK trial (224 patients with AAAs of 3.0 to 5.4 cm, 2 years), neither the ACE inhibitor perindopril nor the calcium-channel blocker amlodipine changed growth compared with placebo (1.77 and 1.81 versus 1.68 mm per year), despite greater blood pressure lowering (Bicknell 2016). In the individual-patient meta-analysis, antihypertensive and other cardioprotective drugs had only small, non-significant effects on growth (Sweeting 2012).

Antiplatelet Therapy

The guideline states that low-dose aspirin may be considered in AAA with concomitant atheroma or penetrating aortic ulcer, and that aortic-specific outcome data are limited. It cites one small cohort in which low-dose aspirin was associated with slower growth at 4.0 to 4.9 cm but not below 4.0 cm, and a Danish registry study in which pre-admission aspirin use was associated with a higher case-fatality rate in ruptured AAA (66% versus 57%) and no difference in the risk of rupture (Isselbacher 2022).

Doxycycline and Other Anti-MMP Strategies

Doxycycline inhibits AAA formation and progression in preclinical models (Meijer 2013), but two randomized trials did not find the same in people. In a Dutch trial of 286 patients given doxycycline 100 mg daily or placebo for 18 months, growth was 4.1 mm with doxycycline versus 3.3 mm with placebo, and the need for repair did not differ (Meijer 2013). In a US trial of 261 patients given doxycycline 100 mg twice daily or placebo for 2 years, the change in maximum diameter was 0.36 cm in both groups (Baxter 2020).

Decisions about screening, medicines and surgery belong with a clinician.

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Key Research Papers

  1. Chaikof EL, Dalman RL, Eskandari MK, Jackson BM, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg. 2018;67(1):2–77.e2. — PubMed PMID: 29268916 — The full text was not accessed for this review; statements on this page are taken from its abstract.
  2. United Kingdom Small Aneurysm Trial Participants; Powell JT, Brady AR, Brown LC, et al. Long-term outcomes of immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med. 2002;346(19):1445–1452. — PubMed PMID: 12000814
  3. United Kingdom EVAR Trial Investigators; Greenhalgh RM, Brown LC, Powell JT, et al. Endovascular versus open repair of abdominal aortic aneurysm. N Engl J Med. 2010;362(20):1863–1871. — PubMed PMID: 20382983
  4. Becquemin JP, Pillet JC, Lescalie F, Sapoval M, et al. A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg. 2011;53(5):1167–1173.e1. — PubMed PMID: 21276681 — This is the ACE trial; it was previously labelled here as the DREAM trial, which is cited separately below (De Bruin 2010).
  5. US Preventive Services Task Force; Owens DK, Davidson KW, Krist AH, et al. Screening for Abdominal Aortic Aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322(22):2211–2218. — PubMed PMID: 31821437
  6. Jones GT, Tromp G, Kuivaniemi H, Gretarsdottir S, et al. Meta-Analysis of Genome-Wide Association Studies for Abdominal Aortic Aneurysm Identifies Four New Disease-Specific Risk Loci. Circ Res. 2017;120(2):341–353. — PubMed PMID: 27899403 — Replaces an entry credited to Jones GT et al., Eur J Vasc Endovasc Surg 2008;35:458–464, on plasma MMP-9, which could not be found in PubMed or Crossref.
  7. Xiong J, Wu Z, Chen C, Wei Y, et al. Association between diabetes and prevalence and growth rate of abdominal aortic aneurysms: A meta-analysis. Int J Cardiol. 2016;221:484–495. — PubMed PMID: 27414727 — Replaces an entry credited to Thompson MM et al., J Vasc Surg 2013;58:773–779, which could not be found in PubMed or Crossref.
  8. Lederle FA, Johnson GR, Wilson SE, Ballard DJ, et al. Rupture rate of large abdominal aortic aneurysms in patients refusing or unfit for elective repair. JAMA. 2002;287(22):2968–2972. — PubMed PMID: 12052126
  9. Lederle FA, Wilson SE, Johnson GR, Reinke DB, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med. 2002;346(19):1437–1444. — PubMed PMID: 12000813
  10. Carter JL, Morris DR, Sherliker P, Clack R, et al. Sex-Specific Associations of Vascular Risk Factors With Abdominal Aortic Aneurysm: Findings From 1.5 Million Women and 0.8 Million Men in the United States and United Kingdom. J Am Heart Assoc. 2020;9(4):e014748. — PubMed PMID: 32063115 — Replaces an entry credited to Wemmelund H et al., Eur J Vasc Endovasc Surg 2015;50:33–40, on smoking dose, which could not be found in PubMed or Crossref.
  11. Schanzer A, Greenberg RK, Hevelone N, Robinson WP, et al. Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair. Circulation. 2011;123(24):2848–2855. — PubMed PMID: 21478500
  12. Propranolol Aneurysm Trial Investigators. Propranolol for small abdominal aortic aneurysms: results of a randomized trial. J Vasc Surg. 2002;35(1):72–79. — PubMed PMID: 11802135
  13. Isselbacher EM, Preventza O, Hamilton Black J 3rd, Augoustides JG, et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2022;146(24):e334–e482. — PubMed PMID: 36322642 — Also published in J Am Coll Cardiol 2022;80(24):e223–e393 (PMID 36334952); facts on this page were checked against that copy's full text (PMC9860464).
  14. Guirguis-Blake JM, Beil TL, Senger CA, Coppola EL. Primary Care Screening for Abdominal Aortic Aneurysm: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2019;322(22):2219–2238. — PubMed PMID: 31821436
  15. Sweeting MJ, Thompson SG, Brown LC, Powell JT; RESCAN collaborators. Meta-analysis of individual patient data to examine factors affecting growth and rupture of small abdominal aortic aneurysms. Br J Surg. 2012;99(5):655–665. — PubMed PMID: 22389113
  16. RESCAN Collaborators; Bown MJ, Sweeting MJ, Brown LC, et al. Surveillance intervals for small abdominal aortic aneurysms: a meta-analysis. JAMA. 2013;309(8):806–813. — PubMed PMID: 23443444
  17. Greenhalgh RM, Brown LC, Kwong GP, Powell JT, et al. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet. 2004;364(9437):843–848. — PubMed PMID: 15351191
  18. Patel R, Sweeting MJ, Powell JT, Greenhalgh RM, et al. Endovascular versus open repair of abdominal aortic aneurysm in 15-years' follow-up of the UK endovascular aneurysm repair trial 1 (EVAR trial 1): a randomised controlled trial. Lancet. 2016;388(10058):2366–2374. — PubMed PMID: 27743617
  19. De Bruin JL, Baas AF, Buth J, Prinssen M, et al. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med. 2010;362(20):1881–1889. — PubMed PMID: 20484396
  20. Lederle FA, Kyriakides TC, Stroupe KT, Freischlag JA, et al. Open versus Endovascular Repair of Abdominal Aortic Aneurysm. N Engl J Med. 2019;380(22):2126–2135. — PubMed PMID: 31141634
  21. Bicknell CD, Kiru G, Falaschetti E, Powell JT, et al. An evaluation of the effect of an angiotensin-converting enzyme inhibitor on the growth rate of small abdominal aortic aneurysms: a randomized placebo-controlled trial (AARDVARK). Eur Heart J. 2016;37(42):3213–3221. — PubMed PMID: 27371719
  22. Meijer CA, Stijnen T, Wasser MN, Hamming JF, et al. Doxycycline for stabilization of abdominal aortic aneurysms: a randomized trial. Ann Intern Med. 2013;159(12):815–823. — PubMed PMID: 24490266
  23. Baxter BT, Matsumura J, Curci JA, McBride R, et al. Effect of Doxycycline on Aneurysm Growth Among Patients With Small Infrarenal Abdominal Aortic Aneurysms: A Randomized Clinical Trial. JAMA. 2020;323(20):2029–2038. — PubMed PMID: 32453369
  24. Pasternak B, Inghammar M, Svanström H. Fluoroquinolone use and risk of aortic aneurysm and dissection: nationwide cohort study. BMJ. 2018;360:k678. — PubMed PMID: 29519881
  25. Sakalihasan N, Michel JB, Katsargyris A, Kuivaniemi H, et al. Abdominal aortic aneurysms. Nat Rev Dis Primers. 2018;4(1):34. — PubMed PMID: 30337540
  26. Kent KC, Zwolak RM, Egorova NN, Riles TS, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg. 2010;52(3):539–548. — PubMed PMID: 20630687
  27. Morris DR, Biros E, Cronin O, Kuivaniemi H, et al. The association of genetic variants of matrix metalloproteinases with abdominal aortic aneurysm: a systematic review and meta-analysis. Heart. 2014;100(4):295–302. — PubMed PMID: 23813847

PubMed Topic Searches

  1. PubMed: Abdominal aortic aneurysm screening
  2. PubMed: Abdominal aortic aneurysm rupture risk
  3. PubMed: Endovascular aneurysm repair trials
  4. PubMed: Drug trials on aneurysm growth

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