Surgical Treatment of Abdominal Aortic Aneurysms

Definition

Most aortic aneurysms are true aneurysms, involving all layers of the aortic wall, and are infrarenal in location. As shown by Pearce and colleagues, normal aortic diameter gradually decreases from the thorax (28 mm in men) to the infrarenal location (20 mm in men). At all anatomic levels, normal aortic diameter is approximately 2 mm larger in men than in women and increases with age and increased body surface area. Because the average infrarenal aortic diameter was 2 cm for these patients, using a 3-cm definition for an infrarenal AAA was recommended, without the need to consider a more complicated definition based on factors such as gender or body surface area. Although such definitions are useful for large patient groups, in clinical practice with individual patients it is more common to define an aneurysm based on a greater than or equal to 50% diameter enlargement compared with the adjacent, nonaneurysmal aorta. This is particularly true for patients with unusually small arteries, in whom even a 2.5-cm local dilation of the infrarenal aorta might be aneurysmal if the adjacent aorta were only 1.5 cm in diameter.

Decision-Making for elective abdominal aortic aneurysm repair

The choice between observation and elective surgical repair of an AAA for an individual patient at any given point should take into account (1) the rupture risk under observation, (2) the operative risk of repair, (3) the patient’s life expectancy, and (4) the personal preferences of the patient. Two randomized trials have provided substantial information to assist with this decision-making process. The United Kingdom (UK) Small Aneurysm Trial was the first randomized trial to compare early surgery with surveillance of 4- to 5.5-cm diameter AAAs in 1090 patients aged 60 to 76. Those undergoing surveillance underwent repeat ultrasound every 6 months for AAAs 4 to 4.9 in diameter cm and every 3 months for those 5 to 5.5 cm. If AAA diameter exceeded 5.5 cm, the expansion rate was more than 1 cm per year, the AAA became tender, or repair of an iliac or thoracic aneurysm was necessary, elective surgical repair was recommended. At the initial report in 1998, after a mean 4.6 years of follow-up, there was no difference in survival between the two groups. After 3 years, patients who had undergone early surgery had better late survival, but the difference was not significant. It was notable that more than 60% of patients randomized to surveillance eventually underwent surgery at a median time of 2.9 years. The rupture risk among those undergoing careful surveillance was 1% per year.

In 2002 the UK trial participants published results of long-term follow-up. At 8 years there was a small survival advantage in the early surgery group (7.2% improved survival). However, the proportion of deaths caused by rupture of an unrepaired AAA was low (6%). The early surgery group had a higher rate of smoking cessation, which may have contributed to a reduction in overall mortality. An additional 12% of surveillance patients underwent surgical repair during extended follow- up, to bring the total to 74%. Fatal rupture occurred in only 5% of men but 14% of women in the surveillance group. Risk of rupture was more than four times higher for women than for men. This prompted the participants to recommend a lower diameter threshold for elective AAA repair in women.

The Aneurysm Detection and Management (ADAM) study conducted at US Department of Veterans Affairs (VA) hospitals was published in 2002. In this trial 1163 veterans (99% male) aged 50 to 79 with AAAs 4- to 5.4-cm diameter were randomized to surveillance versus early surgery. Surveillance entailed ultrasound or CT scan every 6 months with elective surgery for expansion to 5.5 cm, expansion of greater than 0.7 cm in 6 months or greater than 1 cm in 1 year, or development of symptoms attributable to the AAA. CT was used for the initial evaluation with AAA diameter defined as the maximal cross-sectional measurement in any plane that was perpendicular to the aorta. Ultrasound was used for the majority of surveillance visits, but CT was used when the diameter reached 5.3 cm. Patients with severe heart or lung disease were excluded, as were those who were not likely to comply with surveillance. As in the UK trial, there was no survival difference between the two strategies after a mean follow-up of 4.9 years. Similarly, greater than 60% of patients in the surveillance arm underwent repair. Initial AAA diameter predicted subsequent surgical repair in the surveillance group, because 27% of those with AAAs initially 4 to 4.4 cm underwent repair during follow-up, compared with 53% of those with 4.5 to 4.9 cm and 81% of those with 5- to 5.4-cm diameter AAAs. Operative mortality was 2.7% in the early surgery group and 2.1% in the surveillance group. Rupture risk in those undergoing surveillance was 0.6% per year. This trial confirmed the results of the UK trial, demonstrating the lack of benefit of early surgery for AAAs 4 to 5.5 cm even if operative mortality is low. Compliance with surveillance was high in both trials. Furthermore, Ouriel and colleagues reported results of 728 patients who were randomized to either ultrasound surveillance or early endovascular aneurysm repair (EVAR). Mean follow-up of 20 ± 12 months demonstrated no difference in AAA rupture, aneurysm-related death, or overall mortality between groups.

Taken together, these two large randomized studies indicate that it is generally safe to wait for AAA diameter to reach 5.5 cm before performing surgery in select men who are compliant with surveillance, even if their operative mortality is predicted to be low, even in the endovascular era. However, compliance in these carefully monitored trials of select patients was high. In another VA population, Valentine and colleagues reported that 32 of 101 patients undergoing AAA surveillance were not compliant despite several appointment reminders, and 3 or 4 of these 32 patients experienced rupture. In addition, the increased rupture risk for women seen in the UK trial highlights the need to individualize treatment on the basis of a careful assessment of individual patient characteristics (rupture risk, operative risk, life expectancy, and patient preferences).

Rupture risk

The importance of diameter in determining AAA rupture risk is universally accepted, initially on the basis of a pivotal study reported by Szilagyi and associates in 1966. These authors compared the outcome of patients with large (> 6 cm by physical examination) and small (< 6 cm) AAAs who were managed nonoperatively, even though at least one-half were considered fit for surgery in that era. During follow-up, 43% of the larger AAAs ruptured, compared with only 20% of the small AAAs, although the actual size at the time of rupture is unknown. This difference in rupture rate contributed to a 5-year survival of only 6% for patients with large AAAs compared with 48% for patients with small AAAs. These results were confirmed by Foster and colleagues in 1969, who reported rupture in 16% of AAAs less than 6 cm in diameter, compared with 51% for AAAs greater than 6 cm in patients managed nonoperatively. Modern imaging techniques were not available to accurately measure these aneurysms. Therefore it is likely that diameter was overestimated by physical examination, such that the “large” 6-cm AAAs in these studies were closer to 5 cm by current standards, although exact dimensions remain unknown. Nonetheless, the influence of size on AAA rupture risk was firmly established and has provided a sound basis for recommending elective repair for large AAAs, especially because both these studies demonstrated a marked improvement in survival after operative repair.

Autopsy studies have also demonstrated that larger AAAs are more prone to rupture. In an influential study from 1977, Darling and colleagues analyzed 473 consecutive patients who had an AAA at autopsy, of which 25% had ruptured. Probability of rupture increased with diameter: less than 4 cm, 10%; 4 to 7 cm, 25%; 7 to 10 cm, 46%; and greater than 10 cm, 61%. Sterpetti and associates confirmed these results in a more recent autopsy series of 297 patients with AAAs in which rupture had occurred in 5% of AAAs less than or equal to 5 cm in diameter; in 39% of 5- to 7-cm diameter AAAs; and in 65% of greater than or equal to 7-cm diameter AAAs. Although these autopsy studies have clearly shown the impact of relative AAA size on rupture rate, absolute diameter measurements at autopsy likely underestimate actual size because the aorta is no longer pressurized. Following rupture, size measurement is even more difficult because the AAA is no longer intact. Furthermore, autopsy series are biased toward patients with larger AAAs that rupture and more likely lead to autopsy than smaller AAAs in asymptomatic patients who die of other causes. Thus the rupture rates assigned to specific aneurysm diameters by autopsy studies likely overestimate true aneurysm rupture risk.

Further data regarding rupture risk were obtained from high-risk patients who were deemed too fragile to undergo elective repair. Lederle et al. published on a cohort ( n = 198) of VA patients who had AAAs of at least 5.5-cm diameter but were medically unfit for or refused operative repair. They were followed for a mean of 1.5 years during which 57% died. Aneurysm-related mortality was determined postmortem and reaffirmed once more that rupture risk correlates with aneurysm size and exponentially increased with increasing aortic diameter. The reported 1-year incidence of rupture was 9.4% for AAA diameter of 5.5 to 5.9 cm, 10.2% for AAA of 6.0 to 6.9 cm (19.1% for the subgroup of 6.5 to 6.9 cm), and 32.5% for AAA of 7.0 cm or greater, and 25.7% over 6 months only for AAA measuring 8.0 cm or larger.

The simple observation that not all AAAs rupture at a specific diameter indicates that other patient-specific and aneurysm-specific variables must also influence rupture. Several studies have used multivariate analyses to examine the predictive value of various clinical parameters on AAA rupture risk. The UK Small Aneurysm Trialists followed 2257 patients over the 7-year period of the trial, including 1090 randomized patients and an additional 1167 patients who were ineligible for randomization. There were 103 documented ruptures. Predictors of rupture using proportional hazards modeling (adjusted hazard ratio in parentheses) were: female sex (3), initial AAA diameter (2.9 per cm), smoking status (never smokers 0.65, former smokers 0.59—both vs. current smokers), mean blood pressure (1.02 per mm Hg), and lower forced expiratory volume in 1 second (FEV ₁ ) (0.62 per L). The mean diameter for ruptures was 1 cm lower for women (5 cm) compared with men (6 cm). By comparing patients with ruptured and intact AAAs at autopsy, Sterpetti and colleagues also concluded that larger initial AAA size, hypertension, and bronchiectasis were independently associated with AAA rupture. Patients with ruptured AAAs had significantly larger aneurysms (8 vs. 5.1 cm), more frequently had hypertension (54% vs. 28%), and more frequently had both emphysema (67% vs. 42%) and bronchiectasis (29% vs. 15%). Thus, in addition to AAA size, these reports strongly implicate hypertension, chronic pulmonary disease, female gender, and current smoking status as important risk factors for AAA rupture. Adding to these findings is a recent analysis of the Atherosclerosis Risk in Communities (ARIC) study, which recruited 15,792 participants between 1987 and 1989 and followed them through 2013. The authors noted that smoking, white race, sex, greater height, and greater low-density lipoprotein were associated with increased risk of clinically symptomatic or ruptured AAA.

Women are known to have smaller aortas than men. Intuitively, a 4-cm AAA in a small woman with a 1.5-cm diameter native aorta would be at greater rupture risk than a comparable 4-cm AAA in a large man with a native aortic diameter of 2.5 cm. However, the validity of this concept has not been proven. Ouriel and colleagues have suggested that a relative comparison between aortic diameter and the diameter of the third lumbar vertebra may increase the accuracy for predicting rupture risk, by adjusting for differences in body size. However, the improvement in prediction potential was minimal when compared with absolute AAA diameter and the relative risk of gender. A recent analysis of 23,245 patients with AAA in the UK National Vascular Registry found no sex-based difference in mortality from rupture. However, when checked against the UK Hospital Episode Statistics dataset, there was a slightly higher rate of in-hospital mortality following ruptured open AAA repair for women (33.6%) compared with men (27.1%, P < .001).

Because AAA diameter size by itself and other patient biochemical parameters remain unreliable in predicting AAA rupture, there is evolving work using computer-assisted biomechanical profiling of AAAs in an attempt to better predict AAA expansion and rupture. Wall stress measurements using finite element analysis, computational analysis, rupture index, rupture potential index, severity parameter, and geometric factors all may offer improved prediction of AAA expansion and rupture. However, to date, these novel predictive tools remain difficult to validate in vivo and are still some time away from widespread clinical use. Furthermore, the amount of aortic mural thrombus and the presence of aortoiliac outflow occlusive disease may raise the risk of aortic rupture, as evidenced by small series compiled by Moneta et al. ; however, more conclusive evidence yet remains elusive in this regard.

Although a positive family history of AAA is known to increase the prevalence of AAAs in other first-degree relatives (FDRs), it also appears that familial AAAs have a higher rupture risk. Darling and colleagues reported that the frequency of ruptured AAAs increased with the number of FDRs who have AAAs: 15% with two FDRs, 29% with three FDRs, and 36% with greater than or equal to four FDRs. Women with familial aneurysms were more likely (30%) to present with rupture than men with familial AAAs (17%). Verloes and colleagues found that the rupture rate was 32% in patients with familial versus 9% in patients with sporadic aneurysms and that familial AAAs ruptured 10 years earlier (65 vs. 75 years of age). These observations suggest that patients with a strong family history of AAA may have an individually higher risk of rupture, especially if they are female. However, these studies did not consider other potentially confounding factors, such as AAA size, which might have been different in the familial group. Thus further epidemiologic research is required to determine whether a positive family history is an independent risk factor for AAA rupture in addition to a risk factor for increased AAA prevalence.

In summary, AAA rupture risk requires more precise definition. Currently available data suggest the following estimates for rupture risk as a function of diameter: less than 4-cm AAAs, 0% per year; 4- to 5-cm AAAs, 0.5% to 5% per year; 5- to 6-cm AAAs, 3% to 15% per year; 6- to 7-cm AAAs, 10% to 20% per year; 7- to 8-cm AAAs, 20% to 40% per year; and greater than 8-cm AAAs, 30% to 50% over 6 months ( Table 37.1 ). For a given-sized AAA, sex, hypertension, chronic obstructive pulmonary disease (COPD), current smoking status, and wall stress appear to be independent risk factors for rupture. Family history and rapid expansion are probably risk factors for rupture, whereas the influences of thrombus content and diameter ratio remain less certain.

Expansion rate

Estimating expected AAA expansion rate is important to predict the likely time when a given AAA will reach the individual threshold diameter for elective repair. Expansion rate is most accurately represented as an exponential rather than a linear function of initial AAA size. Limet and colleagues calculated the median expansion rate of small AAAs to be e ^0.106t , where t equals years. For a 1-year time interval, this formula predicts an 11% increase in diameter per year, nearly identical to the 10% per year calculation reported by Cronenwett and colleagues in 1990. Several more recent studies have confirmed this estimate of approximately 10% per year for clinically relevant AAAs in the size range of 4 to 6 cm in diameter. In particular, a literature review by Hallin and colleagues found mean expansion rates of 0.33 cm/year for AAAs 3 to 3.9 cm, 0.41 cm/year for AAAs 4 to 5 cm, and 0.51 cm/year for AAAs greater than 5 cm. Studies that have identified small AAAs, usually through screening, suggest that the expansion rate may be less than 10% a year for AAAs smaller than 4 cm.

Although average AAA expansion rate can be estimated for a large population, it is important to realize that individual AAAs behave in a more erratic fashion. Periods of rapid expansion may be interspersed with periods of slower expansion. Chang and colleagues found that in addition to large initial AAA diameter, rapid expansion is independently associated with advanced age, smoking, severe cardiac disease, and stroke. The influence of smoking has been confirmed by others. The UK trialists showed that current smoking is predictive of more rapid expansion, whereas former smoking is not. In addition to these factors, hypertension and pulse pressure have been identified as independent predictors of a more rapid expansion rate. In the VA ADAM trial, 567 patients were randomized with small AAA to surveillance and followed. Risk factors for expansion specifically included elevated diastolic blood pressure and active smoking, whereas diabetes mellitus was protective of aneurysm expansion. Finally, Krupski and others have shown that increased thrombus content within an AAA and the extent of the aneurysm wall in contact with the thrombus are associated with more rapid expansion.

β-Blockade has been postulated to decrease the rate of AAA expansion. This was first demonstrated in animal models. Subsequent retrospective analyses in humans appeared to corroborate this. However, two subsequent randomized trials failed to demonstrate any reduction in growth rate with β-blockade. Furthermore, the randomized trial from Toronto demonstrated that patients taking β-blockers had worse quality of life and did not tolerate the drug well. Even when they analyzed only those who tolerated their medication, there was no effect of propranolol on AAA expansion rate.

The role of statin therapy in preventing AAA expansion and rupture has been the subject of ongoing work. Multiple studies have previously correlated dyslipidemia with coronary disease and peripheral vascular disease alike. Interestingly, it appears that the clinical salutary effects of statin therapy persist irrespective of their effect on lipid lowering. These presumptive “pleiotropic” effects appear to involve numerous events at the cellular level which may impact vascular wall biology and hence their potential benefit on AAA expansion and/or rupture. These effects may involve endothelial cells, smooth muscle cells, platelets, monocytes and macrophages, and finally inflammation. A meta-analysis by Takagi et al. collectively pooled 697 patients from five large observational studies in which patients with small AAA were grouped by statin therapy versus no statin therapy. Accordingly, the authors documented that the patients undergoing statin therapy demonstrated significantly diminished AAA expansion compared to the untreated group.

Doxycycline, 150 mg daily, was shown to slow the rate of AAA expansion in one small randomized trial, whereas roxithromycin, 30 mg daily, was shown to reduce expansion rate in another. These antibiotics have activity against Chlamydia pneumoniae , which has been shown to be present in many AAAs. Vammen and colleagues showed that antibodies to C. pneumoniae predicted expansion in small AAAs and suggested that antibody-positive patients may benefit from anti– C. pneumoniae treatment. Doxycycline has also been shown to suppress matrix metalloproteinase expression and to improve proteolytic balance in human AAAs and to reduce aneurysm formation in animal models. A pharmacologic systematic literature review of eight human studies concluded that the existing literature remains sparse (< 300 patients total) with multiple confounding variables that were uncontrolled, varying drug dosages, lack of compliance, and lack of sufficient follow-up to determine safety and efficacy of doxycycline in AAA patients and thus cannot recommend it for treatment. Further research in this area remains necessary before routine treatment with these antibiotics can be recommended routinely.

Elective operative risk

As expected, considerable variation in operative risk occurs among individual patients and depends on specific risk factors. A meta-analysis by Steyerberg and colleagues identified seven prognostic factors that were independently predictive of operative mortality after elective AAA repair and calculated the relative risk for these factors ( Table 37.2 ). The most important risk factors for increased operative mortality were renal dysfunction (creatinine > 1.8 mg/dL), congestive heart failure (CHF) (cardiogenic pulmonary edema, jugular vein distension, or the presence of a gallop rhythm), and ischemic changes on resting electrocardiogram (ECG) (ST depression > 2 mm). Age had a limited effect on mortality when corrected for the highly associated comorbidities of cardiac, renal, and pulmonary dysfunction (mortality increased only 1.5-fold per decade). This explains the excellent results reported in multiple series in which select octogenarians have undergone elective AAA repair with mortality comparable with younger patients.

On the basis of their analysis, Steyerberg and colleagues developed a clinical prediction rule to estimate the operative mortality for individual patients undergoing elective AAA repair ( Box 37.1 ). This scoring system takes into account the seven independent risk factors plus the average overall elective mortality for a specific center. To demonstrate the impact of the risk factors on a hypothetical patient, it can be seen that the predicted operative mortality for a 70-year-old man in a center with an average operative mortality of 5% could range from 2% if no risk factors were present to more than 40% if cardiac, renal, and pulmonary comorbidities were all present. Obviously, this would have a substantial impact on the decision to perform elective AAA repair. A similar Bayesian model for perioperative cardiac risk assessment in vascular patients has been reported by L’Italien and colleagues, which demonstrated the added predictive value of dipyridamole- thallium studies in patients with intermediate risk for cardiac death. This study also demonstrated the protective effect of coronary artery bypass surgery within the previous 5 years, which reduced the risk of myocardial infarction or death following AAA repair by 2.2-fold. Although this type of statistical modeling cannot substitute for experienced clinical judgment, it helps to identify high-risk patients who might benefit from further evaluation, risk factor reduction, or medical management instead of surgery if AAA rupture risk is not high.

The review of Hallin and colleagues supports the findings of Steyerberg that renal failure is the strongest predictor of mortality with a fourfold to ninefold increased mortality risk. Cardiac disease (a history of either coronary artery disease [CAD], CHF, or prior myocardial infarction) was associated with a 2.6- to 5.3-fold greater operative mortality risk. Older age and female gender appeared to be associated with increased risk, but the evidence was not as strong. Valuable data regarding predictors of operative risk have been generated by prospective trials. In the Canadian Aneurysm Study, overall operative mortality was 4.8%. Preoperative predictors of death were ECG evidence of ischemia, chronic pulmonary disease, and renal insufficiency. The randomized UK Small Aneurysm Trial found older age, lower FEV ₁ , and higher creatinine to be associated with mortality on univariate analysis. With multivariate analysis the effect of age was diminished, whereas renal disease and pulmonary disease remained strong predictors of operative mortality. The predicted mortality ranged from 2.7% for younger patients with below-average creatinine and above-average FEV ₁ to 7.8% in older patients with above-average creatinine and below- average FEV ₁ . The UK trial participants noted that the Steyerberg prediction rule did not work well for the UK trial patients. However, they did not gather information on a history of CHF (one of the strongest predictors in Steyerberg’s analysis) in the randomized UK trial. Female gender has also been found to be associated with higher operative risk in several population-based studies using administrative data. However, these databases may suffer from inaccurate coding of comorbidities and thereby lack of ability to fully adjust for comorbid conditions. Gender has not been found to be associated with operative mortality in prospective trials.

A study by Beck et al., from the Vascular Study Group of New England, assessed risk factors associated with 1-year mortality following open AAA repair and EVAR. In this study, 1387 consecutive patients underwent elective AAA repair in whom 748 underwent open repair and 639 underwent EVAR between 2003 and 2007. Consistent with other studies, factors independently associated with 1-year mortality following open AAA repair included age (> 70), COPD, chronic renal insufficiency (Cr > 1.8 mg/dL), and suprarenal aortic clamp site. Likewise, factors associated with 1-year mortality following EVAR included CHF and AAA diameter. One-year mortality correlated linearly with the number of risk factors present and, accordingly, should likely be factored into decision-making when considering elective AAA repair. This predictive model has since been externally validated and shown to be more sensitive and robust (C-statistic = 0.82) than other predictive models derived from Medicare or center-based datasets and is now widely available on handheld device applications and electronic medical records for real-time assessment of mortality risk for AAA patients at the time of decision-making regarding AAA repair.

Life expectancy

Assessment of life expectancy is crucial to determine if an individual patient will benefit from prophylactic repair of an AAA. Many patients with AAAs have been long-term smokers. Most AAA patients also have extensive comorbid disease, particularly CAD, COPD, hypertension, hyperlipidemia, cerebrovascular disease, and cancer. Many of these chronic conditions increase operative risk, as noted earlier. In addition, these factors impact life expectancy. Patients who survive elective AAA repair have a reduced life expectancy compared with age- and gender-matched populations. In 2001 Norman and colleagues reviewed 32 publications over 20 years that described long-term survival after AAA repair. They found that the mean 5-year survival after AAA repair was 70%, compared with 80% in the age- and gender-matched population without AAA. Predictors of late death after successful AAA repair include age, cardiac disease, chronic pulmonary disease, renal insufficiency, and continued smoking. The UK trial participants found (after adjustment for age, gender, and AAA diameter but not cardiac disease) that both FEV ₁ and current smoking status (plasma cotinine) predicted late death. Table 37.3 shows US census data that have been adjusted to reflect the life expectancy of an average patient surviving elective AAA repair. These numbers should be adjusted according to the relative severity of comorbid disease but may be used to guide clinical decision-making.

Surgical decision-Making

In patients with symptomatic AAAs, operative repair is nearly always appropriate because of the high mortality associated with rupture or thrombosis and the high likelihood of limb loss associated with peripheral embolism. Occasionally, high-risk patients or those with short life expectancies may choose to forego emergency repair of symptomatic AAAs, but in general, surgical decision-making for symptomatic AAAs is straightforward. A contemporary analysis of outcomes of symptomatic AAAs by De Martino et al. from the Vascular Study Group of New England assessed 2386 AAA repairs in whom 1959 were elective, 156 were symptomatic, and 271 were ruptured. EVAR was successfully performed in 945 elective patients, 60 symptomatic patients, and 33 ruptured AAA patients, respectively. The hospital mortality was 1.7% for elective AAA as compared with 1.3% for the symptomatic cohort. One- and 4-year survival was determined to be 83% and 68%, respectively, among the symptomatic group which compared favorably to the elective group with 89% and 73% 1- and 4-year survival.

For those with asymptomatic AAAs, randomized trials have provided assurance that the typical male patient can generally be safely monitored with careful ultrasound surveillance until the AAA reaches 5.5 cm, at which time elective repair can be performed. However, decision analyses and cost-effectiveness modeling have previously demonstrated that individual patient rupture risk, operative risk, and life expectancy need to be considered to determine the optimal threshold for intervention. Both the UK and ADAM trials excluded patients who were considered “unfit” for repair, highlighting the fact that those with high operative risk and short life expectancy should have a threshold diameter greater than 5.5 cm. In the UK trial, the rupture risk for women was 4.5-fold higher than for men, prompting the authors to recommend a lower threshold for women than men. It seems logical to consider other factors that may make rupture more likely during surveillance as well. In both randomized trials, 60% to 75% of patients undergoing surveillance eventually underwent AAA repair. In the UK trial, 81% of those with initial diameters 5 to 5.4 cm eventually underwent repair. Clearly, for many patients with this size AAA, the question is not whether to perform AAA repair but when. Therefore, in patients with AAA diameters approaching 5.5 cm whose life expectancy is expected to be more than 5 years and whose operative risk is estimated to be low, the patient should be informed that AAA repair would likely be required within the next few years. This subgroup of patients could be offered surgery at a time when it is convenient for them, with the understanding that waiting for expansion to 5.5 cm has little risk. In these cases, patient preference should weigh heavily in the decision-making process. For those with multiple risk factors for rupture, long life expectancy, and low operative risk, it would seem prudent to recommend AAA repair at less than 5.5 cm. In addition, the ability of the patient to comply with careful surveillance should be considered.

Although the recent randomized trials have provided a great deal of information to guide decision-making, clinicians should not adopt a “one-size-fits-all” policy for treating patients with AAA. Moreover, with a progressively aging population in mind, quality-of-life assessments should likely also be factored into decision-making analyses. Suckow et al. recently developed and validated a disease-specific quality- of-life instrument to assess the impact of aneurysm surveillance and repair on AAA patient quality of life. The instrument was found to be both sensitive and specific to determine quality of life in patients under surveillance for small AAA and for those who had undergone repair. Validation of the instrument, which is a patient survey, highlighted that few AAA patients are adequately educated about their pathology and thus lack insight into the natural history and subsequent treatment options. Furthermore, physicians play a critical role in educating patients and remain the primary source of information for them. With improved knowledge about AAA, a patient’s quality of life appears improved with regards to worry and stress. Furthermore, this work may implicate that the effect of AAA on patient quality of life could potentially be a factor to play into the shared decision-making process as it relates to how and when to repair a AAA. A prospective trial (Preferences for Open versus Endovascular Repair for Aortic Abdominal Aneurysm [PROVE-AAA] trial) is currently underway to investigate how education about aneurysm repair options affects patient preference for type of repair, and whether patient and physician preferences for the type of repair better align with patient education.

Preoperative assessment