Annals of Vascular Surgery
Volume 22, Issue 1 , Pages 37-44, January 2008

Analysis of Expansion Patterns in 4-4.9 cm Abdominal Aortic Aneurysms

Department of Angiology and Vascular Surgery, Hospital de Galdakao-Usansolo, Barrio Labeaga S/N, 48960 Galdakao-Usansolo (Bizkaia), Spain

published online 17 December 2007.

Article Outline

Our objective was to analyze the growth pattern of 4-4.9 cm infrarenal abdominal aortic aneurysms (AAAs). We used an observational, longitudinal, prospective study design. We followed 4-4.9 cm AAAs with 6-monthly abdominal computed tomographic (CT) scans (January 1988-August 2004). AAA growth was defined as an increase in aortic diameter ≥2 mm in each surveillance period. We established the aortic expansion pattern in AAA with three or more CT scans as continuous, discontinuous. The latter includes at least one period of nongrowth (<2 mm/6 months). We studied the influence of cardiovascular risk factors (CVRFs), comorbidity, and AAA anatomical characteristics using the chi-squared test, t-test, life tables, and Kaplan-Meier for statistical analysis. We included 195 patients: 183 (93.8%) men, age 71 ± 8.3 years (50-90). The follow-up period was 50 ± 36.4 months (6.5-193.7). The growth pattern (n =131) was continuous in 15 (11.5%) and discontinuous in 116 (88.5%) AAA. The mean expansion rate was higher in AAAs with continuous expansion (7.92 ± 3.74 vs. 2.74 ± 2.94 mm/year, p < 0.0001). No CVRFs or comorbidity influenced the expansion pattern (p > 0.05). The eccentric thrombus was associated with a greater incidence of continuous growth (p = 0.05), with no influence of aortic calcification (p > 0.1). The expansion of 4-4.9 cm AAA is mostly irregular and unpredictable. We have not found any modifiable risk factors which influence their growth pattern. The eccentric distribution of the thrombus is associated with continuous expansion.

 

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Introduction 

The growth rates of small abdominal aortic aneurysms (AAAs) have been established as 3-6.9 mm/year.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 This is a practical way of evaluating AAA expansion and rupture risk, but it assumes a linear or at least a continuous and stable pattern of growth. However, AAAs have been reported to grow exponentially or even irregularly rather than linearly,4, 6, 8, 9, 10, 12, 13, 14 although there is only very limited evidence on this issue.

There is currently much debate on the best management for patients with small (<5 cm) AAAs. The UK Small Aneurysm Trial (UKSAT) and the Aneurysm Detection and Management Trial (ADAM) recommended conservative treatment due to very small rupture risk in 4-5.5 cm AAAs.15, 16 Two trials comparing surveillance versus endovascular aortic repair (EVAR) for small AAAs are currently being conducted (Comparison of Surveillance vs. Aortic Endografting for Small Aneurysm Repair [CAESAR] in Europe and PIVOTAL in the United States),17 and their results are expected by the end of 2007.

Besides defining AAA growth rates and possible influencing factors, in order to accurately learn about the natural history of AAAs, to help predict AAA enlargement, and to make precise surgical or endovascular indications, we believe it is important to study the pattern of growth of these small AAAs.

The objective of our study was to establish the growth pattern in our series of 4-4.9 cm AAAs. We also analyzed some clinical and anatomical factors which may have influenced these expansion patterns.

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Patients and Methods 

This is an observational, prospective study, run from January 1988 until August 2004. We followed 195 consecutive patients diagnosed with a 4-4.9 cm asymptomatic infrarenal AAA. We included in the study all patients with 4-4.9cm infrarenal AAAs who were followed for at least 6 months (two or more consecutive scans). Our exclusion criteria included <4 cm and ≥5 cm AAA, location of the AAA other than infrarenal (juxtarenal, suprarenal, thoracoabdominal aneurysms), follow-up fewer than two CT scans, and symptomatic aneurysms. All the patients were followed until surgery or death. AAAs were repaired when they reached a 5 cm diameter, they suffered a >1 cm/year expansion, or they became symptomatic. No patients were lost to follow-up.

We registered demographic data, clinical characteristics, the usual cardiovascular risk factors (tobacco use, hypertension, diabetes mellitus, and hypercholesterolemia), and other comorbidities which could influence aneurysm expansion, such as chronic obstructive pulmonary disease (COPD), coronary artery disease (CAD), cerebrovascular disease, peripheral artery disease (PAD), chronic renal failure, or cancer.

We only included active smokers in the category of “tobacco use.” Patients were regarded as hypertensive when they were being treated (diet or medication) or their blood pressure was registered above 140/90 twice in basal conditions. We included complete blood tests in the study of all our patients. Diabetes mellitus was defined if the blood glucose was ≥126 mg/dL or if the patient was already being treated by an endocrinologist (diet, oral hypoglucemiants, insulin). Hypercholesterolemia was defined as total basal cholesterol levels ≥200 mg/dL, low-density lipoprotein levels ≥100 mg/dL, or the patient's receiving specific medication or a supervised diet.

COPD was diagnosed when maximal voluntary ventilation (MVV) was <80% or the patient was already under treatment. Chronic renal failure was defined as serum creatinine ≥1.5 mg/dL. PAD was diagnosed when the patient complained of ischemic symptoms and had an ankle-brachial index (ABI) <0.90. We routinely performed a carotid duplex scan on all the patients. We considered that cerebrovascular disease was present when we detected an asymptomatic significant (>50%) carotid stenosis or the patient had a positive history of transient ischemic attack or minor or major stroke.

All the patients were followed with an abdominopelvic contrast computed tomographic (CT) scan every 6 months. We measured the greatest transverse and anteroposterior outer diameters of the infrarenal abdominal aorta perpendicular to the aortic axis. All scans were performed in the Department of Radiology of our center, evaluated by two radiologists blind to previous CT scans, and reevaluated by one staff member of our Department of Vascular Surgery. The CT scans were routinely performed at 8 and 5 mm slices.

We registered the serial AAA diameters in each patient. We calculated the mean aneurysm growth by dividing the total growth (mm) throughout the follow-up by the number of years of follow-up for every patient. We expressed the mean growth ± standard deviation (SD) in the complete series and in each group. We also registered the number and percentage of patients whose AAA reached 5 cm, and we calculated the mean number of months it took to reach this surgical size.

In order to establish a growth pattern, we need at least three consecutive AAA size measurements. We classified the expansion pattern as continuous (group CG) or discontinuous (group DG) (Fig. 1). We defined AAA growth for each observation period (6 months) as an increase in aortic diameter ≥2 mm. We consider a 1 mm difference in AAA size between two consecutive CT scans as a possible margin of error of the image technique. The continuous growth pattern implies an increase in AAA diameter ≥2 mm in each consecutive CT scan. This pattern includes a linear expansion, when the growth rate remains stable throughout the follow-up, and an exponential pattern, when the expansion rate increases constantly with every control. The discontinuous growth pattern includes at least one period of nongrowth (<2 mm/6 months) throughout the follow-up (Fig. 1).

We retrospectively revised the follow-up CT scans in order to analyze the influence of certain AAA anatomical characteristics on the aneurysm growth pattern. We specifically evaluated the presence or absence of intraluminal thrombus (ILT) as well as its location (concentric vs. eccentric). The thrombus was considered concentric when it encircled and fully covered the aortic wall in all quadrants, with no direct contact between the lumen and the AAA wall. It was considered eccentric when it did not cover all the quadrants of the wall (Fig. 2). We quantified the calcification of the aortic wall in three different sites: the aortic neck, the area of maximum diameter of the AAA, and the aortic bifurcation. We classified aortic wall calcification as minimal (<10% of the aortic circumference), moderate (10-50%), and severe (>50%) (Fig. 2).

We performed a descriptive statistical analysis, using the mean ± SD for quantitative variables and the number and percentage of patients for nominal variables. The expansion rates follow a normal distribution, as assessed by the Kolmogorov-Smirnov statistical test (p < 0.001). Averages were compared with the independent-samples t-test, and proportions were compared with the chi-squared test and Fisher's exact test. We also used life tables, Kaplan-Meier, and univariate Cox regression. The patient information was introduced in a FileMaker Pro 6 (File Maker, Inc. www.filemaker.com) database, and the statistical analysis was performed using SPSS 10.0 software (www.spss.com). We accepted p < 0.05 as significant.

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Results 

We followed a total of 195 4-4.9 cm AAAs in our center. The clinical characteristics of the series are reflected in Table I. The mean initial AAA size was 42.5 ± 2.8 mm (40-49). The mean follow-up period was 50 ± 36.4 months (6.5-193.7). During the follow-up, 49 patients (25.1%) died, one (0.5%) after AAA elective repair and two (1%) because of AAA rupture. One additional AAA ruptured during the follow-up at size 5.6 cm in a patient who was considered unfit for elective surgery due to severe CAD and who survived the urgent AAA repair. The survival rates were 98.9% at 1 year, 94.1% at 2 years, and 75.1% at 5 years (Fig. 3). The mean expansion rate for the overall group was 3.95 ± 6.02 mm/year (0-48). Half of the AAAs (n = 103, 52.8%) reached ≥5 cm throughout the follow-up, in a mean time of 23.6 ± 18.3 months (6-78.3). At 1, 2, and 5 years, the rates of AAA which remained small (<5 cm) were 83.6%, 60.9%, and 29.8%, respectively (Fig. 3).

Table I. Clinical characteristics of the series (n = 195)
n%
Age (range)71 ± 8.3 years (50-90)
Gender (M/F)183/1293.8%/6.2%
Tobacco use6533.3%
HT10654.4%
Diabetes mellitus2814.4%
Hypercholesterolemia5729.2%
CAD8845.1%
COPD6734.4%
CRF3819.5%
PAD7236.9%
Carotid artery disease3417.4%
Neoplasia4322.1%

HT, arterial hypertension; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; PAD, peripheral artery disease.

  • View full-size image.
  • Fig. 3 

    Survival rates of the patients included in the study (unbroken line) and curve of the AAAs which remained small (<5 cm) throughout the follow-up (broken line) (n = 195) (statistical analysis life tables).

We had only two follow-up CT scans of 64 (32.8%) AAAs. Thirty of these (46.9%) had suffered no expansion (0-1 mm) in the interval between the two controls, and the other 34 (53.1%) had undergone ≥2 mm growth. We obtained three or more CT scans of the rest (n = 131, 67.2%) of the AAAs included in the series. The growth pattern was continuous (group CG) in 15 (11.5%) and discontinuous (group DG) in 116 (88.5%) patients. There was no expansion at all throughout the follow-up in eight (10.5%) AAAs. The patients in group CG included 10 (7.7%) AAAs with linear expansion and five (3.8%) with exponential growth. The AAAs included in group DG experienced a single period (≥6 months) of nongrowth in 87 (75%) patients and several periods of 6-month stability in 29 (25%) cases. The mean time of nongrowth in group DG was 20 ± 11.6 months (6-60), with a median of 18 months and a mode of 12 months.

The mean growth rate was significantly greater in group CG (7.92 ± 3.74 vs. 2.74 ± 2.94 mm/year, p < 0.0001). All 15 (100%) AAAs reached 5 cm in group CG and only 66 (56.9%) in group DG (relative risk [RR] = 1.23, 95% confidence interval [CI] 1.11-1.36; p = 0.001). The AAAs which remained small (<5 cm) in groups CG and DG were 73.3% and 84.4% after 1 year, 20% and 64.7% after 2 years, and 6.7% and 26.9% after 5 years, respectively. There is a very significant difference between both groups (hazard ratio [HR] = 2.77, 95% CI 1.57-4.89; p = 0.0004) (Fig. 4). The time it took for the AAAs which enlarged up to ≥5 cm to reach this surgical size was similar in both groups (22.1 ± 17.8 vs. 25.2 ± 18.3 months, p = 0.56).

  • View full-size image.
  • Fig. 4 

    Curves of the AAAs which remained small (<5 cm) throughout the follow-up in groups CG (n = 15) and DG (n = 116) (statistical analysis Kaplan Meier, univariate Cox regression).

We analyzed the influence of the cardiovascular risk factors and comorbidities on the AAA growth pattern and found no influence of any of them (p > 0.05) (Table II).

Table II. Analysis of the AAA growth pattern (– group CG vs. group DG) according to gender, cardiovascular risk factors, and comorbidities (n = 131) (statistical analysis chi-squared, Fisher's exact test, t-test)
Group CG (n = 15)Group DG (n = 116)p
Age (years)69 ± 6.472 ± 7.70.16
Gender (M/F)15 (100%)/0 (0%)108 (93.1%)/8 (6.9%)0.29
Tobacco use6 (40%)37 (31.9%)0.53
HT9 (60%)64 (55.2%)0.72
Diabetes mellitus1 (6.7%)15 (12.9%)0.49
Hypercholesterolemia3 (20%)38 (32.8%)0.32
CAD7 (46.7%)57 (49.1%)0.86
COPD4 (26.7%)40 (34.5%)0.55
CRF3 (20%)23 (19.8%)0.99
PAD5 (33.3%)38 (32.8%)0.96
Carotid artery disease0 (0%)22 (19%)0.064
Neoplasia5 (33.3%)22 (19%)0.19

HT, arterial hypertension; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; PAD, peripheral artery disease.

We were able to retrieve the follow-up CT scans of only 90 patients, eight included in group CG and 82 in group DG. All 24 (100%) thrombus-free AAAs experienced a discontinuous growth pattern compared to 87.9% (n = 58) ILT-covered AAAs, although the difference did not reach statistical significance (p = 0.074). The eccentric distribution of the ILT, however, has been associated in our series with a greater incidence of continuous growth (p = 0.05) (Table III). The degree of aortic calcification, irrespective of its location within the AAA, has not proved any influence on the growth pattern (p > 0.1) (Table III).

Table III. Analysis of the AAA growth pattern (groups CG and DG) according to AAA anatomical characteristics (ILT, aortic calcification) (n = 90) (statistical analysis chi-squared)
Group CG (n = 8)Group DG (n = 82)p
ILT (n = 90)
Absence/presence0 (0%) / 8 (12.1%)24 (100%) / 58 (87.9%)0.074
Eccentric/concentric/no thrombus8 (14.8%) / 0 (0%) / 0 (0%)46 (85.2%) / 12 (100%) / 24 (100%)0.05
Aortic calcification (n=90)
Aortic neck
Minimum (<10%)3 (7%)40 (93%)0.79
Moderate (10-50%)4 (11.1%)32 (88.9%)
Severe (>50%)1 (9.1%)10 (90.9%)
AAA maximum diameter
Minimum (<10%)1 (4.3%)22 (95.7%)0.13
Moderate (10-50%)6 (15.8%)32 (84.2%)
Severe (>50%)1 (3.4%)28 (96.6%)
Aortic bifurcation
Minimum (<10%)1 (7.1%)13 (92.9%)0.78
Moderate (10-50%)5 (10.9%)41 (89.1%)
Severe (>50%)2 (6.7%)28 (93.3%)

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Discussion 

The growth rate of AAA is usually reported using the ratio of the difference between the final and the initial CT AAA diameters and the time interval in between (mm/year). However, this rate does not really express the natural history of the AAA, and it does not precisely predict the sequential changes in AAA size. Hirose et al.13 expressed the AAA growth curve as a monoexponential equation for electively repaired AAAs and a biexponential equation for AAAs which eventually ruptured. The former showed different growth rates both depending on the location of the aneurysm and during different time periods. The aneurysms which eventually ruptured showed a slow initial growth and a rapid expansion at about 3 months before rupture.14 Brady et al.8 noticed irregular AAA expansion in conservatively managed patients, especially those with the longest follow-up, and suggested a quadratic model rather than a linear one to describe the growth pattern. They also described a tendency of AAA expansion to accelerate with time. Stonebridge et al.9 described exponential AAA expansion, with growth rates increasing with AAA size. Vardulaki et al.4 assumed a linear or exponential growth pattern to describe the data in their series, although the study was not specifically designed to analyze this point. Cronenwett et al.12 reported a diameter increase of 10% yearly (0.4-0.5 cm/year) but found a high degree of individual patient variability in aneurysm expansion rate over time. Reed et al.18 and Delin et al.19 also reported variable growth rates during different time periods which could not be predicted by any given parameter.

This is the first study, to our knowledge, that has systematically evaluated the growth pattern of a complete cohort of infrarenal AAAs. We believe it reflects the spectrum of the disease and the natural history of 4-4.9 cm AAAs. This might be the only group of AAAs where this kind of study is feasible. It could be inappropriate to observe >5 cm AAAs in patients fit for elective repair, and the analysis of large AAAs managed conservatively because of the patients' comorbidities or refusal would only reflect a biased and incomplete sample. It could be done in 3-3.9 cm AAAs, but these AAAs are usually followed with ultrasound techniques, which are operator-dependent and convey a larger possible error of the aortic measurements, usually overestimating AAA size. CT has been repeatedly reported to be very accurate and reliable for the surveillance of AAA expansion, with intraobserver variation not exceeding 1 mm.12, 19, 20, 21 Our study proves that the expansion of small AAAs is mostly irregular and unpredictable. The growth pattern is characterized by periods of expansion and nongrowth. Only about 10% have shown continuous expansion up to AAA repair. Kurvers et al.6 reported a 77% rate of discontinuous expansion in a limited series of 52 3.1-6.5 cm AAAs. The mean duration of nongrowth in their patients was 15 months. The reason small AAAs behave in such a way remains unknown. There might be structural, metabolic, or inflammatory changes within the aortic wall which cause interrupted weakening and expansion.

Chronic inflammation, proteolysis, and degradation of the extracellular matrix are key factors in the development and evolution of AAA.8, 22, 23, 24 Increase in the production of matrix metalloproteinases (MMPs) 2 and 9 and decrease in elastin and collagen content have been associated with aortic wall weakening, AAA expansion, and rupture.6, 8, 25 Serum elastin peptides (SEPs), plasmin–antiplasmin complexes (PAP), and procollagen-IIIN-terminal propeptide (PIIINP) were independently associated with AAA expansion rate and could predict cases reaching 5 cm in diameter within 5 years in the reports of Lindholt et al.22, 26 Cystatin C, an inhibitor of cysteine proteases, has been linked to the development and growth of 4-5.5 cm aortic aneurysms.23 AAA expansion has also been correlated with indicators of chronic infection with Chlamydia pneumoniae.24, 27

The tension on the arterial wall is proportional to intraluminal pressure and radius and inversely proportional to wall thickness, according to Laplace's law. It has been used to explain AAA expansion.6 In Cronenwett et al.'s series12 increased pulse pressure was associated with increased AAA expansion. However, recent studies have not proved hypertension to have any significant effect on small AAA expansion,1, 3, 8, 28 and it did not influence the AAA growth pattern in our series. Kurvers et al.6 suggested that tension may build up gradually in an AAA wall with no change in diameter, and sudden expansion occurs when the tension overcomes the resistive shear stress, reaching a new balance which will again be broken when the wall tension increases once more, in a cycle comparable to plate tectonics and earthquakes.

Peak wall stress, which can predict AAA rupture risk fairly accurately, varies with the AAA diameter and shape and is influenced by blood pressure.13, 29, 30 However, it is not evenly distributed over the AAA wall, due mainly to the fact that AAAs are complex geometrical structures and the intraluminal pressure is not constant.13 The morphology of the ILT adds to this complexity. ILT has been reported to alter the AAA wall stress distribution and to reduce the AAA peak wall stress, with some contradictory results in different studies. It has been considered both a risk factor and a protective factor against AAA rupture.30, 31, 32, 33 The association we have found between the eccentric distribution of the thrombus and continuous expansion could be explained by the mechanical properties of the ILT, the irregular transmission of intraluminal pressure on the AAA wall. This reduction has been reported to be much greater in AAAs with concentric fully covering ILT compared to eccentric partially covering ILT.31 Wang et al.31 associated ILT with local weakening of the aortic wall, possibly from hypoxia, reducing the AAA wall strength and thus increasing rupture risk. ILT also has significant metabolic activity, being intimately linked to wall cell proliferation and inflammatory infiltrate and protein production, which might alter the local elastin and collagen degradation. Kazi et al.32 reported an upregulation of MMPs 1, 7, 9 and 12; urokinase plasminogen activator (uPA); uPA receptor; plasminogen activator inhibitor (PAI)-1; and cathepsin S with increased gelatinolytic activity in aortic thrombus-free wall. The thrombus-covered wall is usually thinner and contains fewer elastin fibers and smooth muscle cells but a greater T-cell and B-cell infiltration than thrombus-free wall. This suggests a chronic inflammatory process in the vessel wall, irregularly distributed and regulated depending on the presence or absence of mural thrombus. The ILT location was mostly eccentric in our series. Hans et al.33 also found that ILT is usually anterior and eccentric in both intact and ruptured AAAs. Eccentric ILT can be expected to alter the aortic wall in irregular patches and so influence the growth pattern.

The methods of quantification of abdominal aortic calcification vary in different published reports,34, 35, 36 and they include some complex and hardly reproducible calcification indexes. We used a simple and widely applicable method. We considered the possibility of the aortic calcification acting as a protective element against aortic expansion because it is likely to affect the distribution of wall stress, but no effect was proved on AAA growth pattern in our series.

Active smoking has been associated with faster AAA expansion in some studies8, 15, 23, 25, 28 but not in others,1, 3 and it has not been associated with continuous expansion in the present series. PAD and diabetes have repeatedly proved to slow down AAA growth,1, 8 but they have shown again no effect on the growth pattern of 4-4.9 cm AAAs. There was a tendency toward discontinuous AAA expansion in our patients with cerebrovascular disease (p = 0.064), but it did not quite reach statistical significance. Englund et al.3 and Chang et al.25 observed a significantly greater AAA growth rate in patients with a history of cardiac disease, but this comorbidity did not influence the AAA growth pattern.

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Conclusions 

The expansion of 4-4.9 cm AAAs is mostly irregular and unpredictable. A 6-month period of expansion does not necessarily imply additional continuous rapid growth. The expansion rates may differ greatly between one observational period and the next, but eventually almost half of them will reach a surgical size after 2 years and 70% after 5 years. The patients can be evaluated and prepared for elective AAA repair, but hasty surgical decisions cannot be made on the asumption that <5 cm AAAs expand linearly or exponentially and could cause an immediate threat. Operative decisions must be made according to AAA size, expectations of AAA growth, patient's overall health status, and life expectancy on an individual basis. We have not found any modifiable risk factors which influence the AAA growth pattern. The eccentric distribution of the ILT is associated with continuous expansion. The prospects of pharmacological treatment of small AAAs must be based on the knowledge and proper understanding of the natural history and biological process of AAA expansion.

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References 

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PII: S0890-5096(07)00357-3

doi:10.1016/j.avsg.2007.07.036

Annals of Vascular Surgery
Volume 22, Issue 1 , Pages 37-44, January 2008

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