Abdominal Aortic Aneurysm

Abstract

An abdominal aortic aneurysm (AAA) is defined as a localized dilation of the artery that is 1.5 times the diameter of the normal segment. The most common location for an aortic aneurysm is the infrarenal segment where a diameter that exceeds 3 cm in diameter is considered aneurysmal. Duplex ultrasonography and spiral computerized tomography are the imaging modalities most commonly performed to detect the longitudinal and transverse diameter of the aorta. The prevalence of AAA may be increasing. Smoking, male gender, and increasing age are the most powerful predictors of AAA. Considering the higher prevalence of hypertension, it is surprising that the prevalence of AAA among African‐American men is 39% less than white men. The risk of rupture is independently associated with female gender, large initial aneurysm diameter, lower forced expiratory volume in the first second, current smoking, and higher mean blood pressure. Inflammation rather than atherosclerosis may be essential to the development of AAA. Treatment is directed at smoking cessation and control of blood pressure and lipids. Beta blockers (propranolol) have not been shown to modify aneurysm growth rates, but drop out rates in the studies have been high. Antibiotics do show a modest benefit. Surgery is generally performed when the aneurysm exceeds 5.5 cm in men. For women, an AAA size between 4.5 cm and 5.0 cm is recommended for elective repair.

Figure 1 displays an abdominal computerized tomography (CT) of a patient with a 6‐cm abdominal aneurysm. An abdominal aortic aneurysm (AAA) is conventionally defined as a segment of aorta that exceeds 3 cm in diameter or the ratio of the abnormal to normal segment of aortic diameter is 1.5 or greater. Most AAAs are infrarenal. Surgery is recommended when the diameter exceeds 5.5 cm. An undetected rupture is a recognized cause of sudden death. Hospital discharges since 1979 with a first‐listed diagnosis of an AAA with or without rupture are shown in Figure 2. ¹

Figure 1.

A 68‐year‐old obese male smoker with long‐standing, poorly controlled hypertension was examined for complaints of nonspecific abdominal cramps. No specific finding was observed on physical examination of the abdomen. A computerized tomographic scan of the abdomen was ordered. What is your diagnosis?

Figure 2.

Number of hospital discharges with a first‐listed diagnosis of abdominal aortic aneurysm (international classification of diseases 441.3 and 441.4). Adapted from Detailed Diagnoses and Procedures, National Hospital Discharge Survey, 1979–2000. Hyattsville, MD: National Center for Health Statistics; 2001.

PREVALENCE AND EPIDEMIOLOGY

Among 4734 men and women older than 65 years, the prevalence of AAA was 8.8%, ² and 87.7% of the AAAs were 3.5 cm or less. The incidence is reported to be increasing, which is in part due to technological improvements in detection and the aging population. ³ , ⁴

The prevalence of AAA for male veterans is displayed in Figure 3. Smoking, male gender, and increasing age are the most powerful predictors of AAA as detected by abdominal ultrasound. ⁵ The prevalence of an AAA 3.0 cm or greater was 4.3% among 122,272 men and 1.0% among 3450 women aged 50–79 years. ⁶ Considering the higher prevalence of hypertension, it is surprising that the prevalence of AAA among African‐American men is 39% less than white men (Figure 4). Although smoking accounts for 78% of the excess prevalence of AAA, other independent predictors include age, height, coronary artery disease, any atherosclerosis, hypercholesterolemia, hypertension, and family history. ⁵ In a case‐control study, smoking, male gender, diastolic blood pressure and family history were risk factors for AAA. ⁷ Of interest is that the prevalence of AAA is significantly less among patients with diabetes mellitus. ⁵ , ⁷

Figure 3.

Prevalence of abdominal aortic aneurysm 4.0 cm or greater detected by screening in male US veterans by age and smoking status. Adapted from Ann Intern Med. 1997;126:441–449. ⁵

Figure 4.

Prevalence of abdominal aortic aneurysm 4.0 cm or greater detected by screening in male US veterans by race and gender. Adapted from Ann Intern Med. 1997;126:441–449. ⁵

Over 24 months the rupture rate of a large AAA among 198 veterans who were unfit for surgery or who refused elective surgery was very high: 22.1% for an aneurysm diameter 5.5–5.9 cm (n=61), 18.9% for 6.0–6.9 cm (n=85), and 43.4% for ≥7.0 cm (n=52). ⁸ The risk of rupture is independently associated with female gender, large initial aneurysm diameter, lower forced expiratory volume in the first second (FEV₁) (poor pulmonary function), current smoking, and higher mean blood pressure. ⁹

The mortality associated with a ruptured AAA is high. The rate of death before admission was 50% among women and 41% among men (p=0.02). ¹⁰ For patients hospitalized with a ruptured aneurysm but not undergoing a surgical repair, the mortality rate was 37% for men and 63% for women (p=0.003). ¹⁰ Overall mortality is related to aneurysm diameter: 11% over 3 years for 3.0–4.1 cm (n=851), 17% for 4.2–4.7 cm (n=779), and 24% for 4.8–9.7 cm (n=675). ¹¹ A similar relationship exists with cardiovascular events.

PATHOGENESIS

AAAs are commonly viewed as atherosclerotic, although there are traumatic, hereditary (e.g., Marfan's and Ehlers‐Danlos syndromes), and infectious causes. ¹² Pulse pressure increases directionally from the thoracic aorta to the abdominal aorta. Hypertension has been viewed as a key factor in the development of AAA by alteration of endothelial permeability and connective tissue metabolism, pressure augmentation of the reflected pulse waves, and intimal injury. ¹² This could damage elastin and collagen. Growth of the AAA possibly follows the law of Laplace:

Wall stress=(Pressure × Radius) ÷ (2 × Wall thickness)

However, neither systolic nor diastolic blood pressure had an effect on aneurysm growth rates among 5032 men and women aged 65–79 years. ¹³

The role of atherosclerosis is being challenged. Proteolytic degradation of aortic wall connective tissues by increased local production of matrix metalloproteinases or other proteinases could destroy elastin and collagen. ¹⁴ Inflammatory cells are present, suggesting that chronic inflammation or an autoimmune response is a factor in destruction of the aortic wall. In addition, familial aggregation of AAA suggests that there are candidate genes that contribute to the development of AAA.

DETECTION

A pulsatile mass in the epigastrium can be detected by bimanual exam using each index finger to determine the width of the aorta. ¹⁵ Success at detection is enhanced by abdominal relaxation, lack of obesity, and focused effort by the examiner. In asymptomatic patients, the sensitivity of physical examination as assessed by ultrasonography is a function of the diameter of the aneurysm: 29% for 3.0–3.9 cm, 50% for 4.0–4.9 cm, and 76% for 5 cm or greater. ¹⁵ Interobserver agreement between two examinations is 77%. ¹⁶ Abdominal girth diminishes sensitivity. ¹⁶ The positive predictive value is only 43%.

Duplex ultrasonography and spiral CT are the imaging modalities most commonly performed to detect the longitudinal and transverse diameter of the aorta. Magnetic resonance imaging is an alternative imaging technique. ³ Biplane angiography may be performed before surgical intervention. It is most commonly used to define concomitant occlusive disease in patients with claudication or suspected renal artery involvement in patients with hypertension. The angiogram can be misleading because the image displays the internal lumen only rather than the true aneurysm diameter. CT scanning is increasingly being used as the alternative to angiography.

The repeatability of ultrasound measurements of aneurysm diameter is ±0.2 cm. ¹⁷ Of 258 paired measurements, the mean difference between CT and ultrasound was −0.119 (p<0.0001). ¹⁸ However, among 28% of the pairs, there was difference of 0.5 cm or greater. Blinded duplicate readings of CT measurements of AAA at a central laboratory differed by only 0.003 cm.

MEDICAL TREATMENT

Smoking amplifies the enlargement of AAA by 20%–25%. ¹⁹ Thus, smoking cessation is mandatory. There are limited data on the treatment of hypertension or lipids in modifying aneurysm growth rates.

The α‐Tocopherol, β‐Carotene Cancer Prevention (ATBC) study examined effects of α tocopherol and β carotene supplementation in male smokers (N=29,133) for cancer prevention and also evaluated outcome on cardiovascular diseases, including ruptured or nonruptured AAA. ²⁰ After 5.8 years of follow‐up, 181 men developed AAA. The incidence per 10,000 person‐years was 11.5 for placebo, 10.6 for α tocopherol, 11.8 for β carotene, and 8.6 for both antioxidants (p=0.52). Thus, antioxidants were not protective.

Two small, randomized, double‐blind studies examined the role antibiotics to reduce the growth rate of AAA. ²¹ , ²² Doxycycline 150 mg daily or placebo was given to 32 subjects with AAA 3.0–5.5 cm for 3 months. ²¹ After 18 months, the AAA in placebo group expanded by 3 cm compared with 1.5 cm in the doxycycline group (not significant). Between 6–18 months, the expansion rate was significantly less with doxycycline. Roxithromycin 300 mg daily or placebo was given to 92 subjects with a small AAA for 4 weeks. ²² After 1 year, the macrolide antibiotic reduced expansion rate by 43% compared with placebo (p=0.02), but no benefit was observed in the second year.

There are three reports using propranolol to reduce expansion of AAA. ²³ , ²⁵ In a 2‐year randomized, double‐blind study, 54 subjects with a small AAA were randomized to 40 mg propranolol twice daily or placebo. ²³ Sixty percent of the propranolol group and 25% in the placebo group dropped out due to side effects resulting in premature trial termination. There was no reduction in the expansion rate for the subjects who remained in the study. A larger study randomized 477 patients with an AAA 3.0–4.5 cm to either propranolol 40 mg or placebo dosed once daily. ²⁵ There was no difference in the growth rate of aneurysms according to treatment. A benefit was seen with propranolol for aneurysms 4.0 cm or greater. The Propranolol Aneurysm Trial was a multicenter, randomized, placebo‐controlled trial of 548 subjects with an AAA 3.0–5.0 cm. ²⁴ Propranolol 20–120 mg twice daily or placebo was titrated according to medication tolerance and heart rate. Forty‐two percent of patients in the propranolol group and 27% in the placebo group stopped their study medication. There was no difference in the aneurysm growth between the two groups after a mean follow‐up of 2.5 years; however, there were fewer elective aneurysm resections for patients who did not stop propranolol (p=0.02). In summary, for all these studies, compliance was poor and benefits were marginal. However, new trials need to be undertaken with long acting β blockers that are better tolerated.

SURGICAL TREATMENT

Two procedures are commonly performed for AAA: open repair with a polyester or expanded polytetrafluoroethylene graft and endovascular repair. ²⁶ Endovascular repair has reduced blood loss, fewer complications, and faster recovery than open repair, but it is not associated with improved survival after 2 years. ²⁷ One complication of endovascular repair is an “endoleak.” An endoleak is a poor seal at an attachment site (type I); retrograde filling of the aneurysm sac via a patent collateral, such as the inferior mesenteric or lumbar artery (type II); or device failure (types III and IV). The end result is exposure of the aneurysm sac to arterial pressure, leading to continued aneurysm expansion and possible rupture. This potential complication requires lifetime follow‐up after the repair. Whether endovascular repair is a durable procedure requires longer follow‐up.

Two important randomized studies assessed the affect of surveillance vs. immediate surgery in patients with AAA 4.0–5.5 cm. ¹⁷ , ²⁸ Both studies were similar in design. The United Kingdom Small Aneurysm Trial randomized 1090 asymptomatic patients aged 60–76 years to either early open prosthetic inlay graft surgery or surveillance by ultrasound for 3–6 months. ¹⁷ Surgery was recommended to the surveillance group if the AAA exceeded 5.5 cm, became tender, or enlarged greater than 1 cm per year. The average follow‐up was 4.6 years for the primary end point of total mortality. The 30‐day operative mortality was 5.8%. The 30‐days operative mortality was 7.1% for the 321 (61%) patients in the surveillance group who underwent surgical repair. There was no difference in overall total mortality between the two groups. After 8 years of follow‐up there was a significant survival advantage of immediate surgical repair compared with surveillance (p=0.05). ²⁹ This surgical advantage, however, may have been related to smoking cessation or other lifestyle changes.

The Aneurysm Detection and Management Study randomized 569 veterans aged 50–79 years to immediate open surgical repair or surveillance by ultrasound or CT. ²⁸ Surgery was performed in 62% the surveillance group, using similar guidelines as the United Kingdom Small Aneurysm Trial. The average follow‐up was 4.9 years. There was no difference in overall mortality. The 30‐day operative mortality in immediate operative group was 2.0%, which was similar to the surveillance group.

New guidelines for the treatment of AAA recognize 5.5 cm as a threshold for surgery for the “average” patient. ²⁶ However, for women, an AAA size 4.5 cm–5.0 cm is recommended for elective repair. Patient preference should also be considered for AAA 4.5 cm–5.5 cm if the surgeon's operative mortality is low. When anatomy is appropriate, endovascular repair is appropriate treatment for patients at high risk for an open aneurysm repair.