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Fleming C, Whitlock E, Beil T, et al. Primary Care Screening for Abdominal Aortic Aneurysm [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2005 Feb. (Evidence Syntheses, No. 35.)

  • This publication is provided for historical reference only and the information may be out of date.

This publication is provided for historical reference only and the information may be out of date.

1Introduction

Primary Care Screening for Abdominal Aortic Aneurysm

An abnormal bulging of the abdominal aorta, called an abdominal aortic aneurysm (AAA), is a serious condition that often leads to death. The normal diameter of the aorta below the take-off of the renal arteries is approximately 2.0 cm. By consensus, an AAA is present when the infrarenal diameter exceeds 3.0 cm.1 Based on US vital statistics data, aortic aneurysms accounted for approximately 15 000 deaths in the year 2000.2 Abdominal aortic aneurysms account for approximately 9000 of these deaths, and the remainder are related to thoracic aneurysms.3 These estimates also include operative mortality from elective AAA repair. These figures may underestimate the true mortality rate due to AAA. Since the majority of those with ruptured AAAs die before reaching a hospital, 4 these sudden deaths may be attributed to other causes.5

The prevalence of AAAs found in population-based ultrasound screening studies from various countries ranges from 4.2–8.8% in men, and 0.6–1.4% in women.6–12In a screening study of 126 696 US veterans, 97% of whom were male, the prevalence of AAAs rose 1.99% at 55–59 years to 4.75% at 65–69 years to 5.95 at 75–79 years.13 The peak of the age-prevalence curve for AAAs in women occurs about ten years later than for men.14

Risk factors for an AAA include age, a history of regular smoking, family history, coronary artery disease, hypercholesterolemia, hypertension, and cerebrovascular disease.13, 15 Significant negative risk factors include female gender, diabetes mellitus, and black race. Although women with AAA are on average older than men with AAA, the increased risk associated with age, smoking, and family history are similar for women and men.

Almost all deaths from ruptured AAAs occur after the age of 65 years.14, 16 The highest mortality rates for AAA are found in white males over 65 years, and increase rapidly from 60 per 100 000 at ages 65–74 to 160 per 100 000 at age 85 and older.3 AAA-related death rates in white females, black females, and black males are about one-third less at the same ages. Most AAA-related deaths in men occur before the age of 80 and most AAA-related deaths in women occur after the age of 80.14

Although age-adjusted death rates for AAA have remained stable in the US over the last several decades, studies based on hospital discharge data indicate an increasing rate of interventions for AAAs.17 Based on US National Hospital Discharge Survey data,3 the rate of hospital discharges for a first-listed AAA diagnosis in those aged 65 years or older rose from 11.2 per 100 000 in 1979 and to 20.5 per 100 000 in 1984, and remained steady from 1984 through 1992. The rate per 100 000 of surgical AAA repairs also rose by the same proportion over this period. Several retrospective population cohort studies from Europe have cited similar findings as support for a possible increase in the true incidence of AAA, but note that increasing use of diagnostic ultrasound over time, changes in coding of death registry data, and aging of the population may also contribute to this increase.18–20

The prognosis for ruptured AAAs is grim. In community-based studies, an estimated 59 to 83% of patients with ruptured AAAs die out-of-hospital or prior to surgery.4 The operative mortality (in-hospital or 30-day) of those who survive to surgery was estimated to be 41% in the year 2000.21 Thus, at most 10–25% of individuals with ruptured AAAs survive to hospital discharge.

The pathogenesis of AAA formation is complex and multifactorial.22 The aorta is an elastic vessel, which primarily depends on elastin and collagen in the vessel wall for support. Physiological remodeling of the aortic wall maintains the integrity of the vessel wall over time. AAA seems to form after a breakdown in this process diminishes the elasticity of the aorta. The aorta becomes inflamed as macrophages and lymphocytes infiltrate the vessel wall, which then accelerates pathologic changes in the vessel wall. Proposed triggers for the inflammatory process include elastin degradation products in the vessel that attract macrophages, autoimmune responses, infectious agents, or damage from free-radicals. Familial clustering of AAAs suggests that their formation may also be influenced by genetics. Biomechanical forces may then expand the aorta to form an aneurysm.

The pathogenesis of AAA formation appears to differ from that of atherosclerosis in other vessels. From 1979 to 1990, age-adjusted death rates for AAA in the US remained unchanged.3 By contrast, deaths rates for both cardiovascular and cerebrovascular disease have declined rapidly over the past several decades.23, 24 The finding that the association between smoking and AAA-related mortality is 2.5 times greater than for smoking and cardiovascular disease mortality also favors this hypothesis.25

The strongest predictor of rupture risk for AAAs is maximal diameter. 26, 27 The natural history of AAAs ≥ 5.5 cm is difficult to determine since most large aneurysms are surgically repaired. In a 5-year prospective study of 198 male veterans with large AAAs who refused or were unfit for surgery, one-year incidence rates of rupture were 9.4% for 5.5–5.9 cm AAAs; 10.2% for 6.0–6.9 cm AAAs; and 32.5% for AAAs ≥ 7.0 cm.28 A rapid rate of aneurysm expansion > 1 cm/year is also commonly used in decision making about elective repair of AAAs <5.5 cm, however, the predictive value of expansion as an index of rupture risk is less clear.17

Estimates of the rupture risk for AAAs < 5.5 cm from population and cohort studies range from 0.3% to 5.3% per year,26, 27, 29, 30 and may be related to current management practices. Two recent clinical trials compared immediate surgical repair to surveillance with delayed repair for individuals with 4.0–5.4 cm AAAs. The one year incidence rate of rupture was 0.6–1.0% for those undergoing surveillance, although over five years, two-thirds of patients being surveyed underwent surgical repair because of aneurysm expansion.31, 32 AAAs < 4.0 cm rarely rupture.26, 33, 34

In 1996, the United States Preventive Services Task Force found insufficient evidence to recommend for or against routine screening of asymptomatic adults for abdominal aortic aneurysm (AAA) either with abdominal palpation or ultrasound.35 The USPSTF recognized that selective screening of high-risk patients might be beneficial, for example, in men with peripheral vascular disease or a family history of AAA. The USPSTF stated that at the time, however, no direct evidence showed that screening for AAA reduces mortality or morbidity in any population.

Since 1996, four large trials of population-based screening for AAA have been reported.11, 14, 36, 37 The purpose of this review is to update the evidence on the effectiveness of AAA screening since the second United States Preventive Services Task Force considered it in 1996.

Cover of Primary Care Screening for Abdominal Aortic Aneurysm
Primary Care Screening for Abdominal Aortic Aneurysm [Internet].
Evidence Syntheses, No. 35.
Fleming C, Whitlock E, Beil T, et al.

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