Epidemiology
Epidemiology varies by region, age, ethnicity, and sex, with large screening studies offering the closest approximation. Prevalence among men is 4 to 6 times higher than in women.[1][14] Prevalence in the first 5 years of the UK National Health Service (NHS) AAA screening programme (2009-2013) was 1.34% (AAA >2.9 cm) among men invited for screening in their 65th year.[15]
According to data from the UK NHS AAA screening programme, of the 291,904 men eligible for their initial AAA screen between 1 April 2019 and 31 March 2020, 76.1% were screened by 31 March 2020 and 0.92% had an aneurysm. There were 8340 men aged over 65 who self-referred into the UK NHS AAA screening programme and 88.9% were screened by 31 March 2020; the aneurysm detection rate in self-referred men was higher than cohort men, at 3.8%.[16] Thirty patients who had AAA detected in this screening year had a subsequent ruptured AAA, 25 of which were fatal.[16]
A systematic review of studies reporting screen-detected AAA in women found that the pooled prevalence of AAA increased with age (>1% for women >70 years of age) and with smoking status (>1% for female ever-smokers; >2% for current smokers).[17] The prevalence of aneurysms among men increases by about 6% per decade of life.[13]
In the UK, deaths from AAA declined sharply from 1997 to 2009, with mortality in men aged >65 years falling from 65.9 to 44.6 per 100,000 population.[18] Admissions for ruptured AAA fell from 18.6 to 13.5 per 100,000 in all age groups. The reduction in mortality and admissions has been attributed to the fall in smoking prevalence and the rise in elective AAA repair in older age groups.[18]
Prevalence is low in Asian populations, though reaches that of Western populations when adjusted for cardiovascular risk factors.[19] Current data from the AAA screening programme in the UK show AAA to be more common in white British (and, in particular, white Irish) men than in black or Asian men.[20]
Risk factors
This is the risk factor most strongly associated with AAA.[1][3][9][13][14][22][23][24][25] Therefore, smoking cessation is key to management.[3][42]
Active cigarette smoking is independently associated with histological high-grade tissue inflammation.[43]
The duration of smoking is significantly associated with an increased risk in a linear dose-response relationship.[24] Each year of smoking increases the relative risk by 4%.[23]
Studies support a familial aggregation of and genetic predisposition to AAA.[1][3][13][25][44][45]
In a large population-based study, a positive first-degree family history for AAA was more common among cases than among controls (8.4% vs. 4.6%, P = 0.0001).[46] The risk of AAA associated with family history was approximately doubled compared with no family history (odds ratio [OR] 1.9, 95% CI 1.6 to 2.2).
A Swedish twin registry study found that the twin of a monozygotic twin with AAA had a risk of AAA approximately 70 times greater than that of the twin of a monozygotic twin without AAA.[39]
Aortic degeneration is accelerated in patients with Marfan syndrome and during pregnancy.[52][53][54][55][56]
Marfan syndrome specifically is associated with cystic medial necrosis of the aorta secondary to an autosomal dominant anomaly in fibrillin type 1, a structural protein that directs and orients elastin in the developing aorta.[52][53] As a result, the mature aorta demonstrates abnormal elastic properties, progressive stiffening, and dilation.[54]
Lipoproteins are elevated in patients with AAA independent of cardiovascular risk factors and extent of atherosclerosis.[57] Patients with AAA have a high incidence of genetically determined dyslipidaemia.[58]
AAA patients have significantly lower levels of apolipoprotein AI and HDL cholesterol than matched controls with aorto-iliac occlusive disease.[57]
High low-density lipoprotein (LDL) cholesterol is associated with a high risk of AAA, whereas high high-density lipoprotein (HDL) cholesterol is strongly associated with a low risk of AAA.[14] Statin therapy may reduce AAA growth rates and mortality.[59]
Hypertension may be a weak independent risk factor.[1][13][14][62] Patients taking blood pressure-lowering medications have a small reduction in risk of AAA repair or rupture.[63]
There is a relation between systolic blood pressure and AAA in women, and an association with previous or present use of antihypertensive medication and AAA risk for both sexes.[14]
One study of more than 12,000 men demonstrated an independent association between central obesity and AAA.[64]
Evidence suggests that diabetes protects against the growth and enlargement of AAA.[26][27] However, the protective mechanism is yet to be determined.[27][28] Operative and long-term survival is lower among AAA repair patients with diabetes than those without, suggesting an increased cardiovascular burden.[26][29]
Co-prevalence of aneurysms is common; 1 in 6 patients with a primary aneurysm also has another aneurysm elsewhere. Screening for AAA in patients with intracranial aneurysms may be clinically indicated and cost-effective.[68]
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