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Dr. Ignacio Bluro
Dr. Fernando Garagoli
Dr. Norberto Fiorini
Dr. Rodolfo Pizarro
Clinical knowledge pertaining to the prevention of the development and rupture of abdominal aortic aneurysm (AAA) is essential in daily medical practice, given the significant prevalence of this pathology and its impact on public health. As smoking is considered the main risk factor in its pathogenesis, anti-smoking advice is crucial in preventing the development of this disease. Smoking cessation, adequate control of arterial blood pressure and pharmacological intervention are the mainstays of delaying the growth of AAA. Echographic screening of high-risk groups and surveillance of small AAAs are fundamental to prevent AAA rupture.
Keywords: aneurysm, abdominal aorta, prevention, smoking, screening
Abdominal aortic aneurysm (AAA) is a pathology that has a significant impact on public health. In the USA, it is responsible for approximately 14,000 deaths per year, a figure that is probably underestimated given that 5% of the 200,000 sudden deaths per year may have an undiagnosed AAA as the cause of death . Therefore, knowledge of the prevention of the development and rupture of AAA is essential in daily medical practice. The objective of this article is to analyse the evidence and recommendations about the prevention of AAA and its rupture through an updated literature review.
Table 1 summarises the main recommendations regarding the prevention of the development of AAA and its rupture.
Table 1. Recommendations regarding the prevention of AAA.
Ultrasound screening is recommended in the following population groups:
Ultrasound surveillance is indicated in patients with small AAAs (30-54 mm) and those subjects with a slow velocity of growth (<10 mm/year).
AAA: abdominal aortic aneurysm
The main risk factors for the development of AAA include advanced age, male sex, smoking and a family history of AAA .
Smoking is the only modifiable variable in the aforementioned risk factors, in addition to being deemed the most important factor in the genesis and growth of AAA . Statistically, more than 90% of AAA patients have smoked at some point in their life . The pathophysiological mechanism that explains the association between smoking and AAA is based on the smoking of tobacco causing inflammation of the arterial wall by promoting the generation of free radicals. This in turn stimulates the proteolytic activity of the extracellular matrix, consequently degrading the elastin and collagen present in the aortic wall and thus contributing to the formation of AAA .
The prevalence of this disease is seven times higher in tobacco users than in those who do not smoke. There is a strong association between the risk of developing an AAA and the duration of smoking history, more so than the total number of cigarettes smoked . The relative risk of the appearance of AAA increases by 4% for each year of smoking. For its part, smoking cessation and smoking-free duration have been shown to reduce the prevalence of AAA . A recent meta-analysis that included 23 prospective studies established that the probability of developing an AAA in current and ex-smokers is 4.87 and 2.10 times higher, respectively, than in those who have never smoked. Likewise, the relative risk of those who have stopped smoking for 25 years was similar to that in those who have never smoked . Therefore, smoking cessation advice during each medical consultation has the highest yield in preventing the development of AAA.
The prevalence of high blood pressure in patients with AAA is approximately 82% . A meta-analysis that included 21 cohort studies with data on 28,162 AAA patients and 5,440,588 individuals showed that high blood pressure increases the risk of developing AAA by 66%. In addition, this study showed that, for every 20 mmHg of increase in systolic blood pressure and for every 10 mmHg of increase in diastolic blood pressure, there is a relative risk of AAA development of 14% and 28%, respectively . Thus, it is reasonable to achieve an adequate control of blood pressure as a measure to prevent the development of AAA.
A cohort study involving more than 3 million individuals published an association between the development of AAA and the presence of certain comorbidities such as dyslipidaemia, overweight, obesity and coronary, cerebrovascular or peripheral vascular disease. Although the impact of these diseases on the development of AAA is weak , they play a greater role in indicating the long-term prognosis of patients with AAA. A British study found a higher 5-year survival rate in those AAA patients treated with statins, antiplatelet therapy or antihypertensive drugs . Therefore, adequate control and treatment of cardiovascular risk factors in patients with AAA is crucial.
Paradoxically, unlike what occurs in subjects with atherosclerotic pathology, the prevalence of AAA and the speed of their growth are lower in diabetic subjects [2,3].
The risk of rupture depends on multiple factors - the diameter of the aneurysm, the growth rate, its morphology (saccular aneurysms have a worse prognosis) and a positive family history [2,7].
Strong epidemiological evidence points to smoking as the main risk factor in the enlargement of AAA. In current tobacco users, the rate of growth of an AAA is 0.35 mm per year, a figure that is double the rate of expansion relative to non-smokers or those who have quit smoking . In recent decades, the decline in smoking among American adults has followed a similar trend with a reduction in deaths from a ruptured AAA. In contrast, in those countries where the prevalence of smoking remains high, mortality associated with AAA continues to increase . Therefore, stopping smoking is the most important intervention to prevent AAA growth . Thus, it is recommended to use all available resources, both pharmacological and non-pharmacological, to achieve smoking cessation .
High blood pressure increases the risk of AAA rupture, mainly due to elevated aortic wall stress. In a study by Bhak et al, an increase in the AAA expansion rate of 0.02 cm per year was evidenced for every 10 mmHg of increase in diastolic blood pressure . Therefore, it is advisable to achieve adequate control of blood pressure in patients with AAA to prevent rupture.
A retrospective cohort study showed that a cardiac rehabilitation programme reduces the growth rate of small AAAs . In keeping with this, an improvement in cardiopulmonary capacity has been demonstrated in patients with AAA less than 55 mm who perform regular physical activity. Therefore, regular aerobic physical activity should be encouraged in these patients for its beneficial effect on general cardiovascular risk and for improvement of cardiopulmonary capacity. On the other hand, the practice of intense isometric exercises is not recommended in these patients .
Diseases are suitable for screening when they meet certain criteria: 1) the pathology is a common cause of morbidity and mortality; 2) it is both detectable and treatable during the pre-symptomatic stage; 3) the tests used to diagnose the presence or absence of the condition must be effective, efficient and safe; 4) early diagnosis and treatment should provide better outcomes than those achieved in subjects treated during the symptomatic phase; and 5) the potential damage or side effects of the intervention during the asymptomatic phase should be less than those of the intervention in the symptomatic phase. Applying these principles to screening for AAA, it is a frequent pathology occurring in men over 65 years of age; subjects are asymptomatic for many years; detection of the disease using a test such as ultrasound is cheap, safe and readily available; and the use of screening and early intervention demonstrates an observable reduction in morbidity and mortality . As a result, AAA constitutes a disease that could be screened for.
Palpation of a pulsating abdominal mass is the classic clinical sign; however, the sensitivity of physical examination to diagnose AAA is very low due to the retroperitoneal location of the abdominal aorta. Furthermore, it is extremely difficult to detect small or saccular aneurysms via physical examination, especially in patients who are obese or have a large body surface area .
Almost three quarters of AAAs are asymptomatic at the time of diagnosis and are incidental findings on routine physical examination or are a supplemental finding in studies requested for other medical reasons .
The test of choice to diagnose, track and monitor AAA is ultrasound, due to its high sensitivity (95%) and specificity (close to 100%), in addition to the fact that it is a safe, low-cost technique with high availability in the different medical centres . Factors limiting the diagnostic performance of ultrasound include the presence of suprarenal or juxtarenal aneurysms, compromised iliac arteries, obesity and the presence of abdominal distention. These limiting factors are exacerbated when the ultrasound is performed by practitioners with limited experience .
In subjects whose ultrasound shows a finding of an AAA, the iliac, femoral and popliteal arteries should also be assessed to rule out any concomitant aneurysms, due to their frequent association with AAAs [2,7].
In subjects in whom AAAs are found to be expanding rapidly, or in those subjects with borderline diameters for surgical intervention, a second imaging method is recommended, preferably computed tomography (CT) .
The use of other imaging techniques such as CT and magnetic resonance imaging (MRI) for screening purposes is discouraged due to its high cost compared to ultrasound, and radiation exposure and the use of iodinated contrast (in the CT case). However, these imaging modalities can detect the presence of an AAA when requested for other reasons .
It is important to assess the impact of screening programmes on reducing the occurrence of events linked to AAAs. To answer this question, multiple randomised clinical studies have been performed. Here we provide a literature review of their findings.
Ultrasound screening in males: there are four randomised clinical trials that included more than 125,000 participants older than 65 years of age, who were randomised to ultrasound scan or regular follow-up. Two of these trials were carried out in the United Kingdom (MASS and Chichester), one in Denmark (Viborg) and the other in Australia (Western). The mean prevalence of AAA across these studies was approximately 5.5%. The results of these four randomised clinical trials were recently analysed in a systematic review by Ali et al, which showed a 42% reduction in mortality associated with AAA and a 38% decrease in the rupture rate in the population tracked at a 15-year follow-up. Based on this analysis, approximately 200 people had to be screened to avoid one death from AAA. After 15 years of follow-up, the implementation of a screening programme resulted in a 2% reduction in total mortality. Elective treatment procedures for an AAA doubled among patients enrolled in active and systematic screening programmes, while halving the need for emergency procedures. This translated into a 54% decrease in 30-day surgical mortality .
Ultrasound screening in females: the Chichester trial is the only randomised trial to have examined aneurysm screening in women. This included approximately 9,300 women. A much lower prevalence of AAA was found compared to men (1.3% versus 7.6%). The conclusion was that, in the female population, systematic screening showed no effect on AAA-related mortality or on the aneurysmal rupture rate at 10 years of follow-up . Due to the low prevalence of AAA in women, there is a lack of data regarding the benefit of systematic screening in females . On the other hand, aneurysmal ruptures in women occur with aortic diameters 5-10 mm smaller than in males, and the risk of death due to rupture of an AAA is 4 times greater in relation to men with similar aneurysmal diameters . In this sense, there is a high-risk subgroup (those older than 65 years with a current or past smoking history, or those with first-degree relatives with a history of AAA), where screening can be considered .
Since the conduct of randomised studies evaluating the efficacy of systematic screening at the end of the last century and the beginning of this century, a change in the epidemiology of AAA appears to have occurred. This is evidenced in data derived from the Swedish and British screening programmes, which showed an AAA prevalence of 1.5% and 1.34%, respectively [17,18]. This may be due to a decrease in smoking today , as well as the fact that both programmes are applied when men turn 65 and are not carried out in the age range of 65 to 74 years as in randomised studies. However, both the British and Swedish reports conclude that screening programmes continue to be effective in reducing mortality associated with AAA in men [17,18].
In a cost-effectiveness analysis performed with data from the MASS study and the Swedish screening programme, it was concluded that the programmes will continue to be cost-effective until an AAA prevalence of 0.5% is reached . Cost-effectiveness has also been demonstrated in relation to other commonly used screening programmes such as cervical and prostate cancer screening .
Ultrasound screening in patients with a family history of AAA: a positive family history of AAA, particularly among first-degree relatives, is associated with a twofold to fivefold increased risk of developing this disease . Therefore, screening is recommended in first-degree relatives (older than 65 years) of patients with an AAA .
Patients with an abdominal aortic diameter less than 25 mm are considered to be at a very low risk of experiencing significant growth in the next 10 years. In those patients with borderline enlargement of their abdominal aorta (25-29 mm), follow-up imaging should be repeated after 4 years . According to data from a meta-analysis that evaluated repeated abdominal aortic diameter measurements, it is feasible to propose an ultrasound monitoring scheme every 3, 2 and 1 years for AAA of 30-39 mm, 40-44 mm and 45 -54 mm, respectively. Using these follow-up intervals, the risk of a spontaneous rupture of an AAA would be less than 1%  (Table 2).
As stated earlier, an association exists between the velocity of growth of an AAA and its risk of rupture. An AAA is deemed to be growing rapidly when its rate of expansion exceeds more than 10 mm per year .
Table 2. Recommended follow-up of small and borderline AAAs.
AAA: abdominal aortic aneurysm; CT: computed tomography
AAA is a pathology with a significant impact on public health. It is therefore essential to recognise patients at high risk of having this condition in order to implement appropriate prevention measures. Strong evidence exists justifying smoking cessation, adequate blood pressure control, and statin use with the aim of slowing the rate of expansion of known aneurysms as well as the establishment of screening programmes in at-risk population groups. Also, ultrasound surveillance in subjects with small AAAs is recommended to guide timely elective repair to improve clinical outcomes. Given the frequent association of atherosclerotic disease in patients with AAA, adequate control of cardiovascular risk factors has demonstrated improvements in the long-term survival in this patient group.
Ignacio Bluro, MD, MSc, MTSAC; Fernando Garagoli, MD; Norberto Fiorini, MD; Rodolfo Pizarro, MD, MSc, MTSAC
Department of Cardiology, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina
Address for correspondence:
Dr. Ignacio Bluro, Hospital Italiano de Buenos Aires, Presidente Juan Domingo Perón 4190, Ciudad Autónoma de Buenos Aires, C1199ABB, Argentina
Telephone: +541149590200 (5303)
The authors have no conflicts of interest to declare.
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