Epidemiology of Abdominal Aortic Aneurysms

Aneurysms of the abdominal aorta (AAA) are a common cause of death. Ruptured AAA accounts for 1.3% of the deaths in men over 65 years of age. 1 In principle, most of these deaths are preventable because an asymptomatic AAA can be treated surgically. In 1952, Dubost 2 was the first to replace an abdominal aortic aneurysm with a graft. Since then the prognosis of the aneurysm of the abdominal aorta has changed dramatically. Nowadays the elective perioperative mortality is less than 5% 3 and a patient surviving aortic grafting has a life expectancy similar to that of men and women of the same age category. 4 In the case of ruptured AAA only one patient in three reaches the hospital alive. The reported mortality rates for emergency surgery for ruptured AAA vary from 30 to 63%.4-7 Despite the importance of aneurysms of the abdominal aorta, little is known about its prevalence, incidence, risk indicators and prognostic factors. Studies dealing with the epidemiology of AAA have only recently been performed. This may be related to the development of ultrasound diagnosis in the midseventies, a technique which provides an easy, inexpensive and accurate method to detect AAA. In this article the available literature on etiology, diagnosis, prevalence, incidence, risk indicators, and prognosis of AAA is reviewed. The objective of this review is to detect gaps in the knowledge on the epidemiology of the aneurysm of the abdominal aorta and to make suggestions as to the direction of future research in the light of the question as to whether screening of the general population for aneurysms of the abdominal aorta should be advocated. Three theories of the aetiology of AAA have emerged: 13 the genetic theory; the proteolytic enzyme theory; and the trace metal theory. Aneurysms of the abdominal aorta were first thought to be atherosclerotic in origin, s-ll Martin 12 was the first to question this concept, suggesting that atherosclerosis may not be the cause but rather the consequence of aortic degeneration. Sterpetti and co-workers 13 proposed the existence of two types of abdominal aneurysms: the first type associated with atherosclerotic occlusive disease and the other not. In their study of 526 patients undergoing aneurysmal resection, 25% were believed to be non-atherosclerotic. There were significantly more ruptures in this group, compared to the atherosclerotic group. A positive family history of AAA was also reported more frequently in the group of the non-atherosclerotic patients. Other differences between atherosclerotic and non-atherosclerotic patients with AAA suggest a generalised weakness of the aortic wall in the non-atherosclerotic type AAA. This may explain the higher risk of rupture and the increased incidence of false aneurysms after operative repair in these patients. They also appear to have a higher risk of aneurysms at other sites of the arterial tree. The finding that men with a first degree relative with AAA experience a 10-fold increased risk of developing an AAA, 14-2° provides a strong argument for a genetic component. Genetic variation on chromosome 16 in patients with AAA has been reported. 21 This has been related to an increased activity of alpha-2 haptaglobulin leading to an acceleration of the hydrolysis of elastin fibres by elastase.