In the United States, aortic aneurysms are the 13th leading cause of deathsee 1, 2 About 15,000 individuals die every year due to the rupture of aortic aneurysms. Based on autopsy studies it has been estimated that 1-2% of the population harbor aneurysms in their aorta with up to 10% prevalence in older age groups.1, 2 Most aortic aneurysms go undetected until rupture and the mortality from ruptured aneurysms is as high as 90%.1, 2
Along the length of the aorta, significant heterogeneity occurs in the distribution of aneurysm disease. The prevalence of abdominal aortic aneurysms (AAAs) located in the infrarenal section of the aorta is at least three times higher than that of thoracic aortic aneurysms and dissections (TAAD).1, 2 In TAAs, about 50% involve the ascending aorta, 10% the arch and 40% the descending thoracic aorta.1, 2 Only about 25% of patients with TAAD have a concomitant AAA, and multisegmental disease is found in only about 10% of cases.1, 2
There are also other differences between TAAD and AAA: 1) age-at-onset for TAAD (65 years) is approximately 10 years earlier than for AAA (75 years); and 2) AAAs are predominantly a disease of Caucacian males with 6:1 male:female ratio, whereas TAADs occur only slightly more frequently in males (1.7:1). Additional differences can be found in the pathobiology of these aneurysms. AAAs are characterized by signs of local chronic inflammation of the aortic wall, decrease in the number of smooth muscle cells in the aortic media layer and fragmentation of the extracellular matrix of the aorta at the site of the aneurysm see 3. Increased local expression of proinflammatory cytokines and matrix metalloproteinases (MMPs) have also been demonstrated.3 Furthermore, AAAs can be induced in a surgical experimental model in which elastases are infused into rodent aorta.4 TAADs are characterized by medial necrosis also known as “Erdheim’s cystic medial necrosis” and more recently referred to as “medial degeneration”, mucoid infiltration, and cyst formation with elastin degradation and vascular smooth muscle cell apoptosis.1
Both TAAD and AAA are silent diseases often without symptoms.2 They can, however, be readily identified through imaging techniques. TAADs can be detected by echocardiography or CT, and family members of TAAD-patients will benefit from imaging by identifying their TAADs before catastrophic consequences. Presently, there are no recommendations about large scale screening of populations for TAAD. On the other hand, for AAA ultrasonography screening studies have demonstrated cost-effectiveness of population-based ultrasonography screening programs and a decrease in the number of aneurysm-related deaths.see,5 Several recommendations have been made including a recent consensus statement, in which Kent et al.6 recommended ultrasonography screening for AAA for all individuals over 60 years of age and for those over 50 years of age with family history for AAA and the recommendation by the US Preventive Service Task Force7 to screen for AAA in men aged 65 to 75 years who have ever smoked.