Pathology of the Thoraco-Abdominal Aorta

Abstract

The aorta is the great systemic artery of the human body. It is composed of three layers or tunicae — the intima, media, and adventitia. The strength of the aorta lies in the tunica media, with the so-called lamellar units that represent the basic structural and functional components in the aortic wall. The pathology of the thoraco-abdominal aorta is traditionally classified into congenital, heredofamilial, inflammatory, degenerative, traumatic, and neoplastic. All the above-mentioned aortic diseases, although with different rates of prevalence, can account for both aortic dissection and aneurysm. Surgical pathology examination of resected aortic specimens, or autopsy investigation, are essential to reach the underlying etiologic diagnosis. Both congenital (coarctation, bicuspid aortic valve) and heredofamilial disease (such as Marfan syndrome) can be associated with degenerative changes of the aortic tunica media (cystic medial necrosis) with the risk of aortic aneurysm formation and dissection. Aortitis, i.e. inflammatory diseases of the aorta, can be subdivided in two main groups — infectious and non-infectious. Syphilitic or luetic aortitis, historically one of the major causes of aortic diseases, is now exceedingly rare. Nowadays, the most common causes of aortitis are large-vessel vasculitides such as giant cell arteritis and Takayasu arteritis. Moreover, aortitis is often associated with collagen/rheumatologic systemic diseases and may also be idiopathic. The inflammatory infiltrate is aspecific and the final diagnosis relies mainly on the clinical features. Atherosclerosis and the so-called “cystic medionecrosis” are traditionally regarded as the main degenerative diseases affecting the aorta, involving the intima and the media, respectively. Complications of atherosclerotic plaque at the level of the aorta can account for progressive atrophy of the underlying tunica media due to release of matrix metalloproteinases, with collagen and elastic degradation and aneurysm formation; thrombosis, systemic embolism, and penetrating atherosclerotic ulcer, as well as superimposed infection with mycotic aneurysm formation.