The thoracic aorta, which is the initial part of the descending aorta, arises from the aortic arch without any clear boundary. It courses initially in a caudal direction in the posterior mediastinum, lying close to the vertebrae on the left, and gradually turns in the lower chest area toward the anterior side of the vertebral column. Apart from a few small branches to the mediastinum, it gives off nine intercostal arteries on each side, as well as a number of unpaired small arteries to the trachea, the bronchi, the esophagus, and the diaphragm. Small branches go off dorsally to the vertebral column and to the back muscles (Fig. 2.1-4).
The abdominal aorta, descending slightly obliquely from the left, lies anterior to the vertebral column together with the inferior vena cava and divides into the common iliac arteries directly in front of the lumbosacral joint. Like the thoracic aorta, just below the diaphragm it gives off the inferior phrenic artery on the right and left and four lumbar arteries to the dorsal body wall. Paired arteries pass to the adrenal glands, kidneys and ovaries or testicles. The latter arteries descend steeply in the direction of the lesser pelvis. The right renal artery usually reaches the kidney along a course posterior to the inferior vena cava (Fig. 2.1-5).
Fig. 2.1–4 Branches of the thoracic aorta.
Three arteries emerge ventrally from the aorta to the unpaired intestines. The celiac trunk already arises in the aortic hiatus and divides into the left gastric artery, the common hepatic artery, and the inferior gastric artery (Fig. 2.1-6). Approximately 1 cm caudal from it, the superior mesenteric artery arises. A further 1 cm caudally, approximately at the level of the lower margin of the second vertebra, the two renal arteries arise-the right renal artery in a ventrolateral direction and the left renal artery dorsolaterally. The inferior mesenteric artery arises at the left ventrolateral side of the aorta approximately at the level of the fourth lumbar vertebra.
Fig. 2.1–5 Branches of the abdominal aorta.
Fig. 2.1–6a, b Variations of the branches of the celiac trunk (adapted from Lippert and Pabst 1985).
The aortic bifurcation normally lies at the level of the fifth lumbar vertebra, but may also be slightly lower. The common iliac artery arises from it on the right and left sides, dividing further on each side after about 4–5 cm into the external and internal iliac arteries. In the area of the bifurcation, the unpaired median sacral artery arises from the posterior surface of the aorta and courses caudally along the anterior surface of the sacrum.
2.1.2 Clinical pictures and epidemiology of arteriosclerotic and acquired diseases of the thoracic aorta
2.1.2.1 Aortic aneurysms
The most frequent diseases of the aorta are aortic aneurysms. These may be limited to an isolated segment of the aorta (ascending aorta, aortic arch, descending aorta) or may affect several segments (ascending aorta and aortic arch; aortic arch and descending aorta; or thoracoabdominal aortic aneurysms). The Crawford classification is now usually used specifically for thoracoabdominal aortic aneurysms (Fig. 2.1-7).
The incidence of thoracic aortic aneurysms is estimated at 5.9 per 100,000 population per year. Among these, the ascending aorta segment is the one most frequently affected (approximately 50%), followed by the descending aorta (approximately 40%). The aortic arch is affected least often, at around 10% (Bickerstaff et al. 1982).
Multisegmental degenerative aortic aneurysms occur in approximately 12.6% of cases (Crawford and Cohen 1982). Some 1% of cases of sudden death are caused by aortic rupture (dissection 62%, aneurysm 37%, pseudoaneurysm 1%). Atherosclerosis is the principal cause of aortic aneurysms (90%).
The normal diameter of the ascending aorta in adults is < 3.5 cm; in the descending aorta, the normal diameter is < 3.0 cm. In asymptomatic patients, surgery (in the ascending aorta) or endoprosthesis implantation (in the thoracic aorta) is indicated at diameters of 5.0 cm or more.
2.1.2.2 Aortic dissection
Aortic dissection is a frequent disease of the thoracic aorta. It is nowadays usually divided into types A and B using the Stanford classification (Fig. 2.1-8). The frequency of aortic dissection is estimated at 10 per 100,000 population per year (Svensson and Crawford 1992). Aortic dissection involves a longitudinal split in the arterial wall, with separation of the intima–media complex from the adventitia. This gives rise to an original “true” lumen, lined with endothelium, and a “false” lumen surrounded by adventitia. It was earlier thought that aortic dissection was based on an aneurysm with additional Erdheim–Gsell cystic medial degeneration. However, an important role is now ascribed to arterial hypertension; 75% of the patients are hypertensive. Additional risk factors include nicotine abuse and hypercholesterolemia. Hereditary diseases such as Marfan syndrome, Ehlers–Danlos syndrome (with an incidence of one in 5000) and annuloaortic ectasia (5–10% of valve replacement operations in patients with aortic valvular regurgitation) are associated with an increased risk of dissection (Erbel et al. 2001). The prevalence is 0.5–3.0 per 100,000 population per year.
Intramural hematoma is an early stage of dissection. This involves hemorrhage into the media on the aortic wall, starting in the vasa vasorum. Dissection develops from this in 15–41% of patients, and rupture in 5–26% (Erbel et al. 2001). There is a high rate of mortality, at 20–80%. Penetrating ulcer, mainly in the descending aorta, can lead to the development of intramural hematoma and dissection, false aneurysm, and perforation.
In the acute stage, there is fluid blood in the dissection fissure, and this coagulates during the subsequent course within hours, or sometimes only after several weeks. The resulting thrombosis in the dissection fissure is the starting point for “spontaneous healing” of the dissection. When there is strong flow through the dissection channel, thrombosis may not take place, and the false lumen becomes endothelialized. The false lumen then often undergoes aneurysmal dilation and may compress the true lumen.
Fig. 2.1–7 The Crawford classification of thoracoabdominal aortic aneurysms. Type I starts distal to the subclavian artery and ends above the renal arteries; type II also starts distal to the subclavian artery and ends below the renal arteries; type III starts in the region of the distal descending aorta (below T6) and extends to underneath the renal arteries; type IV covers most of the abdominal aorta; type V stretches from the distal thoracic aorta to above the renal arteries.
Fig. 2.1–8 The Stanford classification of acute aortic dissection.
The aortic wall destroyed by the dissection may rupture either immediately or during the later course.