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Descending thoracic aortic aneurysms (TAAs) are categorized into three types. In type A the descending TAA starts at the level of the left subclavian artery and ends at the level of T6. Type B starts at T6 and ends at the level of the diaphragm. Type C involves the total descending thoracic aorta. It is not uncommon for descending TAAs to involve the distal aortic arch. In degenerative aneurysms, the more proximal arch is usually not dilated.
Most patients with TAAs are asymptomatic. Elective treatment of degenerative aneurysms is usually advised if the diameter exceeds 6.0 cm. Risk factors for rupture beside diameter and pain include age, presence of chronic obstructive pulmonary disease, renal insufficiency, extent of the aneurysm, and expansion rate of the aneurysm. The average growth rate of descending TAAs (0.42 cm/yr) is greater than that for abdominal aortic aneurysms (AAAs) (0.28 cm/yr). Symptoms like chest or back pain, dyspnea, or dysphagia are also indications for treatment. For patients with aneurysms secondary to inherited connective tissue disorders, the recommended threshold for repair is an aneurysm diameter exceeding 5.0 cm. These patients have a higher incidence of dissection and rupture in descending aortic aneurysms compared with other patients with degenerative aneurysms. Marfan’s syndrome and Ehlers–Danlos syndrome type IV are the most significant disorders causing aneurysmal dilatation of the thoracic aorta.
Chronic type B dissections are the second most common cause of descending TAA formation. Up to 39% of patients with descending TAAs exhibit this pathology. Of all patients with aortic dissections, 20% to 40% will require subsequent aortic replacement during the follow-up. The growth rate of thoracic aortic dissections is significantly greater compared with that of AAAs but comparable to those of degenerative descending TAAs. Diameter indication for asymptomatic post-dissection descending TAAs is the same as for degenerative aneurysms (6.0 cm), except for patients with syndromic conditions such as Marfan’s (5.0 cm).
False aneurysms in the thoracic aorta can be the result of previous aortic surgery or trauma. Anastomotic aneurysms as well as acute traumatic aneurysms immediately distal to the left subclavian artery can often be treated by endovascular means. Failure of thoracic endovascular aneurysm repair (TEVAR) is a new challenging entity in open aortic surgery. Most complications after endovascular stent graft treatment are repaired by an additional endovascular procedure. However, progression of dilation after endovascular treatment of post-dissection aneurysms is the most common reason for open aneurysm repair.
The most common complications during descending TAA surgery include myocardial infarction, pulmonary insufficiency, kidney failure, and stroke. A careful evaluation of factors contributing to these complications is essential for preoperative risk reduction. Patients with these aneurysms are older and have more cardiovascular risk factors than the younger post-dissection patients. Impaired left ventricular ejection fraction appears to be the strongest predictor of perioperative mortality. Cardiac function can be evaluated by electrocardiogram, echocardiography, and stress testing. The threshold for coronary arteriography and antecedent mechanical intervention for coronary artery disease is lower in preparation for TAA surgery compared with that for other general surgical procedures.
Chronic pulmonary disease and a history of smoking are important predictors for postoperative pulmonary complications. Preoperative pulmonary function is impaired in up to 36% of these patients, which can induce oxygenation problems during operation in case of single lung ventilation, and it elevates the risk of prolonged postoperative ventilation and pneumonia. Cessation of cigarette smoking for at least 4 weeks before surgery is mandatory. In patients with marginal pulmonary reserve, a period of pulmonary rehabilitation with appropriate medications is indicated. However, it is important that preoperative therapy does not include the addition of systemic steroids, because steroids might be associated with aneurysm rupture.
Preoperative kidney impairment is the single most powerful predictor of postoperative kidney failure and is associated with a high rate of postoperative mortality. Although kidney dysfunction cannot be modified before operation, identification can influence adjunctive measures regarding protection of the kidneys during surgery. In case of anticipated cross clamping in the aortic arch, duplex imaging of the carotid arteries is advised to minimize the risk of stroke.
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