Chapter30 Aorta

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Chapter 30: Thoracic Aorta

up to 30% of patients. Treatment options in these patients include endovascular stenting, surgical resection, aortoplasty, and bypass grafting.

Pseudocoarctation Congenital elongation with prominent kinking of the aorta at the aortic isthmus can mimic the appearance of coarctation and is termed pseudocoarctation (Fig. 30.23). Pseudocoarcta- tion lacks the hemodynamic changes of true coarctation, such as a significant pressure gradient and arterial collateral forma- tion. Although usually asymptomatic, pseudocoarctation can be associated with hypertension and aortic aneurysm. Like coarctations, it is associated with a bicuspid aortic valve. On chest radiograph, the superior mediastinum may appear wid- ened with a superiorly positioned aortic arch (Fig. 30.23A). Atheroma The pathogenesis and consequences of atherosclerotic dis- ease are more thoroughly discussed in the section of this text dedicated to coronary artery disease; however, it warrants mentioning here as it is so highly prevalent in the aorta. Risk factors for the development of aortic atherosclerotic disease include advanced age, heredity, hypertension, diabetes, smok- ing, hyperlipidemia, sedentary lifestyle, and endothelial dys- function. Atheroma formation is a cyclical process that starts with lipoprotein phagocytosis by macrophages, which are then incorporated into the subintima of the aortic wall. Intra- cellular processes within the macrophage lead to the forma- tion of “foam cells.” Eventually, the macrophages die, with a resultant influx of additional white blood cells and fibro- blasts. The result of this cycle is an intramural mass consist- ing of the inner extracellular lipid core with an outer layer of inflammatory cells and connective tissue that can narrow the arterial lumen. Similar to coronary artery plaques, non- calcified or mixed plaques with a thin fibrous cap and a large necrotic core are more likely to rupture and are termed vul- nerable plaques. As plaques age and calcify, they generally become less prone to rupture. Atherosclerotic disease involving the thoracic aorta is a common finding on chest radiograph and should follow the

Figure 30.22.  Aortic Coarctation. Four-dimensional phase-contrast, sagittal MPR demonstrates flow acceleration, indicated by

red color flow ( yellow arrow ) across the coarctation in the proximal thoracic aortic; pressure gradient quantified as 31 mm Hg.

demonstrates anatomy, MRI and echocardiography allow quantitative evaluation of severity, including pressure gradient and flow acceleration across the coarctation (Fig. 30.22). Aortic coarctation is treated with surgical repair, which typically involves resection of the narrowed segment and pri- mary anastomosis or interposition graft. Additional repair techniques include subclavian flap or prosthetic patch aor- toplasty to augment the coarcted segment, extra-anatomic bypass grafting, and endovascular balloon dilation. Interven- tion is recommended when the coarctation pressure gradient exceeds 20 mm Hg. Following surgical repair, there is a 72% to 74% reported 30-year survival. Postoperative complica- tions include aneurysm formation, rupture with pseudoan- eurysm formation, accelerated atherosclerotic disease, and increased cardiovascular morbidity. Restenosis can occur in

C

A

B

Figure 30.23.  Pseudocoarctation. PA chest radiograph ( A ) demonstrates a rounded density ( white arrow ) superior to the aortic arch ( black arrow ). On sagittal CT (B), the aortic arch and proximal descending thoracic aorta are elongated and folded on themselves ( white arrow ), pro- ducing focal kinking ( white arrow ) but without significant narrowing. 3D VR of same patient ( C ).