SPECIFIC LESIONS OF THE AORTA
In an aortic dissection an intimal tear allows blood to track into the aortic wall (the media), creating a new pathway for blood flow. In many cases, a primary degenerative process called cystic medial necrosis predisposes for dissection to occur. Patients with hereditary connective tissue defects such as Marfan syndrome and Ehlers–Danlos syn-drome eventually develop cystic medial necrosis and are at risk for aortic dissection. Propagation of the dissection is thought to occur as a result of hemodynamic shear forces acting on the intimal tear; indeed, hypertension is a common finding in patients with aortic dissection. Dissection can also occur from hemorrhage into an atheromatous plaque or at the aortic cannulation site following cardiac surgery.
Dissections may occlude the orifice of any artery arising directly from the aorta; they may extend into the aortic root, producing incompetence of the aortic valve; or may rupture into the pericar-dium or pleura, producing cardiac tamponade or hemothorax, respectively. TEE plays an important role in diagnosing and characterizing aortic dissec-tions. Dissections are most commonly of the proxi-mal type (Stanford type A, De Bakey types I and II) involving the ascending aorta. Type II dissections do not extend beyond the innominate artery. Distal dis-sections (Stanford type B, De Bakey type III) origi-nate beyond the left subclavian artery and propagate only distally. Proximal dissections are nearly always treated surgically, whereas distal dissections may be treated medically. In either case, from the time the diagnosis is suspected, measures to reduce systolicblood pressure (usually to 90–120 mm Hg) and aortic wall stress are initiated. This usually includes intravenous vasodilators (nicardipine or nitroprus-side) and β-adrenergic blockade (esmolol or a lon-ger acting agent). The latter is important in reducing the shear forces related to the rate of rise of aortic pressure (dP/dt), which may actually increase with nitroprusside alone.
Aneurysms more commonly occur in the abdominal than in the thoracic aorta. The vast majority of aortic aneurysms are due to atherosclerosis; cystic medial necrosis is also an important cause of thoracic aortic aneurysms. Syphilitic aneurysms characteristically involve the ascending aorta. Other etiologies include rheumatoid arthritis, spondyloarthropathies, and trauma. Dilation of the aortic root often produces aortic regurgitation. Expanding aneurysms of the upper thoracic aorta can also cause tracheal or bronchial compression or deviation, hemoptysis, and superior vena cava syndrome. Compression of the left recurrent laryngeal nerve produces hoarse-ness and left vocal cord paralysis. Distortion of the normal anatomy may also complicate endotracheal or endobronchial intubation or cannulation of the internal jugular and subclavian veins.
The greatest danger from untreated aortic aneu-rysms is rupture and exsanguination. A pseudoaneu-rysm forms when the intima and media are ruptured and only adventitia or blood clot forms the outer layer. Acute expansion (from leaking), manifested as sud-den severe pain, may herald rupture. The likelihood of catastrophic rupture is related to size. The normal aorta in adults varies from 2 to 3 cm in width (it is wider cephalad). The data are clear for abdominal aortic aneurysms; rupture occurs in 50% of patients within 1 year when an aneurysm is 6 cm or greater in diameter. Elective treatment is generally performed in most patients with aneurysms 5 cm or greater. Most often this is accomplished with an intravascular stent; less often, open surgery and a prosthetic graft is used. The operative mortality rate is about 2–5% in good-risk patients and exceeds 50% if leaking or rupture has already occurred. The risks are much less with intravascular stenting, which has become the preferred procedure whenever the anatomy permits.
Atherosclerotic obliteration of the aorta most com-monly occurs near the aortic bifurcation (Leriche’s syndrome). Occlusion results from a combina-tion of atherosclerotic plaque and thrombosis. Atherosclerosis is usually generalized and affects other parts of the arterial system, including the cere-bral, coronary, and renal arteries. Treatment may be accomplished by intra-vascular stenting or by open surgery with an aortobifemoral bypass graft; proximal thromboen-darterectomy may also be necessary.
Aortic trauma may be penetrating or nonpen-etrating. Both types of injuries can result in mas-sive hemorrhage and require immediate operation. Whereas penetrating injuries are usually obvious, blunt aortic trauma may be easily overlooked if not suspected and the appropriate diagnostic test-ing performed. Nonpenetrating aortic trauma typi-cally results from sudden high-speed decelerations such as those caused by automobile accidents (eg, in which the driver’s chest impacts the steering wheel) and falls. The injury can vary from a partial tear to a complete aortic transection. Because the aor-tic arch is relatively fixed whereas the descending aorta is relatively mobile, the shear forces are great-est and the site of injury most common just distal to the subclavian artery. The most consistent initial finding is a widened mediastinum on a chest radio-graph. Definitive diagnosis can be accomplished with magnetic resonance or computed tomographic imaging or TEE.
Th is congenital heart defect may be classified according to the position of the narrowed segment relative to the position of the ductus arteriosus. In the preductal (infantile) type, the narrowing occurs proximal to the opening of the ductus. This lesion, which is often associated with other congenital heart defects, is recognized in infancy because of a marked difference in perfusion between the upper and lower halves of the body; the lower half is cya-notic. Perfusion to the upper body is derived from the aorta, whereas perfusion to the lower body is primarily from the pulmonary artery. Postductal coarctation of the aorta may not be recognized until adulthood. The symptoms and hemodynamic sig-nificance of this lesion depend on the severity of the narrowing and the extent of collateral circula-tion that develops to the lower body (internal mam-mary, subscapular, and lateral thoracic to intercostal arteries). Hypertension in the upper body, with or without left ventricular failure, is usually present. So-called “rib notching” may be present on the chest radiograph as a result of dilated collateral intercostal arteries.
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