Thoracic Aorta

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Chapter 11 Thoracic Aorta

There are four main lesions of the thoracic aorta that present for management: dissection, aneurysm, rupture, and aortic coarctation. The focus in this chapter is on the first two of these conditions; traumatic aortic rupture is covered in Chapter 25, and aortic coarctation is covered briefly in Chapter 15.

Dissection and aneurysm of the aorta are now considered part of a spectrum of diseases known as aortic syndromes. The two conditions commonly overlap; acute dissection may complicate a chronic aneurysm, and aneurysmal dilatation may occur within a chronic dissection. Both conditions may rupture acutely. Aortic syndromes also include intramural hematoma and penetrating atherosclerotic ulcer, which are closely related to aortic dissection.

Surgery of the thoracic aorta is typically complicated and prolonged and is associated with high morbidity and mortality rates. Endovascular stent grafting has been introduced as a less invasive approach for the management of thoracic aortic syndromes, and its role continues to evolve.

In the first part of this chapter, thoracic aortic aneurysm and aortic dissection are discussed separately. In the subsequent sections on intraoperative management and postoperative care, the conditions are considered as a single entity: aortic syndromes.

ANEURYSMS OF THE THORACIC AORTA

An aortic aneurysm is a dilatation of the aorta to more than 50% above its normal size. Aneurysms may be fusiform, in which the dilatation is symmetric and involves the entire circumference of the aorta, or saccular, in which the dilatation is more localized and involves an outpouching of only a portion of the wall.

Etiology

The causes of thoracic aortic aneurysms are summarized in Table 11-1. Atherosclerotic degeneration is the most common cause of aneurysms involving the descending thoracic and thoracoabdominal aorta. Risk factors include increased age, smoking, and hypertension.

Table 11-1 Causes of Thoracic Aortic Aneurysms

Degeneration
Hypertension
Atherosclerosis
Cystic medial necrosis
Genetic or congenital origin
Marfan syndrome
Ehlers-Danlos syndrome
Bicuspid or unicuspid aortic valve
Inflammation
Takayasu arteritis
Behçet arteritis
Kawasaki disease
Polyarteritis
Infection
Aortic stenosis

Cystic medial necrosis is a degenerative condition characterized by fragmentation of the elastic fibers and loss of smooth muscle within the medial layer of the aortic wall, resulting in a loss of tensile strength. Cystic medial necrosis typically affects the ascending aorta and can lead to aneurysm and dissection. The condition is more common in males than females and typically develops in people over 40 years of age. Some degree of medial degeneration of the aorta is part of the normal aging process and accounts for the age-related increase in aortic dimensions. Marfan syndrome is an autosomal-dominant connective tissue disorder characterized by defective synthesis of the glycoprotein fibrillin, predisposing to cystic medial necrosis. Patients with Marfan syndrome are at high risk for developing early-onset aneurysms and dissections of the thoracic aorta.

Aneurysms of the proximal ascending aorta may result from chronic flow turbulence due to aortic valve stenosis (poststenotic dilatation). In addition, patients with bicuspid or unicuspid aortic valves are at increased risk for aortic aneurysm formation due to primary structural abnormalities of the aortic wall.1 Thoracic trauma, usually a sudden deceleration injury, is a rare cause of chronic aneurysm formation. This is usually caused by intimal disruption in the area of the aortic isthmus. A pseudoaneurysm (false aneurysm) is a collection of thrombus and connective tissue outside the aortic wall that occurs as a result of a contained rupture. Pseudoaneurysms typically occur secondary to infection, trauma, or previous aortic surgery.

Clinical Features and Investigations

Thoracic aortic aneurysms are commonly asymptomatic and are usually discovered incidentally when a chest radiograph or echocardiogram is performed for some other reason. A proportion of patients experience chest pain, which is caused by rapid expansion of the aneurysm itself or, rarely, by bony erosion. Occasionally, a large aneurysm causes symptoms that result from pressure on adjacent structures. Hoarseness may develop due to stretching of the recurrent laryngeal nerve. Pressure on the trachea and left main bronchus can cause stridor, dyspnea, atelectasis, or pneumonia. Pressure on the esophagus may cause dysphagia.

Aneurysms involving the aortic root commonly cause aortic regurgitation secondary to annular dilatation. Thus, an aortic aneurysm may be identified in a patient who presents with aortic regurgitation or congestive cardiac failure.

The aneurysm may be apparent on a chest radiograph. With an ascending aneurysm, there may be a prominent right aortic border on the frontal projection and filling in of the upper substernal space on the lateral projection. With an arch aneurysm there may be widening of the mediastinum on the frontal projection. An enlarged descending thoracic aorta may be seen behind the heart on the frontal and lateral projections (Fig. 11-2).

Imaging of thoracic aortic aneurysms may be undertaken by echocardiography, computed tomography (CT), or magnetic resonance (MR) imaging. Echocardiography allows accurate assessment of aortic regurgitation, aortic leaflet morphology, and ventricular function, but it may not fully delineate the anatomic extent and relationships of the aneurysm. Echocardiography is particularly poor at imaging the distal ascending aorta and aortic arch. To image the aneurysm itself accurately, either a contrast CT scan (Fig. 11-3A) or MR imaging scan is required. For patients undergoing aneurysm surveillance, conventional axial CT scanning is sufficient. For operative planning, CT or MR imaging with three-dimensional reconstruction is extremely helpful (Fig. 11-3B).

AORTIC DISSECTION

Unlike aortic aneurysms, which develop slowly and are often asymptomatic, aortic dissection usually has an abrupt onset, is acutely painful and, if untreated, may be rapidly fatal. Aortic dissection is caused by a tear in the intima of the aortic wall followed by delamination of the wall. Blood, under pressure, strips the intima from the adventitia, creating a blood-filled space within the aortic wall (false lumen). The intimal flap may spread proximally and distally from the entry tear as well as up side branches of the aorta.

Intramural hematoma is due to a burst vessel in the media, causing a hematoma, which may then lead to a tear and communication with the aortic lumen. A penetrating atherosclerotic ulcer is ulceration within an atherosclerotic plaque that extends down to the level of the media. Both intramural hematoma and penetrating atherosclerotic ulcer have high incidences of dissection and rupture.7,8

Etiology

The causes of aortic dissection are similar to the causes of aortic aneurysm (see Table 11-1). Indeed, dissection, intramural hematoma, and atherosclerotic plaque rupture can all complicate an aortic aneurysm. An additional cause of aortic dissection is iatrogenic aortic injury due to surgical manipulations such as the placement of aortic cannulas during cardiopulmonary bypass.

Clinical Features and Investigations

Acute aortic dissection (type A and B) classically presents with the abrupt onset of excruciating chest pain that is commonly described as having a tearing quality. Anterior chest pain is more likely with type A dissection; back pain is more common with type B dissection. However, there is wide variation in presenting symptoms, and aortic dissection should be considered in all patients who present with acute severe chest pain.

Imaging

Patients who present with symptoms and signs consistent with aortic dissection require urgent diagnostic imaging. Options include transesophageal echocardiography (TEE), CT scanning, MR imaging, and aortography, all of which have a sensitivity and specificity greater than 90%.10 Intramural hematoma may be difficult to diagnose with any of these techniques. The preferred initial investigation varies according to the institution, but CT scanning is the most widely used modality.11 CT scanning has the advantage of being rapid (unlike MR imaging) and does not require sedation or general anesthesia (unlike TEE). Aortography is rarely indicated other than as part of a stenting procedure. CT scanning demonstrates the extent of the dissection (Fig. 11-6) and the presence of any pericardial blood but does not usually demonstrate the entry tears or any associated aortic regurgitation.

TEE is the most useful investigation for determining the severity of any associated aortic regurgitation (Fig. 11-7

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