Aortic Wall

The aortic wall consists of three layers: outer adventitia, middle media, and inner intima. Under normal circumstances, TEE cannot distinguish these layers. Diseases such as dissection and atheroma alter aortic wall anatomy. In aortic dissection, the intimal layer separates from the adventitia as the false lumen develops. Aortic atherosclerosis injures the intima to cause thickening, calcification, and ulceration.

The aortic adventitia is the thin outermost collagenous layer that contains the vasa vasorum and nerves. Although it is thin, its rich collagen content gives the adventitia the greatest tensile strength of the three aortic wall layers. The aortic media is the thick middle layer between the adventitia and intima. The media normally accounts for up 80% of the aortic wall thickness and consists of elastic tissue intertwined with muscle fibers. The aortic intima is the thin inner wall layer, characterized histologically by a basement membrane lined with endothelium that is in direct contact with the blood. Because of its delicate structure, the intima is most susceptible to injury.

Aortic Segments

The aorta begins at the ventricular-aortic junction with the aortic valve and terminates in the abdomen when it bifurcates into the common iliac arteries. The major aortic segments are the aortic root, ascending aorta, aortic arch, descending thoracic aorta, and abdominal aorta.

The aortic root begins at the ventricular-aortic junction and terminates at the sinotubular junction. The aortic root complex consists of the aortic valve annulus, aortic valve cusps, sinuses of Valsalva (sinus segment), and sinotubular junction, where the sinus segment joins the tubular ascending aorta. The aortic root and proximal ascending aorta lie within the pericardium. The weakest area of the aortic wall is the sinus segment. These anatomic relationships are important because aortic rupture at this level will be intrapericardial and cause acute cardiac tamponade. The aortic root components are clearly demonstrated by TEE in the midesophageal (ME) aortic valve long-axis view, where their diameters can be precisely quantified ( Fig. 19-1). ¹³ The aortic valve cusps and their corresponding sinuses of Valsalva are described by their anatomic relationship to the coronary artery ostia as follows: right coronary, left coronary, and noncoronary. The aortic root complex is also known as the functional aortic annulus, since alterations in one or more of its components can produce aortic regurgitation. ¹³

The ascending aorta is defined as the tubular aorta that ascends from the sinotubular junction to join the aortic arch at the origin of the innominate artery. The ascending aorta can be imaged in both short and long axis at the level of the right pulmonary artery ( Fig. 19-2). As explained earlier, TEE fails to interrogate the distal ascending aorta and proximal aortic arch owing to the attenuation of ultrasound imaging across the air-filled trachea. ²

The aortic arch contains the origins of the brachiocephalic vessels—the innominate, left carotid, and left subclavian arteries ( Fig. 19-3). Anatomic variations in aortic arch branch vessel anatomy have a collective incidence as high as 25%. ¹⁴ The most frequent variant pattern (with a 20% incidence) is the bovine arch, defined as a common origin for the innominate and left common carotid arteries. ¹⁵

The descending thoracic aorta extends from the left subclavian artery to the diaphragmatic hiatus ( Fig. 19-4). Its major branches are the paired intercostal arteries that contribute substantially to the spinal cord collateral network. The aortic isthmus lies just beyond the origin of the left subclavian artery at the site of the ligamentum arteriosum, a vestige of the fetal ductus arteriosus. The aortic isthmus is the most common location for aortic coarctation, patent ductus arteriosus (PDA), and traumatic intimal disruptions.

The abdominal aorta begins at the diaphragmatic hiatus and terminates at the aortic bifurcation where it gives rise to the common iliac arteries. Its major branches include the celiac trunk, superior mesenteric artery, renal arteries, inferior mesenteric artery, and lumbar segmental arteries.

Aortic Segmental Anatomy for Thoracic Endovascular Aortic Repair

Definitions of Aortic Enlargement

According to recent guidelines, the spectrum of aortic enlargement is clearly defined. ⁶ An aortic aneurysm (or true aneurysm) is defined as a focal permanent aortic dilation with a diameter greater than 50% the normal diameter for that aortic segment. ⁶ Although a true aneurysm has all three aortic wall layers, the intima and media may be so attenuated in giant aneurysms that they are undetectable. An aortic pseudoaneurysm (or false aneurysm) results from aortic rupture, and its wall consists of periarterial connective tissue rather than all the aortic wall layers. ⁶ If a pseudoaneurysm freely communicates with the intravascular space, it is also termed a pulsating hematoma. Aortic ectasia is defined as aortic dilation less than 150% of the expected diameter for that aortic segment. ⁶ Aortomegaly is defined as aneurysmal involvement of two or more aortic segments. ⁶

A Systematic Stepwise Approach ( Box 19-1)

First, image the aortic root in the ME short-axis aortic valve view. Identify the aortic valve cusps, their calcification pattern, their mobility profiles, and measure the aortic valve area. Interrogate the aortic valve with color flow Doppler to assess for aortic regurgitation in relation to the valve cusps. Furthermore, examine the origins of the right and left coronary arteries.

Second, image the aorta in the ME long-axis aortic valve view ( Fig. 19-9; also see Fig. 19-1, A). Measure the aortic root diameters from intima to intima (see Fig. 19-1, B). Analyze aortic valve cusp mobility, aortic root calcification, and the extent of sinotubular junction disease. Interrogate the aortic valve with color Doppler imaging to assess for presence and severity of aortic regurgitation.

Third, image the proximal ascending aorta in short axis at the level of the right pulmonary artery by withdrawing and anteflexing the TEE probe from the aortic valve level (see Fig. 19-2, A). Determine the diameter of the ascending aorta at this level. Examine the aortic wall for signs of atheroma, calcification, and dissection. Remember that the distal ascending aorta and the proximal aortic arch lie in the blind spot of TEE.1,2 Image the proximal ascending aorta in long axis at this level by multiplane rotation to about 90 degrees (see Fig. 19-2, B). Measure the ascending aortic diameter, and assess the aortic wall for signs of atheroma, calcification, and dissection.

Fourth, image the descending thoracic aorta in short axis (see Fig. 19-4, A). Determine the aortic diameter and assess for atherosclerosis, aneurysm, dissection, and pleural effusion (see Fig. 19-4, A). Image the descending thoracic aorta in long axis at this level, with multiplane rotation to approximately 90 degrees (see Fig. 19-4, B). This view facilitates close examination of the aortic intima for signs of disease.

Fifth, interrogate the distal descending thoracic aorta to the diaphragmatic level as the TEE probe is gradually advanced and rotated counterclockwise. The proximal descending thoracic aorta can be interrogated as the TEE probe is gradually withdrawn and rotated clockwise. In this fashion, the entire extent of this aortic segment can be examined, noting that the distal aortic arch is typically 20 to 25 cm from the incisors, the mid-descending thoracic aorta at 30 to 35 cm from the incisors, and the diaphragm at 40 to 45 cm from the incisors. As the aorta is imaged distally, its pulsatility and diameter decrease, especially in the setting of aortic valve disease.24,25 The TEE descending aortic short-axis views also permit detection of left pleural effusions that layer adjacent to the aorta in a supine patient.

Sixth, examine the distal aortic arch as the TEE probe is withdrawn from imaging the distal descending thoracic aorta, noting the distances from the incisors. A long-axis view of the distal aortic arch is typically depicted at a 0-degree multiplane angle (see Fig. 19-3, A). A short-axis view of the distal aortic arch will be displayed by multiplane rotation to 90 degrees (see Fig. 19-3, B). The origins of the brachiocephalic vessels (most often the left subclavian artery) can be sought by rotating the TEE probe clockwise from left to right as the aortic arch is imaged. Color flow Doppler imaging can frequently image blood flow in the brachiocephalic vessels by decreasing the Nyquist limit as needed, since flow is often laminar and off-axis to the ultrasound beam. These views allow detailed assessment of the distal aortic arch with respect to diameter, aneurysm formation, dissection, and atheroma. The upper esophageal aortic arch short-axis view may also display the long-axis view of the pulmonic valve and main pulmonary artery as well as the innominate vein in short-axis ( Fig. 19-10).

Imaging Artifacts During Echocardiographic Aortic Imaging

Imaging artifacts during echocardiographic evaluation are common, especially in the lumen of a dilated ascending aorta. Since motion artifacts are possible during CT aortic imaging, it is possible they, together with ultrasound imaging artifacts, may be misdiagnosed as the intimal flap of an acute aortic dissection. Artifacts can readily be recognized because they often cross anatomic boundaries and are often not visible in multiple imaging planes.

Linear artifacts result from reverberations between chamber or vessel walls. These reverberations between the walls of the left atrium and/or right pulmonary artery may create a linear artifact in the ascending aortic lumen, resembling an intimal flap of aortic dissection. Note that in Figure 19-8 the linear artifacts course outside the aortic boundaries. Linear artifacts of this type also result from reverberations between a vessel/chamber surface and an intravascular catheter, as in the example of a Swan-Ganz catheter in the pulmonary artery.

Side-lobe artifacts can be generated by calcified aortic plaques or intravascular catheters, such as a Swan-Ganz catheter. Side-lobe artifacts can produce linear artifacts within the aortic lumen. Linear artifacts from side lobes appear as curvilinear shadows at a constant depth and often extend outside the aorta.

Mirroring artifacts are generated when ultrasound is reflected by acoustic interfaces such as the aortic wall. This process results in a mirror image of the aorta adjacent to the interface of interest. A mirror-image artifact juxtaposed to the descending thoracic aorta can mimic aortic dissection. See Chapter 6 for a more detailed explanation of imaging artifacts.

Imaging Pitfalls During Echocardiographic Aortic Imaging

Vessels adjacent to the aortic wall can mimic the appearance of an aortic dissection. The innominate vein appears adjacent to the aortic arch in upper esophageal views and may mimic aortic dissection during long-axis imaging (see Fig. 19-10). The innominate vein can be readily identified by imaging in multiple views and by imaging luminal echocontrast injected into a peripheral vein of the left upper extremity.

Para-aortic effusions may also mimic aortic dissection. A left pleural effusion adjacent to the descending thoracic aorta is readily distinguished from aortic dissection during ME short-axis imaging to depict the characteristic crescent-shaped effusion in the left pleural cavity ( Fig. 19-11). A right pleural effusion can be imaged by rotating the TEE probe to the right, looking for a crescent-shaped fluid collection oriented to the right.

Epiaortic Imaging of the Aorta

The aortic root, ascending aorta, and aortic arch can be imaged directly with a 5- to 7-MHz ultrasound transducer in sterile sheath against the anterior aortic wall ( Fig. 19-12).^4,5 Epiaortic imaging during cardiac operations is typically feasible after sternotomy, with a systematic comprehensive examination as the standard.^3–5 To improve the image quality of near-field structures, an acoustic standoff is typically utilized by filling the mediastinum with warm sterile saline and/or filling the sterile sheath with fluid or ultrasound gel.

An important indication for epiaortic ultrasound is for assessment of ascending aortic atheroma or calcification prior to manipulation and instrumentation of the ascending aorta during cardiac surgery. Typical ascending aortic events that are associated with cerebral atheroembolism include cannulation for cardiopulmonary bypass and aortic clamping. Risk factors for significant ascending aortic atheroma include prior embolic stroke, severe peripheral vascular disease, severe aortic stenosis, aortic atheroma on preoperative radiographic imaging, and severe atherosclerosis of the descending thoracic aorta detected by TEE.26,27 Epiaortic imaging can also assess for aneurysm and dissection in the ascending aorta and aortic arch where TEE imaging is inadequate, such as in the TEE blind spot and in patients with contraindications to TEE.^1–5

According to recent guidelines, epiaortic imaging planes are oriented as short axis or long axis in relation to the direction of blood flow along the length of the vessel. ⁵ The aortic walls are designated as anterior, right lateral, left lateral, or posterior (see Fig. 19-12). ⁵ The proximal ascending aorta is imaged in short axis at a level proximal to the right pulmonary artery. The mid-ascending aorta short axis is imaged at the level of the right pulmonary artery. The distal ascending aorta short axis is imaged at a level distal to the right pulmonary artery and proximal to the aortic arch. The ascending aorta long axis is imaged at the level of the right pulmonary artery, showing portions of the proximal, mid-, and distal ascending aorta. The aortic arch long axis is imaged at the level of the innominate, left carotid, and left subclavian arteries.

Classification of Aortic Dissection

Aortic dissection can be classified according to intimal tear site and dissection extent ( Fig. 19-16). The DeBakey scheme has three main subtypes. The Stanford scheme has two main subtypes. The classification of aortic dissection is clinically important for clinical management, including prognosis. Acute aortic dissections that involve the ascending aorta are typically surgical emergencies, since delays in surgical management are associated with high mortality risk.^32,33

The Stanford classification emphasizes the clinical importance of ascending aortic dissection (see Fig. 19-16). Stanford type A aortic dissection is defined as any dissection involving the ascending aorta, regardless of intimal tear site (surgical repair typically recommended). Stanford type B dissection is defined as any dissection that does not involve the ascending aorta (medical management recommended unless complicated by threatened/frank aortic rupture and/or malperfusion).^28,29

The DeBakey classification focuses on intimal tear site and dissection extent (see Fig. 19-16). DeBakey type I dissection is characterized by an intimal tear within the ascending aorta complicated by dissection involving the ascending aorta, aortic arch, and descending aorta (surgical repair recommended). DeBakey type II dissection is characterized by an intimal tear within the ascending aorta complicated by dissection confined to the ascending aorta (surgical repair recommended). DeBakey type III dissection is characterized by an intimal tear within the descending thoracic aorta complicated by dissection of the descending aorta (medical management recommended unless complicated by threatened/frank aortic rupture and/or malperfusion). If dissection in this setting is confined to the descending thoracic aorta, it is defined as DeBakey type IIIa. If dissection in this setting involves the descending aorta and abdominal aorta, it is DeBakey type IIIb.

Although ascending aortic dissection is a surgical emergency, perioperative mortality depends significantly on clinical presentation, specifically the presence of branch vessel malperfusion (regional ischemia) and/or circulatory compromise (generalized ischemia).34,35 Recently, the Penn classification of clinical presentation in acute type A dissection has been derived and validated to focus future interventions on clinical presentations in this life-threatening disease as part of the collective effort to improve clinical outcomes yet further.^34,35 Penn Class A presentations are characterized by the absence of ischemia, specifically the absence of malperfusion and circulatory compromise. Penn Class B presentations are characterized by branch vessel malperfusion (e.g., stroke, cold pulseless upper extremity). Penn Class C presentations are characterized by circulatory compromise including shock and/or cardiac arrest. Penn Class B&C presentations are characterized by both branch vessel and circulatory compromise. The clinical presentation in acute type A dissection as defined by the Penn classification independently predicts perioperative mortality.^34,35 An integrated Penn classification of Stanford acute type A aortic dissection has recently been proposed to encourage a comprehensive management strategy of this acute aortic syndrome by considering Penn clinical presentation and DeBakey extent of dissection. ³⁶ This integration of the three classifications of ascending aortic dissection will likely frame future advances in diagnosis and management of this surgical emergency. ³⁶

The European classification of acute aortic dissection consists of five classes and focuses on the anatomic spectrum of aortic dissection, including its variants ( Fig. 19-17). ³⁷ Class I is defined as classic aortic dissection with an intimal tear, complicated by an intimal flap separating the true and false aortic lumens. Class II is defined as IMH with hematoma formation within the medial layer. An intimal tear is not usually detected by echocardiography. Class III is defined as limited dissection confined to a short aortic segment. A partial tear of the inner aortic wall is termed a subtle dissection, and scar formation at this partial tear site is termed an abortive discrete dissection. Class IV is defined as a penetrating atherosclerotic ulcer (PAU) with localized hematoma or pseudoaneurysm. Class V is defined as traumatic or iatrogenic aortic dissection, typically associated with aortic catheterization or surgical aortic manipulation.

As a variant of aortic dissection, IMH is characterized by a medial hematoma that may also be subadventitial. ³⁸ It accounts for up to 30% of patients presenting with an acute aortic syndrome (see Fig. 19-13), especially in Asia.^39,40 The typical patient with IMH is elderly, hypertensive, and has established peripheral vascular disease.^38,39 The genesis of IMH is still debated as to whether it is aortic dissection with a thrombosed false lumen or whether it is intramedial hemorrhage from rupture of the vasa vasorum.^38,41 The extent of IMH is classified by the Stanford approach as type A and type B. Indications for surgery in type A IMH include refractory pain, ascending aortic diameter 5 cm or greater, hematoma thickness greater than 1 cm, and hemodynamic instability. ³⁸

As a variant of aortic dissection, PAU is a focal atherosclerotic plaque that corrodes through the internal elastic lamina into the media.38,39

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