Applied Radiology

Dr. Gotway is an Assistant Professor of Radiology at the University of California, San Francisco and Chief of Thoracic Imaging at San Francisco General Hospital, San Francisco, CA.

The development of helical CT and, recently, multidetector-row CT technology, has revolutionized the ability to image the thoracic aorta non-invasively. Helical CT aortography (HCTA) possesses several advantages over other modalities frequently used to investigate thoracic aortic disease, such as transesophageal echocardiography (TEE), MRI, and aortography. The speed, ease, and widespread availability of helical CT make it the examination of choice for acute aortic pathologies such as dissection, intramural hematoma, aneurysm, and acute traumatic injury. Helical CT is less operator-dependent than TEE and is easier and faster to perform than either MRI or aortography. These considerations are particularly advantageous in acutely ill patients. Another benefit of helical CT that these other methods do not provide is the ability to image the entire thorax. This is particularly important because cardiovascular abnormalities frequently present with nonspecific symptoms, and nonvascular etiologies of the patient's presentation may be obvious with helical CT. Finally, the volumetric data obtained with helical CT aortography is readily processed using two-dimensional, three-dimensional, or volume-rendering techniques to provide angiogram-like images or images in any desired plane or obliquity.

Helical CT aortography technique

Although no standardized techniques exist for helical CT evaluation of the thoracic aorta, and practices vary from institution to institution, certain general principles may be applied to optimize techniques. Variables that must be considered include collimation, pitch, field-of-view, reconstruction increment, amount, rate and timing of contrast administration, distance to be scanned, kVp, mA, and tube rotation time. These variables must be optimized to provide the highest possible scan quality. Occasionally, a compromise among these parameters is required to achieve this goal.

Collimation and pitch--When a scan protocol is constructed, one must generally strike a compromise between the collimation and the pitch. Recall that pitch reflects the ratio of table speed to slice thickness (collimation) per tube rotation, or:

Pitch = Table transport distance

Collimation

A useful general rule of thumb is that effective slice thickness increases by 30% when the pitch is doubled. Thus, a 3-mm scan with a pitch of 2 has an effective slice thickness of 3.9 mm. Apply this concept to the following situation:

What technical parameters provide the best scan quality if the distance to be scanned is 10 cm? If one uses 5-mm collimation with a pitch of 1, the scan will take about 20 seconds (depending on tube rotation time) with an effective slice thickness of about 5 mm. If 3-mm collimation with a pitch of 2 is employed, the scan will require just under 17 seconds with a 3.9 mm effective slice thickness. Thus, whenever possible, it is preferable to maximize spatial resolution using thinner collimation while increasing the pitch to cover the entire scan distance more expediently. A faster scan will in-crease scanner throughput and minimize respiratory motion degradation.

Field-of-view--The field-of-view (FOV) deserves special consideration for two reasons. First, because the conditions that prompt helical CT examination of the aorta are often nonspecific, evaluation of the entire thorax is important. The diagnosis may be found in the pleural space or peripheral lung parenchyma, not the aorta. Additionally, using small FOVs will decrease photon flux in the imaging volume, contributing increased image noise. This may be partially compensated for by increasing the mA, but the scanner may not permit a sufficient increase in mA if the length of the scan is long. For these reasons, it is advisable to measure the FOV from outer rib to outer rib at the widest portion of the thorax. This FOV creates a good compromise between a large enough FOV to visualize the entire thorax yet provides a larger image with improved resolution that is easier to read.

Reconstruction increment--A reconstruction increment that provides nearly a 50% overlap in slice thickness is generally sufficient to generate excellent quality images. Recent work suggests that there is limit at which overlapping the reconstructions no longer provide improved longitudinal resolution. ¹ Beyond this point, further overlap only generates more images and thus only increases scan reconstruction time and storage requirements. The optimal overlap depends on the pitch employed. As a compromise, a 50% overlap generally provides optimal resolution and enhances the quality of post-processing techniques. One should avoid using reconstruction increments that are exact harmonics of the collimation employed (i.e., a 2.5-mm reconstruction increment with a 5-mm collimation scan). In such circumstances, artifacts may be introduced if post-processing techniques are used.

Iodinated contrast--Amount and concentration: There is no consensus regarding what iodine concentration should be routinely employed for helical CTA of the aorta. The common practice of using undiluted (300 mg I/mL or 360 mg I/mL) is usually sufficient. In one study, an iodine concentration of 125 mg I/mL was found to be unacceptable at any flow rate. ² In this same study, an iodine concentration of 150 mg I/mL provided satisfactory images, when the flow rate was adjusted. This iodine concentration had the added benefit of decreasing the amount of streak artifact emanating from thoracic venous structures. However, questions regarding the safety of diluted contrast preparations remain because such dilute mixtures are not generally commercially available. Obviously, there are issues of practicality as well. Generally, we employ undiluted contrast (300 mg I /mL) for all thoracic helical CTA applications.

Rate: There is considerable variation among investigators regarding the rate at which contrast is delivered for helical CTA of the thorax. Generally speaking, a rate of 3 cc/sec is sufficient, although some investigators use rates as high as 5 cc/sec. Some consider higher rates as less practical because they may require larger bore catheters; however, rates of 4 to 5 cc/sec may be achieved using 20-gauge catheters. Generally, an injection rate of 3.5 cc/sec is satisfactory for helical CTA applications in the chest. For such injection rates, 22-gauge catheters are adequate. Indeed, flow rates of 4 to 4.5 cc/sec may be used through such catheters when required. It should be noted that when higher injection rates are used, a larger volume of contrast must be delivered to maintain the injection throughout the scan acquisition.

Injection timing: An appropriate scan delay is critical for excellent vascular imaging. As a general rule of thumb, a standard delay of 25 seconds for helical CTA of the thoracic aorta will usually suffice. Patients with cardiomyopathy or an unsuspected stenosis of the injected vein may require longer delays to achieve optimal aortic opacification. Patients with hyperdynamic cardiac function may require a shorter delay. The time to peak aortic opacification from patient to patient varies considerably. Van Hoe et al ³ found that this delay varied from 11 to 30 seconds, with an average of 20 seconds. One may perform a test injection to determine the time to optimal aortic opacification in a given patient. With this method, a 20-cc bolus of contrast is administered, followed by a 10 second delay. After the 10 second delay, one image every 2 seconds is acquired at the same level (often the cranial aspect of the descending thoracic aorta) for a total of 30 seconds. The image with the greatest contrast density is used to select the proper scan delay. This method is somewhat cumbersome to perform routinely, and has the added detraction of an increased radiation dose as well as a slight increase in visceral background attenuation due to the injected contrast.

As an alternative, bolus timing software packages may be purchased for most modern CT scanners. Such programs allow the time to peak enhancement to be monitored without a separate test injection. These programs monitor the attenuation of the vessel in question during the contrast injection, and display the attenuation graphically in real-time. Once the graph demonstrates a sharp rise in attenuation, the scan sequence is triggered manually. When possible, we prefer to use bolus timing software to ensure proper arterial opacification. With even minimal experience, the CT technologist can learn to achieve excellent arterial opacification without the direct supervision of the radiologist.

Distance to be scanned--The entire distance to be scanned is important for several reasons. Perhaps, most importantly, the contrast injection must be maintained for all but the last few seconds of the scan acquisition. Failure to do so may allow unopacified blood to enter the imaging volume, thus creating artifacts and diminishing the quality of the study. Second, the longer the distance to be scanned, the greater the heat loading on the tube, necessitating a lower mA be used. This is particularly problematic in larger patients, who may require all the photons the tube can muster. Third, imaging beyond the desired structures will provide additional information, but at the expense of more tube exposures. As the x-ray tube has a finite life span, extra tube exposures may come at significant cost. Finally, imaging beyond the desired volume also contributes to increased patient radiation dose.

kVp and mA--There is usually no reason to adjust the kVp from the standard values of 120 to 140 kVp. However, the mA used is critically important for achieving excellent quality studies. While it is preferable to keep mA as low as possible to reduce patient dose, little is accomplished if the patient receives a somewhat lower radiation dose at the expense of a poor quality study. The contrast resolution on CT scanners is heavily dependent on mA. Noisy images resulting from increased quantum mottle often result from using mA values that are too low for a particular patient. Although for the average patient, mA is often not a major consideration, for larger patients, an upward adjustment in the mA is critical to achieve a high quality study. Often this adjustment must be performed manually because modern CT scanners are often programmed to minimize the mA to reduce tube heat loading and patient dose. When larger patients are being scanned, the mA should be adjusted manually to near maximum to diminish image noise and provide the highest quality imaging. Careful attention to FOV and scanning distance in this circumstance is also required.

Tube rotation time--Modern scanners now allow tube rotation times as low as 0.5 seconds. GE scanners (GE Medical Systems, Milwaukee, WI) have a minimum tube rotation time of 0.8 seconds. There are options to increase the tube rotation time that may have a role in other thoracic applications (e.g., HRCT). Helical CTA of the aorta, however, is best accomplished with the fastest allowable tube rotation time.

Normal aortic anatomy

An extensive discussion of mediastinal anatomy is beyond the scope of this review, but normal aortic anatomy will be considered briefly. Of course, the size and shape of the aorta differs significantly among individuals and even within the same individual at different ages. The thoracic aorta may be divided into 5 segments: the aortic root, the ascending aorta, the proximal aortic arch, the posterior aortic arch, and the descending thoracic aorta.

The aortic root is the short segment of the aorta arising from the base of the heart and containing the valve, the annulus, and the sinuses of Valsalva. The right and left coronary arteries arise from the right and left sinuses of Valsalva, respectively. The third, posteriorly located, sinus of Valsalva is termed the noncoronary sinus. The normal diameter of the adult aorta just cranial to the root averages 3.6 cm (range 2.4 to 4.7 cm). ^4,5

The ascending aorta extends from the root to the origin of the right brachiocephalic artery. The average diameter of the adult ascending aorta is 3.5 cm (range 2.2 to 4.7 cm). ^4,5

The aortic arch begins at the origin of the right brachiocephalic artery and ends at the attachment of the ligamentum arteriosum. It is divided into two segments: the proximal arch and the posterior (distal) arch. The proximal arch extends from the origin of the right brachiocephalic artery to the origin of the left subclavian artery, also giving rise to the left common carotid artery. The posterior or distal arch encompasses that segment of the arch from the origin of the left subclavian artery to the ligamentum arteriosum and is also known as the aortic isthmus. This segment is occasionally slightly narrower than the proximal descending thoracic aorta, particularly in infants.

The descending thoracic aorta begins after the ligamentum arteriosum and extends to the aortic hiatus in the diaphragm. The most cranial aspect of the descending thoracic aorta may appear slightly dilated and is known as the "aortic spindle." This finding is more commonly encountered in children than adults. The mid-portion of the descending thoracic aorta has an average diameter of 2.48 cm (range 1.6 to 3.7 cm). The distal descending thoracic aorta (just above the diaphragm) has an average diameter of 2.42 cm (range 1.4 to 3.3 cm). ^4,5

Obviously, the average aortic diameters are less in children. Normal aortic diameter measurements for children have been published. ^5,6 The ascending aorta is normally always larger than the descending aorta. ⁵

Generally, the aortic wall is only a few millimeters thick, and usually is not separable from the unenhanced aortic blood pool. Occasionally, the wall of the aorta is visible in anemic patients, appearing as a thin rim of increased attenuation that is smooth and of uniform thickness around the circumference of the vessel. ⁵

Thoracic aorta: Normal variants

Congenital anomalies of the aorta and the great vessels are beyond the scope of this review. The frequency and imaging appearance of such anomalies have been well described elsewhere. ^5,7 Normal variations in the aortic contour that will be discussed include the aortic spindle, ductus diverticulum, branch vessel infundibula, and pseudocoarctation.

Aortic spindle--As mentioned previously, the aortic spindle is the region of the posterior aortic arch located between the origin of the left subclavian artery and the ligamentum arteriosum. It appears as a circumferential bulge below the region of the isthmus (figure 1). ⁸

Ductus diverticulum--The ductus diverticulum is the term applied to a focal, convex bulge along anterior undersurface of the isthmic region of the aortic arch (figure 2). The major significance of this structure lies in distinguishing it from a posttraumatic pseudoaneurysm. The ductus usually is a smooth convexity that creates obtuse angles with the aortic wall, as opposed to the acute angles created by a pseudoaneurysm. Additionally, a ductus diverticulum does not cause delayed contrast washout, as might a posttraumatic pseudoaneurysm. ^8,10

Branch vessel infundibula--Infundibula of aortic branch vessels, including the brachiocephalic artery, left common carotid artery, left subclavian artery, and intercostal arteries may simulate traumatic injuries or aneurysms. Infundibula are recognized by their anatomic configuration and smooth margins and by the presence of a vessel emanating from the apex of the infunibulum. Infundibula also tend to occur in characteristic locations, commonly affecting the left subclavian artery and the third right intercostal artery. ⁸

Pseudocoarctation--Pseudocoarctation results from elongation of the aortic arch and kinking at the site where the aorta is tethered by the ligamentum arteriosum (figure 3). Although the configuration of the aorta in pseudocoarctation somewhat resembles true coarctation, because there is no pressure gradient across this region, collateral circulation does not develop.

Pitfalls in helical CT aortography: Normal anatomic structures

Normal pericardial recesses, the left brachiocephalic vein, the left inferior pulmonary vein, the left superior intercostal vein, the right atrial appendage, and normal thymus constitute the most frequently encountered normal anatomic structures that may simulate aortic pathology such as dissection or acute traumatic aortic injury. ¹¹

Pericardial recesses--The preaortic and retroaortic portions of the superior pericardial recesses are intimately related to the ascending aorta and may occasionally simulate dissection or hematoma. ¹² The preaortic recess is found along the anterior aspect of the ascending aorta, and the retroaortic portion of the superior pericardial recess is located posterior to the ascending aorta near the level of the left pulmonary artery. The homogeneous water attenuation and characteristic locations are clues to the proper diagnosis. ¹¹

Left inferior pulmonary vein--The left inferior pulmonary vein is in close proximity to the descending thoracic aorta near the former's entry into the left atrium. Where it is in close contact with the aorta, this structure may mimic dissection of the descending thoracic aorta. Knowledge of the normal appearance and course of this vessel and following it superiorly to its termination in the left atrium ensure the proper diagnosis. ¹¹

Left brachiocephalic vein--The unopacified left brachiocephalic vein may simulate a mediastinal hematoma in the setting of trauma. When opacified and low-lying, the left brachiocephalic vein may occasionally mimic a Stanford type A dissection of the ascending aorta. ¹¹

Left superior intercostal vein--Occasionally, the left superior intercostal vein is visible adjacent to the left lateral aspect of the aortic arch as it courses anteriorly from the left-sided accessory hemiazygos vein to the left brachiocephalic vein (figure 4). When the left upper extremity is injected, this vessel may enhance vigorously and can mimic dissection. The focal nature of the abnormality as well as knowledge of the normal course of this vessel will allow the proper diagnosis. ¹¹

Right atrial appendage--The right atrial appendage is normally visible on helical CT aortography anterior to the proximal ascending aorta just above the aortic root, where it may simulate aortic pathology (figure 5). Following this structure into the right atrium on contiguous images will demonstrate its true nature. ¹¹

Thymus--The thymus is normally located anterior to the aortic arch and ascending aorta. In younger patients, residual thymus may resemble hematoma or a false lumen of an aortic dissection. The characteristic location and triangular configuration in a younger patient are clues to the correct diagnosis. ¹¹ Although the lack of mass effect and focal nature of the thymus help to distinguish it from mediastinal hematoma, differentiating the normal thymus from mediastinal hematoma in pediatric trauma patients may be difficult.

Pitfalls in helical CT aortography: Periaortic pathology

Periaortic pathology such as medial left lower lobe atelectasis, left pleural effusion, mediastinal masses or adenopathy, and pericardial effusion may simulate aortic dissection, ¹¹ intramural hematoma, or mediastinal hematoma. Additionally, anemia may render the aortic wall visible and may resemble intramural hematoma.

Left lower lobe atelectasis--Enhanced, atelectatic lung immediately adjacent to the descending thoracic aorta may simulate dissection (figure 6). Additionally, atelectatic lung in this location on unenhanced scans may resemble intramural hematoma. Lack of a constant relationship to the aorta as well as the presence of air bronchograms visible on lung windows ¹¹ will suggest the proper diagnosis.

Left pleural effusion--Left pleural effusion may resemble periaortic hematoma, particularly in the acutely injured patient. Usually effusion is apparent elsewhere, and occasionally attenuation measurements may be useful for distinguishing effusion from aortic pathology. When required, decubitus views may allow the proper diagnosis.

Mediastinal masses and adenopathy--Mediastinal masses and adenopathy may mimic mediastinal hematoma in the trauma patient. Usually the focal and lobulated appearance and location of mediastinal masses and adenopathy will suggest the correct diagnosis. ¹¹

Pericardial effusion--Pericardial effusion may simulate aortic dissection or mediastinal hematoma. Pericardial fluid is usually of homogeneous low attenuation, unless complicated by hemorrhage. Knowledge of the normal pericardial recesses also aids in diagnosis.

Anemia--The aortic wall may become visible as a thin, uniform ring of high attenuation in anemic patients (figure 7). ⁵ This appearance may occasionally cause diagnostic difficulty on unenhanced scans because it may resemble intramural hematoma. The smooth, uniform, homogeneous appearance and absence of periaortic fat stranding or hematoma as well as the tendency to primarily affect the ascending aorta allow the proper diagnosis.

Normal aortic anatomy: Technical difficulties

Poor contrast enhancement--Poor contrast enhancement may result from improper contrast bolus timing due to a wide variety of factors, including poor cardiovascular function, stenosis of the injected vein, or slow administration of contrast media. Poor vascular opacification could obscure the diagnosis of dissection (figure 8). ¹¹ A timing bolus or bolus timing software are useful techniques for ensuring proper contrast delivery.

kVp and mA--As discussed previously, kVp, section thickness, FOV, and, especially, mA have a profound influence on image quality. Careful attention to the technical parameters of the scan can improve image quality by reducing noise.

Streak artifacts--Streak artifact results from dense, highly concentrated contrast causing beam hardening and obscuring photon transmission. When high-density contrast material markedly reduces photon transmission, the scanner detectors may record no transmission. CT scanner reconstruction programs do not recognize this phenomenon, and streak artifacts will result. Streak artifact commonly affects the left brachiocephalic vein and superior vena cava, potentially obscuring the aortic arch and ascending aorta. Streak artifacts may also result from pacemakers, surgical staples, external monitoring devices, or positioning the patient's arms at their sides during the scan. ¹¹ These artifacts are readily recognized by the radial orientation of the artifact and by observing that the dense contrast column is the source of the artifact (figure 9). Streak artifacts may be reduced by using dilute contrast mixtures, scanning caudal to cranial, or injecting via the right upper extremity. ¹¹

Motion artifact--Motion artifacts can be quite problematic, particularly at the base of the heart. Motion artifacts may either obscure the diagnosis or simulate the appearance of aortic dissection (figure 10). Noting motion elsewhere on the scan, as well as the fact that the artifact is usually absent or markedly different on immediately adjacent levels, may allow recognition of the abnormality.

Aortic pathology: Atherosclerotic vascular disease

Aortic atherosclerotic vascular disease (ASVD) is increasingly recognized as a source of stroke and visceral and lower extremity ischemia resulting from peripheral embolization. ^13-21 Ulcerated atherosclerotic plaques in the ascending aorta and aortic arch have been noted with increased frequency in patients with stroke or death due to cerebrovascular disease, ^14,20 and contribute to cerebrovascular events among patients undergoing cardiovascular surgery. ^5,17 Features of aortic ASVD include smooth intimal plaques, ulcerated plaques, calcified plaques, mobile thrombi, and "protruding" atheromas (figure 11). ^13,21 Plaques thicker than 4 mm have been associated with an increased risk of stroke. ^13,19 While calcified plaque may be relatively stable, uncalcified or ulcerated plaque may pose an increased risk for embolization. ^14,22 Thrombi may be superimposed on atherosclerotic plaques; in particular, protruding atheromas are prone to embolize. ^15,21,23 Such thrombi may resolve with anticoagulation. ^13,24

HCTA nicely demonstrates the location and morphology of atherosclerotic plaque. Atherosclerotic plaque typically appears as low attenuation material internal to the aortic wall (figure 11). Calcified plaque is readily apparent, and plaque ulceration may also be seen. Although TEE is used more commonly for the specific investigation of aortic ASVD, disease in the cranial aspect of the ascending aorta and arch may be difficult to identify with TEE. In contrast, HCTA demonstrates plaque in the ascending aorta and aortic arch well. ²⁵

Aortic pathology: Aortic dissection

Aortic dissection results from a primary tear in the intima of the aorta that allows blood to gain access to the aortic media; blood may then propagate proximally and/or distally within the media, creating a false lumen. The false lumen may or may not re-enter the true aortic lumen at a point removed from the primary intimal tear. The intimal tear itself may be a primary inciting factor in aortic dissection ²⁶ or it may be the result of primary weakening of the aortic media due to a spontaneous intramural hematoma. ⁵

Aortic Dissection: Etiologies--Predisposing factors for aortic dissection include hypertension, aortic valve disease, coarctation of the aorta, connective tissue disorders (e.g., Marfan's syndrome, Ehlers-Danlos syndrome), aortic aneurysm, cystic medial necrosis, cardiovascular surgery, infections (syphilis and bacterial), and non-infectious causes of arteritis. ^5,7

Clinical evaluation--Patients with aortic dissection often present with severe chest pain that may mimic myocardial infarction or pulmonary embolism. Pulmonary edema resulting from cardiac failure may occur due to acute aortic insufficiency. Cardiac tamponade may occur with intrapericardial rupture of the dissection. Neurologic sequelae resulting from aortic branch vessel occlusion, such as paraplegia, stroke, and syncope, may be presenting manifestations of aortic dissection. Although uncommon, branch vessel occlusion may cause mesenteric or limb ischemia to be the initial manifestation of aortic dissection. Differential blood pressures may be noted on physical examination.

Classification schemes--Two well known classification schemes for the extent of aortic dissection exist: the DeBakey ²⁷ and Stanford classifications. DeBakey type I dissections (figure 9B) begin in the ascending aorta and extend for a variable distance beyond the aortic arch. DeBakey type II dissections involve the ascending aorta only, and DeBakey type III dissections involve the descending thoracic aorta beginning distal to the left subclavian artery. The Stanford classification scheme primarily considers involvement of the ascending aorta and has largely replaced the DeBakey classification. A Stanford A dissection involves the ascending aorta, with or without descending thoracic aortic involvement. Stanford B dissection is confined to the descending thoracic aorta, beyond the origin of the left subclavian artery. Classification is important because most Stanford A (DeBakey type I and II) dissections are treated surgically, ²⁸ whereas Stanford B (DeBakey type III) dissections are usually managed medically, provided evidence of end-organ ischemia is not present.

The goals ⁷ of HCTA imaging are to:

1) identify the intimal flap (figures 12-19, 21);

2) identify any branch vessel involvement (great vessels, mesenteric and renal arteries) (figures 13 and 14);

3) identify the presence of pericardial fluid (intrapericardial rupture) (figure 15) or periaortic hematoma (aortic rupture) (figure 16);

4) identify extent of dissection;

5) evaluate size of the aorta (figure 17); and

6) evaluate the patency of the false lumen and degree of true lumen compression (figures 18 and 19).

HCTA findings of aortic dissection--The HCTA diagnosis of aortic dissection is based on findings on both unenhanced and enhanced scans. Unenhanced scans are valuable for demonstrating aortic intramural hematomas (figure 20). Intramural hematomas (IM) appear as focal, eccentric thickening of the aortic wall that is high in attenuation. ^5,29 Unenhanced scans may also demonstrate displacement of aortic intimal calcifications (figure 20). However, this finding may be difficult to assess in the presence of marked aortic tortuosity. ³⁰ Furthermore, the displaced intimal calcifications of aortic dissection are often not easily distinguished from calcified atherosclerotic plaque and thrombus, nor does this sign allow one to reliably distinguish acute from chronic dissections. ³¹

The single best criterion for the diagnosis of aortic dissection on enhanced HCTA scans is the demonstration of an intimal flap separating the true and false lumens (figures 12- 19, 21). Contrast enhanced studies are also valuable for demonstrating the patency of branch vessels as well as revealing differential flow rates between the true and false lumens (figures 17 and 18). Enhanced scans also are useful for estimating the size of the aorta (figure 17).

Occasionally, it can be difficult to distinguish true from false lumen. The most specific indicator for the false lumen is the presence of irregular strands within the lumen, known as "cobwebs." Cobwebs represent residual fragments of aortic media separated during the dissection. ³² Frequently, the true lumen is located anteriorly in the descending thoracic aorta (figures 12, 17-19). Often the true lumen is smaller than the false lumen due to compression by the latter (figures 12, 14-19). It has been reported that the true lumen may assume a concave orientation with respect to the false lumen when the latter generates relatively higher pressure, a situation that is associated with an increased likelihood of impaired end-organ perfusion (figure 19). ³³

Older data suggests that the intimal flap is visualized on dynamic CT in only 63% to 70% of cases; ^34,35 this figure may be higher with the rapid volumetric acquisitions possible with HCTA. ³⁶ In cases when an intimal flap is not seen, the diagnosis of aortic dissection must be made on the basis of ancillary criteria, such as distortion of the aortic contour, intramural high attenuation (figure 20), periaortic hematoma (figures 16 B and 16C), or displaced intimal calcifications (figure 20).

HCTA sensitivity and specificity for aortic dissection--Dynamic, contrast-enhanced CT scanning (a non-volumetric technique) has demonstrated a sensitivity of 93.8% and a specificity of 87.1% for the diagnosis of aortic dissection. ³⁷ Recently, Sommer et al, ³⁸ comparing HCTA with TEE and MRI, demonstrated sensitivities of 100% for all three techniques. Specificity was 100%, 94%, and 94% for HCTA, TEE, and MRI, respectively. Disadvantages of HCTA compared with these other modalities include the inability to demonstrate aortic insufficiency or involvement of the coronary arteries. Multiplanar reformations and rendering techniques (figures 12B, 17, and 21) are useful for demonstrating dissections in a format more familiar to clinicians and surgeons, although such techniques rarely add information that is not apparent on the axial images.

Aortic pathology: Aortic aneurysms

Aneurysm of the aorta is defined as dilation of the aorta involving all three wall layers equaling or exceeding twice the normal diameter. ^5,7,39,40 Pseudoaneurysms (false aneurysms), however, represent saccular dilations that do not contain aortic intima. Typically, such aneurysms are associated with blunt chest trauma or penetrating atherosclerotic ulcers or, less commonly, with infection or cardiovascular surgery. ⁵ Etiologies of true thoracic aortic aneurysms include atherosclerosis, infection (mycotic aneurysms), and cystic medial necrosis (annuloaortic ectasia). ⁷ Certain etiologies of thoracic aortic aneurysms tend to be associated with particular locations. For example, causes of annuloaortic ectasia (figure 22) and syphilis usually affect the ascending aorta, whereas atherosclerotic aortic aneurysms (figure 23) most often affect the descending thoracic aorta. ⁷

Growth rate and risk of rupture--Thoracic aortic aneurysms have been associated with a growth rate of 0.42 cm/year as opposed to the 0.25 cm/ year growth rate suggested for abdominal aortic aneurysms. ^41,42 More than 25% of thoracic aortic aneurysms are accompanied by infrarenal abdominal aortic aneurysms. ^5,40,43 The most dreaded consequence of thoracic aortic aneurysm is rupture (figure 24). The risk of rupture increases with increasing aneurysm size, with ruptured ascending aortic aneurysms often measuring >6 cm in diameter. ⁷ The frequency of rupture varies from 40% to 70% depending on the series, ^5,44 and 30% to 50% of deaths related to thoracic aortic aneurysms are due to rupture. ⁷ Because elective thoracic aortic aneurysm repair is associated with a lower mortality than emergent repair, (9% versus 22%, respectively) ⁴⁵ and the risk of rupture increases with increasing size of the aneurysm, size criteria for operative intervention have been suggested. Coady et al ^45,46 noted that the median size of rupture or dissection of ascending and descending aortic aneurysms was 5.9 cm and 7.2 cm, respectively. Therefore, these authors advocate operative intervention for thoracic aortic aneurysms when aneurysm size exceeds 5.5 cm for ascending and 6.5 cm for descending thoracic aortic aneurysms.

CT evaluation of thoracic aortic aneurysms--HCTA accurately identifies the extent and size of thoracic aortic aneurysms. Atherosclerotic aortic aneurysms typically appear as a fusiform dilation of the aorta, commonly affecting the descending aorta. Causes of cystic medial necrosis, (especially Marfan's syndrome and Ehler's-Danlos syndrome), result in an aorta with a conical appearance that tapers superiorly; this appearance has been likened to the shape of a pear. The sinuses of Valsalva are often involved in such cases. Saccular aortic aneurysms may be due to infections (mycotic aneurysms) (figure 25). The morphology of a saccular aneurysm must always raise the possibility of pseudoaneurysm.

HCTA clearly defines the extent of the enhancing lumen as well as the degree and morphology of associated thrombus. HCTA also clearly delineates the degree and location (intimal or within the thrombus itself) of calcification of the aneurysm. The local effect of thoracic aortic aneurysms (compression or erosion of adjacent structures) is also clearly defined with HCTA. Branch vessel involvement is also clearly depicted with HCTA.

The HCTA findings of rupture of thoracic aortic aneurysms include high attenuation fluid in the pleural or pericardial spaces or within the wall of the aorta. Mediastinal fat stranding representing hematoma also suggests the possibility of aneurysm rupture (figure 24). The "draped aorta" sign has been suggested as a sign of an early, contained rupture. This sign is considered present when the posterior wall of the aorta is either not identifiable as distinct from adjacent structures or when it is closely applied to and follows the contour of the adjacent vertebral bodies. ⁴⁷

Multiplanar reformations and rendering techniques--Multiplanar reformations, shaded surface displays, and volume-rendering techniques (figures 1B to 3, 11C, 12B, 17B, 21, and 25B) are useful methods for providing alternate formats for viewing large data sets. Such techniques are particularly valuable for demonstrating pathology to nonradiologists in a more familiar format (i.e., a sagittal oblique view that resembles conventional angiography). However, such techniques rarely change the initial interpretations of the axial source images. ⁴⁸

Aortic pathology: Intramural hematoma

Intramural hematoma (IMH) represents localized hemorrhage within the aortic media. Several methods for the formation of IMH have been proposed: 1) rupture of the vasa vasorum resulting in weakening of the aortic wall; 2) spontaneous thrombosis of the false lumen of an aortic dissection; and 3) penetrating atherosclerotic ulcer induced by rupture of an intimal atherosclerotic plaque, allowing blood to gain access to the aortic media.

It is unclear which mechanism predominates. Indeed, it is likely that all of the above mechanisms play some role in the development of IMH.

CT of IMH--On CT scans, IMH appears as crescenteric, high attenuation material within the wall of the aorta (figures 20, 26 to 28). Although the hyperattenuation may be perceived on postcontrast images (figures 26B to 28), the finding is usually far better appreciated on unenhanced images (figures 20 and 26A). Thus, protocols for aortic imaging should begin with noncontrast helical images of the chest. IMH may present as focal thickening of the aortic wall with internal displacement of intimal calcifications (figures 20 and 28). Unlike atherosclerotic plaque, IMH generally creates a smooth margin with the contrast-enhanced aortic lumen (compare figures 11 and 26, 28).

Natural history of IMH--The natural history of IMH is not completely clear. Several fates may befall an intramural aortic hematoma. Pathologically, IMH, no matter the mechanism, results in weakening of the aortic wall; this weakening may predispose to dissection or frank rupture. This assertion is evidenced by several series demonstrating IMH associated with either hematoma within the mediastinum or pericardial sac, ⁴⁹ or conversion of IMH to either imaging or surgically proven dissections ^50-55 or saccular ⁵⁴ aneurysms. Factors that predict the conversion of IMH to dissection, rupture, or saccular aneurysm are unclear, and this uncertainty results in ambiguity regarding proper management. Several series indicate that IMH in the ascending aorta (figure 26) portends a poor prognosis and thus requires urgent surgical repair. ^49-51,53 IMH involving the descending thoracic aorta is managed as a type B dissection. ^5,50,51 IMH that is not managed surgically should be periodically followed for early detection of complications such as saccular aneurysm, pseudoaneurysm, or classic dissection. Several authors have advocated imaging every 3 months in the first year after diagnosis ^5,51 and continued long-term follow-up to detect the development of fusiform aneurysms. ^5,51

Aortic pathology: Penetrating atherosclerotic ulcer of the thoracic aorta

Penetrating atherosclerotic ulcer (PAU) occurs when atherosclerotic plaque penetrates through the intima and internal elastic membrane of the aorta, allowing blood to gain access to the aortic media. PAU results in IMH (figure 27), and can progress to dissection, ^56,57 saccular aneurysm, ⁵⁸ pseudoaneurysm (figure 29), ^57,59,60 or frank aortic rupture. ^58,59,61-64

Clinical presentation of PAU--PAU, like dissection, may be associated with chest or back pain, ^60,65,66 although this entity is most often detected in asymptomatic patients imaged for some other reason. Patients with PAU are usually older than patients with dissection. ^58,60,62,63 PAU is most often located in the descending thoracic aorta, ^29,60,67,68 although they may present in the arch or, less commonly, the ascending aorta. ⁶⁹

HCTA of PAU--PAU manifests on unenhanced helical CT as an intramural hematoma (figure 27). Aortic wall thickening may be seen, ^5,29,60 and displaced intimal calcifications ⁷⁰ may also be present. Enhanced images demonstrate a focal contrast collection projecting beyond the confines of the lumen of the aorta (figure 29). ^{5,29,60,66,70} Aortic wall enhancement ⁷⁰ and, rarely, active contrast extravasation, may be encountered. ^5,64 PAU is frequently multiple, and evidence of complications, such as dissection ⁵⁶ and pseudoaneurysm (figure 29), ⁵⁸ may coexist. PAU may also be associated with aortic rupture, evidenced by pericardial or pleural high attenuation fluid ⁷⁰ or mediastinal hematoma. ^{5,58, 61}

Natural history of PAU--Early surgical intervention is advocated for patients with PAU of the ascending aorta or cases of complicated PAU who are operative candidates. Conservative therapy is generally employed for patients with PAU of the descending thoracic aorta that is stable or asymptomatic, ⁶⁴ or in patients who are too unstable for operative intervention. ⁶⁹ It should be understood that surgery for PAU is generally more extensive than that for dissection. ^66,70 For cases that are managed conservatively, imaging surveillance is recommended for early detection of potential complications such as saccular or fusiform aortic aneurysm, dissection, or rupture. ^5,60

Aortic pathology: Aortitis

Aortitis usually refers to inflammatory condition affecting the aortic wall. Takayasu's arteritis is the most common such inflammatory disorder, although Reiter's syndrome, psoriasis, ankylosing spondylitis, relapsing polychondritis, giant cell arteritis, and infections (particularly syphilis) are other potential etiologies. ⁷

Takayasu's arteritis is a vasculitis that results in inflammation involving the media and adventitia, with reactive change in the intima. ⁷¹ This condition is commonly associated with, though not limited to, young Asian women and affects women 8 to 10 times as often as men. ^7,71 This disease is may be classified based on the pattern of anatomic involvement: ⁷ 1) aortic arch and branch vessels; 2) segmental involvement of the thoracic and abdominal aorta and branch vessels; 3) a combination of types I and II; and 4) involvement of the pulmonary arteries.

Others classification schemes exist. ⁷¹ Takayasu's arteritis typically results in multifocal stenoses and vascular occlusions, ⁷ although aneurysms (fusiform more than saccular) may occur. ⁷¹ Aortic wall thickening and enhancement has been reported as a manifestation of early disease, whereas calcification of the aortic wall, vascular occlusions, and collateral vessel formation are generally late findings. ⁷¹

Aortic pathology: Mycotic aneurysms

Mycotic aneurysms are the result of infection of the aortic wall and occlusion of the vasa vasorum by septic emboli that results in weakening of the aortic wall (figure 25), predisposing to aneurysm formation. Etiologies of mycotic aneurysm include septic emboli from intravenous drug use and in-dwelling catheters, infection of prosthetic valves, or infection of atherosclerotic plaque. Common infectious agents include Salmonella (figure 25), Staphylococcus aureus, streptococci, tuberculosis, and fungi, such as Candida and Aspergillus. ⁷

Mycotic aneurysms are commonly saccular (figure 25) and may grow rapidly. They may be associated with surrounding periaortic fat infiltration and inflammatory changes or even gas formation. A mycotic etiology of a saccular aneurysm is often suggested when an aneurysm is found in an atypical location. However, the most common location is the undersurface of the aortic arch, near the ligamentum arteriosum, ⁷ where a mycotic aneurysm may be mistaken for a post-traumatic pseudoaneurysm. Mycotic aneurysms are prone to rupture.

Aortic pathology: Acute traumatic aortic injury

Acute traumatic aortic injury (ATAI) is usually the result of severe deceleration injury, such as high speed motor vehicle accidents (MVA) or falls from significant heights. ATAI accounts for 10% to 20% of fatalities in MVAs and results in immediate death in 80% to 90% of cases. ^72-78 Among patients with ATAI who survive transport from the initial trauma scene, the mortality of untreated ATAI is high: 30% die in the ensuing 6 hours, ^{72, 77, 78} nearly 50% by 24 hours, ^72,77 and 90% within the following 4 months. ^72,77 Chronic pseudoaneurysm may result in the small fraction of untreated long-term survivors. ^72,74

Several mechanisms for ATAI have been postulated. Theories such as the "osseous pinch," the "water-hammer effect," and horizontal and/or vertical deceleration have been proposed. The osseous pinch theory holds that the aorta is "pinched" between the bones of the anterior thorax and the spine, resulting in injury. The "water-hammer" theory suggests that blunt trauma causes aortic compression, resulting in an acute and dramatic rise in intravascular pressure. Horizontal and vertical deceleration mechanisms cause injury by creating bending forces and shear stress at sites where the aorta is relatively fixed (especially the isthmus). All of these possibilities may play some role in any given patient.

The most common site of injury is the aortic isthmus (90%), followed by the ascending aorta (5% to 10%), and the descending thoracic aorta near the diaphragmatic hiatus (1% to 3%). ^7,72 Great vessel injuries may coexist. Pathologically, a nearly circumferential laceration is usually present, although partial tears may occur. ^7,72

HCTA of ATAI--HCTA findings of ATAI are classified as direct or indirect (figures 30 to 34). One of the most commonly encountered direct signs of HCTA is a pseudoaneurysm (figure 30). Other direct findings include abnormal aortic contours or abrupt caliber changes, pseudocoarctation, occlusion of a segment of aorta (figure 31), and an intimal flap. Indirect findings of ATAI include mediastinal or retrocrural hematomas. Though indirect findings suggest the possibility of ATAI, they may be the result of mediastinal venous bleeding. When a mediastinal hematoma is encountered, its relationship to the aorta is of paramount importance (figures 32 and 33). Hematomas that obliterate the fat plane surrounding the aorta or great vessels remain suspicious for occult ATAI and are usually evaluated with aortography (figure 32). Mediastinal hematomas that do not directly contact the aorta or great vessels usually represent mediastinal venous bleeding, and aortography is not required (figure 33). In the rare circumstance that a patient survives undiagnosed ATAI, a chronic pseudoaneurysm may result (figure 34).

Overall, HCTA is 100% sensitive and 82% specific for the diagnosis of ATAI. ⁷⁹ Pate et al ⁸⁰ recently evaluated 6169 patients with blunt chest trauma, of whom 47 were diagnosed with ATAI. None of the cases in which the CT scan was read as "normal" were associated with proved ATAI, and the use of HCTA resulted in significantly reduced utilization of aortography. ⁸⁰

The postoperative aorta

Aortic aneurysms and dissections are often repaired using one of two general methods: an interposition graft or an inclusion graft. Use of the interposition graft technique implies resection of the pathologic aortic segment and reconstruction of the vessel with graft material, commonly made of Dacron. Composite interposition Dacron grafts containing a mechanical aortic valve may be used when required. ⁸¹ When an interposition graft is used, necessary vasculature, such as the coronary arteries, is reimplanted into the graft. Occasionally, high attenuation felt rings (figures 35 and 36) are employed to reinforce the anastamosis of interposition grafts; these rings indicate the site of anastamosis. ⁸¹ If such rings are not used, the site of the anastomosis may be surmised by noting an abrupt change in caliber of the aorta or an abrupt change in an atherosclerotic native aorta versus a disease-free graft. ⁸¹ Felt pledgets are also sometimes employed with interposition grafts to reinforce the sites of cannula placement. These felt pledgets, like felt rings, are high in attenuation and can resemble a pseudoaneurysm to the unwary. ⁸¹ The coronary artery anastomoses represent another pitfall of composite interposition grafts that may simulate pathology. Often the coronary arteries are reimplanted into the aortic graft with a portion of native aortic root known as coronary buttons. These buttons may occasionally appear somewhat prominent and may simulate a pseudoaneurysm if the true nature of the finding is not understood. ⁸¹

The use of inclusion graft technique entails insertion of graft material within the native, diseased aorta. This form of reconstruction creates a potential space between the graft material and aorta. ⁵ This potential space may thrombose or contain flowing blood. Blood flow within the perigraft space does not mandate surgery unless the situation is associated with hemodynamic instability. ⁵

Serious postoperative complications include dehiscence of the surgical suture line, more commonly at the proximal site. ⁸¹ Dehiscence may result in pseudoaneurysm formation. Pseu-doaneurysm at the site of coronary artery reimplantation may result in myocardial ischemia and infarction. Aneurysm formation and dissection may also occur, particularly in patients with cystic medial necrosis. CT or MR surveillance of aortic grafts is therefore routinely recommended. ⁵

Innocuous findings commonly encountered following aortic repair include left lower lobe atelectasis, pleural and pericardial effusions, and mediastinal adenopathy. These findings usually resolve slowly. ⁸¹ With interposition grafts, low attenuation material within the mediastinum surrounding the graft is often encountered, even months or years following surgery. This material may represent hematoma organizing into fibrous tissue, and it may never completely resolve in some patients. ⁸¹ An intimal flap is often identified beyond the graft site in patients following dissection repair because surgical reconstruction frequently intentionally maintains blood flow to both the true and false lumens. If the false lumen continues to enlarge, a pseudoaneurysm of the false lumen may result.

Conclusion

Helical CT aortography is a rapid and accurate method for the evaluation of a wide variety of diseases affecting the thoracic aorta. Recent advances in CT technology have mandated careful attention to scan acquisition parameters. Proper scan methodology will ensure excellent scan quality, and an awareness of diagnostic pitfalls and the imaging findings of aortic diseases should allow an accurate scan interpretation in the vast majority of cases. AR