State

The radiologic assessment of patients suspected of having an aortic disseclion must be based on an understanding of the treatment options and how these are to be employed in any clinical setting. The appropriate selection and timing of imaging studies is crucial. The diagnosis of dissection must be quickly confirmed, other diseases that mimic dissection must be excluded, and the type and extent of dissection must be established so that appropriate therapy can be instituted. Although computed tomography, magnetic resonance (MR) imaging, and echocardiography greatly enhanced the ability to evaluate the aorta by noninvasive means, aortography remains the examination of choice for defining the vascular anatomy, especially when surgical intervention is considered. MR imaging may become the primary examination for the initial and subsequent evaluation of acute and chronic dissections as MR angiographic techniques improve and changes are made in monitoring equipment to allow the safe examination of acutely ill patients. Index terms: Aorta, CT, 56.1211 #{149} Aorta, section, 56.74,94.74 #{149} Aorta, MR studies, 94.1214 #{149} Aorta, surgery #{149} Aortography, 56.1243 #{149} State-of.art reviews Radiology

1991;

dis-

180:297-305

‘From the Department of Diagnostic Radiology and Nudear Medicine, Rush-Presbyte. rian.St Luke’s Medical Center, 1653W Congress Pkwy, Chicago, IL 60612. Received January 14, 1991; revision requested March 13; revision received April24; accepted April 30. Address reprint requests to the author. #{176}RSNA, 1991

dissection is the most cornmon catastrophe involving the aorta, occurring two to three times more frequently than acute rupture of the abdominal aorta (1). Few medical emergencies are more dramatic at onset or more fulminating in their course (2). If left untreated, the disease is often rapidly fatal (3-5). The importance of prompt recognition, differentiation from myocardial infarction, and institution of appropriate treatment cannot be overemphasized. Advances in medical and surgical therapy have resulted in current 30-day survival rates of 80%-90% (612) and overall 5- and 10-year survival rates of 57%-66% and 32%..-44%, respectively, with treatment (6,7,10). Patients with aortic dissection present with signs and symptoms resulting from the unpredictable alterations in end-organ blood supply that occur as the dissection propagates proximally and distally (2,13-18). Diagnosis is further complicated by the fact that acute aortic dissection may mimic many other entities including myocardial infarction, pericarditis, acute cholecystitis, and inflammatory conditions involving the costochondral region. The diagnosis can often be suspected from the clinical findings; however, the patient’s signs and symptoms correlate poorly with the site of origin and the extent of dissection. Although the plain radiographic findings are rarely diagnostic, a chest radiograph should be obtained in all patients suspected of having an aortic dissection. An abnormal chest radiograph may lend support to the diagnosis of aortic dissection in the appropriate clinical setting, however, normal findings do not exdude a dissection (19-21). Moreover, the chest radiograph does not delineate the location of the dissection, which is crucial for the selection of appropriate therapy. When aortic dissection is suspected, the selection and timing of imaging ORTIC

of the

Art

studies are crucial. The diagnosis must be quickly confirmed-thereby excluding other diseases that may mimic dissection-and the type and extent of dissection established so that appropriate treatment can be instituted. The widespread use of thrombolytic therapy for patients with impending myocardial infarction makes it imperative to rule out the presence of a dissection. Such therapy can be fatal if the patient’s symptoms are due to an acute dissection involving the ascending aorta or if myocardial infarction is present as a complication of aortic dissection. Although the diagnosis of myocardial infarction can usually be established clinically, in cases in which the dinical findings or the results of coronary arteriography are equivocal, further workup to rule out an aortic dissection is essential. Unfortunately, despite substantial advances in diagnosis and treatment in recent years, many patients die before a diagnosis is made (2,22) or after an incorrect diagnosis is made, such as myocardial infarction, pulmonary embolus, cerebrovascular accident, or an acute surgical abdomen (23). Aortography has long been the procedure of choice for evaluating aortic dissection. Recently, however, crosssectional modalities such as computed tomography (CT), echocardiography, and magnetic resonance (MR) imaging have proved useful in the noninvasive diagnosis of aortic dissection. Their role in management is less certain. This review will consider the role of these newer modalities and compare their utility to that of aortography. Each modality will be evaluated with regard to its ability to enable correct diagnosis of the presence and extent of a dissection, as well as its role in treatment planning, particu-

Abbreviation: giography.

DSA

=

digital

subtraction

IIIIIUII011111 1111111011 IIliiiII CLAG-J3U-

FXNN

an-

larly when surgical intervention contemplated. Additionally, the of each in subsequent management will be assessed.

is role

proximally into the ascending aorta or distally into the abdominal aorta or iliac vessels (2,4,24). TREATMENT

CLASSIFICATION The various classification systems were developed primarily for their therapeutic implications. Nevertheless it is imperative that the radiologist be aware of the essential features of each type of dissection so as to appropriately direct the radiologic evaluation. DeBakey et al (4) dassified disseclions as type I (originating in the ascending aorta and extending to the aortic arch and a variable distance beyond), type II (confined to the ascending aorta), and type Ill (originating beyond the origin of the left subclavian artery and extending a variable distance distally). Reul et al (12) further divided type III dissections into four categories, called lilaIfid depending on their distal extent. More recently, the Stanford classification system originally proposed by Daily et al (24) has gained wide acceptance. This system designates all dissections involving the ascending aorta as type A (proximal) regardless of the site of the intimal tear or the distal extent of the dissection. All other dissections are called type B (distal). Hirst et al (2) found that approximately 60% of dissections are type A and 40% are type B. In type A disseclions, aortic insufficiency may be present as a result of extension of the dissection into the perivalvular region with dislocation of the aortic valve (7). The most common and fatal complication of this type of dissection is rupture into the pericardial sac with resultant tamponade. The branches of the aortic arch may become occluded (4,7). In type A dissections the intimal tear can be located anywhere in the aorta. In type B dissections it is located in the descending aorta usually 2-5 cm distal to the origin of the left subclavian artery or, rarely, in the abdominal aorta. There may be retrograde extension of the dissection into the ascending aorta (2,4,24). Haverich et al (25) found that the primary intimal tear was located in the ascending aorta in 85(89%) of their 96 patients with type A disseclions. Six were in the aortic arch and the remaining five were in the descending aorta. In 33 of their 39 type B patients (85%), the primary intimal tears were in the descending aorta. Type A dissections may extend distally; type B dissections can extend 298

#{149} Radiology

The radiologic assessment of patients suspected of having an aortic dissection must be based on an understanding of the treatment options and how these are to be employed in any clinical setting. It is generally accepted that the most important factor in the management of aortic disseclion is whether the ascending aorta is involved irrespective of the site of the primary intimal tear or the distal extent of the dissection. This is the primcipal determinant of the subsequent clinical course, the patient’s prognosis, and the method of treatment. Therefore, any modality used to evaluate the aorta must allow accurate assessment of the ascending aorta, the competency of the aortic valve, the site of intimal tear, the presence or absence of aortic branch involvement, and the proximal and distal extent of the dissection. The definitive treatment of acute dissections involves the use of antihypertensive therapy possibly with surgery, depending on the type of dissection, the age and overall condition of the patient, and the hospital setting in which treatment is performed (26). There is general agreement that acute proximal or type A dissections require immediate surgical intervention once the patient’s condition has been stabilized (4,6-8,10,11,15,18,24,26-29). The goal is to resect the entire dissected segment and replace it with a synthetic graft, possibly with replacement of the aortic valve. If this cannot be accomplished, the entry site is eliminated and an attempt is made to obliterate the distal false lumen. Additional surgical procedures such as coronary artery bypass grafting are performed as indicated. The diversion of blood flow into the true lumen is intended to decompress the false lumen. However, the false lumen often remains patent distal to the surgical site because multiple entry sites are present. In such cases the false channel may continue to expand, and additional surgical procedures are necessary to prevent rupture of the false lumen. The surgical risk in these patients has decreased considerably in recent years so that surgical mortality of less than 10% has been reported in some series (6-10). Miller et al (8,30) found that the operative mortality is not affected by the location or successful resection of the primary inti-

mal tear, the presence of aortic insufficiency, dilatation of the aorta, prior cardiovascular surgery, or the need for aortic valve replacement or coronary artery bypass grafting. However, renal dysfunction, cardiac tamponade, visceral ischemia, or surgical intervention before the patient’s conchlion could be stabilized increased the operative mortality. There is less agreement about the optimal treatment of patients with acute distal or type B dissections. The high surgical mortality in early series led to the successful development of medical therapy for patients with stable distal dissections, aimed at reducing the velocity of left ventricular contractions and reducing systolic blood pressure to the lowest level compatible with sustaining adequate cerebral, renal, and cardiac perfusion (11,18,26, 29,31-35). Surgery is usually reserved for patients in whom medical therapy fails, as evidenced by persistent symptoms; progression of the dissection; development of visceral, renal, or peripheral ischemia; and the formation of aneurysms of the false lumen, which can rupture. The high operalive mortality of patients in whom medical therapy fails has led to earlier surgical intervention, and results have been excellent (6-8,10,12,30). The treatment of chronic disseclions is more conservative. Chronic type A dissections are uncommon, since most patients with acute type A dissections are treated surgically, and less than 10% of untreated patients survive (2,3). Surgery is usually reserved for patients who develop postoperative complications or those with progression of the dissection as evidenced by the development of aortic insufficiency, progressive enlargement of the false lumen, or development or aneurysms (6,9,19,30). Chronic type B dissections are treated medically unless there is evidence of treatment failure or a major complicalion such as progressive dilatation of the false lumen (6,7,10,29,30). Extension of the dissection with occlusion of multiple major branches may occur, and sudden death due to rupture is a potential complication in either type A or B dissections. Regardless of the method of treatment, potential complications make careful follow-up essential. If the aortic valve and aortic anulus have not been replaced, the dissection can extend proximally to produce aortic insufficiency. There may be progressive enlargement of the false lumen with subsequent rupture into the pericarAugust

1991

ized or diffuse aneurysms may develop, and these may rupture. DeBakey et a! (7) found that late aneurysm formation occurred in 30% of proximal (type I) and 38% of distal (type III) dissections; rupture of these aneurysms was responsible for 29% of all late deaths in their patients.

DIAGNOSIS Chest

Figure 1. Type A dissection. The proximal true (1) and false (F) channels are equally opacified. Note the faint intimal flap (arrows) along the right side of the catheter (arrowhead), which is in the true lumen. There is no opacification of the false lumen beyond the left subclavian artery; however, the true lumen is compressed. Mild aortic insufficiency (Al) is present.

.

a..,

Radiography

The most common findings on chest radiographs in patients with proved aortic dissection are widening of the superior mediastinum and aorta, disparity in the size of the ascending and descending aorta, change in the aortic configuration between successive examinations, and displacement of a calcified plaque by 10 mm or more (2,19,37-39). A pleural effusion, usually on the left, may be present, and there is often cardiomegaly. Widening of the superior mediastinum is difficult to evaluate, since most patients suspected of having an aortic dissection are examined with portable radiography, and it may be difficult for the patient to hold his/her breath in full inspiration. Displacement of aortic calcification may be misleading. The calcified plaque and the most lateral border of the aorta may not be at the same localion. Processes that widen the superior mediastinum-such as fat, neoplasm, or hemorrhage-may create a false impression of calcium displacement and aortic wall thickening. A false-positive diagnosis of aortic dissection can also be made when there is calcification of a mural thrombus or when the aortic wall is thickened due to aortitis.

Aortography Figure 2. Type A dissection. Contrast medium has been injected into a dilated false lumen. The sharp proximal border (arrows) is characteristic of the false lumen. Note that the aortic valve and coronary arteries are not depicted.

dial sac and cardiac tamponade. Patients with Marfan syndrome can develop aneurysms of the sinuses of Valsalva; these aneurysms can rupture into the pericardial sac. Yamaguchi et al (36) found that there was a persistent false channel distal to the site of surgical repair in 26 of 33 patients (79%) with type A dissection and that progressive dilatation of the false channel occurred in four. LocalVolume

180

Number

#{149}

2

Aortography has long been considered indispensable in the diagnosis and evaluation of aortic dissection (11,15,17,19-21,26,37-39,40-44). It is well tolerated by even critically ill patients and can be performed by experienced personnel with minima! risk. Its diagnostic accuracy approaches 98% in some series (36). The major advantage of aortography results from its ability to enable evaluation of the aortic valve and the extent of involvement of the major aortic branches. As with most imaging modalities, the aortographic findings do not allow classification of the dissection as acute or chronic on any one examination. The clinical findings,

follow-up studies, or both are more reliable in this regard. Historically, the initial angiographic studies of dissection used intravenous angiographic techniques (21,45,46). While these studies were limited because of poor opacification of the aorta, particularly in the presence of cardiac decompensation, they demonstrated the value of aortography in management and made it possible to establish the diagnosis in many patients. Retrograde aortography, either from the femoral or axillary artery, is the preferred method of evaluating the aorta in patients suspected of haying a dissection (19,20,39,40-44). The complication rate of catheter aortography in these patients does not differ greatly from the rate in patients with no dissection; initial concerns about the inadvertent passage of the catheter into the false lumen or the injeclion of contrast material into the false lumen have been unfounded (43). Although cut film is most commonly used, cineangiography (47) and digital subtraction angiography (DSA) have been used with direct aortic injection of contrast medium. While the image detail is not as good as with cut film, these methods, particularly if used with a large-field-of-view image intensifier and rapid filming, can shorten the examination time and decrease the amount of contrast medium necessary for examination. These techniques may make it easier to identify the site of intimal tear and the degree of aortic insufficiency because of their higher frame rate. Intravenous DSA has been advocated by some as a noninvasive method of assessing the aorta (48). However, its usefulness is limited because it cannot be used to assess aortic valve competency, and misregistration artifacts often obscure the aortic root and ascending aorta. Angiographic signs in aortic dissection can be categorized as direct or indirect (Figs 1-4) (37). Direct signs, which are pathognomonic of dissection, include demonstration of a double lumen or an intima! flap. Indirect signs, which provide supporting evidence of dissection, include compression of the true lumen, thickening of the aortic wall, aortic insufficiency, branch abnormality, or a small ulcerlike projection beyond the aortic wall (49). The last finding is seen when contrast material escapes from the true aortic lumen through the intimal tear into the false lumen. This may be confused with penetrating atherosclerotic ulcers, which occur in atherosclerotic plaques, disrupt the internal Radiology

#{149} 299

elastic lamina, media (50,51). sive intramural

and extend into the They may cause extenhemorrhage, and false aneurysms or aortic rupture have been reported (50,51). Most lesions have an angiographic appearance resembling a gastric ulcer. The clinical presentation may mimic aortic dissection; however, the lesions are usually localized to the descending or abdomma! aorta and an intimal flap or false lumen is rarely seen. Earnest et a! (19), in reviewing the angiographic findings in 52 confirmed cases, found that the most common angiographic finding was opacification of the false lumen. There was local or complete opacification of the false lumen in 45 (87%) cases, identification of an intimal flap in 41 (79%), demonstration of the intimal tear in 29 (56%), and aortic insufficiency in 17 (33%). The false lumen was not opacified in seven (13%). In all cases the proximal extent of the dissection was accurately determined with angiography; however, the distal extent was not identified in all patients. Of interest is the fact that nine patients (18%) had no findings on plain chest radiographs to suggest dissection. Although aortography is highly sensitive in the diagnosis of aortic dissection, at times it may not readily allow the diagnosis (23,52-54). One such case is when the false lumen is not opacified or there is simultaneous and equal opacification of the true lumen and the false lumen so that the intimal flap is not visualized. The false lumen may thrombosed,

not be opacified when it is when there is no intimal

tear, or when the catheter tip is located distal to the site of the intimal tear. If the intimal tear is located distal to the site being imaged, the false lumen will be seen only if there is sufficient retrograde flow in the false lumen to allow the contrast material to reach the imaged area. When the false lumen is not opacified, the aortic wall frequently appears thickened. This finding by itself is not indicative of aortic dissection, since aortic wall thickening can be caused by diffuse atherosclerosis,

aortitis,

or mural

thrombus. Apparent thickening of the aortic wall can be produced by mediastinal fat, neoplasm, or hemorrhage. Aortic wall thickening may be the only finding when an aneurysm has thrombosed. At times a dissection may be oriented so that the false channel is not shown in proper the case in Marfan

relief. This syndrome

is often or annu-

loaortic ectasia, in which the dissection occurs in a dilated ascending 300

#{149} Radiology

1 b.

a.

Figure 3. Type B dissection. (a) Aortogram demonstrates the entry site into the false lumen (arrow) just distal to the left subclavian artery. The true lumen (7) is compressed by the false lumen. (b) CT scan demonstrates the intimal flap separating the true (7) and false (F) lumina much better than the aortogram. Note that the true lumen is compressed and the false lumen is dilated.

aorta. This problem can be minimized by the use of more than one projection. Although the right posterior oblique projection is usually sufficient to document the presence of a dissection, orthogonal projections must be obtained before a conclusion can be reached that the aortogram is normal. Our practice is to begin the angiographic evaluation of the thoracic aorta with biplane anteroposterior and lateral projection imaging and to obtain additional oblique projections when the results of the initial examination are normal. At times, the diagnosis can be established only by moving the catheter tip into the descending thoracic or abdominal aorta and demonstrating that the dissection involves these regions. CT

and

MR

Imaging

CT and MR imaging have been used with increasing frequency in the evaluation of patients suspected of having an aortic dissection (54-78). Because they are noninvasive, these techniques are frequently used to evaluate patients with chest pain when the clinical findings are nonspecific and do not enable distinction of myocardial infarction from aortic dissection. Both modalities have been highly successful in identifying aortic dissection; tages and

however, disadvantages.

CT scanning-CT an accurate method aorta, mediastinum, pleural

spaces

each has

has

advan-

proved

of evaluating pericardium,

in patients

suspected

to be

the and

of having

an aortic

Diagnostic

accuracy

dissection

(55-67).

of 88%-100%

been reported with dynamic techniques (57,60,61,66,79,80). compares

favorably

of aortography spread diagnosis

referral when

use

with

of CT has and initiation

are

not

accuracy

The

led

wide-

to earlier

of therapy center cardiovascular

to an appropriate aortography and

surgery

the

(19,60,80).

has

scanning This

available

at the

or

pri-

mary hospital. Many authors now recommend that a contrast materialenhanced CT study should be performed as the initial examination in all cases of suspected aortic dissection (27,57,60,62,66,77). universally accepted,

are being

treated

While this is not more patients

on the basis

of the

CT findings if the tent of dissection lished (15,27,57,66).

diagnosis and exare clearly estabAs is the case with

aortography,

the

CT diagnosis

tic dissection

requires

the

of aor-

identifica-

tion of two or more channels separated by an intimal flap (Figs 3, 4) (5665). Indirect signs of dissection (5762) frequently seen with CT include compression

and

deformity

of the

true lumen, dilatation of the aorta, thickening of the aortic wall, and ulcerlike projections of contrast material (49). CT is helpful in differentiating the ulcerlike projections of aortic dissection from penetrating atherosclerotic ulcers (51). The entry site of the

atherosclerotic ulcer is well outlined and located in the descending or upper abdominal aorta. An intramural hematoma may be seen; however, as with aortography, identification of a August

1991

It

I

iI,

b.

a.

C.

Figure 4. Type A dissection with extension into the right innominate artery. (a) Aortogram demonstrates the intimal flap (arrows) between the true (7) and false lumina. The dissection begins just above the aortic valve and extends into the right innominate artery. (b) Postcontrast CT scan through the ascending and descending aorta. The intimal flap (arrows) separating the true (7) and false (F) lumina can be identified. Note that the true lumen in the ascending aorta is small and compressed. (c) Postcontrast CT scan through the aortic arch. Although the intimal flap (arrows) between the true and false (F) lumina is clearly identified, the involvement of the innominate artery is best seen on the aortogram.

false lumen or intimal flap is rare (50,51). Evidence of pericardial or

wall may also in attenuation;

pleura! fluid is a bad prognostic sign and suggests that the aorta has ruptured into the pericardial or pleural

ally

spaces.

CT is often better than aortography in identifying two channels, particularly when the two are equally opacifled, since the axial plane is the optima!

projection

for

detecting

an

intimal flap (Fig 3). The detection of true and false lumina is best accomplished by means of single-level, contrast-enhanced, dynamic scanning techniques, because these make it easy to detect differences in the degree and sequence of opacification of the two channels (55,56,62). The true lumen is usually better opacified than the false lumen and is usually seen earlier. If contrast medium does not enter the false lumen, differentiation between an aortic dissection with a thrombosed false lumen and a clotfilled atherosclerotic aneurysm may be difficult. In either case, the single opacified lumen may be deformed or narrowed, and the aortic wall appears thickened. The best indirect sign of aortic dissection is increased attenuation of a thickened aortic wall (65). This is thought to be due to the increased attenuation of blood within the aortic wall. It is usually seen in the acute phase, since the attenuation decreases in chronic dissections as the hematoma liquefies. In patients with atherosclerotic aneurysms, the aortic Volume

180

Number

#{149}

2

due

rotic

appear to be increased however, this is usu-

to calcification

plaques

(65,81). thickness intimal

of atheroscle-

or mural

nosis

thrombus

Although an increase in wall and central displacement of calcification are commonly

seen in aortic dissection, Tones et a! (81) found that 24% (33 of 136) of their patients with aortic aneurysms presented with similar findings due to calcification

within

Numerous diagnostic

the

pitfalls accuracy

62,64,66,82).

The

thrombus.

can reduce the of CT (55,56,61,

most

frequent

reason

for misdiagnosis is a failure to identify the true and false lumina or the intima! flap because of motion artifacts or insufficient opacification of the aorta. Streak

artifacts

may

simulate

an

inti-

ma! flap, particularly at the level of the diaphragm. If the false channel does not fill, the aortic wall must be carefully

evaluated

for

signs

suggest-

ing intramural hematoma. This may require one to vary the window width and level to appreciate differences in wall thickness and attenuation. The most common cause of falsepositive diagnoses is failure to appreciate normal anatomic variations, particularly about the ascending aorta and aortic arch (66). The left innominate vein, the left superior intercostal vein, and the left upper lobe pulmonary vein lie close to the aortic arch and descending aorta and are often separated from the aorta by a thin cleavage plane. If one does not carefully

observe

the

sequence

ing of these vessels course on adjacent

of fill-

of dissection

or evaluate their scans, a false diagwill

be

made.

Simi-

lar problems may occur when the pericardial recesses around the ascending aorta or thickened pleura adjacent to the descending aorta are mistaken for a thrombosed false lumen. The major disadvantage of CT is its inability to depict abnormalities of the aortic valve or the major aortic branches (Fig 4). Although the site of the intimal tear and the location of reentry points are difficult to assess, Haverich et a! (25) have found that failure to resect the site of intima! tear does not affect survival. While the role of CT in the management of acute dissections has not been clearly established, CT has proved to be of great value in the subsequent

have

follow-up

been

treated

cally. The disease progress in spite

therapy

or resection

of patients

medically process of intense

of the

who

or surgimay medical

involved

segment of the aorta. Patients with type A dissection who have undergone surgical repair of the ascending

aorta may develop progressive enlargement of the false lumen with rupture into the pericardial sac, dilatation of the sinus portion of the aorta, aortic insufficiency if the aortic valve is still present, or local or diffuse dilatation of the aorta distal to the graft. The importance of obtaining a baseline CT study is demonstrated by the persistence of the false lumen disRadiology

301

#{149}

b. Figures. Type B dissection. (a) Aortogram demonstrates origin of the dissection just beyond the left subclavian artery. The true lumen (7) is compressed. (b) Axial electrocardiogram-gated MR image (RR interval = 1 second, echo time = 30 msec, 128 x 256 matrix, four signals averaged). There is a signal void in the true lumen and increased signal in the false lumen. (c) Oblique electrocardiogram-gated MR image (RR interval = 1 second, echo time = 30 msec, 128 x 256 matrix, four signals averaged). The extent of dissection is clearly delineated; however, the brachiocephalic vessels are better evaluated on the aortogram. F = false lumen. a.

tal to the graft in 26 of 33 (79%) patients studied after resection and grafting of the ascending aorta (36). Impending rupture of the false lumen should be suspected when an aneurysm develops acutely, if there is a rapid increase in the size of the false lumen, if blood is present in the pericardia! or pleura! spaces, or if the patient’s pain cannot be controlled by means of intensive drug therapy (11). Patients with acute type B dissections who have been treated medically should be carefully observed, since progression of the dissection, deve!opment of an aneurysm of the false lumen, or signs of compromise or occlusion of a major branch are indications for surgical intervention (11). In 14%-20% of patients with acute aortic dissection treated by means of drug therapy alone, one should anticipate the development of aneurysms of the false lumen (11). MR imaging-MR imaging can provide much the same information as that obtained from CT without the need for intravenous administration of contrast medium (68-78,83). Numerous studies have demonstrated an excellent correlation among MR, CT, and aortography; the reported accuracy for detecting a dissection with MR varies from 83% to 100% (68,75, 84). As is the case with CT, a specific diagnosis of aortic dissection requires the identification of a double lumen and an intima! flap (Fig 5), although indirect signs similar to those seen 302

#{149} Radiology

with CT may suggest the diagnosis in the appropriate clinical setting. The major advantage of MR in vascular imaging results from the high contrast among the blood pool, the vascular wall, and the adjacent soft tissues.

Movement

of blood

through

an imaged volume causes alteration in its signal, which tends to enhance the contrast between the blood and surrounding stationary tissue. Rapidly flowing blood tends to emit little or no intralumina! signal in spin-echo imaging (85-87), but it tends to be very bright on gradient-echo images (88,89).

However,

slowly

moving

blood may exhibit areas of increased signal intensity on spin-echo images, and complex patterns of flow frequently cause intralumina! signal voids on gradient-echo images (88,89). Anatomic abnormalities are best seen on the images obtained with e!ectrocardiogram-gated spin-echo techniques, whereas functional information is best displayed with gradientecho cine techniques that use small flip angles (88,89). The true and false lumina are best identified when there is rapid blood flow in each lumen (Fig 5). On a spinecho image, each lumen then appears devoid of signal, and the intimal flap is seen as a linear structure of medium intensity clearly outlined by the flow void in the two channels (68,69, 71,75). An intimal flap is readily seen in most patients; an exception is those

in whom the false lumen is thrombosed, since it is not outlined on both sides

by

moving

blood.

Consequently,

the intima! flap is more likely to be seen in an acute dissection than in a chronic one (75). The false lumen can usually be differentiated from the true lumen because the flow is slower in the false lumen and thrombus is more likely to form. The true lumen is usually devoid of signal at some time during the cardiac cycle. Slowly flowing blood in the false lumen tends to have an intra!uminal signal intensity that is higher on the second-echo image than on the first-echo image. Although MR is superior to CT or angiography in depicting the presence of blood flow, in some cases it is difficult to differentiate slowly flowing blood from thrombus in the false !umen. Various methods of overcoming this problem have been suggested (68,74,83,88,89).

Techniques

such

as

phase-contrast display (90-94) or gradient-echo imaging (95-97) may be helpful in differentiating between the signal arising from intravascular thrombus and that due to complex or slow blood flow. A major advantage of MR imaging over CT is the quality of the images obtained in the sagittal, coronal, and oblique planes. This is particularly helpful in determining the type and extent of the dissection and its relationship to the major aortic branches, particularly those arising from the aortic arch. Although axial sections August

1991

are best for determining whether the major abdominal vessels arise from the true or false lumen, the origins of the brachiocephalic arteries are best seen in the left anterior oblique equivalent projection. In many instances there is sufficient detail to determine if the dissection extends into a major branch; however, the extent of involvement is not seen as clearly as with aortography (Fig 5). As spatial resolution improves and newer MR angiographic techniques are developed, it is expected that more reliance will be placed on the MR assessment of the major aortic branches. The use of MR imaging in the management of dissections has been limited by its inability to provide the necessary preoperative information in type A dissections regarding the status of the aortic

valve,

the

coronary

arteries,

and the sites of intimal tears. However, the development of gradientecho cine imaging techniques has made it possible to evaluate the competence of the aortic valve (88,89). Failure to recognize normal anatomic structures or artifacts may lead to a false-positive diagnosis of dissection with MR imaging as with CT. This most commonly results from a failure to recognize normal anatomic structures

such

as the

left

superior

intercostal vein or the superior pericardial recess or to assess correctly the origins of major arteries (98). Motion or truncation artifacts may be mistaken for a dissection if only sagittal or coronal images are obtained. This problem can be minimized by acquisilion of axial planes or by reversing the direction of the phaseand frequency-encoding axes (98). Atherosclerotic plaques may cause focal thickening of the aortic wall and can be confused with a thrombosed false lumen. At times it may be difficult to differentiate this from an acute dissection, in which the only finding is an area of high intensity along the aortic wall on T2-weighted images. Yamada et al (99) found this to be the case in eight patients with acute dissection. These areas usually appeared as low-attenuation regions on CT scans and in four of eight patients were associated with displacement of intimal calcification. The use of MR imaging is limited in that only hemodynamically stable patients can be examined, since it is not possible to examine patients with pacemakers and it is difficult to study patients who require electronic support systems. Awareness of the problems inherent in imaging patients on life support systems should enable these to be overcome, particularly in Volume

180

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2

cases in which the use of aortography or contrast-enhanced CT is contraindicated. Despite these limitations, MR will likely play a major role in the evaluation of patients with chronic dissections, particularly in assessing the results of medical or surgical therapy and in detecting postoperative complications (100,101).

specfficity was 98%, with a positive predictive value of 98% and a negalive predictive value of 99%. Echocardiography, particularly transesophageal echocardiography, can rapidly enable a diagnosis of aortic dissection (105-107). Moreover, echocardiography may facilitate an alternate

senting

Echocardiography Transthoracic and transesophageal echocardiography have been successfully used to evaluate the aorta in patients suspected of having an aortic dissection (102-107). As with other imaging modalities, a diagnosis of aortic dissection can be made with echocardiography if two lumina separated by an intimal flap can be identifled (102-104). In patients with proximal dissection, the true lumen can usually be identified by noting its relationship to the left ventricular outflow tract and aortic valve. Pulsed Doppler can be used to assess flow patterns within the true and false lumina and can also aid in the detection of aortic insufficiency. Aortic regurgitation produces diastolic flow signals above the Doppler baseline immediately after aortic valve dosure. Aortic regurgitation can also be identified with two-dimensional echocardiography on the basis of (a) abnormal flow patterns within the left ventricular outflow tract during diastole or (b) diastolic fluttering of the anterior mitral

valve

leaflet

ventricular septum, live of ventricular Transthoracic

and/or

the

which overload echocardiography

intra-

is sugges(102). is

most successful in evaluating the ascending aorta (102-104). The interposition of lung between the anterior chest wall and the aorta, coupled with increasing distance between the transducer and the aorta, limits its ability in assessment of the aortic arch and descending aorta. Transesophageal echocardiography has increased the accuracy of assessment of the aortic arch and the descending aorta (105-107). The entire thoracic aorta is better delineated because of the proximity of the thoracic aorta to the esophagus. Moreover, the transesophageal approach eliminates most of the problems caused by the interposition of the highly reflective lung and mediastinal structures between the transducer and the aorta. Erbel et al (107), after assessing the accuracy of echocardiography in 164 patients suspected of having an aortic dissection, reported that the sensitivity of echocardiography was 99% and the

diagnosis

with

in patients

pre-

chest

pain. Since it is highly successful in demonstrating abnormal cardiac wall motion, it can be reliably used to establish a diagnosis of myocardial infarction, particularly when the findings do not support the diagnosis of aortic dissection (108,109).

The major advantages of echocardiography relate to the fact that it is noninvasive and can be performed at the patient’s bedside. However, the examination is highly dependent on the operator’s skill and experience in evaluating the aorta. In most cases sedation is required, and perforation of the esophagus is a potential complication when transesophageal transducers are used. Although the use of some other method such as CT or MR imaging may be necessary to assess the extent of the dissection (110), the ability of echocardiography to identify involvement of the ascending aorta makes it potentially useful in determining which patients require urgent surgery. CONCLUSION The introduction of CT, MR imaging, and echocardiography has greatly enhanced our ability to assess the aorta by nonrnvasive means. Although each modality can accurately demonstrate the presence of aortic dissection, their use must be considered in the context of disease management. If an aortic dissection is suspected, the diagnosis must be quickly established, other diagnoses must be excluded, and a determination must be made about whether urgent surgery is indicated. When the presence of an aortic dissection cannot be confirmed, other diagnoses-such as myocardia! infarction, which can mimic dissection-must be identified. The use of these modalities may vary with the environment in which the patient is initially seen. In a community hospital where cardiovascular surgery is not available, it is essential to identify patients with aortic dissection who require urgent surgery and who therefore must be transferred to a center where cardiovascular surgery is available. A patient who presents initially to a center where cardiovasRadiology

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cular surgery is available may undergo a different sequence of examinations. Contrast-enhanced CT has become the examination of choice for the initial evaluation of any patient suspected of having an aortic dissection. However, its use as an alternative to aortography when surgery might be appropriate is more controversial. Although great reliance is placed on CT in some institutions (7,56,60,65), most cardiovascular surgeons require aortographic evaluation to accurately assess the extent of dissection, as well as to identify unsuspected abnormalities such as branch occlusion or localized dilatation of the false lumen that will alter their surgical approach. The accuracy of echocardiography in evaluating the aorta may result in its greater use when sufficient experience with the technique has been acquired. Currently, the lack of experience in most institutions has limited its use. MR imaging may replace angiography as MR angiographic techniques improve and changes are made in monitoring equipment to allow the safe examination of acutely ill patients. The development of techniques to evaluate the competency of the aortic valve and improve the assessment of branch vessels might make MR the primary examination for the initial and subsequent evalualion of acute and chronic dissections. CT, MR imaging, and echocardiography can be used to accurately establish the presence of aortic disseclion and in most cases can demonstrate involvement of the ascending aorta. However, because of the limitations of these techniques in evaluating the aortic valve, the aortic arch, and the origins of major aortic branches, aortography remains the examination of choice in the evaluation of all patients with acute disseclions, as well as those with chronic dissections who have developed complications requiring surgical intervention. U

7.

8.

9.

10.

11. 12.

13. 14.

15. 16.

17. 18.

19. 20.

21.

22.

23. 24.

25.

26. 27.

28.

2.. 3.

4. 5. 6.

304

Sorensen HR, Olsen H. Ruptured and dissecting aneurysms of the aorta. Ada Chir Scand 1964; 128:644-650. Hirst AEJr,Johns VJJr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958; 37:217-279. Anagnostopoulos CE, Prabhakar MJS, Kittle CF. Aortic dissections and dissecting aneuysms. AmJ Cardiol 1972; 30:263-273. DeBakey ME, Cooley DA, Creech OJr. Surgical considerations of dissecting aneurysm of the aorta. Ann Surg 1955; 142:586-612. Gore I, Hirst AEJr. Dissecting aneurysm of the aorta. Prog Cardiovasc Dis 1973; 16:103111. Miller DC. Surgical management of aortic dissections: indications, penoperative management, and long-term results. In: Dorog-

#{149} Radiology

34.

Wheat MWJr. Acute dissection of the aorta. Cardiovasc Cliii 1987; 17:241-262.. Reul GJJr, Cooley DA, Hailman GL, Reddy SB, Kyger ER, Wukasch DC. Dissecting aneurysm of the descending aorta. Arch Surg 197; 110:632-640. Sister EE, DeSanCtis RW. The clinical recognition of dissecting aortic aneurysm. AmJ Med 1976; 60:625-633. SIster EE. Aortic dissection: presentation and diagnosis. In: Doroghazi RM, Sister EE, eds. Aortic dissection. New Yorlc McGrawHill, 1983; 61-70. Eagle KA, DeSanctis RW. Aortic dissection. Curr Probl Cardiol 1989; 14:225-278. Cambria RP, Brewster DC, GertlerJ, et a!. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988; 7:199-209. Sister EE, DeSanctis RW. Dissection of the aorta. Med Clin North Am 1979; 63:141-154. Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990; 264: 2537-2541. Earnest F IV, MUhInJR, Sheedy PF 11. Roentgenographic findIngs in thoracic aortic dissection. Mayo Clin Proc 1979; 54:43-50. Stein HL, Steinberg I. Selective aortography, the definitive technique, for diagnosis of dissecting aneurysm of the aorta. AJR 1968; 102:333-348. Dinsmore RE, RourkejA, DeSanctis 1W, Harthorne JW, Austen WG. Angiographic findings in dissecting aortic aneurysm. N EnglJ’Med 1966; 275:1152-1157. Jamieson WRE, Munro A!, Miyagishima RT, Allen P, Tyers GFO, Gerein AN. Aortic dissection: early diagnosis and surgical management are the keys to survival. Can J Surg 1982; 25:145-149. Viljanen T. Diagnostic difficulties in aortic dissection. Ann Chir Gynaecol 1986; 73:328332. Daily P0, Trueblood HW, Stinson EB, Wuerflein 1W, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg 1970; 10:237-247. Haverich A, Miller DC, Scott WC, et a!. Acute and chronic aortic dissections-determinants of long-term outcome for operative survivors. Circulation 1985; 72(suppllll):22-34. Wheat MWJr. Acute dissecting aneurysms of the aorta: diagnosis and treatment-1979. Am HeartJ 1980; 99:373-387. Miller DC. Acute dissection of the aorta: continuing need for earlier diagnosis and treatment. Mod Concepts Cardiovasc Dis 1985; 54:51-55. Meng RL, Najafi H,Javid H, HunterJA, Gotdin MD. Acute ascending aortic dissection: surgical management. Circulation 1981; 64: (supplll)231-234. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N EnglJ Med 1987; 317:1060-1067. Miller DC, Stinson EB, Oyer PE, eta!. Operative treatment of aortic dissections. J Thorac Cardiovasc Surg 1979; 78:365-382. Jex RK, Schaff HV, PiehlerjM, et a!. Early and late results following repair of dissections of the descending thoracic aorta. J Vasc Surg 1986; 3:226-237. Wheat MWJr, Palmer RF, Bartley TD, Sectman RC. Treatment of dissecting aneurysms of the aorta without surgery. J Thorac Cardiovasc Surg 1965; 50:364-373. Wheat ?WJr. Intensive drug therapy. In: Doroghazi RM, SIster EE, eds. Aortic dissection. New York McGraw-Hill, 1983; 165-192.

40.

New Yoric

References 1.

RM, Sister EE, eds. Aortic dissection. McGraw-Hill, 1983; 193-243. DeBakey ME, McCoilum H, Crawford ES, et aL Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982; 92:1118-1134. Miller DC, Mitchell RC, Oyer PE, Stinson EB, Janueson SW, Shuinway NE. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984; 70(suppll):153-164. Crawford ES, Svensson LG, CoselliJS, Safi HJ, Hess KR. Surgical treatment of aneurysm and/or dissection of the ascendirg aorta, transverse aortic arch and ascending aorta and transverse aortic arch. J Thorac Cardiovasc Surg 1989; 98:659-674. Crawford ES, Svensson LG, CoselliJS, Safi EU, Hess KR. Aortic dissection and dissecting tic aneurysms. Ann Surg 1988; 208:254hazi

29. 30. 31.

32.

33.

35.

36.

37.

McFarlandJ,

Willerson

JT, Dinsmore

The medical

treatment

of dissecting

RE, et a!. aortic aneurysms. N EnglJ Med 1972; 286i115-119. Wheat MWJr, Harris PD, MaImJR, Kaiser G, Bowman FOJr, Palmer RF. Acute dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1969; 58:344-351. Yamauchi T, Guthaner DF, Wexler L Natural history of the false channelof type A aortic dissection after surgical repair: CT study. Radiology 1989; 170:743-747. Smith DC,Jang GC. Radiological diagnosis

of aortic dissection. In: Doroghazi RM, Sister EE, eds. Aortic dissection. New Yorlc Mc38.

39.

41.

42.

43.

44.

45.

46.

47.

48.

49.

50.

51.

52.

53.

54.

55.

56.

57.

58.

59.

Graw-Hill, 1983; 71-132. Eyler WR, Clark MD. Dissectin aneurysms of the aorta: roentgen manifestations including a comparison with other types of aneurysms. Radiology 1965; 85:1047-1057. Beachley MC, Rannier K, Roth FJ. Roentgenographic evaluation of dissecting aneurysms ofthe aorta. AJR 1974 121:617-625. Hayashi K, Meaney iT, ZelchJV, Tarar R. Aortographic analysis of aortic dissection. AJR 1q74; 122:769-782. Soto B, Harman MA, Ceballos R, Bards A. Angiographic diagnosis of dissecting aneurysm of the aorta. AJR 1972; 116:146-154. Shuford WH, Sybers RG, Weens HS, Lindsay JJr, HurstJW. Aortoraphic findings in dissectinganeurysm of the aorta. AmJCardiol 1969; 24:111-117. Kirschner U’, Twigg HL, Conrad PW, Hufnagel C. Retrograde catheter aortography in dissecting aortic aneurysms. AJR 1968; 102: 349-353. Itzchak Y, Rosenthall, Adar R, Rubinstein ZJ, Ueberman Y, Deutsch V. Dissecting aneurysm of thoracic aorta: reappraisal of radiologic diagnosis. AJR 1975; 125:559-570. Golden A, Weens Sit The diagnosis of dissecting aneurysm of the aorta by angiocardiography. Am}leartJ 1949; 37:114-118. Steinberg I, Stein HL. Intravenous angiocardiography, abdominal aortography and peripheral arteriography with single arm pressure injection. AJR 1964; 92:893-906. Gutierrez FR, Gowda 5, LudbrookPA, McKnight RC. Cineangiography in the diagnosis and evaluation of aortic dissection. Radialogy 1980; 135:759-761. Guthaner DF, Miller DC. Digital subtraction angiography of aortic dissection. AJR 1983; 141:157-161. TisnadoJ, Cho SR, Beach!ey MC, Vines PS. Ulcerlike projections: a precursor angiographic sign to thoracic dissection. AJR 1980; 135:719-722. Stanson AW, Kazmier FJ, Hoffier LH, et a!. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and dlinicopathologic correlations. Ann Vasc Surg 1986 1:15Welch 17, Stanson AW, Sheedy PF II, Johnson CM, McKusick MA. Radiologic evaluation of penetrating aortic atherosclerotic ulcer. RadloGraphics 1990; 10:675-685. Shuford WH, Sybers RG, Weens HS. Problems in the aortographic diagnosis of dissecting aneurysm of the aorta. NEng1J Med 1969; 280:225-231. Eagle KA, Quertermous T, Kritzer GA, et aL Spectrum of conditions initially suggesting acute aortic dissection but with negative aortograms. AmJCardiol 1986; 57:322-326. Kanick V, Hemley SD, Kittredge R, Finby N. Some prol,lems in the angiographic diagnosis of dissecting aneurysms of the tThoracic aorta. AJR 1964; 91:1283-1287. Godwin Herfkens RL; Skioldebrand CG, Federle M, Upton MJ. Evaluation of dissections and aneurysms of the thoracic aorta by conventional and dynamic CT scanning. Radiology 1980; 136:125-133. Gross SC, Barr I, Eyler WR, Khaja F, Goldstein S. Computed tomography in dissection of l; thoracic aorta. Radiology 1980; 136:135-

m1

Thorsen MX, Lawson U, Foley WD. CT of aortic dissections. CRC Crit Rev Diagn Imag. ing 1985; 26:291-324. Egan TJ, Neiman HI, Herman RJ, Malave SR, SandersJH. Computed tomoraphy in the diagnosis of aortic aneurysm dissection or traumatic injury. Radiology 1980; 136:141146. Larde D, Belloir C, Vasile N, Fri)aJ, FerraneJ. Computed tomography of aortic dissection. Radiology 1980; 136:147-151.

August1991

60.

61.

62. 63.

64. 65.

66.

Moncada R, Churchill R, Reynes C, et a!. Diagnosis of dissectingaortic aneurysm by camputed tomography.l.ancet 1981; 1:238-241. Thorsen MK San Dretto MA, Lawson U, Foley WD, Smith DF, Berland LL Dissecting aortic aneurysms: accuracy of computed tomogr#{231}hic diagnosis. Radiology 1983; 148: Demos TC, Posniak WI, Marsan RE. CT of aortic dissection. Semin Roentgenol 1989; 24: 22-37. Demos TC, Posniak HV, Churchill R. Detection of the intimal flap of aortic dissection on unenhanced CT images. AJR 1986; 146:601603. Heiberg E, Wolverson M, Sundaram M, ConnorsJ, Susman N. CT findings in aortic dissection. AJR 1981; 136:13-17. Heiberg E, Wolverson MK, Sundaram M, ShieldsJB. CT characteristics of aortic atherosderotic aneurysm versus aortic dissection.J Comput Assist Tomogr 1985; 9:78-83. Vasile N, Mathieu D, Keita K Lellouche D, Sloth G, CacheraJP. Computed tomography of thoradc aortic dissection: accuracy

and pitfalls.JComput 67.

68. 69. 70.

71.

72.

73.

7’L

75.

76.

Assist Tomogr

77.

78. 79.

80.

81.

Dinsrnore RE, Wedeen VJ, Miller SW, eta!. MRI of dissection of the aorta: recognition of the intimal tear and differential flow velocities. AJR 1986; 146:1286-1288. Caputo GR, Higgins CB. Advances in cardiac imaging modalities: fast computed tomoraphy, ma$netic resonance imaging and positron emission tomography. Invest Radiol 1990; 25:838-854. Reed JDJr, Soulen RL. Cardiovascular MRI: current role in patient management. Radiol Clin North Am 1988; 26:589-06. PernesjM, Greater P, Desbleds MT, de Brux JL. MR evaluation of chronic sonic dissection.J Comput Assist Tomogr 1987; 11:975Dooms GC, Higgins CB. The potential of magnetic resonance imaging for the evaluation of thoracic arterial diseases. J Thorac Cardiovasc Surg 1986; 92:1088-1095.

95.

96. 97.

98.

99.

Godwin JD, Breiman PS, SpeckmanJM. Problems and pitfalls in the evaluation of thoraac aortic dissection by computed tomor.JComput Assist Tomogr 198Z

Auffermann gins CS. aorticsery.

101.

White RD,Ullyot DJ, Higgins CB. MR imaging of the aorta after surgery for aortic dissec-

102.

83. 84.

85.

86.

87. 88.

89.

90.

91. 92.

93.

94

Glazer H, Gutierrez FR, Levitt RG, Lee JKT, Murphy WA. The thoracic aorta studied by MR imaging Radiology 1985; 157:149-155. Kersting-SommerhoffBA, Higgins CB, White 1W, SommerhoffCP, Upton MJ. Aonic dissection: sensitivity and specificity ofMR imaging. Radiology 1988; 166:651-655. Mills clvi, Brant-Zawadzki M, Crooks LE, et a!. Nudear magnetic resonance: principles flow imaging. AJNR 1983; 4:1161Blood flow effects in magnetic resoimaging. AJR 1984; 143:1157-1166. Bradley WGJr, Waluch V. Blood flow: magnetic resonance imagin Radiology 1985; 154443-450. Sechtem U, Pflugfelder PW, White 1W, et a!. Cine MR imaging potential for the evaluation of cardiovascular function. AJR 1987; 148: 239-246. tood AxelL nance

Sechtem U, Pflugfelder PW, Cassidy MM, et a!. Mitral or aortic regurgitation: quantification of regurgitant volumes with cine MR imaging. Radiology 1988; 167:425-430. Rumandk WM Naidich DP, Chandra R, eta!. Cardiovascular disease: evaluation with MR phase imaging. RadioIogr 1988; 166:63-68. von Schuithess GK, Higgins CB. Blood flow imaing with MR spin-phase phenomenon. Radiology 1985; 157687-695. White EM, Edelman RR, Wedeen VJ, Brady TJ. Intravascular signal in MR imaging. use of phase display for differentiation of blood flow signal from intraluminal disease. Radiology 1986; 161:245-249. Dinsmore RE, Wedeen V, Rosen B, Wismer CL, Miller SW, Brady TJ. Phase-offset technique to distingnish slow blood flow and thrombus on MR images AJR 1987; 148:634-. Wedeen

VJ, Rosen

Wehrli FW. Fast-scan magnetic resonance: principles and applications. Magn Reson Q 1990; 6:165-236. Haacke EM, TkachJA. Fast MR imaging: techniques and clinical applications. AJR 199 155:951-964. FrahmJ, Haase A, Matthaei D. Rapid threedimensional MR imagine using the FLASH technique.J Comput Assist Tomogr 1986; 10: 363-368. Solomon SL, Brown JJ, Glazer HS, MirOWitZ SA, LeeJKT. Thoracic aortic dissection: pitfalls and artifacts in MR imaging. Radiology 1990; 177:223-228. Yamada T, Tada S, HaradaJ. Aortic disseclion without intimal rupture: diagnosis with ;ging and CT. Radiology 1988; 168:

100.

1319. 82.

1986;

10:211-215. Ouokerk M, Overbosch E, Dee P. CT recogmtion of acute aortic dissection. AJR 1983; 141:671-678. Amparo EG, Higgins CD, Hricak H, Sollitto R. Aortic dissection: magnetic resonance imaging. Radiology 1985; 155:399-406. Geisiner MA, Risius B, ODonnellJA, et at. Thoracic aortic dissections: magnetic resonance imaging Radiology 1985 155:407-412. Herfkens RJ, Higms CB, Hricak H, et at. Nudear magnetic resonance imaging of the cardiovascular system: normal and pathologic findings. Radiology 1983; 147:749-759. Amparo ECHiggins CB, HOddiCk W, et aL Magnetic resonance imaging of aortic disease: preliminary results. AJR 1984 143:1203-

White 1W, Dooms GC, Higgins CB. Advances in imaging thoracic aortic disease. Invest Radiol 1986; 21:761-778. Spritzer CE, Blinder PA. Vascular applicalions of magnetic resonance imaging. Magn Reson Q 19B9; 5:205-227. WhIte 1W, Upton MJ, Higgins CB, et a!. Noninvasive evaluation olsuspected thoracic sonic disease by contrast-enhanced camputed tomography. AmJ Cardiol 1986; 57: 282-290. LaasJ, Schluter G, DanielW, Hendrick PH, Haverich A. Acute type-A dissection of the aorta: which diagnostic modes remain for surgical indication? EurJ Cardlothorac Surg 1987; 1:169-172. Torres WE, Maurer DE, SteinbergHV, Robbins 5, Bernardino ME. CT ofaortic aneurysms: the distinction between mural and thrombus calcification. AJR 1988; 150:1317-

103.

104.

105.

tion. AJR 1988; 150:87-9 Mathew T, Nanda NC. Two-dimensional and Doppler echocardiographic evaluation of aortic aneurysm and dissection. AmJ Cardiol 1984; 54:379-385. Granato JE, Dee P, Gibson PS. Utility of two-dimensional echocardiography in suspected ascending aortic dissection. AmJ Cardiol 1985; 56:123-129. Victor MF, Mintz CS, Kotler MN, Wilson AR, Sega! BL Two-dimensional echocardiographic diagnosis of aortic dissection. AmJ Cardiol 1981; 48:1155-1159.

Hashimoto Assessment

echography 106.

W, Olofsson P, Stoney R, HigMR imaging ofcomplications of J Comput Assist Tomogr 1987;

5, Kumada T, Osakada C, eta!. of transoesophageal Doppler in dissecting aortic aneurysm.J

Am CoWCardiol 1989; 14:1253-1262. Turns MA, Gussenhoven WJ, Schippers

LA,

et a!. The value of transesophageaIechocardiography for diagnosis of thoracic aorta pa107. 108.

109.

110.

thology. Eur HeartJ 1988; 9:1308-1316. Erbel1, Daniel W, Visser C, et a!. Echocardiography in diagnosis of aortic dissection. Lancet 1989; 4:457-460. GIbson 85, Bishop HL, Stamm RB. Value of early two-dimensional echocardiography in patients with acute myocardial infarction. Am JCardiol 1982; 49:1110-1119. Horowitz PS, MorganrothJ, Parrotto C. Immediate diagnosis ofacute myocardial infarction by two-dimensional echocardiography. Circulation 198Z 65:323-329. Goldman AP, Kotler MN, Scanlon MH. The complementary role of magnetic resonance imaging. Doppler echocardiography, and computed tomography in the diagnosis of dissecting thoracic aneurysms. Am HeartJ 1986; 111:970-981.

BR, Chester D, Brady TJ. phase display. J 1q85; 9:530-536.

MR velocity imagingby Comput Assist Tomogr

Volume

180

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2

Radiology

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