- Email: [email protected]
Diagnostic imaging of aortic atherosclerosis and its complications
Neuroimag Clin N Am 12 (2002) 437 – 443
Diagnostic imaging of aortic atherosclerosis and its complications Glenn A. Krinsky, MD Department of Radiology, New York University Medical Center, 530 First Avenue, New York, NY 10016, USA
As recently as 1989, large stroke databanks listed up to 40% of strokes as ‘‘cryptogenic’’ [1]. More recently, there has been increasing interest in the thoracic aorta as a source of the cause of many of these strokes as well as peripheral organ damage. This is largely because newer applications of imaging techniques, including transesophageal echocardiography (TEE), CT, MRI, and magnetic resonance angiography (MRA), have allowed for the visualization, characterization, and quantification of atherosclerotic lesions in the thoracic aorta. This article reviews the imaging findings of atherosclerotic disease of the thoracic aorta and its complications with currently available imaging modalities. Because plaque detection and characterization with TEE and MRI are addressed elsewhere in this issue, this article concentrates on plaque detection. In addition, MR contrast agents that aid in the detection of atherosclerotic plaque are reviewed.
Chest radiography The conventional chest radiograph may provide clinically relevant information regarding advanced atherosclerotic disease of the aorta because calcification of the ascending aorta and arch are readily identified. Iribarren et al [2] recently showed that aortic arch calcification (detected on chest radiography) was present in 1.9% of men and 2.6% of women in a study population of more than 115,000 patients. Calcification of the aortic arch was associ-
E-mail address: [email protected]
ated with an increased risk of coronary artery disease in both men and women [2]. Among women, it was also independently associated with an increased risk of ischemic stroke [2]. The presence of aortic calcification is also a significant risk factor for stroke after coronary artery bypass grafting [3]. Aneurysms or pseudoaneurysms resulting from penetrating atherosclerotic ulcers may also be seen on chest radiography when they reach a size of 2 to 3 cm.
Catheter angiography Before the development of cross-sectional imaging techniques and TEE, conventional catheter angiography was the only modality available to evaluate the thoracic aorta for plaque or ulcers. The latter could be readily seen as a focal collection of contrast outside the confines of the aorta. Depending on the concentration of iodine used, plaque can be seen as ‘‘filling defects’’ within the contrast-enhanced lumen or inferred from irregularities of the luminal surface. This invasive procedure is still performed to evaluate for plaque or stenosis in the proximal arch vessels but is rapidly being replaced with gadoliniumenhanced MRA; however, if therapeutic procedures such as brachiocephalic stenting or aortic endarterectomy are contemplated, a catheter angiogram is needed as a ‘‘road map.’’
CT The widely publicized development of electronbeam CT for quantifying coronary artery calcification as a measure of coronary atherosclerotic plaque bur-
1052-5149/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 5 2 - 5 1 4 9 ( 0 2 ) 0 0 0 1 8 - 7
438
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
den [4] has paralleled similar developments using nonenhanced and contrast-enhanced conventional CT to quantify aortic wall thickening and calcifications [5]. Unlike coronary artery imaging, the largersized aorta lends itself to easier quantification of noncalcified plaque, particularly with contrastenhanced imaging. This approach has been proposed as a valuable noninvasive method for following the progression and regression of atherosclerotic disease of the thoracic aorta [6,7]. Using contrast-enhanced CT, Sun et al recently showed that intimal thickening
of the aorta was associated with coronary artery disease [8]. Tenenbaum et al [9] used nonenhanced dual-helical CT to assess for both calcium deposits and areas of hypoattenuation adjacent to aortic wall in 32 patients with recent stroke or embolic events. The authors found that defining a threshold of a 4-mm thickness for protruding atheromatous plaque resulted in the best sensitivity (87%, 13/15) and specificity (82%, 14/17) for CT imaging when compared with TEE. This corresponds well to the threshold of 4 mm that was
Fig. 1. (A) Contrast-enhanced helical CT scan at level of right main pulmonary artery reveals ulcerated plaque in ascending (arrow) and descending aorta. (B) Contrast-enhanced helical CT scan at level of bifurcation of main pulmonary artery shows protruding atheromas of ascending (arrow) and descending aorta. (From Tunick PA, Krinsky GA, Lee VS, Kronzon I. Diagnostic imaging of thoracic aortic atherosclerosis. AJR Am J Roentgenol 2000;174:1119 – 25; with permission.)
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Fig. 2. Contrast-enhanced helical CT scan at level of right main pulmonary artery reveals complex ulcerated plaque in ascending (arrow) aorta.
found in the French Aortic Plaque in Stroke Study [10] to predict a significantly increased risk of stroke. Tenenbaum et al also concluded that while the nonenhanced approach they used is suitable for screening studies, they recommended following any positive nonenhanced dual-helical CT study with a contrastenhanced helical CT (Figs. 1 – 3) or TEE. Notably, the authors also reported six protruding atheromas in the upper ascending aorta and proximal arch that were not seen on TEE. These cases highlight one advantage of CT imaging over TEE, as CT provides complete
439
imaging of the thoracic aorta, whereas with TEE, this area is a blind spot because of interposition of the airfilled trachea and left bronchus. New multidetector CT scanners with image acquisition times less than 1 second are promising because, like electron-beam CT, they may allow imaging to be synchronized with the cardiac cycle, thereby reducing artifacts, particularly in the ascending aorta and aortic root, associated with cardiac motion. Resulting improvements in detection and characterization of atheromatous plaque remain to be demonstrated. In addition, the temporal resolution of CT fluoroscopy may provide the ability to detect the mobile component of atheromas. CT can readily detect penetrating atherosclerotic ulcers (or ulcerlike projections) of the aorta [11]. The ulcer is seen as a focal collection of contrast material that appears outside of the confines of the enhanced lumen. An associated medial hematoma is usually present and localized to a small segment of the contiguous aorta. The hematoma is easily seen on unenhanced CT as a hyperattenuating region, often crescent shaped in the ascending and descending aorta and linear in the aortic arch. Displacement of intimal calcification by the hematoma is a specific sign of intramural hematoma. Although many of these ulcers are detected in asymptomatic patients who undergo chest CT for other purposes, the classic clinical presentation of an acute aortic ulcer may be identical to that of aortic dissection. A potentially lethal complication may
Fig. 3. Contrast-enhanced helical CT scan at the level of the aortic arch shows a large, presumably mobile, thrombus arising from the lateral wall (arrow).
440
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Fig. 4. ECG-triggered T1-weighted spin-echo MR image shows a large aortic arch plaque (arrow).
occur when the ulcer causes aortic rupture. Surgical morbidity and mortality are high because many of these patients have concomitant coronary artery disease and renal insufficiency. Therefore, surgery is indicated only for aortic rupture, rapid expansion, and involvement of the ascending aorta [11]. Yano et al [12] recently reported a patient with an atherosclerotic ulcer of the ascending aorta complicated by cardiac tamponade and aortic valve regurgitation. The natural history of penetrating atherosclerotic ulcers is one of progressive aortic enlargement that includes the development of saccular and fusiform aneurysms or pseudoaneurysms in approximately one third of patients [11]. Whereas most lesions do not increase in size, it is not possible to know a priori which patients will have stable disease. Therefore, surveillance imaging with either CT or MR is recommended.
MR As early as 1983, Herfkens et al [13] showed that MR imaging could be applied to imaging of atherosclerotic disease of the aorta. Using spin-echo imaging at 0.35 T, they were able to visualize aortic wall thickening and protruding atheromas in the abdominal aorta and pelvic vessels of patients in vivo (Fig. 4); however, because of long acquisition times and motion artifacts this technique is no longer used to interrogate the aorta for plaque. More recently, one group has compared TEE and gadolinium-enhanced three-dimensional (3D) MRA for evaluation of protruding atheromas and found that MRA tended to underestimate plaque thickness, presumably because of difficulty in defining aortic wall on the contrast-enhanced MRA images [14].
Fig. 5. Oblique sagittal maximum-intensity-projection image from gadolinium-enhanced 3D MRA shows flat plaques (arrows) in the innominate artery.
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Without ECG-gated cine gradient-echo images, MRI also provides only static views of disease without assessment of clinically significant mobile thrombus. Like CT imaging, however, MRI does have the advantage of visualizing the complete aorta, including blind spots for TEE, as well as assessing great vessel disease, which is commonly seen in patients with aortic atheromatous plaque. When combined with other MRI techniques that can evaluate the heart, aortic plaque morphology, and assessment of plaque mobility, MRI has the potential to provide a comprehensive study for the evaluation of cerebrovascular atheroembolic disease. Gadoliniumenhanced 3D MRA is currently a useful modality to visualize atheromas in the innominate artery (Fig. 5) and contiguous ascending aorta (Fig. 6), which cannot be seen with TEE due to tracheal interposition [15]. It also is the procedure of choice for noninvasive evaluation of the proximal carotid and vertebral arteries for plaque [16]. One limitation is that calcifications cannot be readily seen on MR and may result in overestimation of stenosis. Similar to CT, MR is excellent for the evaluation of atherosclerotic ulcers and their complications (Fig. 7).
MR contrast agents Although only the traditional extracellular gadolinium chelates are currently available for clinical use,
441
there are new contrast agents that will likely increase the sensitivity and specificity of MR imaging of aortic plaque. Blood pool agents such as MS-325 (Epix Medical, Inc, Cambridge, MA) bind to serum albumin and are retained within the intravascular compartment as long as 50 minutes. The long time available for image acquisition may be used to increase signal-to-noise and spatial resolution. In theory, this should lead to a higher sensitivity for plaque detection. Also, the increased imaging time may enable the detection of mobile components. Experimental data have shown that superparamagnetic iron oxide particles (SPIO) and ultrasmall superparamagnetic iron oxide particles (USPIO) accumulate in atherosclerotic plaque [17,18]. When injected intravenously these particles have a long plasma half-life and are also considered blood pool agents; however, unlike MS-325, SPIO particles are similar in diameter to low density lipoprotein (15 – 25 nm) and may enter atherosclerotic plaque with an increase in endothelial permeability and accumulate in plaque with a high macrophage tissue content [17]. For these reasons, SPIO particles may have the potential to assess inflammatory activity of atherosclerotic plaque. While this agent has both T1 and T2 effects, plaque that has taken up SPIO particles demonstrates pronounced signal loss on T2*- weighted imaging [17]. Another potential use for this agent is the ability to determine the age of a thrombus. This may provide clinically relevant information on whether a thrombus will respond to lytic therapy. Using a rabbit model and
Fig. 6. Coronal source image from gadolinium-enhanced 3D MRA shows complex aortic plaque with extension into the innominate artery (arrow). Plaque was not seen on transesophageal echocardiography due to tracheal interposition. The patient had right brain transient ischemic attacks.
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G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
detailed information obtainable, and availability make TEE the procedure of choice for the imaging of thoracic aortic atherosclerosis; however, further technical advances in MR and CT, particularly in MR plaque characterization and the use of plaque specific contrast agents, may allow for a less invasive and more complete evaluation of thoracic aortic atherosclerosis in the near future. Gadolinium-enhanced 3DMRA is the procedure of choice for the noninvasive detection of plaque in the proximal aortic arch vessels. Furthermore, both CT and MRI are better suited to evaluate penetrating atherosclerotic ulcers and their complications such as intramural hematoma, pseudoaneurysm formation, and aortic rupture.
References
Fig. 7. Oblique sagittal maximum-intensity-projection image from gadolinium-enhanced 3D MRA shows penetrating ulcers (or ulcerlike projections) in the ascending aorta, transverse arch, and descending aorta. Note the plaque in the innominate artery (arrow).
T1-weighted imaging, Schmitz et al [18] demonstrated no USPIO uptake in fresh (1-day old) and more organized (9-day old) thrombus; however, USPIO uptake was demonstrated in 3-, 5-, and 7-day old thrombi [18].
Summary Thoracic aortic atherosclerosis has been shown to be an important cause of severe morbidity and mortality. At the present time, the ease of performance,
[1] Sacco RL, Ellenberg JH, Mohr JP, et al. Infarcts of undetermined cause: the NINCDS stroke data bank. Ann Neurol 1989;25:382 – 90. [2] Iribarren C, Sidney S, Sternfeld B, Browner WS. Calcification of the aortic arch: risk factors and association with coronary heart disease, stroke and peripheral vascular disease. JAMA 2000;283:2810 – 5. [3] John R, Choudhri AF, Weinberg AD, et al. Multicenter review of preoperative risk factors for stroke after coronary artery bypass grafting. Ann Thorac Surg 2000; 69:30 – 5. [4] Callister TQ, Raggi P, Cooil B, et al. Effect of HMGCoA reductase inhibitors on coronary artery disease as assessed by electron-beam computed tomography. N Engl J Med 1998;339:1972 – 8. [5] Takasu J, Takanashi K, Naito S, et al. Evaluation of morphological changes of the atherosclerotic aorta by enhanced computed tomography. Atherosclerosis 1992;97:107 – 21. [6] Tsushima M, Koh H, Suzuki M, et al. Noninvasive quantitative evaluation of early atherosclerosis and the effect of monatepil, a new antihypertensive agent: an interim report. Am J Hypertens 1994;7(10):154 – 60. [7] Takasu J, Masuda Y, Watanabe S, et al. Progression and regression of atherosclerotic findings in the descending thoracic aorta detected by enhanced computed tomography. Atherosclerosis 1994;110:175 – 84. [8] Sun K, Takasu J, Yamamoto R, et al. Assessment of aortic atherosclerosis and carotid atherosclerosis in coronary artery disease. Jpn Circ J 2000;64:745 – 9. [9] Tenenbaum A, Garniek A, Shemesh J, et al. Dual-helical CT for detecting aortic atheromas as a source of stroke: comparison with transesophageal echocardiography. Radiology 1998;208:153 – 8. [10] Cohen A, Tzourio C, Bertrand B, et al. On behalf of the FAPS (French study of aortic plaques in stroke) investigators: aortic plaque morphology and vascular events: a follow-up study in patients with ischemic stroke. Circulation 1997;96:3837 – 41.
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443 [11] Quint LE, Williams DM, Francis IR, et al. Ulcerlike lesions of the aorta: imaging features and natural history. Radiology 2001;218:719 – 23. [12] Yano K, Makino N, Hirayama H, et al. Penetrating atherosclerotic ulcer at the proximal aorta complicated with cardiac tamponade and aortic valve regurgitation. Jpn Circ J 1999;63:228 – 30. [13] Herfkens RJ, Higgins CB, Hricak H, et al. Nuclear magnetic resonance imaging of atherosclerotic disease. Radiology 1983;148:161 – 6. [14] Kutz SM, Lee VS, Tunick PA, Krinsky G, Kronzon I. Atheromas of the thoracic aorta: a comparison of transesophageal echocardiography and breath-hold gadolinium-enhanced 3-D magnetic resonance angiography. J Am Soc Echocardiogr 1999;12:853 – 8. [15] Krinsky GA, Freedberg R, Lee VS, Rockman C, Tu-
443
nick PA. Innominate artery atheroma: a lesion seen with gadolinium-enhanced MR angiography and often missed by transesophageal echocardiography. Clin Imaging 2001;25:251 – 7. [16] Krinsky GA, Maya M, Rofsky NM, et al. Gadoliniumenhanced three dimensional MR angiography of the aortic arch vessels in the evaluation of cerebrovascular occlusive disease. J Comput Assist Tomogr 1998;22: 167 – 78. [17] Schmitz SA, Taupitz M, Wagner S, Wolf KJ, Beyersdorff D, Hamm B. Magnetic resonance imaging of atherosclerotic plaques using superparamagnetic iron oxide particles. J Magn Reson Imag 2001;14:355 – 61. [18] Schmitz SA, Winterhalter S, Schiffler S, et al. USPIOenhanced direct MR imaging of thrombus: preclinical evaluation in rabbits. Radiology 2001;221:237 – 43.
Diagnostic imaging of aortic atherosclerosis and its complications Glenn A. Krinsky, MD Department of Radiology, New York University Medical Center, 530 First Avenue, New York, NY 10016, USA
As recently as 1989, large stroke databanks listed up to 40% of strokes as ‘‘cryptogenic’’ [1]. More recently, there has been increasing interest in the thoracic aorta as a source of the cause of many of these strokes as well as peripheral organ damage. This is largely because newer applications of imaging techniques, including transesophageal echocardiography (TEE), CT, MRI, and magnetic resonance angiography (MRA), have allowed for the visualization, characterization, and quantification of atherosclerotic lesions in the thoracic aorta. This article reviews the imaging findings of atherosclerotic disease of the thoracic aorta and its complications with currently available imaging modalities. Because plaque detection and characterization with TEE and MRI are addressed elsewhere in this issue, this article concentrates on plaque detection. In addition, MR contrast agents that aid in the detection of atherosclerotic plaque are reviewed.
Chest radiography The conventional chest radiograph may provide clinically relevant information regarding advanced atherosclerotic disease of the aorta because calcification of the ascending aorta and arch are readily identified. Iribarren et al [2] recently showed that aortic arch calcification (detected on chest radiography) was present in 1.9% of men and 2.6% of women in a study population of more than 115,000 patients. Calcification of the aortic arch was associ-
E-mail address: [email protected]
ated with an increased risk of coronary artery disease in both men and women [2]. Among women, it was also independently associated with an increased risk of ischemic stroke [2]. The presence of aortic calcification is also a significant risk factor for stroke after coronary artery bypass grafting [3]. Aneurysms or pseudoaneurysms resulting from penetrating atherosclerotic ulcers may also be seen on chest radiography when they reach a size of 2 to 3 cm.
Catheter angiography Before the development of cross-sectional imaging techniques and TEE, conventional catheter angiography was the only modality available to evaluate the thoracic aorta for plaque or ulcers. The latter could be readily seen as a focal collection of contrast outside the confines of the aorta. Depending on the concentration of iodine used, plaque can be seen as ‘‘filling defects’’ within the contrast-enhanced lumen or inferred from irregularities of the luminal surface. This invasive procedure is still performed to evaluate for plaque or stenosis in the proximal arch vessels but is rapidly being replaced with gadoliniumenhanced MRA; however, if therapeutic procedures such as brachiocephalic stenting or aortic endarterectomy are contemplated, a catheter angiogram is needed as a ‘‘road map.’’
CT The widely publicized development of electronbeam CT for quantifying coronary artery calcification as a measure of coronary atherosclerotic plaque bur-
1052-5149/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 5 2 - 5 1 4 9 ( 0 2 ) 0 0 0 1 8 - 7
438
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
den [4] has paralleled similar developments using nonenhanced and contrast-enhanced conventional CT to quantify aortic wall thickening and calcifications [5]. Unlike coronary artery imaging, the largersized aorta lends itself to easier quantification of noncalcified plaque, particularly with contrastenhanced imaging. This approach has been proposed as a valuable noninvasive method for following the progression and regression of atherosclerotic disease of the thoracic aorta [6,7]. Using contrast-enhanced CT, Sun et al recently showed that intimal thickening
of the aorta was associated with coronary artery disease [8]. Tenenbaum et al [9] used nonenhanced dual-helical CT to assess for both calcium deposits and areas of hypoattenuation adjacent to aortic wall in 32 patients with recent stroke or embolic events. The authors found that defining a threshold of a 4-mm thickness for protruding atheromatous plaque resulted in the best sensitivity (87%, 13/15) and specificity (82%, 14/17) for CT imaging when compared with TEE. This corresponds well to the threshold of 4 mm that was
Fig. 1. (A) Contrast-enhanced helical CT scan at level of right main pulmonary artery reveals ulcerated plaque in ascending (arrow) and descending aorta. (B) Contrast-enhanced helical CT scan at level of bifurcation of main pulmonary artery shows protruding atheromas of ascending (arrow) and descending aorta. (From Tunick PA, Krinsky GA, Lee VS, Kronzon I. Diagnostic imaging of thoracic aortic atherosclerosis. AJR Am J Roentgenol 2000;174:1119 – 25; with permission.)
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Fig. 2. Contrast-enhanced helical CT scan at level of right main pulmonary artery reveals complex ulcerated plaque in ascending (arrow) aorta.
found in the French Aortic Plaque in Stroke Study [10] to predict a significantly increased risk of stroke. Tenenbaum et al also concluded that while the nonenhanced approach they used is suitable for screening studies, they recommended following any positive nonenhanced dual-helical CT study with a contrastenhanced helical CT (Figs. 1 – 3) or TEE. Notably, the authors also reported six protruding atheromas in the upper ascending aorta and proximal arch that were not seen on TEE. These cases highlight one advantage of CT imaging over TEE, as CT provides complete
439
imaging of the thoracic aorta, whereas with TEE, this area is a blind spot because of interposition of the airfilled trachea and left bronchus. New multidetector CT scanners with image acquisition times less than 1 second are promising because, like electron-beam CT, they may allow imaging to be synchronized with the cardiac cycle, thereby reducing artifacts, particularly in the ascending aorta and aortic root, associated with cardiac motion. Resulting improvements in detection and characterization of atheromatous plaque remain to be demonstrated. In addition, the temporal resolution of CT fluoroscopy may provide the ability to detect the mobile component of atheromas. CT can readily detect penetrating atherosclerotic ulcers (or ulcerlike projections) of the aorta [11]. The ulcer is seen as a focal collection of contrast material that appears outside of the confines of the enhanced lumen. An associated medial hematoma is usually present and localized to a small segment of the contiguous aorta. The hematoma is easily seen on unenhanced CT as a hyperattenuating region, often crescent shaped in the ascending and descending aorta and linear in the aortic arch. Displacement of intimal calcification by the hematoma is a specific sign of intramural hematoma. Although many of these ulcers are detected in asymptomatic patients who undergo chest CT for other purposes, the classic clinical presentation of an acute aortic ulcer may be identical to that of aortic dissection. A potentially lethal complication may
Fig. 3. Contrast-enhanced helical CT scan at the level of the aortic arch shows a large, presumably mobile, thrombus arising from the lateral wall (arrow).
440
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Fig. 4. ECG-triggered T1-weighted spin-echo MR image shows a large aortic arch plaque (arrow).
occur when the ulcer causes aortic rupture. Surgical morbidity and mortality are high because many of these patients have concomitant coronary artery disease and renal insufficiency. Therefore, surgery is indicated only for aortic rupture, rapid expansion, and involvement of the ascending aorta [11]. Yano et al [12] recently reported a patient with an atherosclerotic ulcer of the ascending aorta complicated by cardiac tamponade and aortic valve regurgitation. The natural history of penetrating atherosclerotic ulcers is one of progressive aortic enlargement that includes the development of saccular and fusiform aneurysms or pseudoaneurysms in approximately one third of patients [11]. Whereas most lesions do not increase in size, it is not possible to know a priori which patients will have stable disease. Therefore, surveillance imaging with either CT or MR is recommended.
MR As early as 1983, Herfkens et al [13] showed that MR imaging could be applied to imaging of atherosclerotic disease of the aorta. Using spin-echo imaging at 0.35 T, they were able to visualize aortic wall thickening and protruding atheromas in the abdominal aorta and pelvic vessels of patients in vivo (Fig. 4); however, because of long acquisition times and motion artifacts this technique is no longer used to interrogate the aorta for plaque. More recently, one group has compared TEE and gadolinium-enhanced three-dimensional (3D) MRA for evaluation of protruding atheromas and found that MRA tended to underestimate plaque thickness, presumably because of difficulty in defining aortic wall on the contrast-enhanced MRA images [14].
Fig. 5. Oblique sagittal maximum-intensity-projection image from gadolinium-enhanced 3D MRA shows flat plaques (arrows) in the innominate artery.
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
Without ECG-gated cine gradient-echo images, MRI also provides only static views of disease without assessment of clinically significant mobile thrombus. Like CT imaging, however, MRI does have the advantage of visualizing the complete aorta, including blind spots for TEE, as well as assessing great vessel disease, which is commonly seen in patients with aortic atheromatous plaque. When combined with other MRI techniques that can evaluate the heart, aortic plaque morphology, and assessment of plaque mobility, MRI has the potential to provide a comprehensive study for the evaluation of cerebrovascular atheroembolic disease. Gadoliniumenhanced 3D MRA is currently a useful modality to visualize atheromas in the innominate artery (Fig. 5) and contiguous ascending aorta (Fig. 6), which cannot be seen with TEE due to tracheal interposition [15]. It also is the procedure of choice for noninvasive evaluation of the proximal carotid and vertebral arteries for plaque [16]. One limitation is that calcifications cannot be readily seen on MR and may result in overestimation of stenosis. Similar to CT, MR is excellent for the evaluation of atherosclerotic ulcers and their complications (Fig. 7).
MR contrast agents Although only the traditional extracellular gadolinium chelates are currently available for clinical use,
441
there are new contrast agents that will likely increase the sensitivity and specificity of MR imaging of aortic plaque. Blood pool agents such as MS-325 (Epix Medical, Inc, Cambridge, MA) bind to serum albumin and are retained within the intravascular compartment as long as 50 minutes. The long time available for image acquisition may be used to increase signal-to-noise and spatial resolution. In theory, this should lead to a higher sensitivity for plaque detection. Also, the increased imaging time may enable the detection of mobile components. Experimental data have shown that superparamagnetic iron oxide particles (SPIO) and ultrasmall superparamagnetic iron oxide particles (USPIO) accumulate in atherosclerotic plaque [17,18]. When injected intravenously these particles have a long plasma half-life and are also considered blood pool agents; however, unlike MS-325, SPIO particles are similar in diameter to low density lipoprotein (15 – 25 nm) and may enter atherosclerotic plaque with an increase in endothelial permeability and accumulate in plaque with a high macrophage tissue content [17]. For these reasons, SPIO particles may have the potential to assess inflammatory activity of atherosclerotic plaque. While this agent has both T1 and T2 effects, plaque that has taken up SPIO particles demonstrates pronounced signal loss on T2*- weighted imaging [17]. Another potential use for this agent is the ability to determine the age of a thrombus. This may provide clinically relevant information on whether a thrombus will respond to lytic therapy. Using a rabbit model and
Fig. 6. Coronal source image from gadolinium-enhanced 3D MRA shows complex aortic plaque with extension into the innominate artery (arrow). Plaque was not seen on transesophageal echocardiography due to tracheal interposition. The patient had right brain transient ischemic attacks.
442
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443
detailed information obtainable, and availability make TEE the procedure of choice for the imaging of thoracic aortic atherosclerosis; however, further technical advances in MR and CT, particularly in MR plaque characterization and the use of plaque specific contrast agents, may allow for a less invasive and more complete evaluation of thoracic aortic atherosclerosis in the near future. Gadolinium-enhanced 3DMRA is the procedure of choice for the noninvasive detection of plaque in the proximal aortic arch vessels. Furthermore, both CT and MRI are better suited to evaluate penetrating atherosclerotic ulcers and their complications such as intramural hematoma, pseudoaneurysm formation, and aortic rupture.
References
Fig. 7. Oblique sagittal maximum-intensity-projection image from gadolinium-enhanced 3D MRA shows penetrating ulcers (or ulcerlike projections) in the ascending aorta, transverse arch, and descending aorta. Note the plaque in the innominate artery (arrow).
T1-weighted imaging, Schmitz et al [18] demonstrated no USPIO uptake in fresh (1-day old) and more organized (9-day old) thrombus; however, USPIO uptake was demonstrated in 3-, 5-, and 7-day old thrombi [18].
Summary Thoracic aortic atherosclerosis has been shown to be an important cause of severe morbidity and mortality. At the present time, the ease of performance,
[1] Sacco RL, Ellenberg JH, Mohr JP, et al. Infarcts of undetermined cause: the NINCDS stroke data bank. Ann Neurol 1989;25:382 – 90. [2] Iribarren C, Sidney S, Sternfeld B, Browner WS. Calcification of the aortic arch: risk factors and association with coronary heart disease, stroke and peripheral vascular disease. JAMA 2000;283:2810 – 5. [3] John R, Choudhri AF, Weinberg AD, et al. Multicenter review of preoperative risk factors for stroke after coronary artery bypass grafting. Ann Thorac Surg 2000; 69:30 – 5. [4] Callister TQ, Raggi P, Cooil B, et al. Effect of HMGCoA reductase inhibitors on coronary artery disease as assessed by electron-beam computed tomography. N Engl J Med 1998;339:1972 – 8. [5] Takasu J, Takanashi K, Naito S, et al. Evaluation of morphological changes of the atherosclerotic aorta by enhanced computed tomography. Atherosclerosis 1992;97:107 – 21. [6] Tsushima M, Koh H, Suzuki M, et al. Noninvasive quantitative evaluation of early atherosclerosis and the effect of monatepil, a new antihypertensive agent: an interim report. Am J Hypertens 1994;7(10):154 – 60. [7] Takasu J, Masuda Y, Watanabe S, et al. Progression and regression of atherosclerotic findings in the descending thoracic aorta detected by enhanced computed tomography. Atherosclerosis 1994;110:175 – 84. [8] Sun K, Takasu J, Yamamoto R, et al. Assessment of aortic atherosclerosis and carotid atherosclerosis in coronary artery disease. Jpn Circ J 2000;64:745 – 9. [9] Tenenbaum A, Garniek A, Shemesh J, et al. Dual-helical CT for detecting aortic atheromas as a source of stroke: comparison with transesophageal echocardiography. Radiology 1998;208:153 – 8. [10] Cohen A, Tzourio C, Bertrand B, et al. On behalf of the FAPS (French study of aortic plaques in stroke) investigators: aortic plaque morphology and vascular events: a follow-up study in patients with ischemic stroke. Circulation 1997;96:3837 – 41.
G.A. Krinsky / Neuroimag Clin N Am 12 (2002) 437–443 [11] Quint LE, Williams DM, Francis IR, et al. Ulcerlike lesions of the aorta: imaging features and natural history. Radiology 2001;218:719 – 23. [12] Yano K, Makino N, Hirayama H, et al. Penetrating atherosclerotic ulcer at the proximal aorta complicated with cardiac tamponade and aortic valve regurgitation. Jpn Circ J 1999;63:228 – 30. [13] Herfkens RJ, Higgins CB, Hricak H, et al. Nuclear magnetic resonance imaging of atherosclerotic disease. Radiology 1983;148:161 – 6. [14] Kutz SM, Lee VS, Tunick PA, Krinsky G, Kronzon I. Atheromas of the thoracic aorta: a comparison of transesophageal echocardiography and breath-hold gadolinium-enhanced 3-D magnetic resonance angiography. J Am Soc Echocardiogr 1999;12:853 – 8. [15] Krinsky GA, Freedberg R, Lee VS, Rockman C, Tu-
443
nick PA. Innominate artery atheroma: a lesion seen with gadolinium-enhanced MR angiography and often missed by transesophageal echocardiography. Clin Imaging 2001;25:251 – 7. [16] Krinsky GA, Maya M, Rofsky NM, et al. Gadoliniumenhanced three dimensional MR angiography of the aortic arch vessels in the evaluation of cerebrovascular occlusive disease. J Comput Assist Tomogr 1998;22: 167 – 78. [17] Schmitz SA, Taupitz M, Wagner S, Wolf KJ, Beyersdorff D, Hamm B. Magnetic resonance imaging of atherosclerotic plaques using superparamagnetic iron oxide particles. J Magn Reson Imag 2001;14:355 – 61. [18] Schmitz SA, Winterhalter S, Schiffler S, et al. USPIOenhanced direct MR imaging of thrombus: preclinical evaluation in rabbits. Radiology 2001;221:237 – 43.