| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Head and Neck Imaging |
1 From the Departments of Radiology (T.S., M.S.F., C.Y.) and Surgery (T.S.H.), University of Washington, 815 Mercer St, Box 358050, Seattle, WA 98109; Department of Radiology, People's Liberation Army General Hospital, Beijing, China (J.C., L.M., Y.Q.C.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (T.S.H.). Received March 7, 2005; revision requested May 2; revision received July 18; accepted August 11; final version accepted October 3. Supported by NIH grants R01HL56874, P01HL072262, and R01HL073401. Address correspondence to T.S. (e-mail: Tobias.Saam{at}med.uni-muenchen.de).
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
Materials and Methods: Institutional review board approval and informed consent were obtained for this HIPAA-compliant study. Twenty-three patients (21 men, two women; mean age, 66.1 years ± 11.0 [standard deviation]) with unilateral symptomatic carotid disease underwent 1.5-T time-of-flight MR angiography and 1.5-T T1-, intermediate-, and T2-weighted MR imaging. Both carotid arteries were reviewed. One observer recorded quantitative and morphologic information, which included measurement of the area of the lumen, artery wall, and main plaque components; fibrous cap status (thick, thin, or ruptured); American Heart Association (AHA) lesion type (types I–VIII); and location (juxtaluminal vs intraplaque) and type of hemorrhage. Plaques associated with neurologic symptoms and asymptomatic plaques were compared with Wilcoxon signed rank and McNemar tests.
Results: Compared with asymptomatic plaques, symptomatic plaques had a higher incidence of fibrous cap rupture (P = .007), juxtaluminal hemorrhage or thrombus (P = .039), type I hemorrhage (P = .021), and complicated AHA type VI lesions (P = .004) and a lower incidence of uncomplicated AHA type IV and V lesions (P = .005). Symptomatic plaques also had larger hemorrhage (P = .003) and loose matrix (P = .014) areas and a smaller lumen area (P = .008). No significant differences between symptomatic and asymptomatic plaques were found for quantitative measurements of the lipid-rich necrotic core, calcification, and the vessel wall or for the occurrence of intraplaque hemorrhage or type II hemorrhage.
Conclusion: This study revealed significant differences between symptomatic and asymptomatic plaques in the same patient.
© RSNA, 2006
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
Much of what is currently known about differences between symptomatic and asymptomatic carotid plaques is based on histologic analysis of excised carotid endarterectomy specimens (4). Atherosclerosis research based on histologic analysis, however, is constrained by three factors inherent in its design. First, a histologic examination is invasive; thus, information pertaining to plaque can be obtained at only one time point. Second, during carotid endarterectomy, the tube-like carotid plaque is cut length wise and it is frequently torn, thus preventing accurate gross or microscopic assessment (5). Third, histologic findings from the asymptomatic plaque of the contralateral artery are unavailable; therefore, symptomatic plaques are typically compared with asymptomatic plaques from a different group of patients, thus making it difficult to control for all genetic and environmental atherosclerotic risk factors.
Studying features of asymptomatic and symptomatic plaques in the same patient at the same time is an ideal way to control for all known and unknown risk factors of atherosclerosis. This approach would eliminate the environmental, genetic, and temporal variability inherent in histologic comparisons of lesions in symptomatic patients with those in asymptomatic patients.
Studies have shown that magnetic resonance (MR) imaging can be used to accurately characterize and quantify the composition and morphology of human carotid atherosclerotic plaque in vitro and in vivo, including the lipid-rich necrotic core, calcification, fibrous cap status, age and location of hemorrhage or thrombus, and American Heart Association (AHA) lesion type (6–13). The purpose of this study was to retrospectively determine if in vivo MR imaging can simultaneously depict differences between symptomatic and asymptomatic carotid atherosclerotic plaque.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
Patients
Between April 1998 and February 2003, bilateral carotid arteries of 27 consecutive patients with neurologic symptoms were examined with MR imaging after patients provided informed consent. Patients were included if (a) they had a history of transient ischemic attack, amaurosis fugax, or stroke appropriate to the distribution of the index carotid artery; (b) they had not previously undergone carotid endarterectomy; (c) the time between onset of symptoms and MR imaging was 4 months or less; (d) carotid stenosis, as measured with duplex ultrasonography on the symptomatic side, was at least 50%; and (e) bilateral identical coverage of MR imaging (ie, distance covered by MR imaging in the craniocaudal direction) was at least 1.2 cm. Four patients with an image quality score of less than 3, as scored with a five-point scale (1 = poor, 5 = excellent [10]), were excluded.
The remaining 23 patients (21 men, two women; mean age, 66.1 years ± 11.0 [standard deviation] [Table 1]) underwent a complete neurologic examination performed by a vascular surgeon with more than 10 years of clinical experience (T.S.H.). When clinically indicated, neurologic consultation was provided by faculty members in the department of neurology (University of Washington, Seattle, Wash) and additional diagnostic tests—including brain computed tomography, MR imaging, echocardiography, and Holter monitoring—were used to rule out other potential causes of symptoms. The median interval between symptom onset and MR imaging was 1.5 months, the standard deviation was 1.3 months, and the range was 1 week to 4 months.
|
T1-, intermediate-, and T2-weighted MR imaging and three-dimensional time-of-flight (TOF) angiography were performed. Parameters for black-blood double inversion-recovery two-dimensional fast spin-echo T1-weighted MR imaging were as follows: repetition time msec/echo time msec, 800.0/9.3–11.0; echo train length, eight; acquisition time, 8 minutes; and 12 sections acquired. Parameters for double-echo fast spin-echo cardiac-gated intermediate- and T2-weighted MR imaging were as follows: 2500–3700/10–20 (effective) for intermediate-weighted imaging; 2500–3700/40–70 (effective) for T2-weighted imaging; three or four R-R intervals; echo train length, eight; acquisition time, 3–4 minutes; and 18 sections acquired. Parameters for three-dimensional TOF angiography were as follows: 23.0/3.5; flip angle, 25°; acquisition time, 3 minutes; and 40 sections acquired.
All examinations were performed with a 13–16-cm field of view, a matrix of 256 x 256 pixels, a 2-mm section thickness, and two acquired signals. An intersection space of –1 mm was used for three-dimensional TOF angiography, whereas no intersection space was used for MR imaging. Imaging examinations were centered on the bifurcation. Fat suppression was used for T1-, intermediate-, and T2-weighted MR imaging to reduce the signal from subcutaneous fat. Zero-filled Fourier transformation was used to reduce pixel size, which ranged from 0.25 x 0.25 mm to 0.31 x 0.31 mm, depending on the field of view, and to minimize partial-volume artifacts.
Image Review
Both carotid arteries were reviewed. One radiologist (T.S., with more than 2 years of experience in the interpretation of carotid plaque images) rated the quality of each image before the review by using a previously published five-point scale; scores were dependent on the overall signal-to-noise ratio (13). A score of 1 indicated the arterial wall and vessel margins were unidentifiable. A score of 2 indicated the signal-to-noise ratio was marginal, the arterial wall was visible, and the substructure, lumen, and outer boundaries were indistinct. A score of 3 indicated the wall structures were identifiable but the lumen and outer boundaries were partially obscured. A score of 4 indicated the signal-to-noise ratio was high and the vessel wall and lumen margins were well defined. A score of 5 indicated the signal-to-noise ratio was excellent and the vessel wall and lumen margins could be detected in every detail. For each imaging location, four images obtained with different parameters were available for review. Only the locations of the carotid arteries ipsilateral to symptoms that had corresponding matching locations in the contralateral carotid artery, with regard to longitudinal distance from the bifurcation point, were analyzed. The continuous mean coverage was 1.7 cm for both arteries. All MR images were examined by the same radiologist, who was blinded to patients' clinical information at the time of image analysis.
Plaque composition and quantitative measurements.—Areas of the lumen, outer wall, and plaque tissue components were measured with a quantitative vascular image analysis system, which is a custom-designed image analysis tool (16). The area circumscribed by the outer wall boundary included the lumen, intima, media, and adventitia. The wall area was calculated by subtracting the lumen area from the outer wall area. Plaque tissue components, such as the lipid-rich necrotic core, hemorrhage, calcification, and loose matrix, were identified by using previously published MR imaging criteria (7,10,13). All signal intensities were compared with the sternocleidomastoid muscle at a point adjacent to and at the same depth as the carotid arteries.
Plaque morphology.—Lesion type was determined at each location according to a previously published modified AHA classification scheme (6).
The fibrous cap was categorized as intact and thick (type I), intact and thin (type II), or ruptured (type III) (8). Intact and thick fibrous caps had a uniform continuous dark band adjacent to the lumen on TOF angiograms and a smooth lumen surface on TOF angiograms and T1-, intermediate-, and T2-weighted MR images. Intact and thin fibrous caps had no visible dark band adjacent to the lumen on TOF angiograms and a smooth lumen surface on TOF angiograms and T1-, intermediate-, and T2-weighted MR images. Ruptured fibrous caps had a disrupted dark band or no visible dark band adjacent to the lumen on TOF angiograms; an irregular lumen boundary on TOF angiograms and T1-, intermediate-, and T2-weighted MR images; and a hyperintense area adjacent to the lumen on TOF angiograms. The highest possible rating was assigned to each artery, and plaques were categorized as intact and thick, intact and thin, or ruptured.
Two patients were excluded from fibrous cap analysis: One had a calcified lesion without a fibrous cap, and one had a TOF angiogram with an image quality score of less than 3. Juxtaluminal calcification appeared as a hypointense area on images obtained with all four parameters. It was not discernable from the lumen on black-blood images, but it was clearly distinguishable from the bright lumen on TOF angiograms.
Hemorrhage was differentiated by location (juxtaluminal vs intraplaque) and type (type I vs type II). A hemorrhage or thrombus was considered juxtaluminal if the region of interest was adjacent to the lumen and the dark juxtaluminal band was absent on TOF angiograms (9). Intraplaque hemorrhage was defined as a hemorrhage located deep within the plaque or near the luminal surface, with MR imaging evidence of an intact thick cap (9). Criteria for determining the hemorrhage type were based on previously published MR imaging criteria, with a modification in the terminology. The terms type I and type II rather than fresh and recent, respectively, were used to describe the age of intraplaque hemorrhage (7). Type I hemorrhage was histologically characterized by intact red blood cells with intracellular methemoglobin. A type I hemorrhage appeared hyperintense on TOF angiograms and T1-weighted images and iso- to hypointense on intermediate- and T2-weighted images. A type II hemorrhage was histologically characterized by lytic red blood cells with extracellular methemoglobin and appeared hyperintense on all images (7).
Statistical Analysis
All locations that could be matched with the contralateral artery were used for statistical analysis. Each patient contributed only one set of observations (one study of the symptomatic arteries, one study of the asymptomatic arteries) to the data set for analysis. Area measurements for each artery were calculated as the mean area measured per location for each artery separately. For AHA lesion types, the percentage of sections showing a specific lesion type was calculated for each artery. The mean AHA lesion type distributions calculated for symptomatic arteries were compared with those calculated for asymptomatic arteries. For all other categorical variables, the percentage of arteries that showed the selected feature at one or more locations was calculated separately for symptomatic and asymptomatic arteries. To better accommodate the abnormal distribution of some of the variables, nonparametric tests were used to compare the symptomatic and asymptomatic arteries. The Wilcoxon signed rank test was used to compare variables that were areas or the proportion of sections with a specified AHA lesion type. The McNemar test was used to compare all categorical variables. Because of the limited sample size, the significance of the difference in proportions with the McNemar test was calculated with binomial distribution, as described by Lehman (17). Computation was performed with SPSS for Windows, versions 12 and 13 (SPSS, Chicago, Ill). Differences were considered significant if the P value was less than .05.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
Lumen and Wall Area
The degree of atherosclerotic burden in symptomatic arteries was similar to that in asymptomatic arteries in terms of mean wall area (47.8 mm2 vs 44.0 mm2, P = .3) and mean outer wall area (74.4 mm2 vs 79.1 mm2, P = .3) (Table 2). In contrast, symptomatic arteries had a significantly smaller mean lumen area than did asymptomatic arteries (26.6 mm2 vs 35.1 mm2, P = .008).
|
Lesion Type
In our study, 95.7% of the symptomatic arteries exhibited atherosclerotic lesions classified as AHA type III or greater, whereas 91.8% of the asymptomatic arteries exhibited similar atherosclerotic lesions. Complicated type VI lesions (plaques with a luminal surface defect, hemorrhage, or thrombus) (Figs 1, 2) were found more frequently in symptomatic arteries than in asymptomatic arteries (63.3% vs 40.7%, P = .004) (Table 3). In contrast, uncomplicated type IV and V lesions (plaques with lipid-rich or necrotic cores and surrounding fibrous tissue) (Fig 3) were found more frequently in asymptomatic arteries than in symptomatic arteries (34.5% vs 15.6%, P = .005). No significant differences were found among the other lesion types.
|
|
|
|
|
Type II (recent) hemorrhage was common in patients with symptomatic plaques and in those with asymptomatic plaques; 96% of patients with symptomatic plaques and 78% of patients with asymptomatic plaques had at least one location of type II hemorrhage (P = .2) (Table 4). Type I (fresh) hemorrhage occurred 1.7 times more often in patients with symptomatic plaques than in those with asymptomatic plaques (87% vs 52%, P = .021).
Luminal Calcification
Juxtaluminal calcification with adjacent hemorrhage was slightly more common in patients with symptomatic plaques than in patients with asymptomatic plaques (57% vs 39%); however, this difference was not significant (P = .2) (Table 4).
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
Our findings show that substantial plaque burden was noted in both carotid arteries, as indicated by the mean wall area (47.8 mm2 vs 44.0 mm2, P = .3) and the mean outer wall boundary area (74.4 mm2 vs 79.1 mm2, P = .3) for the symptomatic and asymptomatic sides, respectively. Both carotid arteries exhibited advanced plaque features, such as necrotic core, hemorrhage, loose fibrous matrix, and calcification. Furthermore, the number of locations with AHA type III through type VIII lesions in the symptomatic arteries was comparable with that in the asymptomatic arteries (96% vs 92%).
Plaque composition (measured in square millimeters) was comparable on both sides for lipid-rich necrotic core and calcification. This finding was supported by histologic findings in the carotid arteries, where symptomatic and asymptomatic plaques showed no differences in the size of the lipid-rich necrotic core (18,19) or the amount of calcification (8,18).
Loose matrix and hemorrhage areas were larger in symptomatic arteries than in asymptomatic arteries. Previous work has shown that a loose matrix is produced in plaque healing (ie, repair of a fibrous cap rupture that involves loose matrix) of coronary arteries in patients with silent plaque rupture (20) and that the larger amount of loose matrix formation in the symptomatic artery may occur in response to previous fibrous cap ruptures in this artery.
The association of hemorrhage and symptoms remains a controversial subject (21–24). Lusby et al (23) suggested that intraplaque hemorrhage and surface thrombosis were cardinal features of symptomatic plaques. Sitzer et al (25) demonstrated that ulceration and luminal thrombosis were the main sources of downstream cerebral microemboli in patients with high-grade internal carotid artery stenosis. Kolodgie et al (26) found evidence that showed a hemorrhage might represent a potent atherogenic stimulus. Other studies (4,19,27) found no hemorrhagic differences between symptomatic and asymptomatic plaques, although these studies did not consider the hemorrhage location (intraplaque vs juxtaluminal) or type (I vs II).
In our study, when hemorrhage prevalence was considered independently from hemorrhage location or type, no significant difference was found between symptomatic and asymptomatic plaques. However, when hemorrhages were categorized as type I (fresh) or type II (recent), type I hemorrhages were found significantly more often in patients with symptomatic plaques than in patients with asymptomatic plaques (87% vs 52%, respectively; P = .021). Conversely, the prevalence of type II hemorrhage was comparable in patients with symptomatic plaques and those with asymptomatic plaques. The higher prevalence of type I hemorrhage in patients with symptomatic plaques is characterized by intact red blood cells at histologic analysis and could be caused by either repeated intraplaque hemorrhages or influx of red blood cells from the luminal surface due to a surface defect, such as fibrous cap rupture. We used the terms type I and type II rather than fresh and recent on the basis of an evolving understanding of the distinct time course of intraplaque hemorrhage in the carotid artery. Findings of a recent MR imaging study (28) indicate that atherosclerotic intraplaque hemorrhages may have a longer course for change than that of intracranial hemorrhages because of inherent differences in the tissue environment within the lipid-rich necrotic core. When hemorrhages were categorized according to their location as either an intraplaque hemorrhage or a juxtaluminal hemorrhage or thrombus, the prevalence of intraplaque hemorrhage was comparable between symptomatic and asymptomatic plaques; however, a juxtaluminal hemorrhage or thrombus was found significantly more often in patients with symptomatic plaque than in patients with asymptomatic plaque (61% vs 26%, respectively; P = .039). These findings indicate that the hemorrhage location in relation to the surface and the hemorrhage type and age are important when determining a patient's symptom status.
Symptomatic plaques had significantly more fibrous cap ruptures than did asymptomatic plaques (78% vs 30%, respectively; P = .007). Other authors (29–32) noted that a ruptured or thin fibrous cap is an important feature of vulnerable coronary artery plaque. Our findings indicate that fibrous cap status is also a critical characteristic of high-risk carotid artery lesions. Furthermore, our findings are in agreement with those of Yuan et al (33), who showed that a significant correlation exists between a patient's in vivo fibrous cap status and symptom status.
Complications associated with juxtaluminal plaque structures and luminal surface conditions were reflected by differences in AHA lesion types observed in symptomatic and asymptomatic arteries. Symptomatic arteries had significantly more complicated type VI lesions with possible surface defects, thrombus, and hemorrhage than did asymptomatic arteries (63% vs 41%, P = .004). In contrast, type IV and V lesions were more common in asymptomatic arteries and reflected the absence of complications, such as fibrous cap rupture, hemorrhage, and thrombus.
Our results show that the proximity of the necrotic core to the lumen (expressed as thickness of the fibrous cap), the proximity of hemorrhage to the luminal surface, and the prevalence of type I hemorrhage are associated with neurologic symptoms. Other plaque features, such as the quantitative measurements of lipid-rich necrotic cores and calcifications, or indicators of plaque burden, such as outer wall and wall areas, showed no correlation with neurologic symptoms. These results support the findings of Bassiouny et al (18), who examined a carotid endarterectomy specimen and showed that the topography of individual plaque components in relation to the luminal surface can be used to determine the symptomatic outcome.
A limitation of our study was that the median time between symptom onset and MR imaging was 1.5 months. Lesion characteristics may change during that time. The time between symptom onset and MR imaging should be decreased in future studies.
Although we found highly significant differences between symptomatic and asymptomatic plaques, the predictive value of these findings must be determined in a longitudinal study.
Although both symptomatic and asymptomatic arteries showed features of advanced atherosclerotic disease, the asymptomatic arteries showed less luminal narrowing. It has yet to be determined which of the significant differences in the characteristics of symptomatic and asymptomatic carotid atherosclerotic lesions observed in our study are due to increased luminal narrowing and which produce symptoms.
Only MR images of at least average quality were considered for review; thus, four patients were excluded from analysis. Furthermore, one artery on each side was excluded from fibrous cap analysis because the image quality score of TOF angiograms was less than 3. Improvements in MR imaging protocols, such as time-efficient multisection double inversion-recovery imaging (34) and contrast material–enhanced quadruple inversion-recovery imaging (35), have improved the exclusion rate (36). The exclusion rate should continue to improve in conjunction with improvements in pulse sequence design and hardware (higher-field-strength MR imaging and improved coil design).
In conclusion, the noninvasive imaging approach used in our study revealed significant differences in the composition and morphology of both symptomatic and asymptomatic plaques in the same patient. High-spatial-resolution in vivo MR imaging might be used to characterize high-risk plaque and ultimately identify at-risk patients.
|
ADVANCES IN KNOWLEDGE |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
Abbreviations: AHA = American Heart Association • TOF = time of flight
Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, T.S., C.Y.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, T.S., J.C., M.S.F., N.L.P.; clinical studies, T.S., J.C., L.M., Y.Q.C., T.S.H.; statistical analysis, T.S., N.L.P., T.S.H., C.Y.; and manuscript editing, T.S., J.C., Y.Q.C., M.S.F., N.L.P., T.S.H., C.Y.
|
References |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONADVANCES IN KNOWLEDGEReferences |
|---|
This article has been cited by other articles:
|
|
 |
|
  L. Saba, R. Sanfilippo, L. Pascalis, R. Montisci, and G. Mallarini Carotid Artery Abnormalities and Leukoaraiosis in Elderly Patients: Evaluation with MDCT Am. J. Roentgenol., February 1, 2009; 192(2): W63 - W70. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J M U-King-Im, T Y Tang, A Patterson, M J Graves, S Howarth, Z-Y Li, R Trivedi, D Bowden, P J Kirkpatrick, M E Gaunt, et al. Characterisation of carotid atheroma in symptomatic and asymptomatic patients using high resolution MRI J. Neurol. Neurosurg. Psychiatry, August 1, 2008; 79(8): 905 - 912. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. N. Redgrave, P. Gallagher, J. K. Lovett, and P. M. Rothwell Critical Cap Thickness and Rupture in Symptomatic Carotid Plaques: The Oxford Plaque Study Stroke, June 1, 2008; 39(6): 1722 - 1729. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Yuan Carotid atherosclerosis and magnetic resonance imaging. J. Am. Coll. Cardiol. Img., January 1, 2008; 1(1): 58 - 60. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Leclercq, X. Houard, M. Philippe, V. Ollivier, U. Sebbag, O. Meilhac, and J.-B. Michel Involvement of intraplaque hemorrhage in atherothrombosis evolution via neutrophil protease enrichment J. Leukoc. Biol., December 1, 2007; 82(6): 1420 - 1429. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Y. Tang, S. P. Howarth, S. R. Walsh, M. E. Gaunt, and J. H. Gillard Contralateral Carotid Intraplaque Hemorrhage May Reduce the Predictive Value of Fat-Suppressed T1-Weighted MRI in Symptomatic Carotid Disease Stroke, December 1, 2007; 38(12): e156 - e157. [Full Text] [PDF]
|
|
|
|
 |
|
 L. G. Spagnoli, E. Bonanno, G. Sangiorgi, and A. Mauriello Role of Inflammation in Atherosclerosis J. Nucl. Med., November 1, 2007; 48(11): 1800 - 1815. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Saam, T. S. Hatsukami, N. Takaya, B. Chu, H. Underhill, W. S. Kerwin, J. Cai, M. S. Ferguson, and C. Yuan The Vulnerable, or High-Risk, Atherosclerotic Plaque: Noninvasive MR Imaging for Characterization and Assessment Radiology, July 1, 2007; 244(1): 64 - 77. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A.D. Hardie, C.M. Kramer, P. Raghavan, E. Baskurt, and K.R. Nandalur The Impact of Expansive Arterial Remodeling on Clinical Presentation in Carotid Artery Disease: A Multidetector CT Angiography Study AJNR Am. J. Neuroradiol., June 1, 2007; 28(6): 1067 - 1070. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| RADIOLOGY | RADIOGRAPHICS | RSNA JOURNALS ONLINE |
