| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Technical Developments |
1 From the Department of Radiology, Neuroradiology Division, Johns Hopkins Hospital, 600 N Wolfe St, Phipps B-100, Baltimore, MD 21287-2182 (B.A.W.); the Laboratory of Cardiac Energetics (A.E.A, R.S.B.) and the Cardiology Branch (R.O.C.), National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md; and the Departments of Pathology (W.I.S.) and Surgery (H.H.T.), Suburban Hospital, Bethesda, Md. Received March 22, 2001; revision requested May 1; revision received August 17; accepted September 17. Supported by the intramural program of the National Heart, Lung, and Blood Institute, protocol 98-H-0157. Address correspondence to B.A.W. (e-mail: bwasser@rad.jhu.edu).
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
© RSNA, 2002
Index terms: Arteriosclerosis, 56.754, 9*.7212 • Magnetic resonance (MR), high-resolution, 56.121411, 9*.721 • Magnetic resonance (MR), tissue characterization, 56.121411, 9*.12916 • Magnetic resonance (MR), vascular studies, 9*.12916
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
Findings of in vitro studies have demonstrated the ability of MR imaging to depict the components of plaque (5–7). T2-weighted sequences have been purported to offer the greatest contrast for distinguishing plaque components and interrogating the vessel wall (6,8). Serfaty et al (9) tested the ability of T2-weighted MR imaging alone to depict fibrous cap thickness and lipid core volume. Their study of 41 cadaveric and endarterectomy specimens with T2-weighted imaging alone was limited by overestimation of the lipid core by more than 30% in 43% of the plaques. Therefore the vulnerability of numerous plaques was exaggerated. Shinnar et al (7) similarly found that use of two echo times (30 and 50 msec) was necessary to distinguish the lipid-rich core from fibrocellular areas that contain lipid. One limitation of T2-weighted MR imaging is the inherently low signal-to-noise ratio (SNR). In vivo application of these techniques is supported by the strong agreement demonstrated between in vivo and ex vivo measurements of vessel wall thickness and T2 relaxation of plaque components (10,11).
To our knowledge, there have been no previous reports of contrast enhancement for morphologic characterization of atherosclerosis. Aoki et al (12) report contrast enhancement of the outer extracranial carotid artery wall but not of the atheroma. The authors attributed this enhancement to angiogenesis, which is supported by the report of Lin et al (13) of arterial wall enhancement thought to be related to neovascularity in balloon-injured blood vessels in pigs. One limitation of contrast material–enhanced vessel wall imaging is that enhancement along the inner wall can be obscured. To our knowledge, the mechanism of contrast enhancement in atherosclerosis remains unknown, and the pattern of enhancement of atheroma has not been described with black-blood techniques.
The aims of this study were to determine if atheroma enhances after administration of gadolinium-based contrast agent and if postcontrast MR imaging has the ability to depict the components of atherosclerotic plaque.
|
Materials and Methods |
|---|
|
TOPABSTRACTINTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
MR Studies
MR imaging was performed with a 1.5-T MR imager (CV/i; GE Medical Systems, Milwaukee, Wis) with a dual 3-inch (7.6 cm) phased-array surface coil immobilized by a mechanical support. A two-dimensional time-of-flight MR angiogram was used as a scout image. The vessel wall was imaged with a high-spatial-resolution, black-blood, electrocardiography-gated, double inversion-recovery, fast spin-echo pulse sequence (14,15). Transverse black-blood images were centered at the level of the stenotic carotid bifurcation, and this series was used to orient three or four oblique black-blood sections through the plane of the proximal internal and external carotid arteries to include the bifurcation and area of greatest stenosis. The section that best depicted the carotid stenosis was used to prescribe double-oblique sections through the distal common carotid artery and through the proximal internal carotid artery centered at the level of greatest plaque thickness, with all sections oriented perpendicular to the long axis of the lumen.
Imaging parameters were echo train length, 32; section thickness, 2 mm; field of view, 14 cm; matrix, 256 x 256; and one signal acquired. Chemical fat saturation was applied. The inversion time was set to approximately 600 msec for precontrast images and 300 msec for postcontrast images to minimize the blood pool signal on the basis of estimated T1 values of blood. All images were electrocardiography gated and performed with either a short repetition time (TR) of 32 echoes every heartbeat or a long TR of 32 echoes every other heartbeat. Baseline and postcontrast images were acquired with two TRs (short TR [every heartbeat] with 5-msec echo time and long TR [every other heartbeat] with 5-msec echo time); T2-weighted images (long TR and 60-msec echo time) were also acquired. Gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ), 0.1 mmol per kilogram of body weight, was injected intravenously by using a power injector, and acquisition of postcontrast vessel wall images began approximately 5 minutes after the injection. The center frequency, shim, and receiver gains were consistent before and after administration of gadopentetate dimeglumine to allow comparisons of signal intensity. A three-dimensional MR angiogram was acquired at the arterial phase during administration of gadopentetate dimeglumine.
Analysis of Endarterectomy Specimens
Tissues were fixed in 4% neutral buffered formaldehyde overnight and then decalcified in dilute HCl with chelating agents for 24–48 hours. The arterial specimen was sectioned perpendicular to the long axis of the vessel. The entire specimen was sequentially submitted with separate blocks for the common carotid, bifurcation, and internal and external carotid arteries. The slides were stained with hematoxylin-eosin or Masson trichrome stains. Specimens were evaluated (W.I.S., B.A.W.) with consensus for areas of fibrocellular tissue, lipid, calcium, thrombus, and hemorrhage.
Image Analysis
For the subjects with tissue specimens, areas of enhancement were visually matched with morphologic characteristics seen on specimen slides. The eccentricity of each atheroma and its position relative to the bifurcation allowed us to perform direct comparisons with corresponding MR images. Histologic results were used to determine the location of regions of interest placed on postcontrast images. Regions of interest were drawn (B.A.W.) around the areas of enhancement that corresponded to the fibrous caps, areas of low signal intensity that corresponded to focal calcifications (if present), regions subjacent to the fibrous cap that corresponded to the lipid cores, and the lumina. Regions of interest were made as large as possible and drawn to outline a plaque component and not necessarily an area of greatest enhancement. Regions of interest ranged in size from 3.9 to 14.7 mm2 for the fibrous cap, 19.2–38.6 mm2 for the lipid core, and 1.9–8.5 mm2 for foci of calcification. The regions of interest were copied onto corresponding structures on the baseline precontrast and T2-weighted images, and modified if necessary to account for minor differences from misregistration.
For the subjects without tissue specimens for comparison, the T2-weighted image that best depicted the atheroma was selected, and a region of interest was drawn (B.A.W.) around the area of prolonged T2 relaxation within the plaque that appeared to correspond to the location of the fibrous cap. Regions of interest were also drawn around the lipid core, if identified, and the lumen. Regions of interest ranged in size from 3.0 to 19.0 mm2 for fibrocellular tissue and from 3.2 to 8.4 mm2 for the lipid core. Identical regions of interest were copied onto corresponding structures on the precontrast and postcontrast images at the same location. The position of the region of interest was adjusted if necessary to account for minor differences from misregistration. Areas of questionable composition, such as calcification and thrombus, were not analyzed in this group.
Precontrast and postcontrast images were compared (B.A.W., A.E.) for the short and long TR sequences. The percentage of signal intensity (SI) change from before (pre) and after (post) contrast agent administration that was measured in the regions of interest was calculated (B.A.W,) as follows: [(SIpost - SIpre) x 100]/SIpre. The percentage of signal intensity change was compared among the short and long TR groups by means of a paired Student t test with Bonferroni correction for multiple comparisons.
Background noise was determined by calculating the SD of air and multiplying it by 1.25 (16). The noise was considered constant throughout an examination as there was no variation in bandwidth. SNRs were calculated for the fibrous cap, lipid core, calcification (if present), and lumen for postcontrast and T2-weighted images. SNRs for the short and long TR images were then compared separately with the SNRs for T2-weighted images by using a paired Student t test with Bonferroni correction for multiple comparisons. Contrast-to-noise ratios (CNRs) were calculated (B.A.W.) for the fibrous cap (F) and lipid core (L) as follows: (SIpostF - SIpostL)/SIN, where N is background noise. CNRs were calculated similarly for fibrous cap and lumen.
|
Results |
|---|
|
TOPABSTRACTINTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
|
|
|
|
|
|
|
|
|
|
|
|
The percentage change in fibrous cap signal intensity after administration of contrast agent for all nine subjects was 28.7% ± 9.8 for the short TR images and 21.4% ± 7.8 for the long TR images, although the difference was not statistically significant (P = .14). One patient demonstrated a reversal of this pattern, with a threefold increase in the degree of enhancement on the long TR image relative to the short TR image. This patient was unique in that precontrast images demonstrated considerable T1 relaxation, which was thought to represent intraplaque hemorrhage. This was confirmed histologically.
The mean percentage change in lipid core signal intensity measured in the group with endarterectomy specimens (n = 4) was -9.3% ± 7.0 and 3.9% ± 3.9 for short and long TR images, respectively. In the entire group with lipid cores (n = 8), the percentage change in lipid core signal intensity after administration of contrast agent was 13.9% ± 12.1 and 16.5% ± 9.6 for short and long TR images, respectively.
Although all specimens were decalcified before sectioning, areas of calcification could be identified on the basis of residual blue staining on hematoxylin-eosin slide preparations. In some cases, there was local fragmentation and tissue loss in areas of calcium formation (Figs 3a, 7). In three cases with endarterectomy specimens , areas of calcification were seen that were prospectively identified as areas of low signal intensity on postcontrast and T2-weighted images (Figs 2, 6).
Calcification, when detected histologically, demonstrated the lowest signal intensity on MR images. The mean SNR of calcification in three patients was 5.9 ± 0.8 on T2-weighted images in comparison with 11.6 ± 1.1 and 15.9 ± 0.5 for short and long TR postcontrast images, respectively (difference not significant and P = .013, respectively). CNRs for calcification versus the adjacent lipid core were higher for the postcontrast images, although the differences were not statistically significant.
|
Discussion |
|---|
|
TOPABSTRACTINTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
Our double-oblique section acquisition allowed assessment of plaque volume and fibrous cap thickness by minimizing partial volume averaging from oblique section orientation and facilitated correlation with pathologic cross-sectional slides. The use of a double inversion-recovery sequence with adjustment of the inversion time to account for the increased T1 relaxation of the blood pool after administration of contrast agent provided adequate flow suppression. Flow suppression was optimized by imaging at middiastole to maximize the flow of blood that received the nonselective inversion pulse during the inversion time. The thin sections and the perpendicular orientation of the double-oblique sections to the direction of blood flow contributed to flow suppression by optimizing inflow effects. The adequacy of flow suppression was exemplified by the twofold increase in CNR of the fibrous cap and lumen for the postcontrast images compared with the T2-weighted images. This paralleled the twofold increase in SNR for postcontrast images compared with T2-weighted images and reflects similar suppression of luminal signal intensity on postcontrast and T2-weighted images.
To our knowledge, the use of a contrast agent to help characterize plaque morphology has not been described previously. Gadolinium-based contrast agents are known to distribute to the extracellular fluid space, and a greater degree of enhancement in the vessel wall may be due to (a) increased wash-in of gadolinium-based contrast agent (increased permeability), (b) increased volume of distribution (increased extracellular volume), or (c) decreased washout. Inflammatory changes are known to underlie atherogenesis (17) and may lead to increased extracellular volume or increased endothelial permeability. The latter may also reflect a response to disturbed flow with low shear stress exerted on the wall, such as in areas of arterial branching or curvature (18–20). The areas of low shear stress result in more randomly distributed endothelial cells with cell loss, which allows greater passive diffusion of low-density lipoprotein. This alteration in permeability could also increase entry of a gadolinium-based contrast agent. However, the effect of shear stress on endothelial permeability likely plays a greater role in early vessel wall enhancement before the development of frank atheroma given that these hemodynamic patterns greatly alter as plaque develops.
Angiogenesis may also be postulated as a reason for plaque enhancement. Angiogenesis is thought to have a role in plaque formation (21), and there is evidence that suggests neovascularization is associated with symptomatic carotid disease (22). Aoki et al (12) suggest that the enhancement seen in the outer wall of the extracranial carotid artery after administration of gadolinium-based contrast agent is probably due to neovascularity, but specimens were not available for histologic confirmation in their study.
In our cases, the enhancing tissue clearly corresponded to areas of fibrosis. Enhancement of fibrous tissue has long been observed with MR imaging. A gadolinium-based contrast agent is frequently administered in the evaluation of the postoperative spine to help separate epidural fibrosis from a herniated disk. Enhancement of fibrosis has been extensively described in other organ systems, including fibrosis in breast tissue and myocardium (23). The mechanism of enhancement of epidural fibrosis appears to be due to transgression of gadolinium-based contrast agent through "leaky" intercellular junctions of the endothelial layer, with a rapid diffusion into the extravascular space of the scar tissue (24). Enhancement of fibrous tissue does not seem to depend on blood volume (ie, vessel density); this finding suggests that any neovascularity seen within the vessel wall and thought to underlie enhancement may be coincidental.
There are several technical considerations that should be addressed. First, although T1 weighting was improved by modifying the double inversion-recovery sequence to image at the short TR, the minimum TR achieved ranged from 833 to 1,153 msec. The use of a fast spin-echo technique in the double inversion-recovery sequence provided an inherent magnetization transfer effect that contributed additional T1 weighting. However, additional T1 weighting is possible; on the basis of our results, we believe that the development of a more T1-weighted sequence is desirable. In our T2- and intermediate-weighted sequences, long TRs (every other heartbeat) ranged from 1,714 to 2,666 msec. As a result, there was some T1 weighting on these images. An echo time of 60 msec was used for T2-weighted imaging. Greater T2 weighting was not attempted because of SNR limitations.
The degree of enhancement with the short TR sequence may be limited when preexisting T1 relaxation is present. In one subject, intraplaque hemorrhage was prospectively suspected on the basis of its T1 characteristics and was confirmed histologically. Results of specimen analysis suggested that there had been a plaque disruption with hemorrhage within a few days before our study. The enhancement mechanism may therefore be interrupted in the setting of fibrous cap disruption with hemorrhage, but further investigation is needed.
Although the SDs for lipid core enhancement were high for all plaques and no definite core enhancement was detected, the group without specimens for comparison had a higher mean enhancement. Therefore, core measurements in this group may have included part of the fibrous cap, although this was not evident on images. In the group without correlative specimens, the T2-weighted image was used as a reference image to define regions of interest, which were then applied to corresponding images obtained with other sequences. It is conceivable that contrast enhancement may better delineate the fibrous cap; therefore, the SNR and CNR may be falsely higher for the T2-weighted sequence. The T2-weighted image was used as a reference image to test postcontrast images more rigorously against T2-weighted images.
Incomplete flow suppression can interfere with lesion depiction, particularly of the fibrous cap, because unsuppressed blood signal may blend imperceptibly with the margin of the plaque. Flow suppression is particularly challenging after administration of a contrast agent. We have shown that good flow suppression can be achieved even after administration of contrast agent, although this remains to be tested in the setting of nearly occlusive atheroma.
The SNR of calcification was higher for postcontrast than T2-weighted images, but the number of cases was too small to allow conclusions to be drawn regarding its conspicuity against the adjacent lipid core. This may represent partial volume averaging.
In this study, we found that postcontrast flow-suppressed MR imaging shows promise for determining the presence of the lipid core and the thickness of the overlying fibrous cap. The understanding that a large lipid core with a thin overlying fibrous cap tends to disruption is based on the results of studies of carotid endarterectomy specimens, which are representative of a subpopulation of atherosclerotic disease. To our knowledge, there have been no reliable outcome studies of plaque features that denote vulnerability, specifically the fibrous cap to lipid core ratio, because of technical limitations of in vivo plaque imaging. Compared with current technologies, high-spatial-resolution postcontrast MR imaging offers an improved method of morphologic characterization that has the potential ability to test the current understanding of plaque vulnerability that is based on endarterectomy studies in a broader range of carotid atherosclerotic diseases.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
Abbreviations: CNR = contrast-to-noise ratio, SNR = signal-to-noise ratio, TR = repetition time
Author contributions: Guarantors of integrity of entire study, B.A.W., A.E.A., R.S.B.; study concepts, B.A.W., A.E.A., R.S.B., H.H.T.; study design, W.I.S., B.A.W., A.E.A., R.S.B., R.O.C.; literature research, B.A.W.; clinical studies, B.A.W., H.H.T.; experimental studies, B.A.W., W.I.S.; data acquisition, B.A.W.; data analysis/interpretation, B.A.W., A.E.A., W.I.S.; statistical analysis, B.A.W., A.E.A.; manuscript preparation, B.A.W.; manuscript definition of intellectual content, all authors; manuscript editing and revision/review, B.A.W., A.E.A.; manuscript final version approval, all authors.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMaterials and Methods ResultsDiscussionREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  C. Burtea, S. Laurent, O. Murariu, D. Rattat, G. Toubeau, A. Verbruggen, D. Vansthertem, L. Vander Elst, and R. N. Muller Molecular imaging of {alpha}v{beta}3 integrin expression in atherosclerotic plaques with a mimetic of RGD peptide grafted to Gd-DTPA Cardiovasc Res, April 1, 2008; 78(1): 148 - 157. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. A. Wasserman, A. R. Sharrett, S. Lai, A. S. Gomes, M. Cushman, A. R. Folsom, D. E. Bild, R. A. Kronmal, S. Sinha, and D. A. Bluemke Risk Factor Associations With the Presence of a Lipid Core in Carotid Plaque of Asymptomatic Individuals Using High-Resolution MRI: The Multi-Ethnic Study of Atherosclerosis (MESA) Stroke, February 1, 2008; 39(2): 329 - 335. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. B. Yeon, A. Sabir, M. Clouse, P. O. Martinezclark, D. C. Peters, T. H. Hauser, C. M. Gibson, R. Nezafat, D. Maintz, W. J. Manning, et al. Delayed-Enhancement Cardiovascular Magnetic Resonance Coronary Artery Wall Imaging: Comparison With Multislice Computed Tomography and Quantitative Coronary Angiography J. Am. Coll. Cardiol., July 31, 2007; 50(5): 441 - 447. [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]
|
|
|
|
|
|
E. Touze, J.-F. Toussaint, J. Coste, E. Schmitt, F. Bonneville, P. Vandermarcq, J.-Y. Gauvrit, F. Douvrin, J.-F. Meder, J.-L. Mas, et al. Reproducibility of High-Resolution MRI for the Identification and the Quantification of Carotid Atherosclerotic Plaque Components: Consequences for Prognosis Studies and Therapeutic Trials Stroke, June 1, 2007; 38(6): 1812 - 1819. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. S. Kerwin, K. D. O'Brien, M. S. Ferguson, N. Polissar, T. S. Hatsukami, and C. Yuan Inflammation in Carotid Atherosclerotic Plaque: A Dynamic Contrast-enhanced MR Imaging Study Radiology, November 1, 2006; 241(2): 459 - 468. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. S. Pessanha, K. Potter, F. D. Kolodgie, A. Farb, R. Kutys, E. K. Mont, A. P. Burke, T. J. O'Leary, and R. Virmani Characterization of Intimal Changes in Coronary Artery Specimens with MR Microscopy Radiology, October 1, 2006; 241(1): 107 - 115. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Maintz, M. Ozgun, A. Hoffmeier, R. Fischbach, W. Y. Kim, M. Stuber, W. J. Manning, W. Heindel, and R. M. Botnar Selective coronary artery plaque visualization and differentiation by contrast-enhanced inversion prepared MRI Eur. Heart J., July 2, 2006; 27(14): 1732 - 1736. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Wilensky, H. K. Song, and V. A. Ferrari Role of magnetic resonance and intravascular magnetic resonance in the detection of vulnerable plaques. J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C48 - C56. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. L. Ruberg, J. Viereck, A. Phinikaridou, Y. Qiao, J. Loscalzo, and J. A. Hamilton Identification of cholesteryl esters in human carotid atherosclerosis by ex vivo image-guided proton MRS J. Lipid Res., February 1, 2006; 47(2): 310 - 317. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Nighoghossian, L. Derex, and P. Douek The Vulnerable Carotid Artery Plaque: Current Imaging Methods and New Perspectives Stroke, December 1, 2005; 36(12): 2764 - 2772. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Cai, T. S. Hatsukami, M. S. Ferguson, W. S. Kerwin, T. Saam, B. Chu, N. Takaya, N. L. Polissar, and C. Yuan In Vivo Quantitative Measurement of Intact Fibrous Cap and Lipid-Rich Necrotic Core Size in Atherosclerotic Carotid Plaque: Comparison of High-Resolution, Contrast-Enhanced Magnetic Resonance Imaging and Histology Circulation, November 29, 2005; 112(22): 3437 - 3444. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Y. Desai, S. Lai, C. Barmet, R. G. Weiss, and M. Stuber Reproducibility of 3D free-breathing magnetic resonance coronary vessel wall imaging Eur. Heart J., November 1, 2005; 26(21): 2320 - 2324. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Wasserman, R. J. Wityk, H. H. Trout III, and R. Virmani Low-Grade Carotid Stenosis: Looking Beyond the Lumen With MRI Stroke, November 1, 2005; 36(11): 2504 - 2513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Sirol, V. Fuster, J. J. Badimon, J. T. Fallon, J.-F. Toussaint, and Z. A. Fayad Chronic Thrombus Detection With In Vivo Magnetic Resonance Imaging and a Fibrin-Targeted Contrast Agent Circulation, September 13, 2005; 112(11): 1594 - 1600. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Y. Desai, A. Rodriguez, B. A. Wasserman, G. Gerstenblith, S. Agarwal, M. Kennedy, D. A Bluemke, and J. A.C. Lima Association of Cholesterol Subfractions and Carotid Lipid Core Measured by MRI Arterioscler. Thromb. Vasc. Biol., June 1, 2005; 25(6): e110 - e111. [Full Text] [PDF]
|
|
|
|
|
|
L. V. Hofmann, R. P. Liddell, J. Eng, B. A. Wasserman, A. Arepally, D. S. Lee, and D. A. Bluemke Human Peripheral Arteries: Feasibility of Transvenous Intravascular MR Imaging of the Arterial Wall Radiology, May 1, 2005; 235(2): 617 - 622. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Y. Desai, J. H. Stone, T. K. F. Foo, D. B. Hellmann, J. A. C. Lima, and D. A. Bluemke Delayed Contrast-Enhanced MRI of the Aortic Wall in Takayasu's Arteritis: Initial Experience Am. J. Roentgenol., May 1, 2005; 184(5): 1427 - 1431. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.K. Lovett, J.N.E. Redgrave, and P.M. Rothwell A Critical Appraisal of the Performance, Reporting, and Interpretation of Studies Comparing Carotid Plaque Imaging With Histology Stroke, May 1, 2005; 36(5): 1085 - 1091. [Abstract] [Full Text] [PDF]
|
|
|
|
< |
