Characterization of Hyperintense Plaque With Noncontrast T1-Weighted Cardiac Magnetic Resonance Coronary Plaque ImagingComparison With Multislice Computed Tomography and Intravascular Ultrasound
Tomohiro Kawasaki, MD*,*,
Shoichi Koga, MD ,
Nobuhiko Koga, MD*,
Teruo Noguchi, MD ,
Hidenori Tanaka, MD*,
Hisashi Koga, MD*,
Takeshi Serikawa, MD*,
Yoshiya Orita, MD*,
Shinsuke Ikeda, MD*,
Takahiro Mito, MD*,
Yoshitaka Goto, MD*,
Yoshiaki Shintani, MD*,
Atsushi Tanaka, MD,
Takaya Fukuyama, MD*
* Cardiovascular Center, Shin-Koga Hospital, Kurume, Japan
Department of Cardiology, Koga Hospital 21, Kurume, Japan
Division of Cardiology, Department of Medicine, National Cardiovascular Center, Suita, Japan
 |
Abstract
|
|---|
Objectives: This study sought to characterize coronary hyperintense plaques (HIP) using noncontrast T1-weighted imaging (T1WI) in cardiac magnetic resonance, which was then compared with multislice computed tomography and intravascular ultrasound.
Background: Carotid plaque components such as intraplaque hemorrhages and/or lipid-rich necrotic cores can be detected as HIP by noncontrast T1WI. Although coronary HIPs have been successfully detected using this technique, the properties of hyperintense signals in coronary plaques have not yet been systematically evaluated.
Methods: Thirty-eight lesions from 37 patients with angina pectoris who demonstrated >70% coronary stenosis on multislice computed tomography were evaluated by noncontrast T1WI using a 1.5-T magnetic resonance imager, and 25 lesions were evaluated by intravascular ultrasound. Signal intensity of coronary plaque to cardiac muscle ratio >1.0 was defined as HIP. We divided 25 lesions into the 2 groups, according to the presence or absence of HIP: HIP (n = 18) and non-HIP (n = 7) groups.
Results: In comparison with the non-HIP group, the HIP group demonstrated significantly higher coronary plaque to cardiac muscle ratio (1.7 ± 0.7 vs. 0.9 ± 0.1, p < 0.01), higher frequency of positive remodeling as observed by both multislice computed tomography (89% vs. 0%, p<0.0001) and intravascular ultrasound (94% vs. 14%, p < 0.001) and ultrasound attenuation (100% vs. 14.3%, p < 0.0001). The frequency of spotty calcification tended to be higher in HIP (89% vs. 50%, p = 0.079). The HIP group also exhibited a significantly lower computed tomography density (–23.2 ± 20.7 Hounsfield units [HU] vs. 9.6 ± 20.5 HU, p < 0.01). In addition, the incidence of transient slow-flow phenomena was significantly higher in the HIP group than in the non-HIP group (83% vs. 14%, p < 0.01).
Conclusions: The typical HIP case was associated with ultrasound attenuation, positive remodeling, remarkably low computed tomography density, and a high incidence of slow-flow phenomena. Noncontrast T1WI in cardiac magnetic resonance imaging may be useful for the assessment of coronary plaque characterization in patients with coronary artery disease.
Key Words: coronary plaque imaging • cardiac magnetic resonance • multislice computed tomography • intravascular ultrasound
|
Abbreviations and Acronyms
| | CMR = cardiac magnetic resonance | | HIP = hyperintense plaque | | IVUS = intravascular ultrasound | | MSCT = multislice computed tomography | | PCI = percutaneous coronary intervention | | PMR = coronary plaque to cardiac muscle ratio | | RI = remodeling index | | T1WI = T1-weighted imaging |
|
Cardiac magnetic resonance (CMR) imaging (1–3) and multislice computed tomography (MSCT) (4–7) are attracting attention as new noninvasive imaging techniques for coronary plaque visualization. Noncontrast T1-weighted imaging (T1WI) in CMR enables the identification of the thickened coronary wall (1–3). In addition, contrast-enhanced CMR allows us to identify areas of delayed enhancement that correlate with the severity of atherosclerosis as measured by MSCT and quantitative coronary angiography (8).
In carotid plaques, high signals on inversion recovery-based 3-dimensional T1WI are associated with complicated plaques (type VI as proposed by the American Heart Association) (9) and with recent ischemic cerebrovascular events (10,11). Thus, CMR with T1WI is able to successfully identify vulnerable carotid plaques. Although coronary plaque imaging by noncontrast- and contrast-enhanced T1WI has been successfully demonstrated, and coronary plaques can be visualized as hyperintense signal areas, the properties of hyperintense signals in coronary plaques detected by T1WI have not yet been systematically evaluated.
To address this, we sought to characterize hyperintense coronary plaques visualized by noncontrast T1WI in CMR to compare findings obtained by MSCT and intravascular ultrasound (IVUS).
|
Methods
|
|---|
Study population.
Thirty-seven consecutive angina pectoris patients with a total of 38 lesions were enrolled. In all of these patients, significant coronary stenosis (>70%) was detected on MSCT; all were scheduled for elective percutaneous coronary intervention (PCI) between February 2007 and November 2007. All 38 lesions (37 patients) had been evaluated by noncontrast T1WI in CMR before PCI. Twenty-eight lesions from 27 patients contained areas with hyperintense signals, corresponding to the target lesions on MSCT (defined as hyperintense plaque [HIP]). In contrast, 10 lesions from the remaining 10 patients contained areas without hyperintense signals (defined as non-HIP). We excluded 13 lesions from 13 patients, 10 HIP and 3 non-HIP, who had not undergone IVUS examination during PCI. Thus, 25 lesions from 24 patients (18 HIP and 7 non-HIP) were examined in this study (Fig. 1). Both MSCT and CMR were performed within a month before the IVUS examination. The study protocol was approved by the Institutional Board on Clinical Investigations at Shin-Koga Hospital. Information regarding this study was provided either orally or in written form to all subjects, and written informed consent was obtained from each subject.
View larger version (32K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1 Flow Chart of Inclusion Criteria
A total 38 lesions from 37 patients with significant coronary stenosis (>70%) underwent noncontrast T1W cardiac magnetic resonance; overall, 24 patients (a total of 25 lesions; 18 lesions with hyperintense signal and 7 with nonhyperintense signal) were enrolled in this study. IVUS = intravascular ultrasound; MSCT = multislice computed tomography; T1WI = T1-weighted image.
|
|
CMR coronary plaque imaging.
Coronary plaque imaging was obtained with a 1.5-T MR imager (Intera, Philips Medical Systems, Best, the Netherlands) using 5-element cardiac coils. When heart rates were more than 65 beats/min, the rates were adjusted by administration of 20 to 40 mg of metoprolol 30 min before imaging. Nitroglycerin (0.3 mg) was also administered sublingually immediately before taking images to obtain high-quality CMR images. The survey images were focused around the heart, and the reference images were taken under free breathing to improve the sensitivity of parallel imaging. Coronary plaque images were obtained when patients were breathing freely, with the use of a 3-dimensional, T1W inversion-recovery gradient-echo sequence with fat-suppressed and radial k-space sampling (repetition time: shortest  4.7 ms, echo time: shortest 1.37 ms, flip angle: 20°, excitations per cardiac cycle: 15 to 45, SENSE factor: 2.5, number of excitations: 2, navigator gating window: 5 mm, no drift correction, field of view: 300 x 270 x 112 mm, acquisition matrices: 224 x 224, reconstruction matrices: 512 x 512 x 140). Spatial resolution was 1.34 x 1.34 x 1.6 mm. The same value was set for the acquisition window as in the coronary CMR. The acquisition window was set, according to the movement of the heart, for the time during the diastolic phase at which the heart moves the least. The movement of the heart was confirmed using cine-MR images that had been taken previously. The cine-MR images were obtained with a steady-state sequence as the patient was free breathing (repetition time: 2.6 ms, echo time: 1.3 ms, flip angle: 60°, field of view: 360 x 324 x 7 mm, acquisition matrix: 192 x 192, cardiac phases: 50, SENSE factor: 3.0, imaging time: 2 s).
A coronary CMR image analysis was performed by 2 technicians who were blinded to the plaque information obtained by MSCT. In the coronary CMR image obtained, if the areas that corresponded to the target lesion on MSCT were confirmed, then the signal intensity of coronary plaque to muscle ratio (PMR) (PMR was defined as the signal intensity of the coronary plaque divided by the signal intensity of the cardiac muscle) was calculated. Areas with PMR >1.0 were defined as HIP, whereas areas with PMR  1.0 were defined as non-HIP. The representative cases with HIP and with non-HIP are shown in Figure 2. The signal intensity of the myocardium was measured at a site of the left ventricle near the coronary plaque.
View larger version (114K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2 Representative Case With and Without HIP
(A) Representative case with hyperintense area (white arrow) at distal right coronary artery (left panel). In this case, the intensity of coronary plaque to cardiac muscle ratio (PMR) was 1.76 and it was classified as a hyperintense plaque (HIP) (right panel). (B) Representative case without hyperintense signal area (arrowhead) at proximal right coronary artery (left panel). The PMR was 0.89 and it was classified as non-HIP (right panel).
|
|
Coronary Computed Tomography (CT) angiography.
Coronary CT angiography was performed using MSCT (LightSpeed Volume CT, GE Healthcare, Milwaukee, Wisconsin). A coronary image was acquired with 64 x 0.625-mm slice collimation, a gantry rotation time of 0.35 ms, table feed: 7.2 to 8.2 mm/rotation, tube energy: 120 kV, and effective tube current: 280 mA. The total amount of contrast media (50.1 ± 5.1 ml iopamidol, 370 mgl/ml) (Schering AG, Berlin, Germany) was injected intravenously at a rate of 3.5 to 4.0ml/s. Transaxial images were reconstructed using a medium sharp conventional kernel/standard smooth kernel (B25F) and sharp kernel (B46F). The image matrix was 512 x 512 pixels, with a slice thickness of 0.75 mm and an increment of 0.4 mm using an electrocardiography-gated half-scan algorithm with a resulting temporal resolution of 165 ms in the center of rotation. Image reconstruction was retrospectively gated to the electrocardiogram. The patients with a heart rate >70 beats/min received 20 mg of metoprolol orally 60 min before scanning, and almost all of the patients received 0.3 mg of nitroglycerin sublingually just before scanning. Image reconstruction was performed using a 3-dimensional workstation (Advantage Workstation version 4.2, GE Healthcare). A focal multiplanar reconstruction image and cross-sectional image at the lesion were used for the assessment of coronary plaque morphology, including vessel remodeling index (RI), the minimum CT density of the plaques (expressed by Hounsfield units [HU]), and spotty calcification. The RI on MSCT was calculated by dividing the cross-sectional vessel area at the lesion by the mean of the 2 reference areas, which were obtained within 5 mm proximal to and 5 mm distal to the lesion. Positive remodeling was defined as RI >1.10 (12). Spotty calcification was defined as features <3 mm in size on a focal multiplanar reconstruction image and cross-sectional image in the lesion (13,14). An MSCT image analysis was performed by 2 technicians who were blinded to the plaque information obtained by CMR and IVUS.
IVUS image.
The IVUS image was obtained before the PCI within 1 or 2 weeks after the CMR and MSCT. The IVUS system used a commercially available 40-MHz IVUS catheter (Atlantis Pro 2.9-F, Boston Scientific, Natick, Massachusetts) with 0.5 mm/s auto-pullback. The manual contour detection of the external elastic membrane was performed at the lesion and at the proximal reference site, and the RI was then calculated as the external elastic membrane of the lesion divided by the external elastic membrane of the proximal reference site, as previously described (15,16). Positive remodeling was defined as RI >1.05 (17). In addition, the plaque was checked to determine whether ultrasound attenuation was present. Ultrasound attenuation was defined as backward attenuation of signals behind the coronary atheroma without echogenic deposits or calcium within the plaque (18). The grade of ultrasound attenuation was classified into 3 categories according to the arc of the attenuation as follows: – = no attenuation; + = attenuation <180°; ++ = attenuation  180°(18).
Statistical analysis.
Continuous data were summarized as mean ± SD. Categorical data were summarized as counts and percentages. The comparison of the plaque characteristics between the HIP and non-HIP groups was made using an unpaired t test in continuous data and Fisher exact tests in categorical data. All interpretations of CMR, MSCT, and IVUS imaging were performed in a blinded manner. Interobserver agreement was calculated using kappa statistics. A value of p < 0.05 was considered statistically significant.
|
Results
|
|---|
Of all 25 lesions used in the study, 18 lesions (72%) were classified as HIP and 7 lesions (28%) were classified as non-HIP. The baseline characteristics of those 25 lesions (from 24 patients) are shown in Table 1. Other than in target coronary vessel involvement, there was no statistically significant difference in patient clinical characteristics between HIP and non-HIP lesions. The relationship between the HIP/non-HIP lesions on noncontrast T1WI and the plaque morphology obtained by MSCT and IVUS is shown in Table 2
and is summarized in Table 3. The averaged PMR in HIP lesions was significantly higher than in non-HIP lesions (1.70 ± 0.71 vs. 0.90 ± 0.08, p < 0.001). Positive remodeling on MSCT was observed in 16 (89%) of the 18 patients with HIP as opposed to 0 (0%) of the 7 patients with non-HIP. In addition, minimal CT density was significantly lower in HIP lesions (–23.2 ± 20.7 HU vs. 9.6 ± 20.5 HU, p < 0.01). The frequency of spotty calcification tended to be higher in HIP lesions (89% vs. 50%, p = 0.079). Positive remodeling based on IVUS examinations was observed in 17 (94%) of the 18 patients with HIP, which is significantly higher than in non-HIP patients (14%, p < 0.0001). The frequency of ultrasound attenuation was significantly higher in HIP lesions (100% vs. 14%, p < 0.0001). The kappa statistics for interobserver agreement for ultrasound attenuation was 0.87 (substantial agreement). Transient coronary slow-flow phenomena were observed immediately after either first balloon dilation or stent implantation in 15 (83%) of the 18 patients with HIP, which is significantly higher than in non-HIP patients (14%, p < 0.01). Comparisons of CMR with both MSCT and IVUS of representative cases with HIP are shown in Figures 3 and 4.
View larger version (108K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3 Representative Case of HIP in the Proximal LAD
A 60-year-old patient with a severe coronary stenosis in the proximal left descending artery (LAD) is shown. Multislice computed tomography (MSCT) (A: horizontal, B: sagittal) demonstrates the low-density positive remodeling plaque (–32 Hounsfield units, remodeling index: 1.27) (arrow) with severe coronary stenosis in the proximal LAD. On the corresponding cardiac magnetic resonance (CMR) (C: horizontal, D: sagittal), this low-density plaque was visualized as a "hyperintense spot" (dashed arrow). On the coronary angiography, severe coronary stenosis was observed (E) (arrowhead), and on IVUS examination (F), positive remodeling plaque (remodeling index: 1.29) with ultrasound attenuation (arrowheads) was observed in the proximal LAD, corresponding with the plaque observed by both MSCT and CMR. HIP = hyperintense plaque; IVUS = intravascular ultrasound.
|
|
View larger version (100K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4 Representative Case of HIP in the Mid-RCA
A 60-year-old patient with a severe coronary stenosis in the mid-right coronary artery (RCA) is shown. Multislice computed tomography (MSCT) (A: horizontal, B: sagittal) shows the low-density positive remodeling plaque (–66 Hounsfield units, remodeling index: 1.15, arrow) with severe coronary stenosis in the mid-RCA. On the corresponding cardiac magnetic resonance (CMR) (C: horizontal, D: sagittal), a hyperintense plaque (HIP) can be observed by MSCT in the region with a low-density positive remodeling plaque (dashed arrow). On the coronary angiography, severe coronary stenosis was observed (E). On intravascular ultrasound examination (F), positive remodeling plaque (remodeling index: 1.13) with ultrasound attenuation (white arrowheads) was observed in the mid-RCA, corresponding with the plaque observed both by MSCT and CMR.
|
|
|
Discussion
|
|---|
This is the first report to systematically evaluate the components of HIP detected by noncontrast T1WI in CMR using both MSCT and IVUS examinations. Our findings demonstrate that typical coronary HIP is associated with a high frequency of ultrasound attenuation and positive remodeling, remarkably low CT density, and a high incidence of transient slow-flow phenomena. These results indicate that noncontrast T1WI in CMR is a useful technique for characterization of coronary plaque components.
Coronary plaque imaging with noncontrast T1WI was first reported by Maintz et al. (19) and Yeon et al. (8). These investigators speculated that a hyperintense signal in coronary plaques on noncontrast T1WI indicates the presence of mural or intraplaque thrombus containing methemoglobin. However, these investigators did not systematically evaluate the properties of hyperintense signals in coronary plaques. In our study, the properties of the HIP on noncontrast T1W CMR were examined by using both MSCT and IVUS imaging obtained before PCI. We used noncontrast T1W inversion-recovery and fat-suppressed 3-dimensional black-blood gradient-echo sequence on a 1.5-T MR system. This technique has successfully yielded a description of HIP similar to those observed in the carotid artery (9,20). Recently, our group showed that by using this technique HIP could be observed in the area corresponding to the low-density coronary plaques with positive coronary remodeling observed by MSCT.
Comparison between CMR images and MSCT and IVUS.
Using MSCT, HIP has a significantly higher frequency of positive remodeling and lower CT density in comparison with non-HIP. The frequency of spotty calcification tended to be higher in HIP. Noncalcified plaques <30 HU on MSCT correlated with the presence of a lipid-rich necrotic core (21); the presence of 3 features of coronary plaque on MSCT (positive remodeling, noncalcified plaque <30 HU, and spotty calcification) provided a high level of confidence for the characterization of vulnerable plaques associated with acute coronary syndrome (14). In the present study, all 18 HIP cases displayed significantly lower CT values, and 80% of them presented on MSCT with the aforementioned 3 typical features; in contrast, none of the non-HIP cases exhibited those 3 features. These findings suggest that observation of HIP on noncontrast T1WI may reflect the potential for plaque vulnerability.
In comparisons with IVUS images, HIP also has a significantly higher frequency of positive remodeling and ultrasound attenuation than non-HIP. In this study, positive coronary remodeling was observed with a higher frequency in HIP on both MSCT and IVUS. Positive remodeling associated with a plaque is thought to reflect a compensatory enlargement to avoid the decrease of the coronary lumen (22). On the other hand, Varnava et al. (23) performed a pathological examination of positive remodeling plaques and reported that they have higher lipid content and macrophage count; these 2 findings are recognized pathological markers for plaque vulnerability. Furthermore, positive remodeling plaques have a larger fibro-fatty component according to the IVUS radiofrequency data (24,25); these positive remodeling plaques are observed frequently in patients with acute coronary syndrome (14–16). Therefore, positive coronary remodeling is thought to have a potential for plaque vulnerability. In this study, the rate of positive remodeling was very high. However, in previous studies, the rate of positive remodeling of lesions subjected to elective PCI has not been very high (15,26,27). This discrepancy may relate to the characteristics of HIP. As we have already mentioned, HIP is strongly associated with a remarkably low CT density and a high frequency of positive remodeling. These factors are recognized surrogate markers for vulnerable coronary plaques (14). Thus, the present findings—that in stable angina patients with HIP the rate of positive remodeling was high and similar to those for cases of acute coronary syndrome (15)—may be explained by the possibility that HIP may represent vulnerable coronary plaque. In other words, HIP itself may reflect positive remodeling, which represents a large volume of lipid content.
The mechanism of ultrasound attenuation is thought to involve the existence of microcalcification, thrombus, cholesterol crystals with expansive positive arterial remodeling (20,28), and large lipid-rich necrotic core (29,30). Furthermore, in histological IVUS examination, the necrotic core is significantly larger in plaques with ultrasound attenuation (20). On the other hand, it is well known that slow-flow/no-reflow phenomena may occur with high frequency during PCI treatment of ultrasound-attenuated plaques (18,28,29,31). In our study, transient slow-flow phenomena occurred in 15 (83%) of the 18 lesions with ultrasound attenuation in HIP, in contrast, only 1 (14%) of the 7 lesions without ultrasound attenuation in non-HIP behaved this way. Thus, HIP is thought to represent a great potential for high-risk plaque, which induces transient slow-flow phenomena during PCI.
Clinical impact of HIP on noncontrast T1W CMR.
In the studies of the carotid artery using magnetic resonance imaging, HIP on T1WI has been reported with a histological correlation with methemoglobin in intraplaque hemorrhage (9,10). Because intraplaque hemorrhage is a criterion for complicated plaque (American Heart Association type VI) and patients with this type of carotid plaque exhibited ischemic cerebrovascular events and were therefore recognized as cases of vulnerable carotid plaque (10,11), noncontrast T1WI in CMR may enable noninvasive detection of advanced coronary plaque stages, such as carotid plaque. Based on carotid artery studies and our findings from MSCT and IVUS in this study, we speculate that the observed high signals in coronary plaque generated by noncontrast T1WI may represent intraplaque hemorrhage or lipid-rich necrotic cores and, therefore, may have potential as markers for plaque vulnerability.
Although the characterization of atherosclerotic plaque with a noninvasive imaging modality is still challenging, our findings detected by noncontrast T1WI may be informative findings to identify the plaque characteristics. Noninvasive, easily repeatable, and inexpensive methods that detect instability of coronary lesions are needed for the management of patients with high-risk coronary artery disease. In this regard, coronary plaque imaging using noncontrast T1WI may provide clinically important information regarding plaque vulnerability and clinical outcome. Further prospective studies are warranted to elucidate whether HIP has potential as a marker for vulnerability and clinical outcomes.
Study limitations.
The number of subjects in this study was small. In addition, recruiting patients with significant coronary stenosis might have resulted in a certain bias, because IVUS examination is an invasive technique with associated non-negligible risks, and it is permitted only during PCI. Therefore, patients without significant coronary stenosis were excluded. However, IVUS is the current in vivo gold standard for coronary plaque assessment and is the only way to differentiate plaque characterization. Thus, we have chosen a group of selected patients with significant coronary stenosis. Because no comparison with histopathological data was performed in this study, precise characterization of HIP remains unknown. From the knowledge of carotid plaque evaluation using magnetic resonance imaging and pathological examination, the observed high signals generated by short T1 plaques may represent intraplaque hemorrhage or necrotic lipid cores. These assumptions remain to be investigated in subsequent studies, and histological correlation is required for verification. Furthermore, only T1WI was used in this study. The time-of-flight image was considered to be a useful method for distinguishing intraplaque hemorrhage from lipid-rich necrotic cores (30). Another limitation of this study is that study patients presented with stable angina pectoris but not acute coronary syndrome; therefore, it remains unknown whether HIP detected by T1WI represents really vulnerable coronary plaques.
|
Conclusions
|
|---|
Hyperintense plaque on noncontrast T1WI is strongly associated with positive coronary remodeling, remarkably low CT density, and ultrasound attenuation. Thus, the data suggest that HIP detected by noncontrast T1WI may have potential for identifying vulnerable coronary lesions.
* Reprint requests and correspondence: Dr. Tomohiro Kawasaki, Cardiovascular Center, Shin-Koga Hospital, 120, Tenjin-cho, Kurume 830-8577, Japan (Email: to-kawasaki{at}mug.biglobe.ne.jp).
Manuscript received September 17, 2008;
revised manuscript received January 6, 2009,
accepted January 9, 2009.
|
REFERENCES
|
|---|
- Botnar RM, Stuber M, Kissinger KV, Kim WY, Spuentrup E, Manning WJ. Noninvasive coronary vessel wall and plaque imaging with magnetic resonance imaging Circulation 2000;102:2582-2587.[Abstract/Free Full Text]
- Kim WY, Astrup AS, Stuber M, et al. Subclinical coronary and aortic atherosclerosis detected by magnetic resonance imaging in type 1 diabetes with and without diabetic nephropathy Circulation 2007;115:228-235.[Abstract/Free Full Text]
- Kim WY, Stuber M, Bornert P, Kissinger KV, Manning WJ, Botnar RM. Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with nonsignificant coronary artery disease Circulation 2002;106:296-299.[Abstract/Free Full Text]
- Ferencik M, Nieman K, Achenbach S. Noncalcified and calcified coronary plaque detection by contrast-enhanced multi-detector computed tomography: a study of interobserver agreement J Am Coll Cardiol 2006;47:207-209.[Free Full Text]
- Kopp AF, Schroeder S, Baumbach A, et al. Non-invasive characterisation of coronary lesion morphology and composition by multislice CT: first results in comparison with intracoronary ultrasound Eur Radiol 2001;11:1607-1611.[CrossRef][Web of Science][Medline]
- Ropers D, Baum U, Pohle K, et al. Detection of coronary artery stenoses with thin-slice multi-detector row spiral computed tomography and multiplanar reconstruction Circulation 2003;107:664-666.[Abstract/Free Full Text]
- Schroeder S, Kopp AF, Baumbach A, et al. Noninvasive detection and evaluation of atherosclerotic coronary plaques with multislice computed tomography J Am Coll Cardiol 2001;37:1430-1435.[Abstract/Free Full Text]
- Yeon SB, Sabir A, Clouse M, et al. Delayed-enhancement cardiovascular magnetic resonance coronary artery wall imaging: comparison with multislice computed tomography and quantitative coronary angiography J Am Coll Cardiol 2007;50:441-447.[Abstract/Free Full Text]
- Moody AR, Murphy RE, Morgan PS, et al. Characterization of complicated carotid plaque with magnetic resonance direct thrombus imaging in patients with cerebral ischemia Circulation 2003;107:3047-3052.[Abstract/Free Full Text]
- Murphy RE, Moody AR, Morgan PS, et al. Prevalence of complicated carotid atheroma as detected by magnetic resonance direct thrombus imaging in patients with suspected carotid artery stenosis and previous acute cerebral ischemia Circulation 2003;107:3053-3058.[Abstract/Free Full Text]
- Yamada N, Higashi M, Otsubo R, et al. Association between signal hyperintensity on T1-weighted MR imaging of carotid plaques and ipsilateral ischemic events Am J Neuroradiol 2007;28:287-292.[Abstract/Free Full Text]
- Imazeki T, Sato Y, Inoue F, et al. Evaluation of coronary artery remodeling in patients with acute coronary syndrome and stable angina by multislice computed tomography Circ J 2004;68:1045-1050.[CrossRef][Web of Science][Medline]
- Ehara S, Kobayashi Y, Yoshiyama M, et al. Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study Circulation 2004;110:3424-3429.[Abstract/Free Full Text]
- Motoyama S, Kondo T, Sarai M, et al. Multislice computed tomographic characteristics of coronary lesions in acute coronary syndromes J Am Coll Cardiol 2007;50:319-326.[Abstract/Free Full Text]
- Nakamura M, Nishikawa H, Mukai S, et al. Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study J Am Coll Cardiol 2001;37:63-69.[Abstract/Free Full Text]
- Schoenhagen P, Ziada KM, Kapadia SR, Crowe TD, Nissen SE, Tuzcu EM. Extent and direction of arterial remodeling in stable versus unstable coronary syndromes: an intravascular ultrasound study Circulation 2000;101:598-603.[Abstract/Free Full Text]
- Pasterkamp G, Borst C, Gussenhoven EJ, et al. Remodeling of de novo atherosclerotic lesions in femoral arteries: impact on mechanism of balloon angioplasty J Am Coll Cardiol 1995;26:422-428.[Abstract]
- Okura H, Taguchi H, Kubo T, et al. Atherosclerotic plaque with ultrasonic attenuation affects coronary reflow and infarct size in patients with acute coronary syndrome: an intravascular ultrasound study Circ J 2007;71:648-653.[CrossRef][Web of Science][Medline]
- Maintz D, Ozgun M, Hoffmeier A, et al. Selective coronary artery plaque visualization and differentiation by contrast-enhanced inversion prepared MRI Eur Heart J 2006;27:1732-1736.[Abstract/Free Full Text]
- Yamada R, Okura H, Kume T, et al. Histological characteristics of plaque with ultrasonic attenuation: a comparison between intravascular ultrasound and histology J Cardiol 2007;50:223-228.[Medline]
- Motoyama S, Kondo T, Anno H, et al. Atherosclerotic plaque characterization by 0.5-mm-slice multislice computed tomographic imaging Circ J 2007;71:363-366.[CrossRef][Web of Science][Medline]
- Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries N Engl J Med 1987;316:1371-1375.[Web of Science][Medline]
- Varnava AM, Mills PG, Davies MJ. Relationship between coronary artery remodeling and plaque vulnerability Circulation 2002;105:939-943.[Abstract/Free Full Text]
- Fujii K, Carlier SG, Mintz GS, et al. Association of plaque characterization by intravascular ultrasound virtual histology and arterial remodeling Am J Cardiol 2005;96:1476-1483.[CrossRef][Web of Science][Medline]
- Higashikuni Y, Tanabe K, Yamamoto H, et al. Relationship between coronary artery remodeling and plaque composition in culprit lesions: an intravascular ultrasound radiofrequency analysis Circ J 2007;71:654-660.[CrossRef][Web of Science][Medline]
- Okura H, Hayase M, Shimodozono S, Bonneau HN, Yock PG, Fitzgerald PJ. Impact of pre-interventional arterial remodeling on subsequent vessel behavior after balloon angioplasty: a serial intravascular ultrasound study J Am Coll Cardiol 2001;38:2001-2005.[Abstract/Free Full Text]
- Weissman NJ, Sheris SJ, Chari R, et al. Intravascular ultrasonic analysis of plaque characteristics associated with coronary artery remodeling Am J Cardiol 1999;84:37-40.[Web of Science][Medline]
- Hara H, Tsunoda T, Moroi M, et al. Ultrasound attenuation behind coronary atheroma without calcification: mechanism revealed by autopsy Acute Card Care 2006;8:110-112.[Medline]
- Furuichi S, Itoh A, Ishibashi-Ueda H, et al. Ultrasound attenuated coronary plaque as a risk factor for slow flow or no-reflow during percutaneous coronary intervention: a case report J Cardiol 2007;49:193-197.[Medline]
- Yuan C, Mitsumori LM, Ferguson MS, et al. In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques Circulation 2001;104:2051-2056.[Abstract/Free Full Text]
- Tanaka A, Kawarabayashi T, Nishibori Y, et al. No-reflow phenomenon and lesion morphology in patients with acute myocardial infarction Circulation 2002;105:2148-2152.[Abstract/Free Full Text]
Related Article
-
Coronary Plaque Characterization by T1-Weighted Cardiac Magnetic Resonance
- René M. Botnar
J. Am. Coll. Cardiol. Img. 2009 2: 729-730.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
C. M. Kramer and J. Narula
Atherosclerotic Plaque Imaging: The Last Frontier for Cardiac Magnetic Resonance
J. Am. Coll. Cardiol. Img.,
July 1, 2009;
2(7):
916 - 918.
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. M. Botnar
Coronary Plaque Characterization by T1-Weighted Cardiac Magnetic Resonance
J. Am. Coll. Cardiol. Img.,
June 1, 2009;
2(6):
729 - 730.
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods