Characterization of signal properties in atherosclerotic plaque components by intravascular MRI.

Magnetic resonance imaging (MRI) is capable of distinguishing between atherosclerotic plaque components solely on the basis of biochemical differences. However, to date, the majority of plaque characterization has been performed by using high-field strength units or special coils, which are not clinically applicable. Thus, the purpose of the present study was to evaluate MRI properties in histologically verified plaque components in excised human carotid endarterectomy specimens with the use of a 5F catheter-based imaging coil, standard acquisition software, and a clinical scanner operating at 0.5 T. Human carotid endarterectomy specimens from 17 patients were imaged at 37 degrees C by use of an opposed solenoid intravascular radiofrequency coil integrated into a 5F double-lumen catheter interfaced to a 0.5-T General Electric interventional scanner. Cross-sectional intravascular MRI (156x250 microm in-plane resolution) that used different imaging parameters permitted the calculation of absolute T1and T2, the magnetization transfer contrast ratio, the magnitude of regional signal loss associated with an inversion recovery sequence (inversion ratio), and regional signal loss in gradient echo (gradient echo-to-spin echo ratio) in plaque components. Histological staining included hematoxylin and eosin, Masson's trichrome, Kossa, oil red O, and Gomori's iron stain. X-ray micrographs were also used to identify regions of calcium. Seven plaque components were evaluated: fibrous cap, smooth muscle cells, organizing thrombus, fresh thrombus, lipid, edema, and calcium. The magnetization transfer contrast ratio was significantly less in the fibrous cap (0.62+/-13) than in all other components (P<0.05) The inversion ratio was greater in lipid (0.91+/-0.09) than all other components (P<0.05). Calcium was best distinguished by using the gradient echo-to-spin echo ratio, which was lower in calcium (0.36+/-0.2) than in all plaque components, except for the organizing thrombus (P<0.04). Absolute T1 (range 300+/-140 ms for lipid to 630+/-321 ms for calcium) and T2 (range 40+/-12 ms for fresh thrombus to 59+/-21 ms for smooth muscle cells) were not significantly different between groups. In vitro intravascular MRI with catheter-based coils and standard software permits sufficient spatial resolution to visualize major plaque components. Pulse sequences that take advantage of differences in biochemical structure of individual plaque components show quantitative differences in signal properties between fibrous cap, lipid, and calcium. Therefore, catheter-based imaging coils may have the potential to identify and characterize those intraplaque components associated with plaque stability by use of existing whole-body scanners.

[1]  E. Lakatta,et al.  Increased expression of 72-kd type IV collagenase (MMP-2) in human aortic atherosclerotic lesions. , 1996, The American journal of pathology.

[2]  R. Balaban,et al.  In Vivo 31P Nuclear Magnetic Resonance Measurements in Canine Heart Using a Catheter‐Coil , 1984, Circulation research.

[3]  P A Bottomley,et al.  High resolution intravascular MRI and MRS by using a catheter receiver coil , 1996, Magnetic resonance in medicine.

[4]  R M Henkelman,et al.  Intravascular MR imaging in a porcine animal model , 1994, Magnetic resonance in medicine.

[5]  W. Kucharczyk,et al.  Optimization of gradient-echo MR for calcium detection. , 1994, AJNR. American journal of neuroradiology.

[6]  H C Charles,et al.  Chemical shift imaging of atherosclerosis at 7.0 Tesla. , 1989, Investigative radiology.

[7]  Chun Yuan,et al.  Serial magnetic resonance imaging of experimental atherosclerosis detects lesion fine structure, progression and complications in vivo , 1995, Nature Medicine.

[8]  J L Duerk,et al.  Intravascular (catheter) NMR receiver probe: Preliminary design analysis and application to canine iliofemoral imaging , 1992, Magnetic resonance in medicine.

[9]  R D Kamm,et al.  Mechanical properties of model atherosclerotic lesion lipid pools. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[10]  M. Rekhter,et al.  Does platelet-derived growth factor-A chain stimulate proliferation of arterial mesenchymal cells in human atherosclerotic plaques? , 1994, Circulation research.

[11]  R S Balaban,et al.  Analysis of water‐macromolecule proton magnetization transfer in articular cartilage , 1993, Magnetic resonance in medicine.

[12]  P. Weissberg,et al.  High expression of genes for calcification-regulating proteins in human atherosclerotic plaques. , 1994, The Journal of clinical investigation.

[13]  V. Fuster,et al.  Plaque rupture, thrombosis, and therapeutic implications. , 1996, Haemostasis.

[14]  V. Fuster,et al.  Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. , 1994, Journal of the American College of Cardiology.

[15]  J R Brookeman,et al.  High‐resolution H NMR spectral signature from human atheroma , 1988, Magnetic resonance in medicine.

[16]  F J Schoen,et al.  Circumferential stress and matrix metalloproteinase 1 in human coronary atherosclerosis. Implications for plaque rupture. , 1996, Arteriosclerosis, thrombosis, and vascular biology.

[17]  V. Fuster,et al.  Magnetic resonance images lipid, fibrous, calcified, hemorrhagic, and thrombotic components of human atherosclerosis in vivo. , 1996, Circulation.

[18]  E. Falk Why do plaques rupture? , 1992, Circulation.

[19]  S. H. Koenig,et al.  Calcification Can Shorten T2, but not Tl, at Magnetic Resonance Imaging Fields: Results of a Relaxometry Study of Calcified Human Meningiomas , 1995, Investigative radiology.

[20]  T. Ekfors,et al.  Proton relaxation times in arterial wall and atheromatous lesions in man. , 1986, Investigative Radiology.

[21]  Y. Arad,et al.  Predictive value of electron beam computed tomography of the coronary arteries. 19-month follow-up of 1173 asymptomatic subjects. , 1996, Circulation.

[22]  Ogan Ocali,et al.  Intravascular magnetic resonance imaging using a loopless catheter antenna , 1997, Magnetic resonance in medicine.

[23]  R. Kikinis,et al.  Imaging System for Image-guided Therapy' , 1995 .

[24]  C. Dumoulin,et al.  Active MR tracking on a 0.2 Tesla MR imager. , 1999, Radiation medicine.

[25]  A. Becker,et al.  Fibrous and lipid-rich atherosclerotic plaques are part of interchangeable morphologies related to inflammation: a concept. , 1994, Coronary artery disease.

[26]  R W Günther,et al.  Invited. Visualization of MR‐compatible catheters by electrically induced local field inhomogeneities: Evaluation in vivo , 1998, Journal of magnetic resonance imaging : JMRI.

[27]  V. Fuster Human Lesion Studies , 1997, Annals of the New York Academy of Sciences.

[28]  R. Kikinis,et al.  Superconducting open-configuration MR imaging system for image-guided therapy. , 1995, Radiology.

[29]  J. Pearlman,et al.  Nuclear Magnetic Resonance Microscopy of Atheroma in Human Coronary Arteries , 1991, Angiology.

[30]  R Frayne,et al.  A rapid 2D time‐resolved variable‐rate k‐space sampling MR technique for passive catheter tracking during endovascular procedures , 1998, Magnetic resonance in medicine.

[31]  R. Henkelman,et al.  On MR imaging of atheromatous lipids in human arteries , 1995, Journal of Magnetic Resonance Imaging.

[32]  徐貴淑 Hyaline cartilage: In vivo and in vitro assessment with magnetization transfer imaging(磁気遷移法を利用した硝子軟骨の検討) , 1997 .

[33]  E. Falk,et al.  Histopathology of plaque rupture. , 1999, Cardiology clinics.