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European Heart Journal Advance Access originally published online on June 20, 2006
European Heart Journal 2006 27(14):1732-1736; doi:10.1093/eurheartj/ehl102
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Selective coronary artery plaque visualization and differentiation by contrast-enhanced inversion prepared MRI

David Maintz1,*, Murat Ozgun1, Andreas Hoffmeier2, Roman Fischbach1, Won Yong Kim4, Matthias Stuber5, Warren J. Manning3, Walter Heindel1 and René M. Botnar6

1 Department of Clinical Radiology, University of Muenster, Münster 48129, Germany
2 Department of Thoracic Surgery, University of Muenster Germany
3 Cardiac MR Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
4 Institute of Clinical Medicine and Department of Cardiology, MR Center, Aarhus University Hospital, Skejby Sygehus, Aarhus, Denmark
5 Department of Radiology, Division of MR Research, Johns Hopkins Hospital, Baltimore, MD, USA
6 Department of Nuclear Medicine, Technical University Munich, Munich, Germany

Received 28 November 2005; revised 11 May 2006; accepted 26 May 2006; online publish-ahead-of-print 20 June 2006.

* Corresponding author. Tel: +49 251 8347301; fax: +49 251 8347312.E-mail address: maintz{at}uni-muenster.de


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Aims We sought to evaluate the utility of contrast-enhanced coronary magnetic resonance imaging (CE-MRI) for selective visualization and non-invasive differentiation of atherosclerotic coronary plaque in humans.

Methods and results Nine patients with coronary artery disease (CAD) as confirmed by X-ray angiography and multidetector computed tomography (MDCT) were studied by T1-weighted black blood inversion recovery coronary MRI before (N-IR) and after administration of Gd-DTPA (CE-IR). Plaques were categorized as calcified, non-calcified, and mixed based on their Hounsfield number derived from MDCT. With MDCT, a total of 29 plaques were identified, including calcified (n=6), non-calcified (n=6), and mixed calcified/non-calcified (n=17). On N-IR MRI, 26 plaques (90%) were dark, whereas three plaques (two non-calcified and one mixed) appeared bright. On CE-MRI, 13/29 (45%) plaques, 11 of which were mixed, one non-calcified, and one calcified showed contrast uptake. All others remained dark.

Conclusion In this preliminary study, we demonstrate the potential utility of CE-IR MRI for selective plaque visualization and differentiation of plaque types. The observed contrast uptake may be associated with endothelial dysfunction, neovascularization, inflammation, and/or fibrosis.

Key Words: Magnetic resonance imaging • Coronary plaque • Contrast enhancement • Plaque characterization


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 References
 
Atherosclerosis is a chronic systemic inflammatory disease of the vessel wall affecting large, medium, and small arteries such as the aorta, the carotid, and coronary arteries. During the past decade, progression and complication of coronary artery atherosclerosis has been intensively studied and stages of plaque progression have been defined.1 Evidence has been found that most acute coronary syndromes are caused by rupture of atherosclerotic plaques of AHA stages 3 to 4 without underlying high grade lumen stenosis.2 Invasive X-ray coronary angiography (XCA) is the current gold standard for visualization of the coronary artery lumen, but does not visualize and grossly underestimates the underlying plaque and is therefore not suitable for early disease detection or characterization of plaque components. Potential for non-invasive plaque characterization has recently been assigned to multidetector computed tomography (MDCT) and cardiovascular magnetic resonance (CMR). MDCT can distinguish between calcified plaques, mixed plaques with calcified and non-calcified components, and non-calcified plaques.3 MRI has the advantage of a superior soft tissue contrast. In vivo coronary vessel wall visualization has successfully been demonstrated using CMR and coronary artery remodelling in patients with X-ray confirmed coronary artery disease (CAD) has been shown.4–6

Contrast-enhanced MRI (CE-MRI) has been demonstrated to improve the contrast-to-noise (CNR) ratio between the vessel lumen and the vessel wall, but previous studies using gadolinium (Gd)-based or iron-based contrast agents have been restricted to larger arteries7–9 or animal models.10–12 We sought to examine the potential utility of CE-MRI for plaque visualization and characterization using a T1-weighted CMR technique with an inherent high contrast between contrast enhancing and non-enhancing tissue.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 References
 
Study population and design
The study population included nine prospectively enrolled patients (6 male, 3 female, age 44–72 years, mean 61) with known CAD. All subjects had previously undergone XCA and coronary 16-slice MDCT angiography. The time interval between XCA and CMR was 1–29 days (mean 15 days) and between MDCT and CMR was 1 day. All patients initially assessed for inclusion deemed eligible for the study. The baseline and main clinical characteristics of study patients are summarized in Table 1.


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  		Table 1 Baseline and main clinical characteristics of the patients

 
The study complies with the Declaration of Helsinki and the study protocol was approved by the locally appointed Ethics Committee and all patients gave written informed consent to participate.

Multidetector spiral computed tomography
MDCT imaging was performed on a 16-detector row scanner (Sensation 16, Siemens Medical Systems, Forchheim, Germany) applying a detector collimation of 16x0.75 mm with a table feed of 3.4 mm/rotation at a rotation time of 420 ms. The tube current was 370 mAs and the tube voltage 120 kV. Patients with a heart rate above 65 bpm. received oral medication of 80 mg propranolol 60 min before the examination. Arterial contrast was achieved with intravenous application of 100 mL of a non-ionic contrast medium (Ultravist 300, Schering, Berlin, Germany) injected at a flow rate of 4 mL/s. Transaxial images (slice thickness 1.0 mm, increment 0.5 mm) were reconstructed using an ECG-gated half-scan reconstruction algorithm (temporal resolution 210 ms) and a medium-sharp kernel (B30f). The position of the reconstruction window within the cardiac cycle was individually optimized to minimize motion artifacts.13

CMR imaging
CMR imaging was performed on a 1.5T MR system (Intera, Philips Medical Systems, Best, The Netherlands) using a commercial five element cardiac synergy coil. After a survey scan to localize the heart and diaphragm, a multi-heart phase SSFP cine sequence (TR, 2.9 ms; TE, 1.5 ms; flip angle, 60°; 50 heart phases; matrix, 144x144; SENSE factor 2) was obtained to assess the interval of minimal right coronary artery (RCA) motion for the determination of the trigger delay of the subsequent coronary CMR lumen and vessel wall scans.

Coronary bright-blood MRA was performed with a previously described navigator-gated free-breathing and cardiac-triggered T2-prepared three-dimensional steady-state free-precession sequence allowing visualization of the anatomy of the coronary artery lumen.14

The following coronary plaque scan was a navigator-gated free-breathing and cardiac-triggered T1-weighted inversion-recovery and fat-suppressed 3D black-blood gradient-echo sequence. Parameters of the sequence were: TR, 6.1 ms; TE, 1.9 ms; flip angle, 30°. Spatial resolution of both sequences was 1.0x1.0x3.0 mm. Scans of the proximal left and RCA system were performed in the transverse plane to allow for slice-to-slice comparison with MDCT data. The number of slices was limited to 20 because of time constraints.

After intravenous application of 0.3 mmol/kg body weight of a Gd-based contrast medium (Magnevist, Schering, Berlin, Germany) and a predefined delay time between contrast administration and imaging of 3 h outside the scanner, the above described scan protocol was repeated.

The inversion time (TI) of the inversion recovery sequences was individually assessed according to the T1 of blood using a TI scout (Look Locker sequence, 15). Typically, the inversion time before contrast administration was 450 ms and after contrast application 250 ms.15,16

Data analyses
Two investigators evaluated the MDCT data sets in consensus using axial and multiplanar reformatted images. For every coronary artery segment, identified via side branches, the investigators decided whether calcified plaque, non-calcified plaque, both or neither was present in MDCT.3

Original MDCT- and CMR-source images were evaluated by two experienced readers in consensus on a segment-per-segment basis. Both readers were blinded to the catheter angiography results and clinical data.

Contours were drawn around areas of contrast uptake on post-contrast MR images and copied to the corresponding pre-contrast images. MR contrast enhancement was defined as a signal-to-noise ratio (SNR defined as signal of plaque divided by SD of noise) increase of at least 50% and a CNR (defined as signal of plaque minus signal of blood divided by SD of noise) increase of at least 100% with respect to the native N-IR scan. Blood signal was measured at the root of the aorta in pre- and post-contrast images. Noise was defined as the SD measured in air anterior to the patients chest wall.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 References
 
All nine MDCT and CMR examinations were completed without complication. While the scan volumes of MDCT covered the whole heart, the coronary MRA and the CMR plaque scans were limited in volume covering a total of 55 proximal and mid-coronary artery segments available for further analysis [in all patients the proximal RCA, the left main (LM) coronary artery, the proximal left anterior descending coronary artery (LAD), and proximal circumflex coronary artery (Cx) were covered]. The mid-LAD was included in the scan volumes of six patients, the mid-Cx in four, and the mid-RCA in four patients. In addition, the first diagonal branch (D1) was included in three and the first marginal branch (M1) in two patients.

Within these segments, 29 plaques were identified using MDCT and classified as calcified (n=6), non-calcified (n=6), or mixed calcified/non-calcified (n=17; Table 2). The plaques were located and distributed among the following segments: proximal RCA, 5; mid-RCA, 3; LM, 3; proximal LAD, 6; mid-LAD, 4; proximal Cx, 3; mid-Cx, 3; D1, 1; M1, 1.


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  		Table 2 Differentiation of different plaque types with regard to MDCT morphology and CMR signal intensity before and 3 h after contrast administration

 
The inversion recovery CMR sequence facilitated suppression of both blood and surrounding tissues, thereby enabling selective plaque visualization. After contrast administration, 13 plaques demonstrated enhancement (Figures 1 and 2), including 11 (65%) of 17 mixed calcified/non-calcified but only 1 (17%) of calcified and 1 (17%) of non-calcified plaques.


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  		Figure 1 Detection of coronary artery plaque enhancement. High-grade ostial stenosis of the RCA as demonstrated by catheter angiography (A) and MR-angiography (D). MDCT coronary angiography (B) shows that the underlying plaque is severely calcified, but also has non-calcified components (C). Inversion recovery CMR-images before (E) and after (F) contrast media application demonstrate strong focal enhancement of the plaque and diffuse enhancement of the RCA wall.

 

Figure 1022
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  		Figure 2 Enhancement of coronary artery plaque. Proximal plaque of the RCA with calcified and non-calcified components as demonstrated by MDCT (A) causing medium- to high-grade lumen stenosis in MR-angiography (B). Inversion recovery CMR-images before (C) and after (D) contrast media application demonstrate focal enhancement of the RCA plaque (straight arrow). Please also note strong enhancement of aortic plaque (dotted arrow).

 
Quantitative signal measurements
Of the 29 plaques, 26 (90%) were hypointense on N-IR images with an SNR of 4.9±1.5. Three plaques had a hyperintense appearance on N-IR imaging corresponding to an SNR >10 (14.8±1.6).

After contrast agent administration, 13 of 29 (45%) plaques showed significant enhancement corresponding to an SNR and CNR increase of 233±149 and 445±292%. Average SNR and CNR of those plaques on N-IR were 4.6±1.1, 2.1±1.8, 15.4±7.6, and 12.2±7.1, respectively.

The remaining 16 plaques did not exhibit significant contrast uptake (SNR 33±33% and CNR 60±51%). The three plaques that appeared bright at baseline were among those 16 plaques without significant enhancement. Figure 3 shows one example for each of the plaque types according to their signal intensities before and after contrast agent application.


Figure 1023
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  		Figure 3 Examples of different plaque types. From left to right: catheter angiography, MDCT coronary angiography, coronary MRI, CMR before contrast-media application, and CMR 3 h after contrast-media application. (A) LAD coronary artery plaque with mixed components in MDCT appears dark before and after contrast application (type 1). (B) Marginal branch plaque (non-calcified) appearing bright before and after contrast application (type 2). (C) RCA plaque with low signal before and bright signal after contrast enhancement (type 3).

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 References
 
This study of patients with CAD yielded two important findings:1 The use of black blood CE-IR coronary MRI for the detection of selective contrast uptake in non-calcified and mixed coronary plaque in patients with CAD has been demonstrated.2 The different signal intensities of plaques in N-IR scans in combination with different signal intensities after contrast application facilitates differentiation of three different plaque types (Figure 3): (i) plaques that are hypointense on N-IR and CE-IR (type 1); (ii) plaques that are hyperintense both on N-IR and on CE-IR (type 2); and (iii) plaques that are hypointense on N-IR and hyperintense on CE-IR (type 3).

CMR technique
CMR has been accredited for high potential to non-invasively image the coronary artery vessel wall.4–6 While these previous studies used techniques for unselective visualization of the entire vessel wall (in both healthy and diseased states), our approach facilitates visualization of coronary artery plaque morphology. As the imaging task using the proposed method is reduced to the assessment of the presence or absence of contrast uptake, requirements on spatial resolution are less stringent. Furthermore, image interpretation is reduced to the detection of hot spots similar to radionuclide methods.

Enhancement phenomenon
To our knowledge, this is the first report of in vivo contrast enhancement of coronary artery plaques in human coronary arteries using a Gd-based MR contrast medium. In previous studies, gadolinium uptake has been observed in patients with advanced carotid atherosclerosis using a T1-weighted fast spin-echo imaging technique.8,9 In contrast to the here proposed IR-prepared segmented gradient-echo sequence, contrast uptake is more difficult to appreciate because of the reduced suppression of surrounding tissues. Other investigators have used contrast agents based on iron oxides that lead to a negative contrast on T2-weighted images after phagocytosis by plaque-mediated macrophages. Similar to the Gd-based studies, imaging was performed in human carotid arteries or in animal models.10,17

In our protocol, MR imaging was performed immediately before and 3 h after i.v. injection of contrast medium application. The ‘late enhancement’ approach ensures that the contrast medium had already been renally filtered and that physiologic uptake of contrast medium in healthy tissues has washed out. Previous studies have shown that both inflammation18–20 and fibrosis21 are associated with contrast uptake and may lead to the same visual appearance. This delayed enhancement effect can be explained by an increased extracellular space and by a reduced washout kinetics. These studies also demonstrate a relationship between inflammation and fibrosis, whereby fibrosis was found in patients with chronic or recurrent inflammation.19 Differentiation between these two entities may be possible based on differences in the pharmacokinetics. Thus we hypothesize that the observed contrast uptake may be associated with inflammatory or fibrous coronary plaques and thus may reflect acute as well as chronic vascular inflammation. Inflammation is a known process in the development and progression of atherosclerotic plaques and is suspected to play a key role in plaque rupture, suggesting that plaque enhancement may identify potentially vulnerable plaques. Therefore, plaque enhancement might indicate potentially vulnerable plaques. These assumptions remain to be investigated in subsequent studies and histological correlation is required for verification.

Plaque types
For our study, MDCT was used as the reference standard for the detection of coronary plaques. This method enables classification of plaques as calcified, non-calcified, and mixed calcified and non-calcified. Using our new CE-MR protocol, we found that one group of non-calcified and mixed plaques appear bright on CE-MRI while a substantial minority do not display enhancement. Although our study lacks histological correlation of our findings, we hypothesize on the underlying composition of the plaques that lead to the different MR appearance. Tissue that appears bright in T1-weighting must have a very short T1-relaxation time. One tissue that might fulfil this criterion is haemorrhage containing methemoglobin. Similarly very high signal of certain plaque types on strongly T1-weighted images have been reported for the carotid arteries22 with a histological correlation with methemoglobin in intraplaque haemorrhage. As intraplaque haemorrhage is a criterion of complicated plaque (type VI), our technique may enable non-invasive detection of advanced plaque stages and/or recent plaque rupture. Intraluminal thrombus, with fewer trapped red blood cells, may have different signal characteristics when compared with a haemoglobin-rich intraplaque haemorrhage.23


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
References
 
This study demonstrates selective coronary plaque visualization by CE-MRI that allows for differentiation between MDCT-characterized plaque entities. Further investigations are now warranted to investigate these findings in larger patient studies to assess the methods sensitivity and specificity for the detection of plaque and histological correlation is needed for clarification of the different plaque signal intensities.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Stary HC, Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull W Jr, Rosenfeld ME, Schwartz CJ, Wagner WD, Wissler RW. (1995) A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 92:1355–1374.[Abstract/Free Full Text]
  2. Falk E, Shah PK, Fuster V. (1995) Coronary plaque disruption. Circulation 92:657–671.[Free Full Text]
  3. Achenbach S, Moselewski F, Ropers D, Ferencik M, Hoffmann U, MacNeill B, Pohle K, Baum U, Anders K, Jang IK, Daniel WG, Brady TJ. (2004) Detection of calcified and non-calcified coronary atherosclerotic plaque by contrast-enhanced, submillimeter multidetector spiral computed tomography: a segment-based comparison with intravascular ultrasound. Circulation 109:14–17.[Abstract/Free Full Text]
  4. Kim WY, Stuber M, Bornert P, Kissinger KV, Manning WJ, Botnar RM. (2002) Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with non-significant coronary artery disease. Circulation 106:296–299.[Abstract/Free Full Text]
  5. Fayad ZA, Fuster V, Fallon JT, Jayasundera T, Worthley SG, Helft G, Aguinaldo JG, Badimon JJ, Sharma SK. (2000) Non-invasive in vivo human coronary artery lumen and wall imaging using black-blood magnetic resonance imaging. Circulation 102:506–510.[Abstract/Free Full Text]
  6. Botnar RM, Stuber M, Kissinger KV, Kim WY, Spuentrup E, Manning WJ. (2000) Non-invasive coronary vessel wall and plaque imaging with magnetic resonance imaging. Circulation 102:2582–2587.[Abstract/Free Full Text]
  7. Kramer CM, Cerilli LA, Hagspiel K, DiMaria JM, Epstein FH, Kern JA. (2004) Magnetic resonance imaging identifies the fibrous cap in atherosclerotic abdominal aortic aneurysm. Circulation 109:1016–1021.[Abstract/Free Full Text]
  8. Wasserman BA, Smith WI, Trout HH III, Cannon RO III, Balaban RS, Arai AE. (2002) Carotid artery atherosclerosis: in vivo morphologic characterization with gadolinium-enhanced double-oblique MR imaging initial results. Radiology 223:566–573.[Abstract/Free Full Text]
  9. Yuan C, Kerwin WS, Ferguson MS, Polissar N, Zhang S, Cai J, Hatsukami TS. (2002) Contrast-enhanced high resolution MRI for atherosclerotic carotid artery tissue characterization. J Magn Reson Imag 15:62–67.[CrossRef][ISI][Medline]
  10. Ruehm SG, Corot C, Vogt P, Kolb S, Debatin JF. (2001) Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation 103:415–422.[Abstract/Free Full Text]
  11. Sirol M, Itskovich VV, Mani V, Aguinaldo JG, Fallon JT, Misselwitz B, Weinmann HJ, Fuster V, Toussaint JF, Fayad ZA. (2004) Lipid-rich atherosclerotic plaques detected by gadofluorine-enhanced in vivo magnetic resonance imaging. Circulation 109:2890–2896.[Abstract/Free Full Text]
  12. Barkhausen J, Ebert W, Heyer C, Debatin JF, Weinmann HJ. (2003) Detection of atherosclerotic plaque with gadofluorine-enhanced magnetic resonance imaging. Circulation 108:605–609.[Abstract/Free Full Text]
  13. Ropers D, Baum U, Pohle K, Anders K, Ulzheimer S, Ohnesorge B, Schlundt C, Bautz W, Daniel WG, Achenbach S. (2003) Detection of coronary artery stenoses with thin-slice multi-detector row spiral computed tomography and multiplanar reconstruction. Circulation 107:664–666.[Abstract/Free Full Text]
  14. Spuentrup E, Bornert P, Botnar RM, Groen JP, Manning WJ, Stuber M. (2002) Navigator-gated free-breathing three-dimensional balanced fast field echo (TrueFISP) coronary magnetic resonance angiography. Invest Radiol 37:637–642.[CrossRef][ISI][Medline]
  15. Look D and Locker D. (1970) Time saving measurement of NMR and EPR relaxation times. Rev Sci Instrum 41:250–251.[CrossRef]
  16. Weinmann HJ, Schuhmann-Giampieri G, Schmitt-Willich H, Vogler H, Frenzel T, Gries H. (1991) A new lipophilic gadolinium chelate as a tissue-specific contrast medium for MRI. Magn Reson Med 22:233–237 discussion 42.[Medline]
  17. Kooi ME, Cappendijk VC, Cleutjens KB, Kessels AG, Kitslaar PJ, Borgers M, Frederik PM, Daemen MJ, van Engelshoven JM. (2003) Accumulation of ultrasmall superparamagnetic particles of iron oxide in human atherosclerotic plaques can be detected by in vivo magnetic resonance imaging. Circulation 107:2453–2458.[Abstract/Free Full Text]
  18. Desai MY, Stone JH, Foo TK, Hellmann DB, Lima JA, Bluemke DA. (2005) Delayed contrast-enhanced MRI of the aortic wall in Takayasu's arteritis: initial experience. Am J Roentgenol 184:1427–1431.[Abstract/Free Full Text]
  19. Dill T, Ekinci O, Hansel J, Kluge A, Breidenbach C, Hamm CW. (2005) Delayed contrast-enhanced magnetic resonance imaging for the detection of autoimmune myocarditis and long-term follow-up. J Cardiovasc Magn Reson 7:521–523.[Medline]
  20. Bley TA, Wieben O, Leupold J, Uhl M. (2005) Images in cardiovascular medicine. Magnetic resonance imaging findings in temporal arteritis. Circulation 111:e260.[Free Full Text]
  21. Kim RJ, Wu E, Rafael A, Chen EL, Parker MA, Simonetti O, Klocke FJ, Bonow RO, Judd RM. (2000) The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 343:1445–1453.[Abstract/Free Full Text]
  22. Moody AR, Murphy RE, Morgan PS, Martel AL, Delay GS, Allder S, MacSweeney ST, Tennant WG, Gladman J, Lowe J, Hunt BJ. (2003) Characterization of complicated carotid plaque with magnetic resonance direct thrombus imaging in patients with cerebral ischemia. Circulation 107:3047–3052.[Abstract/Free Full Text]
  23. Corti R, Osende JI, Fayad ZA, Fallon JT, Fuster V, Mizsei G, Dickstein E, Drayer B, Badimon JJ. (2002) In vivo non-invasive detection and age definition of arterial thrombus by MRI. J Am Coll Cardiol 39:1366–1373.[Abstract/Free Full Text]

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