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DOI:10.2214/AJR.06.5023
AJR 2006; 186:1197-1198
© American Roentgen Ray Society

Inflammatory Hyperenhancement Persists in Delayed High-Resolution MRI in Giant Cell Arteritis

T. A. Bley1, M. Markl1 and O. Wieben2

1 Department of Diagnostic Radiology and Medical Physics University Hospital Freiburg, Germany
2 Department of Medical Physics and Radiology University of Wisconsin Madison, WI

We read with great interest the article by Desai et al. [1] reporting on contrast-enhanced MR imaging of delayed hyperenhancement and the pictorial essay by Gotway et al. [2] on imaging findings in patients with Takayasu's arteritis and congratulate the authors on their results. We share the authors' motivation in noninvasive MRI assessment of inflammatory vessel wall disease as we investigated methods to detect mural inflammatory changes in giant cell (temporal) arteritis (GCA), which is a form of vasculitis occurring in large- and medium-sized vessels and is nontrivial to diagnose. Both entities—giant cell arteritis and Takayasu's arteritis—share pathogenic pathways with cellular immune responses involving T cells, antigen-presenting cells, and macrophages [3]. Specifically, we would like to point out that high-resolution MRI has proven to be feasible for the visualization even of small branch vessels such as the superficial temporal arteries. Here we would like to share our findings over the course of the previous 26 months from imaging patients suspected of having GCA.

The depiction of mural inflammatory changes of the rather small-sized superficial cranial arteries requires very high resolution. Therefore, we acquired multislice T1-weighted spin-echo sequences with a submillimeter spatial resolution of 196 µm x 260 µm and a slice thickness of 3 mm before and after IV injection of a contrast bolus (0.1 mmol/kg, Magnevist, Schering) (Figs. 1A and 1B). With this approach, the superficial cranial arteries could be sharply depicted, allowing for an evaluation of their lumen and vessel wall dimensions and the grading of a contrast enhancement score [4]. We found very good agreement with the histologic results and the diagnosis according to the criteria of the American College of Rheumatology. This approach offered valuable information on the intensity of mural inflammatory changes and provided insight into the involvement pattern of the different cranial arteries [5].


Figure 1
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Fig. 1A —65-year-old man with histologically proven giant cell arteritis. Spin-echo MR images planned perpendicular to vessel's track of superficial temporal artery (arrows). Unenhanced image shows subcutaneous tissue thickening.

 

Figure 2
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Fig. 1B —65-year-old man with histologically proven giant cell arteritis. Spin-echo MR images planned perpendicular to vessel's track of superficial temporal artery (arrows). Image acquisition initiated 1 min after venous injection of gadolinium-based contrast agent. Pronounced hyperenhancement of thickened vessel wall and perivascular tissue indicating acute inflammation is readily revealed.

 
In our experience, it is not necessary to restrict vascular delayed enhancement imaging to a specific time delay. We found that T1-weighted vessel wall imaging is quite insensitive to the selected delay following contrast agent administration. MRI signal intensity behavior with respect to the timing of the spin-echo acquisition is illustrated for a patient with GCA in Figures 1A, 1B, 1C, and 1D. Associated inflammatory signal changes could be clearly identified in the superficial cranial arteries without significant changes for different delays following contrast agent administration. This illustrates the robustness of T1-weighted imaging of the vessel wall with respect to the delay in the injection of the bolus.


Figure 3
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Fig. 1C —65-year-old man with histologically proven giant cell arteritis. Spin-echo MR images planned perpendicular to vessel's track of superficial temporal artery (arrows). Image acquisition initiated 8 min after injection of contrast agent with same image parameters as in B. Only slightly decreased hyperenhancement.

 

Figure 4
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Fig. 1D —65-year-old man with histologically proven giant cell arteritis. Spin-echo MR images planned perpendicular to vessel's track of superficial temporal artery (arrows). Image acquisition initiated 15 min after injection of contrast agent with same image parameters as in B and C. Mural hyperenhancement is still readily definable.

 

GCA usually affects the superficial cranial arteries. However, involvement of other vascular structures such as the vertebral arteries, the aorta and its branches, the coronary arteries, the mesenteric arteries, and the lower leg arteries also can occur. It is therefore advantageous to know the exact vascular involvement pattern of the individual patient.

Combining high-resolution assessment of the cranial arteries with analysis of the involvement of the aortic wall as presented by Desai et al. [1] should be feasible without the need for additional contrast agent injections or an increase in dosage. In addition, the contrast agent may even be further utilized by combining such studies with first-pass MR angiography for assessment of vascular geometries and potential detection of stenoses associated with inflammatory diseases.


References
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References
 

  1. Desai MY, Stone JH, Foo TK, Hellmann DB, Lima JA, Bluemke DA. Delayed contrast-enhanced MRI of the aortic wall in Takayasu's arteritis: initial experience. AJR 2005;184 : 1427-1431[Abstract/Free Full Text]
  2. Gotway MB, Araoz PA, Macedo TA, et al. Imaging findings in Takayasu's arteritis. AJR 2005;184 : 1945-1950[Abstract/Free Full Text]
  3. Weyand CM, Goronzy JJ. Medium- and large-vessel vasculitis. N Engl J Med 2003;349 : 160-169[Free Full Text]
  4. Bley TA, Wieben O, Uhl M, Thiel J, Schmidt D, Langer M. High-resolution MRI in giant cell arteritis: imaging of the wall of the superficial temporal artery. AJR 2005;184 : 283-287[Abstract/Free Full Text]
  5. Bley TA, Wieben O, Uhl M, et al. Assessment of the cranial involvement pattern of giant cell arteritis with 3 T magnetic resonance imaging. Arthritis Rheum 2005;52 : 2470-2477[CrossRef][Medline]

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This Article
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