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Abstract

  1. Top of page
  2. Abstract
  3. PATIENTS AND METHODS
  4. RESULTS
  5. DISCUSSION
  6. REFERENCES

Objective

Previous studies have confirmed the poor correlation of symptoms, signs, and levels of acute-phase reactants with disease activity in ∼50% of all patients with Takayasu arteritis (TA). Invasive angiographic studies demonstrate vessel lumen anatomy, but do not provide qualitative information about the vessel wall. Moreover, sequential invasive angiographic studies expose patients to high-dose ionizing radiation and catheter/procedure-related morbidity. The aim of the present study was to determine the utility of new developments in vascular magnetic resonance (MR) technology in patients with TA.

Methods

Electrocardiogram-gated “edema-weighted” MR was used to evaluate the aorta and its primary branches with regard to the vascular lumen, vessel wall anatomy, and vessel wall edema in 24 TA patients (77 studies). Inclusion criteria were age <50 years and features of TA on both clinical examination and invasive angiographic studies. Patients were stratified based on clinical and laboratory indications of having either unequivocally active disease, inactive disease, or uncertain disease status.

Results

MR revealed vessel wall edema in 94% (17 of 18), 81% (13 of 16), and 56% (24 of 43) of studies obtained during periods of unequivocally active disease, uncertain disease activity, and apparent clinical remission, respectively. Westergren erythrocyte sedimentation rate and C-reactive protein values did not correlate with either the clinical assessment of disease activity or MR evidence of vascular edema. The frequency of presumed vascular inflammation (edema), as assessed by MR, in patients who appeared to be in remission was similar to the reported frequency of new angiographic lesions and histopathologic evidence of active disease in surgical specimens from patients thought to be in remission. However, the presence of edema within vessel walls did not consistently correlate with the occurrence of new anatomic changes found on subsequent studies.

Conclusion

Inconsistencies in the presence or absence of vessel edema and subsequent anatomic changes have cast doubt on the utility of edema-weighted MR imaging as a sole guide to disease activity and treatment in TA. In this study, the greatest utility of MR was in providing a safe, noninvasive means of assessing changes in vascular anatomy.

Takayasu arteritis (TA) is a chronic, idiopathic inflammatory disease that principally affects the aorta and its primary branches (1, 2). TA typically occurs in women, most often during their reproductive years. Men are a minority in all series. Vessel wall inflammation may cause organ ischemia due to arterial stenosis or occlusion. Less often, aneurysms may produce sequelae such as aortic regurgitation and, rarely, vascular dissection or rupture. It is therefore crucial that active disease be treated before vascular inflammation produces anatomic abnormalities.

It has often been assumed that active vasculitis of any type is usually clinically apparent and correlates with abnormal levels of acute-phase reactants. However, this observation has not withstood rigorous evaluation, especially in regard to TA. In TA, clinical signs and symptoms and measures of acute-phase reactants may not be sufficiently sensitive to identify ∼50% of all patients with active disease (1–4). These observations are based on identification of active vasculitis in >40% of specimens obtained during bypass surgery from patients whose TA was thought to be quiescent, as well as new angiographic abnormalities at previously unaffected sites in 61% of patients whose TA was thought to be in remission (1, 2).

Past attempts to directly visualize large vessel inflammation by indium-111 leukocyte scanning have been shown to be relatively insensitive (5). Basic “edema-weighted” magnetic resonance (MR) imaging has been shown to be highly sensitive in demonstrating areas of extracellular fluid, which manifest as increased signal intensity compared with surrounding normal tissue. These sequences have been used to identify tissue edema, with or without inflammation, in patients with musculoskeletal diseases (6), tumors (7), liver disease (8) and vascular graft infections (9). Recent methodologic developments have permitted tissue characterization, including detection of edema, to be performed rapidly and relatively free of artifacts (10, 11).

Limitations in the assessment of TA activity led to our prospective evaluation of the utility of MR in 24 TA patients. The goal of this study was to assess the performance characteristics of advanced “edema-weighted” MR techniques in imaging large vessel topography and recognizing qualitative features of vessel wall injury that reflect inflammation.

PATIENTS AND METHODS

  1. Top of page
  2. Abstract
  3. PATIENTS AND METHODS
  4. RESULTS
  5. DISCUSSION
  6. REFERENCES

Patients.

Since 1995, all patients who were referred to one of us (GSH) because of TA and who satisfied the American College of Rheumatology diagnostic criteria for TA (12) modified as shown in Table 1 as well as the Chapel Hill Consensus Conference Nomenclature for vasculitis (13), underwent vascular evaluations by MR. Methods used to delineate unequivocally active and inactive disease were based on guidelines reported by Kerr et al (1) (Table 2). The clinical judgment regarding disease activity was not known to the 2 cardiovascular radiologists (SDF and RDW) at the time of MR image review. Clinical evaluation occurred within hours after MR imaging was completed. With the exception of 2 patients in whom the diagnosis of TA was not established prior to imaging, the MR evaluation was not available to the evaluating physician (GSH) prior to clinical assessment. The 2 exceptions were individuals in whom surgery for aortic root reconstruction and/or valve repair/replacement was planned. These patients did not have symptoms or an existing diagnosis of TA, but a routine preoperative MR study of the thoracic aorta had revealed features compatible with TA.

Table 1. Inclusion and exclusion criteria for Takayasu arteritis
  • *

    Modification of the American College of Rheumatology criteria, which arbitrarily required an age ≤40 years.

  • Essential for magnetic resonance study inclusion.

Inclusion criteria (presence of ≥3 features)
 Onset at age ≤50 years*
 Claudication of an extremity
 Decreased extremity artery pulse
 >10 mm Hg difference in blood pressure between arms
 Bruit over extremity arteries or the aorta
 Arteriographic evidence of stenosis or aneurysm of aorta or its primary branches
Exclusion criterion
 Other causes of large-vessel abnormalities
Table 2. National Institutes of Health criteria for active Takayasu arteritis
Unequivocal active disease (new/worsening of 2 or more features)
 Systemic features
 Elevated erythrocyte sedimentation rate
 Worsening ischemia (claudication, diminished/absent pulse, bruit, vascular pain, asymmetric blood pressure)
Typical angiographic features

MR technique. All imaging was performed with a 1.5T MR scanner (Vision or Symphony model; Siemens, Erlangen, Germany). A phased-array torso coil was used to maximize signal-to-noise ratio and electrocardiographic gating was used to “freeze” the moving vascular structures in diastole. The following general acquisition parameters were used: field of view 220–320 mm with and without a rectangular matrix, data matrix size 108 × 256, and slice thickness 5–8 mm. Each image slice was obtained using a single excitation during a single breathhold (∼10–15 seconds) or using 4 excitations without breathholding (∼40–60 seconds). In all cases, T1-weighted imaging (repetition time [TR] minimum R-R interval in milliseconds; echo time [TE] 12 or 32 msec [3 or 9 phase encodings per segment, respectively]) was performed in various orientations, depending on the vessel being imaged, to identify areas of concern in the arterial wall. All examinations included transaxial imaging. T2-weighted (TR ∼1,900–2,200 msec; TE 76 msec) and mixed T1/T2-weighted STIR (TR ∼1,900–2,200 msec; TE 76 msec) images were likewise acquired in all cases, in orthogonal and/or oblique orientations with particular attention to areas of wall thickening (10).

Clinical status and MR assessments of disease activity were available from a standardized database that included clinical, laboratory, angiographic, and MR data for 77 clinical and imaging visits in 24 patients. These studies and patients comprised the study population.

Interobserver agreement. Since two cardiovascular radiologists were involved in the clinical study, we assessed the interobserver variability in the vascular MR interpretations. To accomplish this, an agreement study of MR readings was conducted by having the 2 blinded readers give an enhancement rating of 0 (isointense compared with skeletal muscle), 1 (slightly hyperintense compared with skeletal muscle but greatly hypointense compared with adipose tissue on T2-weighted images and cerebrospinal fluid on STIR images), 2 (moderately hyperintense compared with skeletal muscle but slightly hypointense compared with adipose tissue on T2-weighted images and cerebrospinal fluid on STIR images), or 3 (markedly hyperintense compared with skeletal muscle and isointense compared with adipose tissue on T2-weighted images and cerebrospinal fluid on STIR images) for each of 59 randomly viewed studies of 26 patients. (Two patients included in the interobserver variability study were not part of the clinical study). Subsequently, a second agreement study was performed in which each reader received all MR studies of a patient, sorted by visit date. For each of the 2 studies, readings were made using both the T2-weighted and STIR methods.

Agreement between readers on the 0–3 rating scale was assessed for each method by a weighted kappa statistic that measures the agreement beyond what would be expected by just guessing at disease status. The weighted kappa gives more credit to ratings that are close together (e.g., 2 and 3) and less to those that are far apart (e.g., 0 and 3, which would get no credit). Weighting was done using 2 common methods, one attributed to Fleiss and Cohen and the other attributed to Conchetti and Allison (14, 15). The weighted kappa ranges from 0 (no agreement beyond chance) to 1.0 (perfect agreement beyond chance). Agreement among readers was also assessed on the outcome considered as either positive or negative (reading of >0 or 0, respectively) using the traditional nonweighted kappa statistic.

RESULTS

  1. Top of page
  2. Abstract
  3. PATIENTS AND METHODS
  4. RESULTS
  5. DISCUSSION
  6. REFERENCES

MR findings in the TA patients. There were 5 males and 19 females in the study population. Their ages ranged from 14 to 57 years (mean 34 years). Nineteen (79%) were Caucasian, 3 were Middle Eastern, 1 was Hispanic, and 1 was Indian. Seventy-seven MR examinations were performed on these 24 patients between November 1, 1995 and April 20, 1999 (Table 3). Sequential imaging was performed on 16 patients. MR readings for each examination were performed by the 2 collaborating cardiovascular radiologists, using the aforementioned rating scale.

Table 3. Association between acute-phase reactants and MRI findings in patients with Takayasu arteritis
 Clinical diagnosis*
Active (n = 18)Inactive (n = 43)Uncertain (n = 16)Inactive + uncertain (n = 59)
  • *

    Some patients did not have both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) studies performed on the day of the magnetic resonance (MR) study; therefore, n represents the number of studies.

  • P = 0.009 versus inactive group, and P = 0.013 versus inactive plus uncertain group.

  • See Patients and Methods for an explanation of the rating scale.

% with abnormal ESR (normal ≤30 mm/hour)57293631
% with abnormal CRP (normal ≤2 mg/dl)29291426
ESR, mm/hour (normal ≤30 mm/hour)
 Mean39252725
 SD30242123
 Median34202120
 Range1–1171–1131–611–113
Enhancement on MR
 % of patients94568163
 % with abnormal ESR or CRP62292330
Vessel wall thickening, mm (normal 1–2 mm)
 Mean4.32.93.63.1
 SD1.31.41.01.3
 Median5.03.03.03.0
 Range1–71–72–61–7
Vessel wall edema rating (0–3 scale)
 Mean2.21.21.91.4
 Range0–30–30–30–3

The frequencies of new or progressive features of active disease are presented in Figure 1. Figures 2–4 present examples of vessel wall thickening (Figure 2) and edema (Figures 3 and 4) and response to therapy (Figure 3) as demonstrated by MR.

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Figure 1. Frequency (%) of new-onset or progressive symptoms during disease exacerbations in patients with Takayasu arteritis. BP = blood pressure; CNS = central nervous system.

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Figure 2. Increased aortic wall thickness in Takayasu arteritis, as demonstrated on magnetic resonance images. Transaxial (top) and longitudinal-oblique (bottom) images of the thoracic aorta reveal abnormal vessel wall thickening (arrow). Lobular ectasia is visible in the ascending and descending thoracic aorta, the aortic arch, and the innominate and left subclavian arteries.

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Figure 3. Response of aortitis to effective therapy, as demonstrated on magnetic resonance images. At initial presentation, “edema-weighted” images (top) revealed circumferential wall thickening (5 mm), with moderately increased signal intensity of the thickened wall relative to skeletal muscle (arrow). Following aggressive immunosuppressive therapy (bottom), corresponding images showed improvement in wall thickening and reduced signal intensity. These changes are compatible with diminished inflammation. T2-weighted images are shown on the left; STIR images are shown on the right.

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Figure 4. A, Magnetic resonance images of the aorta of a 35-year-old woman with shortness of breath and angina. The patient underwent surgery for an ascending aortic aneurysm and valvular regurgitation. Images obtained 2 days before surgery showed lobular dilatation of the aorta, increased wall thickening, and increased signal intensity from the aortic root to the level of the diaphragm. Increased wall signal intensity was consistent with active inflammation. STIR = short tau inversion recovery. B, Histopathologic section of the aorta, showing transmural mononuclear cell inflammation, which includes giant cells (hematoxylin and eosin stained).

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Among the 18 patients with clinically unequivocal active disease (Table 3), concurrent MR images revealed increased signal intensity consistent with edema in all but 1 case (94%). The enhancement rating in these patients ranged from 0 to 3 (mean 2.2). Only 62% of these patients had concurrently elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) values.

In 16 instances, MR studies were performed when disease activity was clinically uncertain. In 13 of these 16 studies (81%), vessel wall edema was present. The enhancement rating in these patients ranged from 0 to 3 (mean 1.9). In only 3 of this subset of 13 patients with vascular edema noted on MR was there an increase in levels of acute-phase reactants (23%).

Twenty-four of 43 MR studies obtained during periods of clinically presumed remission demonstrated increased signal intensity consistent with edema (56%). The enhancement rating in these patients ranged from 0 to 3 (mean 1.2). In only 29% of these patients in whom MR results were suggestive of active vasculitis (i.e., vascular edema present) did patients have abnormal ESR or CRP values.

We found no statistically significant associations between clinical characteristics or acute-phase reactant levels and edema-weighted features of vascular enhancement on MR. There was, however, the suggestion of a trend toward higher vessel wall edema on MR (P = 0.07) and abnormal levels of acute-phase reactants (ESR or CRP; P = 0.06) in the group with unequivocal clinically active disease compared with the group with inactive disease.

Sixteen patients underwent several MR studies over time. A total of 12 new anatomic abnormalities (4 occlusions, 7 stenoses, and 1 dilatation) were demonstrated over time in 8 of these patients. The range of MR vessel edema scores concurrent with these new findings was 0–3 (mean 1.25). Among patients in whom sequential MR studies were repeated over at least 5 months, 2 patients did not have vessel edema and did not develop new lesions, 6 did not have disease progression despite the presence of vessel edema on consecutive MR studies, 3 patients developed 6 new lesions in the absence of concurrent edema, and 5 had new lesions after the appearance of vessel edema. Concurrent therapy may have played an important role in modifying these results. Only 3 of the 16 patients were not receiving immunosuppressive therapy at the time the new lesions were demonstrated on MR. One of these 3 untreated patients, who appeared to be in remission, had anatomic progression but did not have vessel edema on sequential studies.

Two of our 24 patients required surgery at the time that MR was being used to evaluate large-vessel inflammation. Both were women (ages 35 and 44) who had severe aortic regurgitation and root dilatation. Neither was systemically or chronically ill or known to have active inflammatory vascular disease before the MR images were obtained. In both cases, MR revealed 3–4 mm of thickening and increased signal intensity of the ascending aorta and aortic arch. The enhancement rating in these patients was 1 and 3, respectively. One patient had wall thickening extending to the descending aorta, with lobular dilatation of the entire thoracic aorta. The other patient had remarkable thickening and signs of edema extending to the proximal arch vessels and pulmonary arteries. The histopathologic specimens from both patients revealed active granulomatous inflammation (Figure 4).

Results of MR interobserver agreement analysis. For one MR interpretation agreement study, random image sampling from 59 visits was employed. In these 26 patients, T2-weighted and STIR images were evaluated by both readers. Results are given below, first for the ordinal outcome (a reading of 0–3) and then for the binary outcome (0 versus 1–3).

Ordinal outcome. Using the Fleiss and Cohen weighting system, the agreement beyond chance (i.e., kappa statistic) was 0.82 (95% confidence interval [95% CI] 0.66–0.99) for T2 and 0.84 (95% CI 0.68–0.92) for STIR readings. These both indicate very good to excellent agreement beyond what would be expected just by chance. Using the Conchetti and Allison weighting scheme, which gives smaller weight to disagreements, the kappa statistics were 0.76 (95% CI 0.55–0.96) and 0.78 (95% CI 0.63–0.86) for T2 and STIR readings, respectively, which is also very good agreement. We found no statistical difference in agreement between the T2 and STIR methods for either the random or followup studies.

Binary outcome. Between-reader agreement was also determined in regard to their assessment of images as showing either positive or negative (reading of >0 or 0, respectively) enhancement. Kappa statistics were 0.84 (95% CI 0.66–1.0) and 0.78 (95% CI 0.56–0.95) for random T2-weighted and STIR readings, and 0.89 (95% CI 0.78–1.0) and 0.83 (95% CI 0.55–1.0) for followup T2-weighted and STIR readings, respectively. Again, no statistical differences were found. For binary outcome analyses, there were few disagreements: only 4 of 59 and 5 of 59 for T2 and STIR readings, respectively, for randomly presented studies, and 2 of 46 and 3 of 46 for T2 and STIR readings, respectively, among studies presented in temporal sequence of acquisition.

We concluded that agreement between the 2 readers was good to excellent, using either the T2-weighted or STIR methods and that neither method stands out as being better than the other in the evaluation of vessel enhancement. These observations provided confidence in the consistency of interpretations of the MR studies obtained in our clinical study group. We used the evaluations of either reader in comparing the clinical status and MR results as shown in Table 3.

DISCUSSION

  1. Top of page
  2. Abstract
  3. PATIENTS AND METHODS
  4. RESULTS
  5. DISCUSSION
  6. REFERENCES

This study is the first prospective analysis of the utility of recent technical advances in MR imaging in patients with Takayasu arteritis. We have demonstrated that this radiation-free, noninvasive means of evaluating large vessels can be an important supplement to following anatomic changes in TA patients. By incorporating edema-weighted images, we had hoped to demonstrate that MR may also be a useful adjunct to clinical and laboratory assessment of disease activity. Patients in our study with unequivocal clinically active TA had a high frequency of vessel wall edema (94% of studies), as determined by increased MR signal. Signs of vessel wall edema by MR were also demonstrated in >50% of all patients in whom TA was judged to be clinically inactive or of uncertain activity status.

Because most of the patients in this series did not require surgery, questions remain about whether the findings of vessel edema include numerous false positives, a product of excessive MR sensitivity. The credibility of the data is supported by independent observations. First, histopathologic evidence of active vasculitis has been noted in 42–44% of vascular bypass specimens from patients who were clinically assessed to be in remission at the time of bypass surgery (1, 2, 4). Second, in a National Institutes of Health report of 60 patients, sequential angiographic studies demonstrated new lesions in 61% of those who were thought to be in remission (1, 2). This proportion of TA cases in whom asymptomatic active arteritis was present is similar to that in our MR study. Nonetheless, these observations offer only indirect, circumstantial evidence that the finding of edema-enhanced vessels on MR represents inflammation. It is theoretically possible that the vessel wall could remain edematous for unknown periods of time after effective treatment of inflammatory lesions. The lack of a consistent correlation between edema and subsequent changes in vascular anatomy introduces further uncertainty about the utility of MR-determined vessel edema as a measure of disease activity.

Since the completion of this study, we have also evaluated vascular MR studies in 34 additional patients who have required aortic root reconstruction, with or without valve replacement (Hoffman G, et al: unpublished observations). In 10 instances, histopathologic findings and edema-weighted MR images could be compared. Previously recognized giant cell arteritis (GCA) was present in 4 patients. Three patients had histologic proof of GCA discovered from their surgical specimens. One patient had relapsing polychondritis and a thoracic aortic aneurysm. Two patients had atherosclerosis. In 4 patients (1 with GCA and 3 with idiopathic aortitis discovered in surgical specimens), the findings of aortic wall edema correlated with histopathologic evidence of aortitis. In 3 patients (2 with atherosclerosis and 1 with relapsing polychondritis in remission), the absence of MR edema correlated with an absence of histopathologic evidence of inflammation. However, in 3 patients (known GCA), vascular edema was present on MR, but histologic evidence of inflammation was absent. Although these 3 cases would appear to be false positives for edema/MR-identified inflammation, this 30% false-positive rate may be related to tissue sampling in a disease that is known for “skip lesions.”

This study differs from other studies that describe wall thickening and luminal changes with MR or CT scanning (16–25) or thrombus formation on vessel walls (25). In TA, luminal abnormalities and wall thickening alone cannot distinguish active inflammation from chronic fibrotic lesions (26). A previous report of MR studies in TA emphasized abnormalities of the vessel wall, based on contrast-enhanced imaging, which required use of an intravenous iodinated agent. That study also emphasized the weak correlation of ESR or CRP values with vessel “inflammation” (edema), as indicated by tissue enhancement on MR (27). Unlike that study, our investigation utilized a form of MR-inherent signal changes that are related to changes in the distribution of tissue water due to edema, rather than differences in the distribution of extracellular contrast agent. The technique utilized in our study does not require contrast agents.

We are not suggesting that vascular MR replace invasive angiography. Each technique has unique advantages and disadvantages (Table 4). Sequential invasive angiography has been very informative in detecting new vascular lesions in TA patients (1, 2). It provides greater image resolution than MR in vessels smaller than the aorta, such as the innominate, renal, mesenteric, and iliac arteries (28), which makes it desirable for the preoperative planning of bypass surgery. Invasive angiography provides opportunities to perform transluminal angioplasty, and it enables the recording of central blood pressure readings and gradient determinations in patients with vessel stenoses, which allows the clinician to assess the reliability of extremity blood pressure cuff measurements. Alternatively, the noninvasive, radiation-sparing qualities of MR with “edema-weighted” imaging techniques may lead to its preferred use for routine followup.

Table 4. Properties of “edema-weighted” magnetic resonance imaging and invasive agniography
Magnetic resonance imagingAngiography
Advantages
 NoninvasiveBetter image resolution
 Defines anatomyAbility to perform interventions
 Can evaluate wall thickness Can determine enhancementCan record intravascular blood pressure and measure gradients
 No radiation exposure
Disadvantages
 Resolution lower than that of angiographyInvasive
 Not quantitative in assessment of signal intensityEvaluates lumen (“lumenogram”)
 Does not provide intravascular pressureIonizing radiation
Impractical for frequent monitoring

Our experience lends further support to past impressions that clinical features of disease activity and levels of acute-phase reactants underestimate active, progressive TA in at least 50% of patients. We have found MRI to be an important adjunct to the assessment of TA. “Edema-weighted” images detect fluid within the vessel wall, which may be due to inflammation. However, it is possible that edema may remain during tissue remodeling, after inflammation has resolved. The finding of new anatomic lesions in conjunction with “edema” would favor the presence of active disease. However, the absence of a consistent correlation between MR findings and clinical and laboratory parameters of disease activity, as well as the development of new lesions, has influenced us to not use MR-determined vessel edema as the sole guide to disease activity and treatment. Additional studies that provide MR images and concurrent histopathologic specimens will be required to determine whether MR vessel “edema” correlates with inflammation and whether treatment based on such findings alters disease prognosis.

REFERENCES

  1. Top of page
  2. Abstract
  3. PATIENTS AND METHODS
  4. RESULTS
  5. DISCUSSION
  6. REFERENCES
  • 1
    Kerr GS, Hallahan CW, Giordano J, Leavitt RY, Fauci AS, Rottem M, et al. Takayasu arteritis. Ann Intern Med 1994; 120: 91929.
  • 2
    Hoffman GS. Takayasu arteritis: lessons from the American National Institutes of Health experience. Int J Cardiol 1996; 54 Suppl: 836.
  • 3
    Hoffman GS, Ahmed AE. Surrogate markers of disease activity in patients with Takayasu arteritis: a preliminary report from the International Network for the Study of the Systemic Vasculitides (INSSYS). Int J Cardiol 1998; 66 Suppl: 191–4.
  • 4
    Lagneau P, Michel J-B, Vuong PN. Surgical treatment of Takayasu's disease. Ann Surg 1987; 205: 15766.
  • 5
    Chen CC, Kerr GS, Carter CS, Read EJ, Carrasquillo JA, Leitman SF, et al. Lack of sensitivity of Indium-111 mixed leukocyte scans for active disease in Takayasu's arteritis. J Rheumatol 1995; 22: 47881.
  • 6
    Bogost GA, Lizerbram EK, Crues JV III. MR imaging in evaluation of suspected hip fracture: frequency of unsuspected bone and soft-tissue injury. Radiology 1995; 197: 2637.
  • 7
    Richardson ML, Zink-Brondy GC, Patten RM, Koh W-J, Conrad EU. MR characterization of post-irradiation soft tissue edema. Skeletal Radiol 1996; 25: 53743.
  • 8
    Bydder GM, Steiner RE, Blumgart LH, Khenia S, Young IR. MR imaging of the liver using short T1 inversion recovery sequences. J Comput Assist Tomogr 1985; 9: 10849.
  • 9
    Hansen ME, Yucel EK, Waltman AC. STIR imaging of synthetic vascular graft infection. Cardiovasc Intervent Radiol 1993; 16: 306.
  • 10
    Simonetti OP, Finn JP, White RD, Laub G, Henry DA. “Black blood” T2-weighted inversion-recovery MR imaging of the heart. Radiology 1996; 199: 4957.
  • 11
    Lim T-H, Hong M-K, Lee JS, Mun CW, Park S-J, Park S-W, et al. Novel application of breath-hold turbo spin-echo T2 MRI for detection of acute myocardial infarction. J Magn Reson Imaging 1997; 7: 9961001.
  • 12
    Arend WP, Michel BA, Bloch DA, Hunder GG, Calabrese LH, Edworthy SM, et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990; 33: 112934.
  • 13
    Jennette JC, Falk RJ, Andrassy K, Bacon PA, Churg J, Gross WL, et al. Nomenclature of systemic vasculitides: proposal of an international consensus conference. Arthritis Rheum 1994; 37: 18792.
  • 14
    Fleiss JL. The measurement of interrater agreement. In: Statistical methods for rates and proportions. 2nd ed. New York: John Wiley & Sons; 1981. p. 2234.
  • 15
    Landis J, Koch G. The measurement of observer agreement for categorical data. Biometrics 1977; 33: 15974.
  • 16
    Hayashi K, Fukushima T, Matsunaga N, Hombo Z-I. Takayasu's arteritis: decrease in aortic wall thickening following steroid therapy, documented by CT. Br J Radiol 1986; 59: 2813.
  • 17
    Matsunaga N, Hayashi K, Sakamoto I, Matsuoka Y, Ogawa Y, Honjo K, et al. Takayasu arteritis: MR manifestations and diagnosis of acute and chronic phases. J Magn Reson Imaging 1998; 8: 40614.
  • 18
    Morita K, Imai H, Saito K, Miura AB, Ishikawa H. The role of gallium scintigraphy, computerized tomogram scan, and magnetic resonance imaging angiography in the diagnosis of Takayasu's disease. J Rheumatol 1993; 20: 16047.
  • 19
    Park JH, Chung JW, Im J-G, Kun SK, Park YB, Han MC. Takayasu arteritis: evaluation of mural changes in the aorta and pulmonary artery with CT angiography. Radiology 1995; 196: 8993.
  • 20
    Park JH. Conventional and CT angiographic diagnosis of Takayasu arteritis. Int J Cardiol 1996; 54 Suppl: 165–71.
  • 21
    Park JH, Chung JW, Lee KW, Park YB, Han MC. CT angiography of Takayasu arteritis: comparison with conventional angiography. J Vasc Interv Radiol 1997; 8: 393-400.
  • 22
    Sharma S, Taneja K, Gupta AK, Rajani M. Morphologic mural changes in the aorta revealed by CT in patients with nonspecific aortoarteritis (Takayasu's arteritis). AJR Am J Roentgenol 1996; 167: 13212.
  • 23
    Tanigawa K, Eguchi K, Kitamura Y, Kawakami A, Ida H, Yamashita S, et al. Magnetic resonance imaging detection of aortic and pulmonary artery wall thickening in the acute stage of Takayasu arteritis: improvement of clinical and radiologic findings after steroid therapy. Arthritis Rheum 1992; 35: 47680.
  • 24
    Yamada I, Numano F, Suzuki S. Takayasu arteritis: evaluation with MR imaging. Radiology 1993; 188: 8994.
  • 25
    Hata A, Numano F. Magnetic resonance imaging of vascular changes in Takayasu arteritis. Int J Cardiol 1995; 52: 4552.
  • 26
    Nasu T. Pathology of pulseless disease: a systematic study and critical review of twenty-one autopsy cases reported in Japan. Angiology 1963; 14: 22535.
  • 27
    Choe YH, Han BK, Koh EM, Do YS, Lee WR. Takayasu's arteritis: assessment of disease activity with contrast enhanced MR imaging. AJR Am J Roentgenol 2000; 175: 50511.
  • 28
    Miller DL, Reinig JW, Volkman DJ. Vascular imaging with MRI: inadequacy in Takayasu's arteritis compared with angiography. AJR Am J Roentgenol 1986; 146: 94954.