J Cardiol 2007 Nov; 50（5）: 317 – 324

Usefulness of Ultrasonography in
Carotid Arteries and Combined
Positron Emission Tomography/
Computed Tomography for Diagnosis of Takayasu Arteritis With
Unusual Presentation as Acute
Myocardial Infarction : A Case
ReportKotaroMIYAGAWA, MD

Jun

SHIRAISHI, MD

Michitaka

NASU, MD＊1

SayukiTORII, MD

Masayasu

ARIHARA, MD＊1

Masayuki

HYOGO, MD

Takakazu

YAGI, MD

Takatomo

SHIMA, MD

Takashi

OKADA, MD

YoshioKOHNO, MD

Hiroaki

MATSUBARA, MD＊2

Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────This unusual case of Takayasu arteritis presenting as acute myocardial infarction could be defined byultrasonography and 18-fluorodeoxyglucose positron emission tomography（18F-FDG PET）coregisteredwith computed tomography（CT）. A 55-year-old male was admitted to our hospital with continuous chest
pain and left-side neck pain. After primary percutaneous coronary intervention, elevation of inflammatory
markers persisted and dull pain in the left side of the neck continued. Ultrasonography revealed characteristic wall thickening of the left common carotid artery and subsequent 18F-FDG PET with CT depicted positive uptake in the left common carotid artery and the vessel wall of the ascending aorta, confirming thediagnosis of Takayasu arteritis. Three months after angioplasty, follow-up cardiac catheterization was performed. Coronary angiography showed no restenosis. During the catheterization, angiography confirmed
the mild stenosis in the long segment of the left common carotid artery and the left subclavian artery as
well as the focal narrowing and the dilation of the abdominal aorta. This case shows that ultrasonography
in the cervical region and combined 18F-FDG PET with CT may be useful in the diagnosis and evaluationof Takayasu arteritis. In addition, we should pay attention to underlying disease even in middle-aged orolder male patients with acute myocardial infarction.
──────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2007 Nov; 50（5）: 317−324──────────────────────────────────────────────
京都第一赤十字病院 循環器科，＊ 1 救急部 : 〒 605−0981 京都市東山区本町 15−749 ; ＊ 2 京都府立医科大学大学院医学研究科
循環器病態制御学，京都
Departments of Cardiology and ＊ 1Emergency Medicine, Kyoto First Red Cross Hospital, Kyoto ; ＊ 2Department of Cardiovascular
Medicine, Kyoto Prefectural University School of Medicine, Kyoto
Address for correspondence: SHIRAISHI J, MD, Department of Cardiology, Kyoto First Red Cross Hospital, Honmachi 15−749,
Higashiyama-ku, Kyoto 605−0981 ; E-mail : sjun@msj.biglobe.ne.jp
Manuscript received June 18, 2007 ; revised July 17, 2007 ; accepted July 20, 2007

317

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Miyagawa, Shiraishi, Nasu et al

Key Words■ Myocardial infarction, pathophysiology■ Ultrasonic diagnosis■ Computed tomography

INTRODUCTION
Takayasu arteritis（TA）is a chronic vasculitis of
unknown etiology, predominantly involving the
aorta and its primary branches that frequently leadto stenotic, occlusive, and aneurysmal change.1,2）
TA usually affects young females and its prevalencein females is approximately 10 times that inmales.3,4）Although conventional angiography has
been the mainstay of diagnostic image analysis for
TA, the diagnosis of early TA is very difficult tomake in the prestenotic stage by this method. In
contrast, recent reports have demonstrated that, in
addition to enhanced computed tomography（CT）
and magnetic resonance imaging, ultrasonography
as well as 18-fluorodeoxyglucose positron emission
tomography（18F-FDG PET）are useful in the diagnosis and the assessment of early TA. 5−10） We
describe an unusual case of TA in a middle-aged
male presenting with acute myocardial infarction,
which could be diagnosed noninvasively by ultrasonography and 18F-FDG PET coregistered withCT.
CASE REPORTA 55-year-old male was admitted to our hospitalwith continuous chest pain for 2 hr. He had no
obvious past history of cardiovascular disease, but
had felt a slight dull pain in the left side of the neckfor 3 months. His coronary risk factors included
smoking and hyperlipidemia. Routine blood test
results were normal, except for C-reactive protein（CRP）of 1.9 mg/dl（normal range 0.0−0.3 mg/dl）.
Electrocardiography showed abnormal ST-segment
elevation in the Ⅱ,Ⅲ, aⅤF leads, and emergency
echocardiography revealed decreased wall motionin the inferoposterior wall of the left ventricle.
Emergency coronary angiography indicated total
occlusion in the mid segment of the right coronary
artery（Fig. 1−A）and a diffuse lesion in the left
anterior descending coronary artery with severe
stenosis in the diagonal branch（Fig. 1−B）. The
left circumflex coronary artery was hypoplastic.
Primary percutaneous coronary intervention was
performed for the mid right coronary artery occlusion. Using a 6F JR4 with side hole guiding
catheter（mach-1, Boston Scientific）and a guidewire（Runthrough NS 0.014 inch, TERUMO）, theocclusion was passed through without difficulties.
After thrombectomy using an aspiration catheter（Export, Medtronic）, Thrombolysis in Myocardial
Infarction（TIMI）
2 flow was observed（Fig. 1−C）.
Then, after dilation using a balloon catheter（Maverick 2, 3.5/20 mm, Boston Scientific）, a baremetal stent（Driver, 4.0/30 mm, Medtronic）was
implanted（Fig. 1−D）. Finally, TIMI 3 flow was
obtained without residual stenosis（Fig. 1−D）. He
began daily treatment with 100 mg aspirin, 200 mg
ticlopidine, 5 mg enalapril, 10 mg carvedilol, and10 mg pravastatin.
After the primary percutaneous coronary intervention, his clinical course was uneventful except
for the continuous dull pain in the left side of theneck. His plasma lipid profile showed that low-density lipoprotein cholesterol level was 221 mg/dl,
high-density lipoprotein cholesterol level was
34 mg/dl, and triglyceride level was 225 mg/dl.
Unexpectedly, the CRP gradually increased up to
18.2 mg/dl and the erythrocyte sedimentation rate
（ESR）was 108 mm in the first hour. The value ofthese inflammatory makers did not decrease significantly and other laboratory data, including rheumatoid factor, antinuclear antibody, and antineutrophil
cytoplasmic antibody did not show any abnormalities.
Ultrasonography of the cervical region was performed to examine the origin of his neck pain,
which revealed diffuse, isoechoic, circumferential
wall thickening of the left common carotid artery（Figs. 2−A, B）. The wall of the right common
carotid artery was also slightly thickened with someatherosclerotic change（Fig. 2−C）. The wall thickening of both carotid arteries spared the external
and internal carotid arteries, findings considered
consistent with TA. In addition, 18F-FDG PET
coregistered with CT was employed to identify the
inflammation of the vasculature directly. Wholebody 18F-FDG PET suggested FDG uptake in thebilateral common carotid arteries as well as ascending aorta, arch, and descending aorta（Fig. 3）. 18FFDG PET coregistered with CT showed elevatedaccumulations in the left common carotid artery,the vessel wall of the ascending aorta, and thelymph nodes（Fig. 4）. TA was highly suspected
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Ultrasonography and 18F-FDG PET /CT in Takayasu Arteritis

319

Fig. 1 Coronary angiograms
A : Left anterior view of right coronary
angiography before primary percutaneous
coronary intervention showing a total
occlusion in the mid segment.
B : Cranial view of left coronary angiography showing a diffuse lesion in the left
anterior descending coronary artery withsevere stenosis in the diagonal branch.
C : Right coronary angiography immediately after thrombectomy showing residual stenosis.
D : Right coronary angiography immediately after coronary stenting showing the
optimal result.

Fig. 2 Ultrasonographic findings of the common carotid arteries
Ultrasound images of the left common carotid artery showing diffuse, circumferential
wall thickening（A : longitudinal view ; B : transverse view）, and the distal end of thewall thickening at the beginning of the carotid sinus（arrow）. Ultrasound images of
the right common carotid artery showing a slight wall thickening with atheromatous
lesion（C : arrowhead）.

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Miyagawa, Shiraishi, Nasu et al

Fig. 3 Whole-body 18-fluorodeoxyglucose（18F-FDG）
positron emission tomography（PET）
A−C : Coronal slices from anterior to posterior showing suspected FDG uptakes in the bilateral common
carotid arteries as well as the ascending aorta, arch, and descending aorta（arrows）.

Fig. 418

F-FDG PET coregistered with computed tomography

A, D : Computed tomography images.
B, E : Coregistered 18F-FDG PET with computed tomography images. 18F-FDG accumulations wereobserved in the left common carotid artery（arrowhead）, the vessel wall of the ascending aorta（arrow）,
and the lymph nodes.
C, F : 18F-FDG PET images of same sections of A and D.
Abbreviations as in Fig. 3.

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Ultrasonography and 18F-FDG PET /CT in Takayasu Arteritis

321

Fig. 5 Angiograms of the branches of the aortic arch（A）
and the abdominal aorta（B）
Angiography of the branches of the aortic arch（A）showing slight stenosis in the long segment of the leftcommon carotid artery and moderate stenosis of the left subclavian artery. Angiography of the abdominal
aorta（B）showing focal narrowing（arrowhead）and dilation.

based on the findings from ultrasonography and
18
F-FDG PET combined with CT. Without specifictreatment, the CRP gradually decreased down to
1.5 mg/dl spontaneously, the ESR to 21 mm in thefirst hour concomitantly, and the neck pain disappeared 2 months after the onset of acute myocardial
infarction.
Three months after the angioplasty, follow-up
cardiac catheterization was performed. Coronary
angiography showed no restenosis. During thecatheterization, angiography of the branches fromthe aortic arch and the abdominal aorta was also
performed to confirm the diagnosis and evaluate the
distribution of the disease. The slight stenosis in thelong segment of the left common carotid artery wasconfirmed（Fig. 5−A）. Slight stenosis of the left
proximal common carotid artery as well as intermediate stenosis of the left subclavian artery were also
found（Fig. 5−A）. Additionally, focal narrowing
and dilation of the abdominal aorta were detected（Fig. 5−B）. These findings confirmed the diagnosis of TA. He has been carefully observed on an
outpatient basis without steroid treatment, because
the inflammatory makers have remained slightly
above the normal laboratory value（ CRP ＜1.5 mg/dl, ESR ＜ 20 mm in the first hour）.
DISCUSSION
TA is an idiopathic granulomatous vasculitis,
occurring predominantly in young females, whichmainly attacks the aortic trunk, its main branches,
and the pulmonary and coronary arteries.1,2）TheJ Cardiol 2007 Nov; 50（5）: 317 – 324

prevalence of coronary involvements in TA is about
9% to 10%.11,12）However, recent studies have indicated that the incidence of coronary lesions in TA isrelatively high（approximately 40%）13,14）and TA isa relatively common underlying disease in young
females with acute myocardial infarction. 15）
Besides aortic regurgitation, heart failure ascribed
to coronary artery disease and hypertension is the
major cause of death in patients with TA.11,13,14,16）
Coronary artery lesions in TA can be classified into
three types based on the pathological findings : 17）
stenosis or occlusion of the coronary ostium andthe proximal segments of the coronary arteries ;
diffuse or focal coronary arteritis（skip lesions）;
and coronary aneurysm. Most coronary involvements in TA are located at the ostium or the proximal segments of the coronary arteries, and this type
frequently affects females. 17）In contrast, mostcases of diffuse or focal coronary arteritis occur in
middle-aged or older males.17−19）According to thisclassification, the present patient might have focal
coronary arteritis in the right coronary artery anddiffuse coronary arteritis in the left anterior
descending coronary artery. On the other hand,recent reports have demonstrated that platelet andcoagulation activities are significantly enhanced inpatients with TA.20−22）Not only coronary stenotic
lesion but also platelet hyperaggreability and hypercoagulability might have contributed to the pathogenesis of acute myocardial infarction in the present case.
Ultrasonography is a noninvasive, repeatable,

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Miyagawa, Shiraishi, Nasu et al

and superior method compared with contrast
angiography for the detection of involvements ofthe common carotid artery, one of the most commonly affected vessels in patients with TA. 23,24）
Ultrasonography can be used to estimate both thelumen and the vessel wall morphology, so can
detect early TA in the prestenotic stage .7,8）The
characteristic findings from ultrasonography associated with early TA are long segmental lesions withhomogeneous, midechoic, circumferential arterial
wall thickening of the common carotid artery.23）
18
F-FDG PET has also been recently reported to be
useful in the diagnosis of early TA.8−10）18F-FDG
PET can directly identify the distribution and theactivity of the inflammation in the aorta and its
main branches. 18F-FDG PET coregistered withenhanced CT is a more appropriate diagnostic tool
than only 18F-FDG PET in cases in which 18F-FDG
accumulation is weak.25）Recent studies have indicated that the inflammation in the atherosclerotic
plaque of the aorta and the carotid artery could also
be detected by 18F-FDG PET.26−28）Inflammation is
an important risk factor for atherosclerosis29）and
vasculitis might be a serious background for secondary atherosclerosis. Indeed, coexisting atherosclerotic changes were observed in some cases ofTA, consistent with our present case. 2,30,31）
Therefore, in the diagnosis of TA, 18F-FDG accumulations in PET should be carefully estimated
together with clinical symptoms, inflammatory
markers, and findings from other imaging techniques.
In the present case, the differential diagnosis
要

included other causes of large vessel vasculitis suchas giant cell arteritis, syphilis, tuberculosis,
Behçet s disease, and Kawasaki disease, in addition
to atherosclerosis. Based on the findings from laboratory data, clinical symptoms, and specific featuresof carotid ultrasonography and PET/CT, the diagnosis of TA could be made without difficulty. TA
has two phases during disease progression ; theacute active phase with arterial wall thickening, andthe chronic inactive phase with occlusive luminalchanges.5,6）Based on the findings from ultrasonography, 18 F-FDG PET combined with CT, andangiography, we cannot rule out the possibility that,in the present case, the recurrent active phase might
be superimposed over the chronic inactive phasewith occlusive luminal changes. Steroid therapy has
been expected to change the course of the disease if
started early. However, steroid treatment may
encourage the development of atherosclerosis,
because it alters lipid metabolism, glucose metabolism, coagulation fibrinolytic system, and bloodpressure. In some cases of TA, arteritis and atherosclerosis have been reported to coexist in the vessel
wall.2,30−32）Therefore, steroid treatment should be
carefully employed, particularly in TA patients withhigh risk of atherosclerosis.
In conclusion, this unusual case of TA presenting
acute myocardial infarction could be promptly
diagnosed by ultrasonography and 18 F-FDG
PET/CT. We should pay attention to the underlying
disease even in middle-aged or older male patientswith acute myocardial infarction.

約

急性心筋梗塞発症を契機に診断された高安動脈炎の 1 例: 頸動脈エコーおよび陽電子放射線断層撮影/コンピューター断層撮影の有用性
宮川浩太郎

白 石

淳

那須

道高

鳥居さゆ希

有原

正泰

兵庫

匡幸

八木

孝和

島

岡 田

隆

河野

義雄

松原

弘明

孝 友

症例は 55 歳，男性．前胸部痛，左側頸部違和感を主訴に救急搬送された．急性心筋梗塞の診断のもと冠動脈造影を施行し，右冠動脈中間部の閉塞に対してステントを留置し再灌流に成功した．
入院経過中に炎症反応の上昇が遷延し，左側頸部違和感が持続していたことから頸動脈エコーを施行したところ，左総頸動脈のび漫性，全周性の壁肥厚を認めた．加えて陽電子放射線断層撮影/コンピューター断層撮影（PET/CT）で左総頸動脈および上行大動脈の壁に一致して集積を認めたことから，高安動脈炎と診断した．3 ヵ月後の冠動脈造影では再狭窄は認められず，大動脈造影により

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Ultrasonography and 18F-FDG PET /CT in Takayasu Arteritis323

左総頸動脈のび漫性狭窄，左鎖骨下動脈の狭窄，腹部大動脈の一部狭小化を確認した．急性心筋梗
塞発症を契機に診断されたまれな高安動脈炎の 1 例を経験した．同疾患の診断に頸動脈エコーおよび PET/CT が有用であった．加えて中年男性の急性心筋梗塞症例においても，基礎疾患の存在について留意する必要性が示唆された．

J Cardiol 2007 Nov; 50（5）: 317−324

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