Title Page:

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Article Title:
Ultrasonography in the diagnosis and follow-up of Giant Cell Arteritis

Corresponding Author:
Chetan Mukhtyar
Rheumatology, Norfolk and Norwich University Hospital, Colney Lane, NR4 7UY
Chetan.mukhtyar@nnuh.nhs.uk

ORCiD iD - 0000-0002-9771-6667

Co-Author:
Fiona Coath
Rheumatology, Norfolk and Norwich University Hospital, Colney Lane, NR4 7UY
Fiona.coath@nhs.net

© The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights
reserved. For permissions, please email: journals.permissions@oup.com
Ultrasonography in the diagnosis and follow-up of

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Giant Cell Arteritis

Fiona L. Coath, Chetan Mukhtyar

Abstract

Colour-doppler ultrasonography is the first measure to allow objective bedside assessment

of Giant Cell Arteritis (GCA). This paper discusses the evidence using the OMERACT filter.
Consensus definitions for ultrasonography changes were agreed by Delphi process, with the
‘halo’ and ‘compression’ sign being characteristic. The ‘halo’ is sensitive to change,
disappearing within 2-4 weeks of starting glucocorticoids. Ultrasonography has moderate
convergent validity with temporal artery biopsy in a pooled analysis of 12 studies including
965 participants (k=0.44, 95% CI 0.38-0.50). The interobserver and intraobserver reliabilities
are good (k=0.6, k=0.76-0.78) in live exercises, and excellent when assessing acquired
images and videos (k=0.83-0.87, k=0.88). Discriminant validity has been tested against
stroke and diabetes mellitus (k=-0.16 for diabetes). Machine familiarity and adequate
examination time improves feasibility. Ultrasonography in follow-up is not yet adequately
defined. Some patients have persistent changes in the larger arteries but these do not
necessarily imply treatment failure or predict relapses.

Keywords

Giant Cell Arteritis, Colour Doppler Ultrasonography

Key Messages

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 Ultrasonography has moderate convergent validity with temporal artery biopsy
(k=0.44, 95% CI 0.38-0.50).
 Discriminant validity has been tested against stroke and diabetes mellitus patients
(k=-0.16 for diabetes).
 Ultrasonography is feasible, with good Interobserver and intraobserver reliabilities
in live exercises ((k=0.6 and k=0.76-0.78).
Main Text:

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Introduction

Giant Cell Arteritis (GCA) was first described as a distinct clinical entity in 1890(1). A
systematic presentation of 39 cases was published in 1946 (2). It is now defined as
“Arteritis, often granulomatous, usually affecting the aorta and/or its major branches, with a
predilection for the branches of the carotid and vertebral arteries. Often involves the
temporal artery. Onset usually in patients older than 50 years and often associated with
polymyalgia rheumatica” (3). With this definition it becomes a distinct pathological entity
rather than being just a phenotype of disease (e.g., temporal arteritis). But this definition
also means that a definitive diagnosis of GCA can only be made with an arterial specimen.
By 1976 it had been recognised that pathological specimens obtained from temporal
arteries were not 100% sensitive. Foci of inflammation as short as 300  in length were
found in otherwise normal specimens.(4) In the first study looking for the incidence and
character of skip lesions, Klein et al found that 28% of their specimens (N=60) had skip
lesions.(4) The presence of skip lesions mean that negative biopsies in the clinical context of
headache with raised inflammatory markers are often considered to be falsely negative.
This in turn raises the question of the value of biopsy as a test that does not affect either
diagnosis or treatment.(5) International recommendations in 2009, advocating the need for
a temporal artery biopsy were based on low quality evidence and were appropriately weak
in their strength of recommendation.(6) No test including histopathology could be
considered a gold standard for the diagnosis of GCA.
In 1982, doppler ultrasonography was first used as a method of improving the sensitivity
and yield of temporal artery biopsy (TAB). The presence of normal or discrete abnormality in
doppler flow was not associated with inflammatory lesions on biopsy (1/23 and 0/14
respectively); but in the presence of stenosis or thrombosis, 12/23 biopsies demonstrated
inflammatory lesions.(7) The real breakthrough in diagnosis of GCA, especially for those with
cranial involvement, was achieved in 1995. The focus of doppler ultraound shifted from
luminal changes to intramural changes. Schmidt et al described 10 cases and 23 controls
who underwent colour doppler ultrasonography. Individuals with suspected GCA had thicker
vessel walls, smaller lumens and lower velocity. But most impressively, all individuals with
suspected GCA had a concentric hypoechoic ‘halo’ around the perfused lumen (Figure 1)

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which disappeared within 2 weeks of commencing glucocorticoid therapy.(8) This paper
describes the development of colour doppler ultrasonography in the diagnosis of GCA and
proposes a role for its use in monitoring of this disease. Most of this data comes from
studies of the superficial temporal artery and its rami. We also describe the evolving role of
imaging the other territories. In our practice we routinely commence ultrasonography of the
superficial temporal artery anterior to the tragus and trace the course of the artery to
include the parietal and frontal rami as distally as possible. Other favoured locations include
the facial artery (over the mandible, anterior to the masseter), the common carotid,
vertebral, subclavian and all three parts of the axillary arteries.

Validating ultrasonography for diagnosis

Doppler ultrasonography is a surrogate marker for histopathology. It cannot demonstrate

giant cells in the vessel wall, but it can be a measure of the inflammation in the vessel wall
for which there are very few causes in the unselected case, and almost no other cause in the
appropriate clinical context.(9) It is uniquely exigent to validate a method for diagnosis
when there is no current standard of diagnosis besides physician verified diagnosis. Prior to
the validation of ultrasonography, we had two imperfect standards for diagnosis – temporal
artery biopsy (TAB) and classification criteria. American College of Rheumatology
classification criteria were developed in 1990.(10) They have been widely misused for
diagnosis where they perform poorly.(11) Meta-analyses of diagnostic colour doppler
ultrasonography have assessed sensitivity and specificity of specific features of colour
doppler ultrasonography against either TAB or classification criteria.(12-16) The sensitivity
of a test is defined as the proportion of people with disease who will have a positive result
and the specificity of a test is the proportion of people without the disease who will have a
negative result. But to interpret that successfully we need to know with certainty who does
or does not have the disease. That level of certainty is not allowed by TAB or classification
criteria. Sensitivity and specificity analysis therefore are blunt and less meaningful tools for
validating colour doppler ultrasonography for diagnosis of GCA.
Developing definitions and reliability testing

Diagnostic ultrasonography for GCA has been around as a technology since the Mid-1990’s.

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Initially, it remained a research tool and a clinical application in pockets of excellence.(8, 17,
18) For it to become widespread as a diagnostic tool, there needed to be consensus on
normal appearances and potential lesions that could be encountered in the process of
imaging an individual with suspected GCA. In 2018, Chrysidis et al. performed a systematic
review of literature to identify all the possible lesions that could be encountered and then
developed definitions for normal images and the lesions that could be encountered in a
temporal artery through a Delphi process (Table 1, Figure 1 and Figure 2).(19) Now images
could be readily reported and the reports could be meaningfully compared for a validation
process.

Ultrasonography Definition
finding
Normal temporal Pulsating, compressible artery with anechoic lumen surrounded by
arteries mid-echoic to hyperechoic tissue. Using US equipment with high
resolution, the intima-media complex presenting as a homogenous,
hypoechoic or anechoic echo structure delineated by two parallel
hyperechoic margins (‘double line pattern’) may be visible.
Halo sign Homogenous, hypoechoic wall thickening, well delineated towards
the luminal side, visible both in longitudinal and transverse planes,
most commonly concentric in transverse scans.
Stenosis A stenosis is characterised by aliasing and persistent diastolic flow by
colour Doppler US. The maximum systolic flow velocity determined
within the stenosis by pulsed wave-Doppler US is ≥2 times higher
than the flow velocity proximal or distal to the stenosis.
Occlusion Absence of colour Doppler signals in a visible artery filled with
hypoechoic material, even with low pulse repetition frequency and
high colour gain.
 Compression sign The thickened arterial wall remains visible upon compression; the
hypoechogenic vasculitic vessel wall thickening contrasts with the

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mid-echogenic to hyperechogenic surrounding tissue.

Table 1. Definitions for the ultrasonography images of temporal arteries developed by

Chrysidis et al. (19)

Convergent validity

The concordance of diagnostic ultrasonography for GCA is best compared with TAB.
Although TAB is an imperfect diagnostic tool, it is nearly 100% specific. It has the advantage
of being the most widely accessed and reported diagnostic modality. There have been
several studies that have tested this concordance with variable results. In one of the first
studies comparing the concordance of the two tests, Salvarani et al reported agreement
between the two modalities in 62 (6 positive by both tests, 56 negative by both tests) out of
the 86 participants (Kappa () = 0.16).(20) At the other end of the spectrum, Karahaliou et al
reported agreement between the two modalities in 43 (18 positive by both tests, 25
negative by both tests) out of 49 individuals ( = 0.75).(21) 12 studies where concurrent TAB
and ultrasonography have been performed for diagnosis of GCA have together reported
outcomes in 965 participants.(20-31) The raw data in Table 2 demonstrates moderate
agreement between the two modalities ( = 0.44, 95% CI 0.38, 0.50). Figure 3 shows the
individual effect of each study on the total pooled analysis.

Study USG+/TAB USG+/TAB- USG-/TAB+ USG-/TAB- Total Proportion Kappa

+ of
agreement
Nesher 2002 7 9 2 14 32 0.65 0.31
Salvarani 2002 6 15 9 56 86 0.72 0.16
Schmidt 2003 24 0 8 4 36 0.77 0.40
Murgatroyd 6 6 1 13 26 0.73 0.44
2003
Reinhard 2004 24 1 9 14 48 0.79 0.58
 Karahaliou 2006 18 3 3 25 49 0.87 0.75
Pfenninger 2012 12 3 15 27 57 0.68 0.35

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Black 2013 2 3 3 13 21 0.71 0.21
Muratore 2013 52 13 11 54 130 0.81 0.63
Luqmani 2016 74 88 27 192 381 0.69 0.35
Bilyk 2017 7 7 10 50 74 0.77 0.31
Mukhtyar 2020 7 7 1 10 25 0.68 0.39
Total 239 155 99 472 965 0.73 0.44

Table 2 Raw data from studies comparing outcomes of ultrasonography (USG) and TAB for diagnosis of GCA

Interobserver and Intraobserver reliability

These can be tested by sonographers assessing still images and videos, or by acquiring the
images themselves. Both measures are important. The review of still images acquired by
high-class equipment and skilled sonographers is important because one does not need
acquisition skills to interpret the images and therefore that exercise has generalisability.
However, to ensure that sonographers can acquire images without drop off in yield is very
important to demonstrate and represents the true utility of the technology.
Schmidt et al reported 100% agreement between 2 sonographers who scanned 30
individuals with GCA for the halo sign, and 95% agreement when considering halo, stenosis
and occlusion.(32) De Miguel et al report two separate exercises where 29 and 43
sonographers interpreted images of 27 and 30 subjects. An average of 6 images were
interpreted for each individual. The inter-observer reliability to reach a diagnosis of GCA was
excellent both times (each  = 0.85).(33) Chrysidis et al tested interobserver reliability in 24
sonographers who applied the consensus definitions in Table 1 to 150 still and video
images. There was excellent agreement for recognising temporal artery halo ( = 0.87) and
compression sign ( = 0.83).(19) Aschwanden et al compared the results obtained by a
vascular specialist and a rheumatologist for interpreting the compression sign; identical
results were obtained in 59/60 subjects (Krippendorf  0.92).(34) Luqmani et al reported
that 12 sonographers who reviewed 30 clinical images had unanimous agreement on 10 of
the 30 images and overall there was good agreement (Intraclass correlation coefficient
0.61).(24) Schafer et al went a step further and tested the interobserver reliability in 12
sonographers who applied the consensus definitions in images acquired live in 6 subjects
who had GCA of varied durations or were healthy controls. There was good agreement for

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temporal artery halo as well as the compression sign (each with  = 0.60).(35)
Chrysidis et al tested intraobserver reliability in 24 sonographers who assessed 150 still and
video images two weeks apart in a different order. The intraobserver reliability was
excellent for temporal artery halo ( = 0.88) and compression sign ( = 0.83). Schafer et al
got 12 sonographers to assess 6 subjects twice on the same day and reported good
reliability for temporal artery halo ( = 0.76) and the compression sign ( = 0.78).

Discriminant validity

Discriminant validity is the ability of a test to discriminate between similarly presenting

diseases and to differentiate activity from quiescent disease state. To test whether
ultrasonography can differentiate accurately between GCA and other differential diagnoses,
we need to have a clear understanding of what conditions might present as GCA.
Vertebrobasilar territory stroke with raised inflammatory markers should have GCA as a
differential diagnosis.(36) Women >65 years of age are the commonest demographic for
incident diabetes mellitus.(37) Diabetes has a higher C-reactive protein level than the
general population, and non-arteritic anterior ischaemic optic neuropathy is a common
complication of that disease.(38, 39) That clinical scenario may also be a mimic for GCA.(40)
Karahaliou et al compared the findings of 55 individuals suspected to have GCA with 15 age
and gender-controlled individuals who had diabetes mellitus and/or stroke. 22/55 were
diagnosed as having GCA clinically and 18 of them had ultrasonography features of GCA, but
none of the 15 controls had any ultrasonography changes of GCA. Mukhtyar et al reported a
study of 112 cases of GCA compared with 336 age and gender-controlled controls where the
vast majority of cases were diagnosed on the basis of ultrasonography signs. In that study
10/62 participants with diabetes mellitus had GCA, compared to 102/274 without diabetes
( = -0.16).(40) The negative kappa suggests an inverse relationship.

The ultrasonography appearance of ‘halo’ appears to respond to treatment with

glucocorticoids. Schmidt et al described that the halo disappeared at a mean of 16 days in
30 patients treated with glucocorticoids.(32) Perez-Lopez et al described their serial
ultrasonographyfindings in 26 patients with evidence of GCA at baseline. The halo

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disappeared in 13 individuals at 6 weeks, and in 3 further people at 6 months.(41) De Miguel
et al have described the ‘halo’ disappearing in 36/38 individual at 10 weeks with a clinically
meaningful and statistically significant fall in the C-reactive protein from 47.2mg/dL at
baseline to 6.8 mg/dL at time of halo disappearance.(42) Ford et al studied the serial
ultrasonography findings in 36 individuals with baseline ‘halo’ sign, of which only 9 had
residual halo at median of 5 months.(43) In all of these studies, the cases appeared to be in
clinical remission. While this means that some patients in clinical remission may continue to
have ultrasonography changes of ‘halo’, there is a much greater probability that the
disappearance of the ‘halo’ is associated with remission. Although, the data are
circumstantial, it does suggest that ultrasonography may be a biomarker that is sensitive to
changing disease states and may become an addition to the precious few validated
biomarkers in systemic vasculitis.(44)

Feasibility

A diagnostic test that is highly concordant with the presence of pathology, repeatable,
reproducible, discriminant and sensitive to change, may still be unacceptable in its mass
utility if it is not feasible to carry out the test easily. ultrasonography requires expensive, but
ubiquitously available equipment. Effective training programmes have been developed.(33,
45) Such training programmes have led to collaborative multi-centre studies.(24) Like any
other aspect of clinical medicine, experience improves results, but even experienced
sonographers need familiarity with machines and adequate time to ensure good results.
Schafer et al reported on the validation of diagnostic ultrasonography for GCA in live
exercises. When 12 sonographers were given just 13 minutes to complete an examination,
the interobserver reliability for halo sign and compression sign in the temporal arteries was
moderate ( = 0.47 and 0.49 respectively). However, when they were allowed to practice on
the machines and had 20 minutes to complete an examination, the interobserver reliability
was good for halo as well as compression sign ( = 0.60 for both).(35) Given equipment,
experience and time for each examination, ultrasonography appears to be an eminently
feasible application in clinical practice. Currently there are no certifications, or
recommendation for minimum number of scans that need to be carried out prior to
launching a service. There is at least one validation of a service based on 25 scans followed

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by long-term follow-up to establish the true diagnosis.(25) Luqmani et al proposed 20
normal scans followed by demonstration of 1 abnormal scan as evidence of experience.(24)
A training programme in Norway consists of 5 hours of theoretical training and 10 hours of
hands-on ultrasonography examination of 12 controls and eight individuals with GCA.(45)
The number of 20-25 scans is probably enough as long as there is auditing against another
validated outcome measure or expert sonographer. But just like the rest of clinical
medicine, greater experience improves performance. CM has now performed >1000
ultrasonography examinations and continues to improve.

The role of extra-cranial ultrasonography

Involvement of the extra-cranial arteries in GCA, especially affecting the upper limb
circulation, has been known about since the mid-1970’s.(46) A biopsy of the subclavian
artery is indistinguishable from that of the temporal artery in this context.(47) Sometimes
the presentation of GCA may only be related to the immediate branches of the aorta, with
complete absence of cranial symptoms, even in the presence of a positive TAB.(48) Schmidt
et al demonstrated ultrasonographic changes of GCA in the branches of the common carotid
and subclavian arteries.(49). In a series of 176 individuals with GCA diagnosed using
ultrasonography, 20 participants had typical vessel wall oedema in the immediate aortic
branches without temporal arterial involvement.(50) In the presence of suspicion of GCA
and a negative temporal artery ultrasonography, additional scanning of the axillary artery
improves the yield of the diagnosis significantly and reduces the need for TAB (Figure 4).(51,
52)

Practically, the authors scan the superficial temporal artery (including parietal and frontal
branches) and all three parts of the axillary artery in all patients. If those arteries do not
demonstrate changes of GCA as defined in Table 1, we also scan the facial artery (if jaw
claudication), subclavian artery (if upper limb girdle stiffness) and carotid artery (if
carotidynia). Other areas that can potentially be scanned include the vertebral arteries and
occipital arteries. Practically the authors find the presence of atherosclerosis in immediate

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branches of the aorta. Intima-media thickening related to atherosclerosis is patchy,
eccentric and hyperechoic. (19) However, it is not unusual to find a mixed picture of
vasculitis and atherosclerosis. We are not aware of a specific exercise testing the
discriminant validity of extra-cranial arterial ultrasonography for diagnosis of GCA versus
atherosclerosis.

Ultrasonography in follow-up imaging

The halo sign disappears within 2-4 weeks of starting glucocorticoids.(15) Some academics
have documented persistence of ultrasonography changes in a small number of individuals
thought to be in clinical remission.(41, 52) However, these changes are observed usually in
the axillary artery rather than the superficial temporal artery or its branches.(53) Persistent
large vessel wall thickening does not necessarily imply treatment failure and does not
necessarily result in clinical relapses. As a bedside imaging modality, ultrasonography may
have a role in the follow-up of people with GCA to diagnose relapsing disease. There is an
evolving research agenda in this field, but a paucity of consistent data means there is no
formal recommendation for its use. The current EULAR LVV recommendations do not
endorse the use of regular imaging for diagnosis of relapse because of lack of evidence.(54)

In practice the ultrasonography probe can take the place of the stethoscope. All patients
with suspected relapsing disease must have a thorough assessment of their arteries,
examining pulses and listening for bruits. The authors do use the ultrasonography probe to
complement the physical examination when relapse is suspected. We have modified the
criteria for diagnosing active Takayasu arteritis published by Kerr et al to diagnose relapsing
GCA.(53) The presence of any 2 of the following 4 helps us to diagnose relapsing disease in
GCA -
 Constitutional symptoms (any one of fever >38°C, weight loss >2kg, loss of appetite,
drenching night sweats) in the absence of any other explanation
  Claudication symptoms (headache, jaw claudication, arm claudication)
 C-reactive protein >10 mg/L (normal range 0-10mg/L), for which there is no other

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explanation
 Ultrasonography changes of GCA

Conclusions

Colour Doppler ultrasonography is the first outcome measure that can objectively allow
bedside assessment for the presence of new GCA. Considering that the first case of GCA was
described 130 years ago, this is an extremely overdue and highly welcome technology. It is
now convention that all new outcome measures are validated using the OMERACT process.
Outcome Measures in Rheumatoid Arthritis Clinical Trials (OMERACT) is an international
effort to achieve consensus on the use clinical / laboratory / imaging tools, at first in
rheumatoid arthritis clinical trials, and later in all of rheumatology.(55) The OMERACT filter
to validate an outcome measure includes ‘Truth’, ‘Discrimination’ and ‘Feasibility’.(56)
Newer iterations of this filter have been published which extend into suggested lines of
questioning, but these basic three pillars remain constant. Can an outcome measure find or
measure what it seeks? Can it differentiate between conditions of interest? Is it easy to use
and roll-out for mass use? If an outcome measure can answer these three questions in an
affirmative way, it is considered as a valid outcome measure. This review has shown that the
sum of evidence for the role of colour doppler ultrasonography for the diagnosis of GCA
meets the OMERACT filter. We accept that these data are from different studies and not
from one exercise. Up to very recently, clinical trials have not accepted ultrasonography
findings as evidence of diagnosis.(57) But that is changing. There are currently (on Nov 18,
2020) two interventional clinical trials in GCA registered on clinicaltrials.gov, that are
actively recruiting subjects, which accept ultrasonography as a diagnostic modality for GCA
(NCT03725202 and NCT03726749). Outside of clinical trials, ultrasonography is a validated,
readily available bedside modality and the update of the EULAR recommendations for
managing large vessel vasculitis approve its use as the primary diagnostic modality.(54)
There is no current consensus on the threshold size of the intima-media complex that would
tip us towards a definite diagnosis of GCA. Schafer et al have reported a hypoechoic halo of
≥0.4mm at the superficial temporal artery to be highly sensitive and specific.(58) But
without replication the overall image remains more important than the size. Its use in
follow-up is less certain and requires further work. The clinical follow-up of an individual

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with GCA requires inspection, palpation and auscultation. Where available, the addition of
insonation can only add to the acquisition of information. The validation of the
ultrasonography probe has been more far more rigorous than the signature instrument of
the physician – the stethoscope.

Competing interests:
There are no relevant associations with commercial or non-financial entities that provided
support for this work, either for the authors or their family members.

Contributorship:

Both authors meet the ICMJE recommendations for authorship in that they have provided
substantial contribution to the analysis of relevant literature, drafting and critical revision of
the manuscript, approval of the final version submitted and agreement to be accountable
for all aspects of this work.

Acknowledgements:

There are no other contributors or collaborators for this manuscript.

Funding information:

No funder involvement for this work and manuscript.

Ethical Approval Information:

This manuscript is a case report, there was no research which required an ethics approval
process.
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All data relevant to this case report is are included in the article.
Data sharing statement:
References:

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Figure Legends:

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Figure 1. A) Normal section of superficial temporal artery seen in longitudinal view; B) ‘Halo’
sign at the common temporal branch, intima-medial thickness 0.5mm in a longitudinal view,
GE LOGIQ e with 22mHz probe; C) Normal section of superficial temporal artery seen in
transverse view; D) ‘Halo’ active vasculitis in a section of superficial temporal artery seen in
transverse view, GE LOGIQ e with 22mHz probe

Figure 2. A) ‘Halo’ sign - Homogenous, hypoechoic wall thickening, well delineated towards
the luminal side of the frontal branch of the temporal artery, intima-medial thickness
measures 0.6mm GE LOGIQ e 22mHz probe; B) ‘Compression’ sign - The thickened arterial
wall remains visible upon compression with the ultrasonography probe, GE LOGIQ e 22mHz
probe
 Downloaded from https://academic.oup.com/rheumatology/advance-article/doi/10.1093/rheumatology/keab179/6143584 by Universidad de los Andes user on 21 February 2021
Figure 3. Bubble chart of kappa values from various studies comparing ultrasonography
(USG) with TAB
Figure 4. A) Normal axillary artery seen in longitudinal view, intima-medial thickness 0.06cm;
B) Normal axillary artery seen in longitudinal view with colour doppler, GE LOGIQ e with

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14mHz probe; C) Active vasculitis in a segment of axillary artery seen in longitudinal view,
intima-medial thickness 0.21cm; D) Active vasculitis in a segment of axillary artery seen in
longitudinal view with colour doppler, intima-medial thickness 0.14cm, GE LOGIQ e with
14mHz probe; E) Normal axillary artery seen in transverse view, intima-medial thickness
0.06cm, GE LOGIQ e with 14mHz probe; F) Active vasculitis in the axillary artery seen in
transverse view, intima-medial thickness 0.15cm, GE LOGIQ e with 14mHz probe
 Downloaded from https://academic.oup.com/rheumatology/advance-article/doi/10.1093/rheumatology/keab179/6143584 by Universidad de los Andes user on 21 February 2021
Figure 1. A) Normal section of superficial temporal artery seen in longitudinal view; B) ‘Halo’ sign at the
superficial temporal artery, in a longitudinal view, intima-medial thickness 0.5mm, GE LOGIQ e with 22mHz
probe; C) Normal section of superficial temporal artery seen in transverse view; D) ‘Halo’ active vasculitis in
a section of superficial temporal artery seen in transverse view, intima-medial thickness 0.6mm, GE LOGIQ
e with 22mHz probe

95x95mm (600 x 600 DPI)

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Figure 2. A) ‘Halo’ sign - Homogenous, hypoechoic wall thickening, well delineated towards the luminal side
of the frontal branch of the temporal artery, intima-medial thickness measures 0.6cm, GE LOGIQ e 22mHz
probe; B) ‘Compression’ sign - The thickened arterial wall remains visible upon compression with the
ultrasound probe, GE LOGIQ e 22mHz probe

126x64mm (600 x 600 DPI)

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Figure 3. Bubble chart of kappa values from various studies comparing ultrasonography (USG) with TAB

127x80mm (600 x 600 DPI)

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Caption : Figure 4. A) Normal axillary artery seen in longitudinal view, intima-medial thickness 0.6mm; B)
Normal axillary artery seen in longitudinal view with colour doppler, GE LOGIQ e with 14mHz probe; C)
Active vasculitis in a segment of axillary artery seen in longitudinal view, intima-medial thickness 2.1mm; D)
Active vasculitis in a segment of axillary artery seen in longitudinal view with colour doppler, intima-medial
thickness 1.4mm, GE LOGIQ e with 14mHz probe; E) Normal axillary artery seen in transverse view, intima-
medial thickness 0.6mm, GE LOGIQ e with 14mHz probe; F) Active vasculitis in the axillary artery seen in
transverse view, intima-medial thickness 1.5mm, GE LOGIQ e with 14mHz probe

84x126mm (300 x 300 DPI)