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Abstract

Imaging has become a cornerstone in the clinical management of giant cell arteritis (GCA), with its role extending beyond diagnosis to include disease monitoring, risk stratification of relapse, and therapeutic decision-making. While imaging modalities have been well-established for diagnostic purposes, growing evidence supports their utility in tracking disease activity and stratifying the risk of relapse. In this narrative review, we discuss the available evidence on the prognostic and therapeutic implications of imaging-guided stratification in GCA, and highlight areas that require further research. Ultrasound assessment of intima-media thickness shows measurable improvement following treatment. While this response is relatively rapid in the cranial arteries, it occurs slowly or very slowly in extracranial vessels. Moreover, ultrasound signs and quantitative indices may be useful for distinguishing remission from relapse. Similarly, arterial inflammation assessed by ¹⁸F-fluorodeoxyglucose positron emission tomography (¹⁸F-FDG PET) also improves with treatment. However, persistent large vessel vascular uptake is often observed in patients deemed to be in clinical remission. The clinical relevance of such subclinical imaging abnormalities remains unclear, underscoring the need for further research before imaging can be routinely employed for disease monitoring. Imaging may also provide valuable prognostic information. Evidence remains conflicting as to whether patients with large-vessel involvement detected by imaging may relapse more frequently, require glucocorticoid-sparing agents more often, and have an increased risk of cardiovascular events compared to those with isolated cranial GCA. However, quantifying vascular inflammation by ultrasound at diagnosis could support risk stratification and inform individualized treatment decisions. Moreover, elevated arterial uptake on ¹⁸F-FDG PET at baseline has been associated with a higher likelihood of late vascular complications, such as aneurysm formation.

Keywords

giant cell arteritis imaging large vessel vasculitis MRI PET-CT risk stratification ultrasound

Background

Giant cell arteritis (GCA) is the most common systemic vasculitis in patients older than 50 years. Glucocorticoids are the cornerstone of treatment,¹ although the use of other glucocorticoid-sparing agents is increasingly common. Currently, tocilizumab² and upadacitinib³ have been approved for use in GCA. Nevertheless, relapses are common—reported in up to 68% of patients⁴—even when treatment guidelines are properly applied. To date, we do not have clinical or laboratory markers that help us stratify the risk of relapse in patients with GCA. In addition, patient monitoring is challenging, as it is primarily based on symptoms and inflammatory markers. This is particularly relevant in patients treated with tocilizumab, where IL-6 blockade limits the reliability of acute-phase reactants.

Imaging is recommended by EULAR for the diagnosis of GCA and, in cases of high clinical suspicion, it may allow the diagnosis to be established without the need for temporal artery biopsy or additional confirmatory tests.⁵ Ultrasound is the first imaging modality to be performed in cases of suspected GCA, whether with cranial or extracranial involvement, but other modalities such as ¹⁸F-fluorodeoxyglucose positron emission tomography (¹⁸F-FDG PET)-computed tomography (CT), magnetic resonance imaging (MRI), or CT are also valid for diagnosis.⁵ In addition, imaging has recently been included in the 2022 EULAR/ACR classification criteria for GCA,⁶ representing a major milestone in its adoption in clinical practice^7,8 and in patient selection for clinical trials.

Despite improvements in diagnosis, relapses and late complications remain a concern in GCA. EULAR does not recommend the routine use of imaging in patients in clinical and biochemical remission. However, it may be useful in cases of suspected relapse or when acute-phase reactants are unreliable (e.g., in patients receiving tocilizumab).⁵ Imaging can also be useful for long-term monitoring of structural damage, although the frequency of screening is not well defined.⁵ Nevertheless, it is very important to stratify the risk of relapse to guide treatment strategies. Imaging may help define disease phenotypes and quantify the extent of arterial wall abnormalities, and it is possible that, in the future, it may assist in patient risk stratification.

In recent years, growing evidence has highlighted the role of imaging in both monitoring disease activity and supporting risk stratification in GCA.^9–12 In this narrative literature review, we examine current evidence on the use of imaging for disease monitoring and its potential contribution to outcome prediction, particularly regarding relapse and vascular complications, while discussing its evolving role in informing therapeutic decisions.

Methods

This study was conducted as a narrative review aimed at providing a comprehensive overview of current evidence on the use of imaging for disease monitoring and outcome prediction. A literature search was performed in PubMed, Scopus, and Web of Science using combinations of the following keywords: “[giant cell arteritis],” “[imaging]” “[ultrasound],” “[magnetic resonance imaging],” “[positron emission tomography],” “[monitoring],” and “[prognosis].” The search covered the period from 1995 to 2025 and included only articles published in English. Relevant data were synthesized thematically, focusing on the role of imaging in monitoring disease activity and risk stratification of relapse and ischemic complications in GCA.

Current monitoring strategies in GCA

The treatment target in GCA is remission, defined as the absence of clinical symptoms and signs as well as systemic inflammation.¹³ Disease activity should be monitored regularly, as frequently as every 1–4 weeks until remission has been achieved, and at longer monitoring intervals (e.g., between 3 and 6 months) in patients who are in stable remission on therapy.¹³ Although tocilizumab has been shown to reduce the frequency of relapses,² less than a quarter of patients in the GIACTA extension study achieved drug-free remission at 2 years.¹⁴ Although rare (0%–6%), ischemic complications such as blindness or stroke can still occur during relapses.⁴ Additionally, aortic aneurysms and arterial dissection occur more frequently in areas with active inflammation and in patients with a higher number of relapses.^15,16 Current monitoring of GCA is based on clinical assessment and evaluation of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). However, inflammatory markers have limited value when evaluating patients undergoing treatment with tocilizumab. To date, there are no reliable tools for monitoring disease activity in GCA.

Role of imaging in the monitoring of GCA

According to the latest EULAR recommendations, the routine use of imaging in patients with GCA in clinical and biochemical remission is not recommended.⁵ This is based on the difficulty in interpreting the persistence of positive imaging findings after the initiation of treatment, as these may not fully resolve during follow-up. A key challenge lies in determining whether such findings represent subclinical inflammation with prognostic relevance or merely post-inflammatory vascular remodeling without therapeutic implications. While establishing cut-off values may assist in standardization, interpretation should integrate not only quantitative thresholds but also the temporal evolution, distribution, and morphological characteristics of vascular changes.¹⁷ Nonetheless, imaging is still recommended if relapse is suspected or in situations where inflammatory markers are unreliable.⁵

Ultrasound

Its availability, low cost, and non-invasive nature make ultrasound a potentially useful tool for monitoring disease activity. Once treatment is initiated, it has been reported that the temporal arteries normalize faster than the extracranial arteries.^18–20 In Table 1, the percentage of pathological findings at the patient level is shown according to the evolution time of different imaging tests. In the earliest ultrasound studies in GCA, the temporal artery halo sign persisted for an average of 16 days.²¹ However, the probes used at that time were much less sensitive than those currently available. Subsequent studies have shown that the sensitivity of ultrasound to detect abnormalities decreases as early as the second day after treatment initiation.¹⁹ More recently, a prospective study confirmed this rapid decline, reporting a 27% relative reduction in temporal artery ultrasound sensitivity after just 10 days of glucocorticoid therapy.²² In general, vasculitic abnormalities in the temporal arteries tend to resolve around 8 weeks after the initiation of therapy.²³ Involvement of the axillary arteries may persist longer, with improvement typically seen after several months of treatment¹⁸ (Figure 1). We cannot know for certain, given the difficulty of obtaining histological studies, whether these changes reflect persistent inflammation or vascular wall remodeling. In a longitudinal study of 40 patients with large-vessel GCA, follow-up ultrasound of the proximal arm arteries revealed changes suggestive of vasculitis in 70% of patients after a mean follow-up period of 39 months.²⁴ Similarly, persistent increases in intima media thickness (IMT) of axillary arteries have been reported for up to 4 years in patients with long-standing disease, even in the absence of clinical relapse.²⁵ However, the IMT cut-off values have been validated for the diagnosis of GCA,^26–29 and their usefulness in monitoring disease activity should be investigated further. In addition, caution is needed when interpreting the findings, especially in the presence of atherosclerosis. Over time, chronic lesions of the axillary arteries may exhibit a hyperechogenic appearance with multilinear bands, which has been recognized as a potential marker of structural damage rather than active vasculitis³⁰ (Figure 2). These findings underscore the importance of integrating imaging morphology and temporal evolution, rather than relying solely on wall thickness or other quantitative parameters, to distinguish between active and chronic vascular changes.

Table 1.

Persistence of any pathological abnormalities at the patient level in different imaging tests for the assessment of disease activity in GCA.

Exam	Location	Percentage of positive findings	Follow-up	Number of patients	Reference
Ultrasound	Temporal arteries	94	3 days	16	Seitz et al.³¹
		68	3 days	37	Hansen et al.²²
		53	10 days	47	Hansen et al.²²
		50	16 days	22	Schmidt et al.²¹
		91	4 weeks	11	Seitz et al.³¹
		30	8 weeks	47	Nielsen et al.³²
		92	8 weeks	12	Seitz et al.³¹
		85	12 weeks	13	Seitz et al.³¹
		77	24 weeks	13	Seitz et al.³¹
		30	24 weeks	47	Nielsen et al.³²
		54	52 weeks	13	Seitz et al.³¹
	Axillary arteries	57	3 days	37	Hansen et al.²²
		60	10 days	48	Hansen et al.²²
		57	8 weeks	47	Nielsen et al.³²
		66	24 weeks	47	Nielsen et al.³²
¹⁸F-FDG/PET	Extracranial arteries	100	3 days	10	Nielsen et al.³³
		36	10 days	14	Nielsen et al.³³
MRI	Temporal arteries	60	24 weeks	11	Christ et al.³⁴
		0	52 weeks	11	Christ et al.³⁴
	Aorta	67	12 weeks	9	Reichenbach et al.³⁵
		80	24 weeks	11	Christ et al.³⁴
		83	52 weeks	12	Christ et al.³⁴

¹⁸F-FDG/PET, ¹⁸F-fluorodeoxyglucose positron emission tomography; GCA, giant cell arteritis; MRI, magnetic resonance imaging.

Figure 1.

Longitudinal ultrasound scan of the right superficial temporal artery (a and b) in a patient with GCA at diagnosis (a) and after 2 months of treatment (b). Longitudinal ultrasound scan of the left axillary artery (c and d) in a patient with GCA at diagnosis (c) and after 6 months of treatment (d). Although the halo sign persists, note the appreciable decrease in IMT measurement following treatment. Improvement in IMT in axillary arteries is generally slower than in temporal arteries.

Figure 2.

Longitudinal examination of the right axillary artery in a patient with long-standing giant cell arteritis. Note the hyperechoic appearance of the arterial wall and the presence of multiple lines.

The GUSTO clinical trial has provided important evidence on the arterial changes observed by ultrasound following the initiation of treatment.³¹ In this trial, an ultra-short course of glucocorticoids was administered (500 mg IV methylprednisolone for 3 days) to 18 patients, followed by IV tocilizumab on day 3 and weekly subcutaneous injections thereafter. A sharp decline in IMT was observed in the temporal arteries by days 2–3, followed by a rebound to baseline levels at week 4, and then a gradual decrease until week 52. In contrast, axillary arteries showed an initial IMT reduction, followed by a transient worsening and then a period of stability until week 24, after which a more progressive decline was detected. These findings may suggest that the axillary arteries have greater remodeling changes after inflammation than the temporal arteries, or that immunosuppressants are less effective at controlling inflammation in the extracranial arteries. Overall, the significance of subclinical ultrasound findings in patients considered to be in clinical remission remains to be determined. Specifically, it must be understood whether positive findings correspond to subclinical inflammation (and therefore deserve treatment escalation), vascular remodeling (which follows inflammation and precedes vascular damage and is probably less influenced by anti-inflammatory agents), or something else.³⁶ The inclusion of other outcome measures such as hospitalization, risk of disability, or mortality, would have a major clinical impact on the evaluation of long-term subclinical findings.

Few published studies have compared ultrasound findings with markers of disease activity in GCA. In a retrospective study, De Miguel et al.²³ showed that resolution of the temporal artery halo sign in 30 patients with new or relapsing GCA was associated with reductions in CRP and ESR during follow-up. More recently, Ponte et al.¹⁸ conducted a prospective study involving 49 patients and demonstrated a correlation between temporal artery IMT and disease activity markers, including CRP, ESR, and the Birmingham Vasculitis Activity Score. Interestingly, no significant correlation was found for axillary artery IMT. In a subsequent prospective study involving 47 patients with GCA, Nielsen et al.³² confirmed that temporal artery ultrasound-based scores correlated moderately with CRP and global disease activity measures, while large-vessel scores showed only weak or no correlation. Nevertheless, a validated definition of remission and disease activity in GCA is needed to assess the correlation between imaging findings and disease activity in future studies.

In recent years, composite ultrasound scores have been proposed to quantify the burden of arterial wall abnormalities, with some designed primarily for diagnosis and others for longitudinal monitoring.^37–41 The Southend Halo Score—which includes six temporal artery segments and both axillary arteries, assigning weighted scores based on IMT—was developed and shown to perform well as a diagnostic tool.^42,43 Although chiefly diagnostic, subsequent studies have assessed its utility for monitoring treatment response and quantifying changes in vascular inflammation over time.^32,44 More recently, the OMERACT ultrasound group has published the OMERACT GCA Ultrasonography Score (OGUS) to standardize the quantification of vascular abnormalities by ultrasound specifically for monitoring purposes.⁴¹ OGUS is based on the same measurements in the same arterial segments as the Southend Halo Score, differing only in the method of calculation. OGUS has demonstrated both intra- and inter-observer reliability, as well as sensitivity to change. Nielsen et al.,³² in a study involving 47 patients with GCA that compared several quantitative ultrasound scores, demonstrated that OGUS was the index with the highest sensitivity to change. In a prospective 1-year cohort of 50 patients, Schäfer et al.⁴⁵ observed improvements in IMT, number of affected arteries, and OGUS after treatment; relapses occurred in four patients, and at relapse mean IMT and OGUS were higher than at the preceding assessment.

Future options to improve disease monitoring, especially in extracranial arteries, include the use of contrast-enhanced ultrasound. In a proof-of-concept study involving 24 patients, Bergner et al.⁴⁶ demonstrated that this technique had high sensitivity (91.7%) and specificity (100%) for detecting active extracranial disease when a >25% increase in the calculated contrast-enhanced area was observed. However, the inter-observer reliability of contrast-enhanced ultrasound of the axillary and carotid arteries for monitoring disease activity is low.⁴⁷ Larger studies are needed to validate these results.

¹⁸F-FDG PET, MRI, and CT

Apart from ultrasound, ¹⁸F-FDG PET is the second imaging modality with the most evidence supporting its usefulness in monitoring GCA, especially for assessing extracranial involvement. However, its cost, exposure to ionizing radiation, and limited availability in many centers restrict its routine use for follow-up. Blockmans et al.⁴⁸ studied 35 patients with ¹⁸F-FDG PET/CT at diagnosis, 3 months, and 6 months. They demonstrated that the Total Vascular Score (TVS) significantly decreased from diagnosis to 3 months, with no further significant reduction observed at 6 months.⁴⁸ Grayson et al. studied 56 patients with large vessel vasculitis (LVV), including 30 with GCA, using serial ¹⁸F-FDG PET/CT at 6-month intervals. ¹⁸F-FDG PET/CT scans were interpreted as showing active vasculitis in most patients who were in clinical remission (41 out of 71 (58%)). Consequently, the specificity of ¹⁸F-FDG PET/CT to distinguish between imaging evidence of LVV and clinical remission was only 42%.⁴⁹ In this study, the PET Vasculitis Activity Score (PETVAS) was developed to assess disease activity by summing the qualitative assessment of arterial ¹⁸F-FDG uptake compared to the liver across nine vascular territories (aorta, subclavian, carotid, and innominate arteries). Clinically active LVV was associated with a higher mean PETVAS (21.5 vs 12.2, p < 0.001), while lower scores were observed in patients in remission. The ability of PETVAS to discriminate between remission and relapse subsequently yielded a sensitivity of 68% and a specificity of 71% using a cut-off value of >20. On the other hand, the presence of atherosclerosis could also represent a confounding factor in patients considered to be in clinical remission, since age was associated with higher uptake. Other PETVAS cut-off points have been proposed to assess disease activity, showing similar performance. In a retrospective study of 100 patients with LVV, Galli et al. demonstrated an association of PETVAS with disease activity (OR for active disease 1.15, 95% CI: 1.11–1.19). A PETVAS ⩾10 provided 60.8% sensitivity and 80.6% specificity in differentiating between clinically active and inactive LVV.⁵⁰ Eshagh et al.,⁵¹ in a small retrospective study of 38 patients with GCA, found no relapses in patients who had a PETVAS ⩽3 during follow-up (sensitivity 1, 95% CI: (1–1)), while relapse occurred in all but 2 patients who had a PETVAS ⩾7 (specificity 0.78, 95% CI: (0.44–1)).

The RIGA study aimed to assess the change in vascular inflammation in 88 patients with large vessel (LV)-GCA under different treatments using ¹⁸F-FDG PET/CT. PETVAS decreased from 18.9 to 8.0 units at follow-up in the overall population (p < 0.001). A numerically greater reduction in PETVAS was observed with combination treatment (methotrexate or tocilizumab vs glucocorticoid monotherapy). However, only 45.12% of follow-up scans were actually considered inactive, defined as the absence of vascular ¹⁸F-FDG uptake ⩾2 in any vascular territory.⁵² These findings are in line with another study by Quinn et al.,⁵³ which showed a significant reduction in PETVAS after treatment, but also found a similar incidence of persistent active vasculitis (44%). These studies suggest that, while ¹⁸F-FDG PET is sensitive to changes in vascular inflammation, persistent uptake is common even in clinically quiescent disease, limiting its utility in routine monitoring. Emerging molecular imaging modalities may improve visualization of disease activity in GCA. Fibroblast activation protein inhibitor PET/CT can detect inflammation of large arteries, although persistent uptake has been observed even in remission, likely reflecting vascular wall remodeling and fibroblast activity.⁵⁴ More recently, a novel inflammation-specific tracer, [⁶⁸Ga]Ga-DOTA-Siglec-9 PET/CT, which is expressed only during active inflammation, has demonstrated the potential ability to accurately depict GCA^55,56 (Figure 3). However, a recent pilot study including eight patients with GCA did not show higher arterial uptake compared to ¹⁸F-FDG uptake.⁵⁷

Figure 3.

Representative [⁶ ⁸ Ga]Ga-DOTA-Siglec-9 PET/CT images showing selected body regions in patients with GCA. (a) Treatment-naïve patient with relapsing GCA demonstrating intense vascular tracer uptake and periarticular signals consistent with concomitant polymyalgia rheumatica. (b) Different patient imaged after 1 week of prednisolone therapy, showing low vascular and periarticular uptake indicative of early treatment response.

MRI, although less studied than ¹⁸F-FDG uptake, has emerged as a promising tool for monitoring disease activity in GCA due to its ability to detect both cranial and extracranial arterial inflammation without ionizing radiation. In cranial GCA, vessel wall enhancement on MRI has been shown to decrease over time with treatment. Christ et al.³⁴ reported complete resolution of cranial vessel wall enhancement at week 52 in 11 patients with GCA who underwent follow-up MRI, following a short-course glucocorticoid regimen combined with tocilizumab. Similarly, Rhee et al.⁵⁸ observed a progressive reduction in vessel wall enhancement on serial orbital and cranial MRI scans performed at 1, 6, and 12 months in 11 patients with confirmed GCA. In extracranial arteries, however, abnormalities on MRI may persist despite clinical remission.⁵⁸ Reichenbach et al.³⁵ investigated the role of MRI in monitoring 30 patients randomized to receive TCZ or placebo, and found that late vessel wall enhancement persisted or increased in one-third of patients at week 52, despite complete clinical and laboratory remission. Taken together, these findings indicate that MRI signal may decline with therapy—especially cranially—yet persistence in LVs is common and complicates interpretation in routine follow-up. In a prospective comparison between MRA and ¹⁸F-FDG PET/CT, Quinn et al.⁵⁹ showed that MRI better documented the anatomical extent of disease, but PET was more closely associated with clinical disease activity. Concordance between the two modalities was present in 68% of scans (Cohen’s kappa = 0.30), and clinical status was associated with disease activity by ¹⁸F-FDG PET/CT (p < 0.01) but not MRA (p = 0.70). Notably, 51% of patients in clinical remission showed active disease on both imaging modalities. To address variability in image interpretation, Froehlich et al.⁶⁰ recently proposed the MRVAS scoring system to standardize assessment of wall thickening and enhancement, demonstrating excellent inter-reader agreement; however, its role in disease monitoring remains to be validated. Overall, MRI appears complementary to PET—offering superior structural mapping—while PET more consistently reflects metabolic activity. However, not all of these abnormalities detected by either modality correlate with clinical findings. The complementary nature of MRI and PET has prompted interest in hybrid ¹⁸F-FDG PET/MRI, with early pilot data from a study of 13 patients with LVV suggesting that combining structural and metabolic imaging may enhance disease activity assessment.⁶¹

The use of CT is not recommended by EULAR for monitoring disease activity or detecting relapses,⁵ but it could be useful for long-term monitoring of vascular damage, especially in regions with preceding vascular inflammation. A prospective study of 35 GCA patients undergoing CT during follow-up showed that contrast enhancement resolves in the majority of patients, but vessel wall thickening persists in 68%.⁶² However, routine assessment of all GCA patients for vascular damage is not recommended.

Current outcome risk stratification in GCA

Treatment selection in GCA should be based on disease severity and activity, the presence of relevant comorbidities, and potential predictors of outcome.¹³ Some identified predictors of relapse include a high level of systemic inflammation at baseline, persistently increased inflammatory markers or imaging signs of inflammation, as well as predominant extracranial disease.^49,63–66 However, current treatment recommendations do not stratify patients based on their risk of relapse, and overall, reliable tools to assess the risk of outcomes in GCA are lacking.

Role of imaging in risk stratification of relapse in GCA

GCA phenotypes detected by ultrasound

From a clinical perspective, at least four distinct phenotypes of patients with GCA can be identified, which are not mutually exclusive: (1) the cranial phenotype, with predominant involvement of the temporal arteries, may present with headache, scalp tenderness, or jaw claudication⁶⁷; (2) the ischemic phenotype mainly includes patients with vision loss, usually due to anterior ischemic optic neuropathy, which can occur in 10%–25% of patients.⁶⁸ In addition, although less frequently, GCA patients may present with cerebrovascular accidents⁶⁹; (3) The extracranial phenotype, known as LV-GCA, predominantly affects the aorta and its major branches, and may cause nonspecific symptoms such as fever, constitutional syndrome, or fatigue,⁷⁰ and (4) patients with GCA may present with symptoms consistent with polymyalgia rheumatica, even in the absence of GCA-related symptoms.⁷¹ Imaging is part of the diagnostic process for GCA and helps us differentiate between the various phenotypes. In the case of LV-GCA, imaging confirmation of extracranial involvement is an essential requirement for diagnosis.

The LV-GCA phenotype has previously been associated with worse outcomes. However, most available data come from retrospective studies. Czihal et al.,⁷² in a retrospective study of 43 patients using baseline ultrasound, reported that patients with subclavian and axillary involvement experienced higher relapse rates (100% vs 35%) and greater need for glucocorticoid-sparing agents (56% vs 24%) compared to those with isolated cranial GCA. Sugihara et al.,⁷³ in another retrospective study of 139 patients, also found that the presence of LV-GCA detected by imaging at baseline was significantly associated with poor treatment outcomes at 24 and 54 weeks of follow-up (HR 3.54, 95% CI: 1.52–8.24). In contrast, two more recent prospective studies did not find baseline LV involvement to predict relapse. Monti et al.,⁷⁴ in a multicenter prospective cohort of 97 patients, and Haaversen et al.,⁷⁵ in a prospective study of 132 patients, both using vascular ultrasound, reported similar relapse rates across cranial, LV, and mixed GCA phenotypes. Another prospective study including 53 LV-GCA patients and 53 GCA patients without LV involvement found no differences in ischemic complications, glucocorticoid use, or treatment duration during follow-up.²⁴ These findings suggest that while retrospective studies consistently associate LV-GCA with worse outcomes, prospective data remain limited and have yet to confirm a clear prognostic impact of LV involvement. Based on these results, recommendations advocate the same treatment strategies for both disease patterns.¹ Nevertheless, imaging plays a central role in identifying LV-GCA, and its incorporation into patient phenotyping remains important for individualizing risk stratification as more robust longitudinal data emerge.

Quantification of arterial wall abnormalities by ultrasound

The quantification of arterial wall abnormalities by ultrasound at diagnosis may also provide relevant information for follow-up. In early studies based on the TABUL cohort, Monti et al.⁴⁰ studied 207 patients and found no significant association between baseline ultrasound findings and 6-month outcomes related to disease activity/burden—including relapse, prolonged glucocorticoid use, and cumulative glucocorticoid exposure. In a separate prospective study, Aschwanden et al. showed in a prospective cohort of 42 patients that those with regression of vascular wall thickening during follow-up had lower baseline CRP and ESR compared to those with persistent thickening. This regression, however, did not translate into significant differences in relapse rates, cumulative glucocorticoid exposure, or need for DMARDs.²⁰ In contrast, the first prospective study from the PROTEA cohort demonstrated in 49 GCA patients that a lower number of arterial segments with halo and reduced IMT in temporal arteries (but not in axillary arteries) were associated with a higher likelihood of being in clinical remission and a lower cumulative dose of prednisone.¹⁸ Addressing relapse specifically, the subsequent prospective study by Schäfer et al.⁴⁵ did not demonstrate a predictive value of OGUS for detecting relapses, likely influenced by the very low number of relapse events (4/50 patients).

In a recent retrospective study, Molina-Collada et al. included 76 patients with 6-month follow-up and showed that less early improvement in OGUS after initiation of treatment was associated with a higher risk of relapse at 6 months. This same research question was recently addressed by Monti et al.⁷⁴ in a prospective study of 97 patients from the PROTEA cohort. They demonstrated that higher OGUS at diagnosis was associated with an increased risk of relapse within 12 months (incidence rate ratio (IRR) per 1 point increase in OGUS 1.85, 95% CI: 1.05–3.32). Additionally, OGUS score <1 within the first 3 weeks was negatively associated with subsequent relapses (IRR 0.44, 95% CI: 0.22–0.88), and not achieving this cut-off predicted shorter time to first relapse. In an ongoing international multicenter, prospective cohort, Molina-Collada et al.⁷⁶ confirmed these results, showing that greater vascular inflammation at diagnosis and lack of normalization of vascular inflammation during the first 3 months of treatment confer higher relapse risk.

¹⁸F-FDG PET and MRI

In the study by Blockmans et al.,⁴⁸ which followed 35 patients with GCA over 6 months, baseline ¹⁸F-FDG PET/CT findings did not predict relapses during follow-up. Patients who relapsed showed similar early decreases in TVS compared to those who did not relapse. Sammel et al.,⁷⁷ using a similar approach with TVS in both cranial and LV territories at diagnosis, also found that PET activity did not distinguish relapsing versus non-relapsing disease. By contrast, Grayson et al.,⁴⁹ in a prospective study of 56 patients with LVV, found that those with high PETVAS (>20) during clinical remission were more likely to experience future clinical relapse than those with low scores (55% vs 11%; p = 0.03) over a median follow-up period of 15 months. Two additional studies, by Schönau et al.⁵² and Quinn et al.,⁵³ also evaluated the prognostic role of PETVAS but failed to demonstrate consistent associations between PET findings—either at baseline or during follow-up—and future relapse. Complementing these PET data, Adler et al.⁷⁸ reported in a randomized trial that MRI-derived mural thickening and enhancement did not correlate with relapse status, suggesting the limited utility of conventional MRI signals for relapse prediction. Taken together, current data do not yet support PET or MRI as standalone tools for relapse risk stratification, although PET-based composite scores (e.g., PETVAS) may hold promise pending further validation.

Role of imaging in risk stratification for ischemic complications in GCA

Another concern in GCA is stratifying the risk of ischemic complications that could benefit from early and more intensive treatment. Imaging may also play a relevant role in this context. In analyses from the TABUL cohort, both Ponte et al.¹⁹ and Monti et al.⁴⁰ found no significant association between baseline ultrasound findings and ischemic complications at 6 months. However, although baseline ultrasound may not predict whether ischemia will occur, ultrasound-defined phenotypes seem to relate to the anatomic pattern of events. Amar Muñoz et al.,⁷⁹ in a retrospective multicenter study of 188 GCA patients, demonstrated that patients with a cranial-predominant ultrasound presentation were more likely to have anterior ischemic optic neuropathy, whereas those with predominantly LV-GCA were more likely to have cerebrovascular accidents. This observation was later confirmed by Martín Gutierrez et al.,⁶⁹ who analyzed cerebrovascular accidents in 1540 patients from the large Spanish GCA registry ARTESER, demonstrating that the presence of LV-GCA on imaging is associated with the risk of cerebrovascular accidents. On the other hand, the imaging subtype of GCA may provide information on the risk of cardiovascular events. De Boysson et al.⁸⁰ prospectively analyzed 183 patients with LV-GCA and 105 controls without LV involvement. During the follow-up period, new cardiovascular events occurred in 49% and 11% of LV-GCA patients and controls, respectively (p < 0.0001). Inflammation of the aorta and/or its branches (HR 3.42, p < 0.0001) and LV stenosis (HR 2.75, p < 0.0001) were independent predictive factors of new cardiovascular events. Additionally, quantification of abnormalities on ultrasound may be associated with ischemic events in GCA. Van der Geest et al.⁸¹ investigated the correlation between the ultrasound Halo Score and the presence of intimal hyperplasia in the temporal artery biopsy. They observed that the presence of intimal hyperplasia, rather than transmural inflammation or giant cells, was associated with elevated Halo Scores in patients with GCA, and these patients more frequently presented with ocular ischemia.

On the other hand, activity on imaging can predict the risk of vascular complications, such as aneurysms. In a retrospective multicenter study of 549 GCA patients, De Boysson et al.¹⁵ found that LV involvement was the strongest independent predictor of aortic dilation during follow-up, with a hazard ratio of 3.16 (95% CI: 1.34–7.48, p = 0.009), and that these dilations occurred in previously inflamed aortic segments in 94% of cases. A higher TVS on ¹⁸F-FDG PET/CT has been associated with an increased yearly growth of the aortic diameter.⁸² In another study, most vascular territories with increased tracer uptake subsequently did not develop stenosis or dilatation, but a lack of baseline ¹⁸F-FDG PET/CT activity was strongly associated with stable angiographic disease.⁶³

Conclusion

Beyond the evidence supporting the validity of imaging in the diagnosis of GCA, there is growing evidence that may support its use in monitoring and the risk stratification of outcomes in GCA. Ultrasound shows improvement of IMT after treatment, with faster changes in cranial than extracranial arteries, and may help distinguish remission from relapse. Vascular inflammation assessed by ¹⁸F-FDG PET also improves, though persistent LV uptake may occur in clinical remission. Moreover, ultrasound may help identifying patients at higher risk of relapse or developing cardiovascular events, particularly in LV-GCA. Elevated arterial uptake on ¹⁸F-FDG PET at baseline has been associated with a higher risk of late vascular complications, such as aneurysms. However, future research should address the significance of subclinical findings in patients considered to be in clinical remission and its prognostic implication, as well as the efficacy of different treatment strategies based on imaging-guided risk stratification. Clarifying these aspects could help optimize treatment decisions, prevent complications, and move toward a more personalized management approach in GCA.

Footnotes

Acknowledgements

None.

Declarations

ORCID iD

Juan Molina-Collada

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Imaging-guided stratification in giant cell arteritis: prognostic and therapeutic implications

Abstract

Keywords

Background

Methods

Current monitoring strategies in GCA

Role of imaging in the monitoring of GCA

Ultrasound

18F-FDG PET, MRI, and CT

Current outcome risk stratification in GCA

Role of imaging in risk stratification of relapse in GCA

GCA phenotypes detected by ultrasound

Quantification of arterial wall abnormalities by ultrasound

18F-FDG PET and MRI

Role of imaging in risk stratification for ischemic complications in GCA

Conclusion

Footnotes

Acknowledgements

Declarations

ORCID iD

References

¹⁸F-FDG PET, MRI, and CT

¹⁸F-FDG PET and MRI