Related Experiment Video
Updated: May 25, 2026
An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Large vessel involvement in biopsy-proven giant cell arteritis: prospective study in 40 newly diagnosed patients
Sergio Prieto-González1, Pedro Arguis, Ana García-Martínez
1Department of Systemic Autoimmune Diseases, Hospital Clínic Barcelona, Barcelona, Spain.
Insights
Large vessel vasculitis (LVV) affects two-thirds of newly diagnosed giant cell arteritis (GCA) patients, often involving the aorta. Early corticosteroid treatment may reduce detectable LVV.
Area of Science:
- Vascular Medicine
- Rheumatology
- Diagnostic Imaging
Background:
- Giant cell arteritis (GCA) is suspected to affect the aorta and its branches.
- Prevalence of large vessel vasculitis (LVV) in GCA remains unclear despite non-invasive imaging capabilities.
Purpose of the Study:
- To prospectively determine the prevalence, characteristics, and location of LVV in new GCA cases.
- To identify associated clinical and laboratory features of LVV in GCA.
Main Methods:
- CT angiography (CTA) was used to examine 40 consecutive patients with newly diagnosed, biopsy-proven GCA.
- Patients were treatment-naïve or had minimal corticosteroid exposure (<3 days).
- Evaluated vessel wall thickness and diameter changes in the aorta and its major branches.
Main Results:
- LVV was identified in 67.5% of patients.
- The aorta (65%) and brachiocephalic trunk (47.5%) were most commonly affected.
- Aortic dilation was present in 15% of patients; LVV was more frequent in treatment-naïve individuals (77%).
Conclusions:
- CTA-defined LVV is prevalent in two-thirds of newly diagnosed GCA patients.
- Aortic dilation is an early finding in 15% of GCA cases.
- Prior corticosteroid use may reduce CTA-detected LVV.
Background:
Necroscopic and surgical studies have suggested that giant cell arteritis (GCA) may target the aorta and its main branches. Imaging techniques are able to detect large vessel vasculitis (LVV) non-invasively in patients, but the prevalence of LVV in GCA has not been clearly established.
Objective:
To assess prospectively the prevalence, characteristics and topography of LVV in patients with newly diagnosed GCA and to determine the associated clinical and laboratory features.
Methods:
CT angiography (CTA) was performed in 40 consecutive patients with newly diagnosed biopsy-proven GCA. Patients were treatment-naïve or had been treated with corticosteroids for <3 days. Vessel wall thickness and vessel diameter (dilation or stenoses) at four aortic segments (ascending aorta, aortic arch, descending thoracic and abdominal aorta) and at the main aortic branches were evaluated.
Results:
LVV was detected in 27 patients (67.5%). The vessels involved were as follows: aorta (26 patients, 65%), brachiocephalic trunk (19 patients, 47.5%), carotid arteries (14 patients, 35%), subclavian arteries (17 patients, 42.5%), axillary arteries (7 patients, 17.5%), splanchnic arteries (9 patients, 22.5%), renal arteries (3 patients, 7.5%), iliac arteries (6 patients, 15%) and femoral arteries (11 patients, 30%). Dilation of the thoracic aorta was already present in 6 patients (15%). Cranial ischaemic events were significantly less frequent in patients with LVV (p=0.029). Treatment-naïve patients had a higher frequency of LVV (77% vs 29%, p=0.005).
Conclusions:
CTA-defined LVV occurs in two-thirds of patients with GCA at the time of diagnosis and aortic dilation is already present in 15%. Previous corticosteroid treatment may decrease CTA-detected LVV.
