Evolution and outcomes of aortic dilations in giant cell arteritis.

• In GCA patients with aortic dilation, scarce data exist on the evolution of aortic morphology. • More than 25 % of GCA patients with aortic dilation showed a fast progression of aorta caliber. • More than 90 % of the aortic dilations on the abdominal portion of the aorta progressed. • Among patients with aortitis, aortic dilation developed on an inflammatory segment in 85 % of them. • Available histologies of patients with fast progression and aortic surgery showed active vasculitis. To identify factors associated with the progression of giant cell arteritis (GCA)-related or associated aortic dilations. In this retrospective study, 47 GCA patients with aortic dilation were longitudinally analyzed. Each patient underwent ≥2 imaging scans of the aorta during the follow-up. Three progression statuses of aortic dilations were distinguished: fast-progressive (FP) defined by a progression of the aortic diameter ≥5 mm/year or ≥1 cm/2 years, slow progressive (SP) by a progression of the aortic diameter >1 mm during the follow-up, and not progressive (NP) when aortic diameter remained stable. Among the 47 patients with aortic dilation, the thoracic section was involved in 87 % of patients. Within a total follow-up of 89 [6–272] months, we identified 13 (28 %) patients with FP dilations, and 16 (34 %) and 18 (38 %) patients with SP and NP dilations, respectively. No differences regarding baseline characteristics, cardiovascular risk factors or treatments were observed among the 3 groups. However, FP patients more frequently showed atheromatous disease (p = 0.04), with a more frequent use of statins (p = 0.04) and antiplatelet agents (p = 0.02). Among the 27 (57 %) patients with aortitis, aortic dilation developed on an inflammatory segment in 23 (85 %). Among the FP patients who underwent aortic surgery with available histology (n = 3), all presented active vasculitis. This study suggests that aortic inflammation, as well as atheromatous disease, might participate in the fast progression of aortic dilation in GCA. [ABSTRACT FROM AUTHOR]