FRI0357 Incidence and Predictors of Thoracic Aortic Damage in Biopsy-Proven Giant Cell Arteritis: A Single-Institution Cohort Study
Authors: M.J. Koster, C. Labarca, C. Crowson, E.L. Matteson, K.J. Warrington
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Patients with giant cell arteritis (GCA) are at an increased risk for aortic structural damage; however, the timing and predisposing characteristics for development of aortic aneurysm is poorly understood. <h3>Objectives</h3> The aim of this study was to evaluate the incidence and predictors of thoracic aortic aneurysm in a large single-institution cohort of patients with biopsy-proven GCA. <h3>Methods</h3> A retrospective review was performed to identify all patients with biopsy-proven GCA from 1998 through 2013. Demographic, clinical, laboratory, radiographic, and treatment data at baseline and subsequent followup visits were collected. Kaplan-Meier methods were used to estimate cumulative incidence and Cox models were used to examine potential predictors of development of aneurysm/dilatation of the thoracic aorta. <h3>Results</h3> The cohort included 286 patients with biopsy-proven GCA (213 females and 73 males, mean [±SD] age 75 [±7.6] years) with a mean (±SD) follow up of 6 (±3.9) years. 130 patients had 280 imaging studies (41% magnetic resonance angiography [MRA], 55% computed tomographic angiography [CTA] and 4% conventional angiography). The median time from diagnosis to first imaging study was 0.2 [interquartile range (IQR) 0.0, 2.7] years. Of the 130 patients, 48% underwent follow up imaging studies. At the first imaging study, 14 (11%) patients had evidence of aneurysm or dilatation of the thoracic aorta and 28 (22%) patients had thoracic aorta thickening. Excluding prevalent cases, the cumulative incidence (±SE) for aneurysm/dilatation of the thoracic aorta during followup was 0% at both 1-yr and 2-yrs but increased to 9% (±0.4) at 5-years. Among all patients with GCA evaluated with vascular imaging, thoracic aortic aneurysm/dilatation was detected in 11% (±3) at 1-yr, 11% (±3) at 2-yrs, and 15% (±3) at 5-yrs. Patient baseline demographics, cardiovascular risk, clinical presentation, laboratory values, and initial treatment were assessed to predict incidence of thoracic aortic damage. Baseline thickening of the thoracic aorta was not a risk factor for subsequent aneurysm/dilatation (p=0.99). Neither the presence of relapse (p=0.99) nor the number of relapses (p=0.65) were associated with development of thoracic aortic damage [HR (95% CI): 0.88 (0.50, 1.54); p=0.65]. Furthermore, there was no difference in initial prednisone dose between patients who did and did not develop aortic damage. The sole predictor for development of thoracic aortic aneurysm/dilatation was a history of smoking [HR (95% CI) 28.1: (1.59, 495.71); p=0.023]. <h3>Conclusions</h3> In our cohort, thoracic aortic aneurysm/dilatation was seen in 11% of patients at baseline evaluation and increased to 15% at 5-yrs after diagnosis. Former smokers were at a 28-fold increased risk for developing thoracic aortic damage. Surveillance for aortic damage should be pursued in all patients with GCA, particularly those with a smoking history. Prospective investigations into screening methods and optimal frequency are warranted. <h3>Disclosure of Interest</h3> None declared