Background/Purpose: 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. 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.

Methods: 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.

Results: 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].

Conclusion: 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

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/incidence-and-predictors-of-thoracic-aortic-damage-in-biopsy-proven-giant-cell-arteritis-a-single-institution-cohort-study/