Background 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.
Objectives 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].
Conclusions 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.
Disclosure of Interest None declared