Aortic and Carotid Complications in Patients With Giant Cell Arteritis.

PURPOSE: To assess the risk of developing aortic aneurysms (AAs) and carotid artery stenosis (CAS) in patients with giant cell arteritis (GCA), particularly among those presenting with and without visual symptoms.

DESIGN

Retrospective cohort study.

SUBJECTS: A total of 7294 patients aged ≥50 years with biopsy-proven GCA (temporal artery biopsy within 2 weeks of diagnosis and ≥3 prednisone refills) were identified and compared with 265 948 control patients presenting with tension-type headache using the TriNetX US Collaborative Network. A secondary comparison was performed between patients with GCA with (n = 2390) and without (n = 5222) visual symptoms (eg, diplopia, amaurosis fugax, vision loss).

METHODS

GCA was defined using International Classification of Diseases, 10th Revision codes M31.5 and M31.6. Patients with a history of other vasculitides, prior AAs, or major thrombotic events were excluded. Propensity score matching was used to balance demographics, socioeconomic factors, comorbidities, substance use, and laboratory/vital parameters, resulting in matched cohorts for each comparison. Adjusted hazard ratios (aHRs) and 95% CIs were estimated using Cox proportional hazards models to account for time to onset of vascular complications.

MAIN OUTCOME MEASURES: Primary outcomes were the 5-year risks of (1) thoracic AAs, (2) thoracoabdominal AAs, (3) abdominal AAs, and (4) CAS.

RESULTS

After matching, 7252 patients remained in each arm for the primary GCA versus control comparison. Patients with GCA had a significantly higher 5-year risk of any AA (3.59% vs 1.75%; aHR, 1.98; 95% CI, 1.59-2.45), including thoracic (2.23% vs 1.02%; aHR, 2.01; 95% CI, 1.59-2.77), thoracoabdominal (0.32% vs 0.14%; aHR, 3.68; 95% CI, 1.50-9.05), and abdominal (1.80% vs 0.82%; aHR, 2.03; 95% CI, 1.49-2.77). CAS was also elevated in GCA (7.20% vs 4.37%; aHR, 1.59; 95% CI, 1.38-1.84). In the subanalysis of patients with GCA, the 5-year risk of any AA was comparable between those with and without visual symptoms (3.58% vs 3.23%; aHR, 1.14; 95% CI, 0.83-1.57). However, CAS occurred more frequently in patients with GCA presenting with visual symptoms (8.95% vs 7.43%; aHR, 1.24; 95% CI, 1.01-1.53).

CONCLUSIONS

Patients with GCA demonstrate a substantially increased risk of AAs, particularly thoracic AAs, compared with matched controls. Although having visual symptoms did not correlate with additional aortic risk, they were associated with a higher risk of CAS.