Key result
Giant cell arteritis is linked to significantly higher aortic stiffness and carotid plaque burden vs controls.
Why the study?
Do patients with giant cell arteritis have increased carotid pulsatility, resistance, atherosclerosis, and aortic stiffness compared to healthy controls?
Cohort (n=159)
Do patients with giant cell arteritis have increased carotid pulsatility, resistance, atherosclerosis, and aortic stiffness compared to healthy controls?
Answers are grounded in this paper and cite their sources.
Patients with giant cell arteritis exhibit increased carotid pulsatility, resistance, atherosclerosis, and aortic stiffness compared to healthy controls, suggesting a higher burden of macroangiopathy.
BACKGROUND: To assess a combination of novel color Doppler ultrasound (CDUS), greyscale ultrasound (GSUS), and oscillometric indices of macroangiopathy and (CV) risk in patients with giant cell arteritis (GCA). Additionally, to explore the relationships between these imaging markers and both patient-specific and disease-related characteristics, as well as traditional CV risk factors. METHODS: CDUS was performed to evaluate arterial compliance markers, specifically the resistance (RI) and pulsatility (PI) indices, in both the common (CCA) and internal carotid artery (ICA) of GCA patients and healthy controls. GSUS examinations were conducted to measure carotid intima-media-thickness (cIMT), identify plaques, and quantify cumulative carotid calcification surface. Oscillometry was utilized to determine aortic stiffness via carotid-femoral pulse-wave velocity (cfPWV). RESULTS: Sixty-six GCA patients and 93 healthy subjects were included. Patients showed significantly higher cfPWV (padj <0.001), cIMT (padj =0.037), CCA-PI (padj =0.009), CCA-RI (padj=0.019), and plaque-area (p < 0.001) compared with controls. cfPWV correlated with traditional CV risk factors, like age (rho = 0.330, p < 0.009), mean-arterial-pressure (rho = 0.257, p = 0.044), and cholesterol (rho = 0.318, p = 0.017). CCA-PI and -RI were lower in patients receiving immunosuppressive therapy [1.5 (1.33–2.04) vs. 1.95 (1.72–2.29); 0.74 (0.68–0.82) vs. 0.80 (0.76–0.85), both; p < 0.05], and CCA-RI was predicted by erythrocyte-sedimentation-rate (rho = 0.343, p = 0.044). cIMT correlated with age (r = 0.619, p < 0.001) and plaque area (rho = 0.305, p = 0.047). CONCLUSION: GCA patients demonstrated increased carotid pulsatility, resistance, atherosclerosis, and aortic stiffness compared to controls. Moreover, key predictors of impaired CV and cerebrovascular surrogates were identified. The combined assessment of CDUS and GSUS could provide a more thorough evaluation of the arterial tree, thereby enhancing the overall assessment of macroangiopathy. TRIAL REGISTRATION: DRKS00031470.
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Triantafyllias et al. (2026) conducted a cohort in Giant cell arteritis (n=159). Giant cell arteritis vs. Healthy controls was evaluated on Carotid-femoral pulse-wave velocity (cfPWV), carotid intima-media-thickness (cIMT), CCA-PI, CCA-RI, and plaque-area (p=<0.001). Giant cell arteritis was associated with significantly higher aortic stiffness (cfPWV, padj<0.001), carotid intima-media thickness (padj=0.037), and plaque area (p<0.001) compared to healthy controls.
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