Background: Large (LVV) and medium (MVV) vessel vasculitis are characterized by life-threatening macro-vascular complications including coronary artery disease, stroke and aneurysm formation [1]. The vascular damage is attributed to tissue and systemic inflammation, immunosuppressive therapy and cardiovascular disease (CVD) risk factors. An acceleration of the three classical types of arterial damage i.e. inappropriate arterial remodeling, atheromatosis and arteriosclerosis, contributing to the increased CVD morbidity and mortality of these patients [2] has been also proposed, raising challenges and potential opportunities for management optimization.

Objectives: To comprehensively explore the functional and structural alterations of both micro- and macro-circulation in LVV/MVV patients, utilizing state-of-the art, non-invasive vascular biomarkers in active and inactive disease state.

Methods: Forty-six LVV/MVV patients were studied (36 giant cell arteritis-GCA, 5 Takayasu arteritis, 1 IgG4 related aortitis and 4 with polyarteritis nodosa) who were strictly matched (at 1:1 ratio), according to age, sex, all CVD risk factors presence and management, with apparently healthy individuals (AH), rheumatoid arthritis (RA) and polymyalgia rheumatica without vasculitis (PMR) disease controls. Atheromatosis (carotid/femoral plaques), arterial stiffness (carotid-femoral pulse wave velocity-cfPWV), pressure wave reflections (augmentation index-AIx) and vascular remodeling (carotid intima media thickness-cIMT and retinal vessel calibers: central retinal venular equivalent–CRVE and central retinal arteriolar equivalent-CRAE) were evaluated at two time points, i.e. active disease and upon remission.

Results: Overall, LVV/MVV patients exhibited higher cfPWV compared to AH (by 1.2 m/sec, p=0.08) and to RA controls (by 1.9 m/sec, p=0.001). Pressure Wave Reflections were mildly lower, irrespectively of disease status and matched control group. Interestingly, accelerated atheromatosis (carotid/femoral plaques) was seen at diagnosis compared to both AH (p=0.016), and RA controls (p=0.02). LVV/MVV patients also displayed increased cIMT when evaluated, independently to baseline disease state (p=0.04 vs AH and p<0.001 vs RA controls), as well as in active disease (p=0.13 vs AH, p=0.003 vs RA controls). Following treatment reduction of the inflammatory bulk, the most sensitive to change biomarker tended to be the cIMT. Moreover, compared to AH, LVV/MVV patients displayed increased both CRVE (for all: p=0.004, for active p=0.005) and CRAE independently to disease activity (for all: p=0.011, for active: p=0.017), but only CRAE compared to RA controls (for all: p=0.018, for active: p=0.054). Both CRVE and CRAE correlated with ESR (r=0.644, p=0.017 and r=0.717, p=0.006 respectively). Further, sensitivity analysis demonstrated that active GCA patients at diagnosis exhibited increased aortic stiffness compared to matched controls (p=0.001 vs RA and p=0.02 vs PMR controls), accelerated carotid/femoral atheromatosis (p=0.03 vs AH, p=0.02 vs RA and p=0.02 vs PMR controls) and carotid hyperplasia (p=0.04 vs RA and p=0.006 vs PMR controls), as well as increased retinal calibers (CRVE: p=0.014 vs AH controls, CRAE: p=0.035 vs AH controls).

Conclusion: Early macro- and micro-vascular damage, which is only partly reversible, may occur in LVV/MVV, suggesting a long preceding subclinical disease course. Incorporation of non-invasive vascular biomarker assessment should be considered in clinical practice to optimize CVD risk reduction strategies.

REFERENCES: [1] Pugh D, et al. Nat Rev Dis Primers 2022;7(1):93.

[2] Argyropoulou OD, et al. Curr Opin Rheumatol 2018;30(1):36-43.

Acknowledgements: Ourania D Argyropoulou and Petros P. Sfikakis are members of the European Reference Network for Rare Immunodeficiency, Autoinflammatory and Autoimmune Diseases (RITA-ERN). The study was partially funded by the Hellenic Rheumatology Society.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.