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  • Title: Increased prevalence of subclinical atherosclerosis in patients with small-vessel vasculitis.
    Author: Chironi G, Pagnoux C, Simon A, Pasquinelli-Balice M, Del-Pino M, Gariepy J, Guillevin L.
    Journal: Heart; 2007 Jan; 93(1):96-9. PubMed ID: 16940394.
    Abstract:
    BACKGROUND AND OBJECTIVE: Although changes in smaller vessels is the hallmark of medium-sized and small-vessel vasculitis, it has been suggested that large arteries of such patients may also be affected by the early atherosclerotic process because of coexisting risk factors or systemic inflammation. This study aimed to bring additional arguments supporting this hypothesis. DESIGN, SETTING AND PATIENTS: 50 consecutive patients with primary systemic necrotising vasculitis and 100 controls matched for age and sex underwent ultrasonic detection of plaque in three peripheral vessels (carotid and femoral arteries and abdominal aorta). Cardiovascular risk factors and inflammation (C reactive protein (CRP)) were concomitantly measured in all participants, and diagnosis of high-risk status was defined by the presence of known history of cardiovascular disease, type 2 diabetes or 10-year-Framingham Risk Score > or =20%. RESULTS: Patients had higher frequency of plaque than controls in the carotid arteries (p<0.05), in the aorta (p<0.01) and in the three vessels examined (p<0.001), and adjustment for high-risk status did not confound such difference in the aorta and in the three vessels. In the overall population of patients and controls, vasculitis was associated with a higher frequency of three-vessel plaques (p<0.05), independently of high-risk status and CRP. In patients, the higher frequency of three-vessel plaques was associated with high-risk status (p<0.05) but not with CRP, or disease and treatment characteristics. CONCLUSIONS: Small-vessel vasculitis is associated with more frequent subclinical atherosclerosis, especially extended to multiple peripheral vessels, and such association is not entirely explained by cardiovascular risk factors and systemic inflammation.
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