Accelerated atherosclerosis in ANCA‐associated vasculitis

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Atherosclerosis is a slowly progressive disease of the arterial wall, responsible of most of cardiovascular events.1 Although the pathogenesis of atherosclerosis is not completely elucidated, is currently accepted a central role of inflammation in all phases of the atherosclerotic process.2 It is well known the existence of an early and accelerated atherosclerosis in the course of autoimmune diseases with higher cardiovascular morbi‐mortality3 probably related to a chronic systemic inflammation superimposed to traditional cardiovascular risk factors (CVRF).4
ANCA (antineutrophil cytoplasmic antibodies)‐associated vasculitis (AAV) are a group of autoimmune disorders characterized by inflammation and necrosis of the small‐sized vessels,6 including granulomatosis with polyangiitis (GP), microscopic polyangiitis (MPA), and granulomatous eosinophilic granulomatosis with polyangiitis (GEPA). In AAV, cardiovascular diseases (CVD) are a major cause of mortality9; prior studies have demonstrated the presence of accelerated subclinical atherosclerosis not explained by traditional CVRF and increased CIMT even in patients in complete remission (CR).10
The common carotid artery intima‐media thickness (CIMT) has been postulated as a surrogate marker of atherosclerosis.11 Several studies have demonstrated that CIMT correlates well with histology, CVRF and the presence of advanced atherosclerosis.12 Moreover, increased CIMT can predict future risk events, especially cardiovascular (myocardial infarction, angina, or coronary intervention) and cerebrovascular events (stroke or TIA).11
Some studies have linked microangiopathy to an increased CIMT. Moreover, a correlation between CIMT with the pulsatility index of the internal carotid artery (PI‐ICA) has been demonstrated14 and related to the presence of microalbuminuria in diabetic and non‐diabetic patients15 and a probable cerebral microangiopathy.14
The aim of our study was to investigate the association of atherosclerosis measured by CIMT and cerebral small vessel disease in AAV‐patients.

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