Abstract
Giant cell arteritis (GCA) is a systemic vasculitis with a direct and indirect increased risk of acute and chronic vascular events, affecting large and medium vessels, and responsible for most of the morbidity and mortality of this disease. We aimed in this review to provide an updated synthesis of knowledge regarding cardiovascular events observed in GCA. By definition, GCA patients are over 50 and often over 70 years old, and subsequently also present age-related cardiovascular risk factors. In addition, the systemic and vascular inflammation as well as glucocorticoids (GC) probably contribute to an accelerated atherosclerosis and to vascular changes leading to arterial stenoses and aortic dilations and/or dissections. GCA-related ischemic complications, especially ophthalmologic events, stroke or myocardial infarcts are mostly observed within the first months after the diagnosis, being mainly linked to the vasculitic process. Conversely, aortic complications, including dilations or dissections, generally occur several months or years after the diagnosis, mainly in patients with large-vessel vasculitis. In these patients, other factors such as atherosclerosis, GC-related endothelial damage and vascular wall remodeling/healing probably contribute to the vascular events. GCA management includes the detection and treatment of these previous and newly induced cardiovascular risk factors. Hence, the use of cardiovascular treatments (e.g., aspirin, anticoagulation, statins, anti-hypertensive treatments) should be evaluated individually. Aortic structural changes require regular morphologic evaluations, especially in patients with previous aortitis. The initial or secondary addition of immunosuppressants, especially tocilizumab, an anti-IL-6 receptor antibody, is discussed in patients with GCA-related cardiovascular complications and, more consensually, to limit GC-mediated comorbidities.
Highlights
Giant cell arteritis (GCA) is the most frequent systemic vasculitis in patients over50, affecting medium- and large-sized vessels
Several studies suggest a link between inflammatory ophthalmologic involvement and atherosclerosis, since visual losses found in GCA were more likely to occur in older patients with past histories of stroke and peripheral arterial disease [36,39,40]
We aimed to underline how giant cell arteritis is a systemic vascular disease, with a direct and indirect increased risk of vascular events that remain the major cause of morbidity and mortality in this disease
Summary
Giant cell arteritis (GCA) is the most frequent systemic vasculitis in patients over. One showed an initial impaired flow-mediated vasodilatation that improved with GC [27] supporting the presence of an endothelial dysfunction in GCA patients before treatment These results were not replicated in another study [28]. Taken together, no specific study has shown accelerated atherosclerosis in GCA patients, there is much evidence that systemic inflammation provides a proatherogenic effect by inducing dyslipidemia, insulin resistance, hypercoagulation, endothelial dysfunction and oxidative stress [22]. Some preclinical studies showed that GC exposure may reduce the recruitment of monocytes and macrophages within the atherosclerotic lesions and reduce the cholesterol accumulation in macrophages It results in a reduction of macrophage-induced pro-inflammatory cytokine release limiting the vascular remodeling [32]. The exact impact of GC and the mechanisms implied in atherosclerosis formation is more complex, since GC may act at different cellular levels resulting in opposite results, either beneficial or detrimental to the development of atherosclerotic plaques
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