Abstract
Giant cell arteritis (GCA) is a primary systemic vasculitis characterized by systemic inflammation and vascular insufficiency of large and medium blood vessels which may lead to end-organ damage in patients age 50 and older. Standard corticosteroid treatment of GCA significantly improves the intima-media thickness while having less influence on vascular endothelial dysfunction. GCA morbidity may be related to both cardiovascular complications and corticosteroid toxicity. Therefore, we aim to discuss 1) characteristic aspects of vascular damage, 2) several mechanisms that cause vascular dysfunction, intima-media ‘nodular’ thickness, progressive narrowing of the arterial lumen and vascular blockage in the context of systemic inflammation, thrombosis and of the cardiovascular complications in GCA and 3) new therapeutic glucocorticosteroid-sparing (GS) agents which might be a more productive way of avoiding the invalidating or life-threatening cardiovascular complications of GCA.