Background: Vascular inflammatory lesions from patients with giant-cell arteritis show a remarkable amount of neovascularization, but its clinical implications have never been investigated.
Methods and results: To assess the clinical relevance of neovascularization in giant-cell arteritis, angiogenesis was measured in temporal artery sections from 31 patients with biopsy-proven giant-cell arteritis by staining endothelial cells with Ulex europaeus lectin. Angiogenesis was highly variable among these patients. Patients without ischemic complications had higher tissue angiogenesis scores than patients with ischemic events (5.69+/-0.6 versus 2.91+/-0.6, P=0.003). Angiogenesis was also more prominent in patients with a strong acute phase response (score: 5.31+/-0.6) compared with those with a weak systemic inflammatory reaction (2.30+/-0.44; P=0.0007). Serum angiogenic activity was studied in an additional series of 38 biopsy-proven patients. Sera from patients without ischemic events tended to be more active in stimulating human umbilical vein endothelial cell growth (optical density x1000, 270+/-15 versus 192+/-14, P=0.065) and differentiation into capillary-like structures (107+/-5 versus 84+/-8 relative units, P=0.0058) than patients with ischemic complications. Sera from patients without ischemic events had more in vivo full angiogenic activity tested in the chick chorioallantoic membrane than sera from patients with ischemic complications.
Conclusion: Inflammation-induced angiogenic activity may play a compensatory role for ischemia in patients with giant-cell arteritis.