Intraluminal assessment of inflammatory factors in patients with intracranial aneurysms.

Abstract

The formation, growth, and rupture of intracranial aneurysms (IA) are due to several pathophysiological mechanisms, including focal hemodynamic injury and inflammation of the arterial wall. We investigated the differences between venous, parent artery, and intra-aneurysmal blood by measuring inflammatory factors and antibodies in patients with ruptured (rIA) or unruptured intracranial aneurysms (uIA). A prospective study was performed in patients who presented with IA and required endovascular treatment. Blood was drawn from the lumen of the aneurysm sac, the parent artery, and the peripheral veins, to determine the serum concentrations of complement factors C3, C4, IgG, IgM, IgA antibodies, and C-reactive protein (CRP). Thirty-six patients (15 with uIA and 21 with rIA) were enrolled in the study. In both groups, C3, C4, IgM, IgG, and IgA showed a gradual decrease from venous to intra-aneurysmal samples, but only IgG in the parent artery and intra-aneurysmal samples reached a significant decrease in uIA compared with venous samples. Accordingly, C3 and IgG concentrations in the intra-aneurysmal samples showed a significant decrease in rIA compared with venous samples. A significant increase in CRP concentrations was observed in parent artery and intra-aneurysmal samples from patients with rIA compared with patients with uIA; a significant increase in C3 concentrations was observed in parent artery samples from patients with rIA compared with patients with uIA, and a significant decrease in IgM concentrations was observed in venous, parent artery, and intra-aneurysmal samples from patients with rIA compared with patients with uIA. A decrease in C3 and IgG in the aneurysm sac indicates activation of the complement system in the arterial wall. CRP in the aneurysm sac and lumen of the parent artery was significantly increased in ruptured compared with unruptured aneurysms, whereas venous, parent artery, and intra-aneurysmal IgM were decreased in ruptured compared with unruptured aneurysms. These results argue for the role of an ongoing inflammatory process in aneurysms leading to their growth and rupture.