Novel in vivo Assessment of Unruptured Intracranial Aneurysm Inflammatory Factors

Abstract

Background and Purpose: The growth and eventual rupture of intracranial aneurysms may be due to an underlying inflammatory process as evidenced by pathological examination of aneurysm walls. We hypothesize that unruptured aneurysms have an increased inflammatory milieu within their lumen in comparison to the rest of the cerebral arterial vascular system. Methods: Blood was sampled from unruptured aneurysms in patients presenting for aneurysm coil embolization and C3 and C4 complement values from this serum were compared with complement values in the parent artery. Results: Ten patients were enrolled over 32 months with a mean aneurysm size of 9.1 mm. Compared to control samples drawn from peripheral circulation, there were significant decreases of both C3 (p = 0.0003) and C4 (p = 0.0063) levels in aneurysmal blood samples. Conclusions: A state of decreased complement indicative of classic pathway activation was found in all tested aneurysms, thus providing evidence of an ongoing process of complement activation in the blood of live, unruptured aneurysm sacs.

Growth and rupture of an intracranial aneurysm: the role of wall aneurysmal enhancement and CD68+

“…In our series, we observed that positive effects for CD68, in line with previous literature reports ( 27 – 29 ), were associated with a high percentage of SAH. These patients exhibited an increase in ECM along with rarefaction of the muscular component through the aneurysm wall.…”

“…CD68 and GFAP ( 25 ) are highly correlated with circulating macrophages, which are typically involved in the inflammatory mechanisms of IA. In recent times, it has been highlighted by various authors ( 19 – 23 , 26 , 27 ) that the percentage of CD68-positive cells in recently ruptured aneurysm domes (within 2 days) is significantly higher compared with the percentage in unruptured aneurysm domes. The presence of foaming elements of macrophagic nature (foam cells) indicates a high concentration of lipid material, similar to that seen in vessels with atherosclerotic plaques, along with an inflammatory process in the aneurysm wall.…”

The Role of Soluble Urokinase Plasminogen Activator Receptor (suPAR) in the Context of Aneurysmal Subarachnoid Hemorrhage (aSAH)—A Prospective Observational Study

“…As a consequence, it remains elusive whether intracranial aneurysm rupture (as a local event with an immediate systemic inflammatory increase) or the preexisting condition of chronic inflammation is causative of higher suPAR levels. However, it is conceivable that a local, compartmentalized inflammatory processes within the cerebral aneurysm wall are probably not detectable systemically, rendering an early inflammatory response caused by the rupture more likely ( 47 ). An alternative hypothesis may be that chronic, low grade, but systemic inflammation may support or even initialized the formation of aneurysm ( 48 ).…”