Outcome prediction with serum intercellular adhesion molecule-1 levels after aneurysmal subarachnoid hemorrhage

Background and Purpose-Chronic cerebral arterial vasospasm is the leading cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). Not all cases of SAH, however, develop chronic vasospasm. Inflammation, specifically leukocyte-endothelial cell interactions, appears to be critical in vasospasm development. Haptoglobin (Hp) is a serum protein that limits the extent of inflammation after a hemorrhagic event. An individual's Hp genotype may predict the severity of the inflammatory response during a hemorrhagic event, and consequently modulate the risk for vasospasm. Methods-Sixty mice (Hp 1-1, nϭ30; Hp 2-2, nϭ30) underwent injection of either autologous blood or normal saline solution into the cisterna magna. An additional 30 mice (15 per genotype) served as controls. The extent and manifestations of vasospasm were assessed by measuring lumen patency, quantifying activity levels, and counting the number of vessel-infiltrated macrophages/neutrophils at 24 hours after injection, which corresponds to the time of peak vasospasm in mice. Results-Genetically

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Haptoglobin 2-2 Genotype Determines Chronic Vasospasm After Experimental Subarachnoid Hemorrhage

Chaichana

Levy

Miller‐Lotan

et al. 2007

“…114 In another study, an association of serum sICAM-1 concentrations with clinical outcome was found in patients with SAH. 115 …”

Section: Inflammatory Adhesion Moleculesmentioning

confidence: 99%

Inflammatory Cell Adhesion Molecules in Ischemic Cerebrovascular Disease

Frijns

Kappelle

2002

353

264

Background — In this review we discuss the role of inflammatory cell adhesion molecules (CAMs) in ischemic stroke and in delayed cerebral ischemia after subarachnoid hemorrhage. Vascular endothelial cells and leukocytes express several inflammatory adhesion receptors, the most important of which are the selectins, immunoglobulin gene superfamily CAMs, and β2 integrins. They mediate the transmigration process of leukocytes to the abluminal side of the endothelium. Summary of Review — There is ample evidence from animal models of middle cerebral artery occlusion that expression of CAMs is associated with cerebral infarct size. Absence of CAMs in knockout animals resulted in reduced infarct size. When middle cerebral artery occlusion in experimental stroke was followed by reperfusion, administration of anti-CAM antibodies decreased infarct size. Thus far, anti-CAM treatment has not been successful in patients with ischemic stroke. Inflammatory CAM may also play a role in the pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage. In animal models, increased expression of CAMs has been observed in vasospastic arteries. Increased concentrations of CAMs have also been found in cerebrospinal fluid of patients with subarachnoid hemorrhage. Conclusions — Further research on the role of inflammatory CAMs in the pathogenesis of ischemic cerebrovascular disorders should lead to new diagnostic and therapeutic strategies.

“…[3][4][5][6][7][8] The most important is the neurological state at onset. 9,10 Except for the initial Glasgow Coma Scale, predictors show a variable relationship with outcome in SAH.…”

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confidence: 99%

Cerebral Venous Flow Velocity Predicts Poor Outcome in Subarachnoid Hemorrhage

Niesen

Rosenkranz²,

Schummer³

et al. 2004