Abstract
Background and Aims : Delayed cerebral vasospasm (DCV) is the leading cause of mortality after subarachnoid hemorrhage (SAH). There is increasing evidence that inflammation, specifically leukocyte-endothelial cell interactions, plays a role in the pathogenesis of DCV. High-density lipoproteins (HDL) are biological molecules that prevent the expression of cell adhesion molecules induced by pro-inflammatory agents in endothelial cells, thus inhibiting leukocyte adhesion. In pathological conditions, HDL undergo quantitative and qualitative changes that have been associated with loss of physiological function.
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