Role of inflammation in stroke and atherothrombosis.

摘要: The onset of cerebral ischaemia triggers a cascade proinflammatory molecular and cellular events. Clinical studies suggest that the strength this acute response is important in early late clinical outcomes, worsening, extent brain damage. Variables are predictors adverse stroke outcome include erythrocyte sedimentation rate, levels C-reactive protein (CRP), interleukin-6, tumour necrosis factor-alpha intercellular adhesion molecule-1. Current data indicate inflammation serves to fuel atherosclerosis can act as link between atherothrombosis. Growing evidence indicates platelets prominent players inflammatory component these disease processes. Thus, upon activation, release series cytokines growth factors express CD40 ligand, which interacts with receptor on other major cell types involved atherosclerosis/atherothrombosis. In healthy volunteers, CD40L expression not significantly inhibited by acetylsalicylic acid (ASA) alone, but after treatment ADP-receptor antagonist clopidogrel or plus ASA. Of range potential biomarkers have been reported literature, best studied CRP. Such may utility for refined identification patients at high risk atherothrombosis different arterial beds monitoring therapeutic agents trials.