How and when do we alter inflammatory mechanisms in stroke? Will it help?
The emerging recognition of atherosclerosis as primarily a chronic inflammatory process opens new possibilities to the treatment options that can reduce the risk of atherothrombotic stroke. The question is, "How do we alter the inflammatory mechanisms in atherosclerosis and will it reduce the risk of stroke?" Investigation into the fundamental pathophysiological mechanisms involved in the initiation, formation, and activation of atherosclerotic plaques is critical if we are to successfully employ pharmacotherapeutic strategies to reduce stroke risk. This article will review the key inflammatory elements associated with atherosclerosis and atherothrombotic stroke, identify potential inflammatory markers associated with the increased risk of stroke, review the effects of currently available medications that may have a beneficial impact on atherosclerosis and stroke, and briefly explore potential future strategies for reducing inflammation.
DeGraba
Thomas J
TJ
Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20889, USA.
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000473:pathology; D015415:Biomarkers; D005819:Genetic Markers; D006801:Humans; D007249:Inflammation / Q000473:pathology* / Q000517:prevention & control*; D020521:Stroke / Q000473:pathology* / Q000517:prevention & control*
D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D005819:Genetic Markers