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(Stroke. 2007;38:631.)
© 2007 American Heart Association, Inc.

Inflammation and Stroke: Introduction

Inflammation and Stroke

Introduction

Bruce M. Coull

From the Arizona Health Science Center, University of Arizona, Department of Neurology, Tucson, AZ.

Correspondence to Bruce M. Coull, Arizona Health Science Center, University of Arizona, Department of Neurology, Rm 6205,1501 N Campbell Ave, PO Box 245023, Tucson, AZ 85724-5023. E-mail coullb@u.arizona.edu

Key Words: brain imaging • inflammation • matrix proteins • neurochemistry • carotid artery

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Inflammation is an all encompassing term for a complex process that entails multiple cellular, hormonal and biochemical alterations that are both systemic and organ-specific. A panalopy of acute and chronic infections as well as many exogenous and intrinsic sources of inflammation is associated with an increased risk for ischemic stroke. The molecular mediators of these processes are the focus of enormous research interest in both vascular and neurobiology and encompass investigatory areas including atherogenesis, vascular autoregulation, endothelial function, hemostasis, leukocyte and bone marrow activation and intrinsic neuroinflammatory mechanisms.

Atherosclerosis affecting precerebral as well as intrinsic brain arteries and arterioles plays a key role in the pathogenesis of stroke. Atherosclerosis producing focal carotid stenosis localized to the carotid bulb and proximal internal carotid artery is a principal cause of atheroembolic ischemic stroke in North America. The development of the atherosclerotic lesion is usually a gradual one taking place over a time scale measured in years and is characterized by chronic inflammation within the vessel wall in a response to the deposition of oxidized LDL cholesterol components. During acute atherothrombosis there is an abrupt transition from a chronic indolent inflammatory process to one that is far more fulminate and giving rise to the so-called hot or active plaque. This response entails increased leukocytosis within the atheroma, activation of the regional vascular endothelium that promotes further recruitment of leukocytes as well as digestion of the fibrous cap by the expression of tissue matrix metalloproteinases (MMPs) that ultimately cause plaque rupture and exposure of . . . [Full Text of this Article]