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(Stroke. 2006;37:291.)
© 2006 American Heart Association, Inc.

Advances in Stroke 2005

The Harms and Benefits of Inflammatory and Immune Responses in Vascular Disease

From the Stroke Unit (A.C.), Institute of Clinical Neurosciences, Hospital Clínic; and the Stroke Branch (J.H.), National Institute of Neurological Disorders and Stroke/National Institutes of Health.

Correspondence to Ángel Chamorro, Stroke Unit, Institute of Clinical Neurosciences, Hospital Clinic, 170 Villarroel, 08036 Barcelona, Spain. E-mail achamorro@ub.edu

Key Words: inflammation

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

Accumulating experimental evidence strongly supports a role for inflammatory, innate immune and adaptive immune mechanisms in many facets of vascular disease.¹ This brief review will highlight recently published insights into inflammation and immune system involvement in stroke biomarker identification, atherosclerosis, abdominal aortic aneurysm (AAA) formation, thrombosis, ischemic tolerance, progression of ischemic brain injury, and peristroke infections.

Inflammatory Biomarkers and Stroke

Inflammation plays a role in the genesis of brain ischemia and inflammatory processes and may facilitate serious and life-threatening complications in stroke patients.² However, efforts to disentangle good from bad effects of inflammation in cerebrovascular disease reveal frequent discrepancies between preclinical and clinical data. A clinical goal for several decades has been the identification of reliable inflammatory biomarkers of impending stroke in asymptomatic subjects and clinical prognosis in stroke patients. So far, most markers have shown moderate utility at the bedside as the result of low sensitivity and specificity. The list of biomarkers includes high-sensitivity C-reactive protein (hsCRP), fibrinogen, serum amyloid A, matrix metalloproteinase (MMP)-9, P-selectin, sCD40L, myeloperoxidase, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, tumor necrosis factor (TNF)-, interleukin (IL)-1, IL-6, and IL-8. Novel markers evaluated in 2005 are PARK7,³ nucleoside diphosphate kinase A (NDKA),³ and adiponectin.⁴ PARK7 is a redox-sensitive molecular chaperone activated by oxidative stress; it increases within 30 minutes to 3 hours of stroke onset. Sensitivities are of 54% to 91%, for PARK7, and 70% to 90%, for NDKA, and specificities are 80% to 97%, for PARK7, and 90% to 97%, for NDKA. Adiponectin is an adipocytokine . . . [Full Text of this Article]

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