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(Stroke. 2002;33:2141.)
© 2002 American Heart Association, Inc.

Editorials

Inflammation, Cell Adhesion Molecules, and Stroke: Tools in Pathophysiology and Epidemiology?

Andrew D. Blann, PhD, MRCPath; Paul M. Ridker, MD Gregory Y.H. Lip, MD

From the Haemostasis, Thrombosis and Vascular Biology Unit (A.B., G.Y.H.L.), University Department of Medicine, City Hospital, Birmingham, UK, and Center for Cardiovascular Disease Prevention (P.M.R.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Dr AD Blann, PhD, MRCPath, Haemostasis, Thrombosis, and Vascular Biology Unit, University of Birmingham, University Department of Medicine, City Hospital, Dudley Rd, Birmingham B18 7QH, UK. E-mail a.blann@bham.ac.uk

Key Words: cell adhesion molecules • inflammation • risk factors • stroke, ischemic

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

Since their development approximately a decade ago, cell adhesion molecules have been attracting interest for a number of reasons. For example, the blockade of the interaction between leukocytes and the endothelium by agents that mimic or inhibit these adhesion molecules may provide the basis for a new class of therapeutic agents, although promising studies in animals^1–3 have yet to be translated into products proven to be effective in humans. Study of the expression of the molecules on the surface of various cells or of the soluble form in the plasma may provide insights into their role(s) in pathophysiology in cardiovascular, connective tissue and neoplastic diseases,^4,5 and differences in levels of soluble cell adhesion molecules in the plasma may be useful tools in stratifying disease severity or prognosis.^6,7 However, these aspects may be related, as soluble forms themselves may interfere with leukocyte/endothelial cell interactions, at least in vitro.^8,9 Despite this, soluble adhesion molecules may be useful in dissecting the pathophysiological events in cardiovascular disease, as it may be presumed that changes in levels may relate to activation or damage to various cells such as the platelet and endothelium.

The selectin family of adhesion molecules has two principal members. Soluble P-selectin is believed to be the product of activated platelets, although the endothelium displays a membrane-bound form.^10,11 Increased levels are found in a number of conditions, including thrombotic disorders, diabetes, and ischemic heart disease,^12,13 and raised levels predict adverse events,¹⁴ even in apparently healthy individuals.¹⁵ Although increased levels of soluble E-selectin are . . . [Full Text of this Article]

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