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Cardiovascular Research 2004 63(2):192-193; doi:10.1016/j.cardiores.2004.05.007
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Angiogenesis and platelets: the clot thickens further

Andrew D Blann*

Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Dudley Road, Birmingham, B18 7QH, UK

* Tel./fax: +44-121-507-5076. Email address: a.blann@bham.ac.uk

Received 10 May 2004; accepted 14 May 2004

The first 10% of the full text of this article appears below.

See article by Brill et al. [15] (pages 226–235) in this issue.

Pathophysiogical aspects of platelet biology have, until recently, focussed on their relatively passive and reactive roles in minimising blood loss after injury, in contributing to the final stages of cardiovascular disease (largely in the inappropriate formation of life-threatening thrombosis), and on attempts in the clinic, the cardiac catheter suite, and on the ward to reduce the latter with anti-coagulant and anti-platelet agents. However, there is currently a growing awareness that another pathophysiological process, inflammation, may be important in atherosclerosis and acute coronary . . . [Full Text of this Article]


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