Editorial
Inflammatory role of platelets in acute coronary syndromes
| The first 150 words of the full text of this article appear below. |
Increasing
evidence shows that inflammatory mediators play a pathogenic role in
atherogenesis and acute coronary syndrome.1 In particular,
several reports suggest that inflammatory cytokines such as tumour
necrosis factor 
(TNF), interleukin (IL)-1 and various chemokines
(for example, IL-8) may enhance degradation of the connective tissue
matrix protein by activating matrix metalloproteinases (MMPs) and
induce apoptosis of cells within the atherosclerotic lesion, promoting
plaque destabilisation and rupture.1 2 These findings
indicate a pathogenic link between persistent immune activation and
plaque rupture in coronary artery disease. It is well established that
platelets also contribute to the pathogenesis of acute coronary
syndromes by promoting thrombus formation. However, recent studies
suggest that these cells also may trigger an acute coronary event
through other mechanisms, such as stimulation of an inflammatory
response within the atherosclerotic plaque.
Several lines of evidence support a role for platelets as
inflammatory cells. Firstly, platelets provide
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