| Abstract: | Our understanding of the mechanisms underlying acute coronary syndromes has evolved beyond the view that this syndrome reflects a progressive collection of lipids and cellular debris in the vascular wall. Current evidence has implicated a role for inflammation in the pathogenesis of this process. Thus, inflammatory cytokines may attenuate interstitial collagen synthesis, increase matrix degradation and promote apoptosis in several atheroma-associated cell types, and all these cellular events may enhance plaque vulnerability. Recently, a series of experimental studies have reported the plaque-stabilising effects of immunomodulatory therapy such as chemokine blockade, anti-CD40 ligand and IL-10. It is conceivable that some of these approaches will be tested clinically and, if successful, they could provide novel treatment strategies for atherosclerotic plaque stabilisation. |
