Strategies such as vaccination against antigens promoting atherogenesis, cyclooxygenase inhibitors, statins and ACE inhibitors may reduce the levels of inflammatory markers and other potential targets, but their impact on overall cardiovascular risk is largely unknown.Things are really heating up in Trove, so stay cool this summer and save big with these super chill offers available for you! Numerous associations have been made, and targets suggested for pharmacotherapy, but few have demonstrated real promise in terms of disease prevention or regression. While some of these factors appear to be independent of traditional risk factors, and some may ultimately prove to be useful as biomarkers for risk of disease progression and clinical events, they do not necessarily represent targets for pharmacotherapy.

Many of these factors are also detectable systemically and have been hypothesised as markers of atherosclerosis and plaque instability. Several cell types within the plaque, in particular monocyte derived macrophages and T-lymphocytes, are known to produce a large range of factors including cytokines, chemokines, proteolytic enzymes, growth factors and disintegrins which perpetuate a cycle of endothelial cell activation, smooth muscle cell proliferation, lipid deposition, inflammation and lesion progression, culminating in acute plaque destabilisation. This review will highlight the local and systemic factors associated with disease progression and acute plaque destabilisation, the current role of therapeutic agents and the potential for targeted plaque modification. However, despite much scientific promise with in vitro cell and animal models, there has been much less success in modulation of these processes in clinical practice. Furthermore, many potential biomarkers of vascular disease have generated interest in terms of monitoring disease activity and the effect of therapeutic agents.

Many potential targets have been identified for therapeutic intervention aimed at disease prevention, plaque stabilisation and regression.

Our understanding of the events that occur within atherosclerotic plaques has improved dramatically over the last 2 decades, particularly with regard to the role of plaque destabilisation and the onset of clinical ischaemic syndromes.

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