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The successful evolution of humans has included a highly complex and interwoven series of pathways that govern the balances of lipid storage and mobilisation, thrombosis and thrombolysis, and inflammation and immunity.1 Atherosclerotic heart disease in many respects represents an ‘abundance of success’ in storing fat, mounting an inflammatory response to oxidised lipids, and producing a prothrombotic response to inflammation and endothelial abnormalities. The culmination of ischaemic heart disease, an acute myocardial infarction (AMI), produces a much larger secondary inflammatory wave in response to tissue injury, and this wave can produce additional myocardial injury and mechanical dysfunction.2 Separately, it is known that states of chronic inflammation, even those remote from the cardiovascular system such as rheumatologic disorders, result in an increased risk of atherosclerotic heart disease and myocardial infarction. It follows, therefore, that potent anti-inflammatory therapies may be of benefit in the setting of AMI.
Cytokines, the so-called ‘hormones of inflammation’, are proteins produced by inflammatory cells to invoke a response in other nearby and remote cells. Tissue necrosis factor α (TNFα), an acute phase cytokine, is produced by macrophages and lymphocytes and stimulates the vascular endothelium to produce cellular adhesion molecules. These adhesion molecules, such as platelet–endothelial cell adhesion molecule and endothelial–leucocyte adhesion molecule, cause reactive cells (platelets and leucocytes) to bind to the endothelium and to each other. Platelets also have surface receptors for TNF, and their stimulation theoretically may promote platelet activation, CD40L release, and aggregation.3 ,4 In cardiovascular medicine, elevated concentrations of TNFα have been demonstrated in worsening ischaemic heart disease, AMI, and decompensated heart failure, and persistently elevated values are predictive of recurrent myocardial infarction.5
Etanercept is a biopharmaceutical agent developed for …
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