In general, the eicosanoids derived from AA have potent prothrombotic and proinflammatory activity. In contrast, the eicosanoids derived from EPA have reduced biological activity and are less prothrombo-tic and proinflammatory. Eicosanoid production is generally tightly controlled through homeostatic mechanisms. However, eicosanoid production can be significantly altered in situations in which endothelial dysfunction, atherosclerosis and plaque rupture, or various thrombotic or inflammatory conditions are present.
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