The proposed biochemical mechanism for the anti-platelet effect of omega n3 fatty acids is based on modifications in platelet prostaglandin metabolism (27-31). Cellular membranes are primarily composed of phospholipids (PL). The backbone of PL's is glycerol. The glycerol hydroxyl groups in position 1 and 2 bind two fatty acid molecules through formation of ester bonds (31). The third hydroxyl binds the so-called head group, which may be choline, inositol, ethanolamine or serine. At least in the case of platelets the fatty acid at the C-2 position is often the unsaturated arachidonic fatty acid (an omega n6 fatty acid). When Lovaza® is ingested (an omega n3 fatty acid), the unsaturated fatty acid at the C2 position can be DHA or EPA. Several important differences result from this substitution including an important effect on platelet function. As part of the platelet activation process, phospholipase A2 clips the fatty acid at the C-2 position, either arachidonic acid or DHA/EPA (31). In the case of the platelet, the fatty acid is then metabolized through an enzyme called COX-1 to a thromboxane (32-35). When the fatty acid is arachidonic acid, thromboxane A2 is synthesized (TxA2). TxA2 is a very potent platelet activator and vasoconstrictor. In the case of DHA or EPA, a series 3 TxA3 is synthesized, a poor platelet activator and vasoconstrictor (32-35). Production of TxA3 underlies the potential anti-platelet effect of Lovaza®.