lerotic plaques and reducing the incidence of thrombus formation (Plutzky, 1999; Thies et al., 2003). Furthermore, n-3 PUFAs can enrich cell membranes and alter the lipid raft structure and function leading to improved organelle and cellular function (Din et al., 2008), autonomic tone (Abuissa, O'Keefe Jr., Harris, & Lavie, 2005; O'Keefe Jr., Abuissa, Sastre, Steinhaus, & Harris, 2006), elevated arrhythmic thresholds (Anand, Alkadri, Lavie, & Milani, 2008) and ameliorating hypertension (Geleijnse, Giltay, Grobbee, Donders, & Kok, 2002; O'Keefe Jr. et al., 2006). Importantly, several experimental, clinical and epidemiological studies hypothesize that the cardioprotective effects of n-3 PUFAs and their metabolites are attributed mainly to their immunomodulatory properties. Notably, emerging evidence demonstrates the ability of n-3 PUFAs to reduce circulating levels of inflammatory chemokines, cytokines, and the pro-inflammatory metabolites derived from n-6 PUFAs (Calder, 2013, Calder,