EPA is an essential fatty acid that we all need.
It has been shown to reduce arterial calcification in rats: www.ncbi.nlm.nih.gov/pubmed/21193197
Arterial medial calcification (NYSE:AMC) was induced by administering warfarin (3 mg/g food) and vitamin K1 (1.5 mg/g food) for 2 weeks in Sprague-Dawley rats (control group), and EPA (1 g/kg/day) was administered for 2 weeks simultaneously with warfarin and vitamin K1 (EPA group) or after initiation of AMC (late EPA group). EPA showed a marked reduction of medial calcification in the EPA group, and showed a similar effect in the late EPA group. Immunohistochemical and RT-PCR analyses showed that EPA lowered the expression of osteogenetic markers, such as osteopontin, alkaline phosphatase and core binding factor-α1 in the aorta. Significant migration of macrophages with expression of matrix-metalloproteinase (NYSE:MMP)-2 or MMP-9 was observed in the aortic adventitia around calcification. EPA also reduced macrophage infiltration, MMP-9 expression as well as gene expression of monocyte chemotactic protein (MCP)-1.CONCLUSIONS:
These observations indicate that EPA attenuates arterial medial calcification through an effect associated with the suppression of MMP-9 activity and inhibition of macrophage infiltration as well as osteogenic protein expression in warfarin-induced rat models.
EPA has been shown to increase the number of Endothelial Progenitor Cells and colony forming units, in vitro: www.ncbi.nlm.nih.gov/pubmed/
Endothelial dysfunction is pivotal in atherosclerosis. Endothelial progenitor cells (NYSE:EPC) predict cardiovascular events and could serve as a cellular biomarker of endothelial function...
Incubation with DHA and EPA, either alone or in combination significantly increased the number of EPCs and colony forming units (CFU). In addition, co-incubation with DHA + EPA, significantly enhanced EPC migratory capacity, adhesive properties and greater incorporation into tubules. Thus, EPA + DHA are effective in improving EPC number and functionality in-vitro.
This study found a correlation between the amount of EPA in a plaque and its stability and decreased inflammation: www.ncbi.nlm.nih.gov/pubmed/20542512
However, the EPA content of plaque phospholipids was inversely associated with plaque instability (P=0.0209), plaque inflammation (P=0.0108), the number of T cells in the plaque (P=0.0097) and a summary score considering a range of plaque features (P=0.0425). Plaques from patients who received n-3 PUFAs had significantly lower levels of mRNA for matrix metalloproteinases (MMP)-7 (P=0.0055), -9 (P=0.0048) and -12 (P=0.0044) and for interleukin-6 (P=0.0395) and intercellular adhesion molecule 1 (P=0.0142).CONCLUSIONS:
Atherosclerotic plaques readily incorporate EPA. A higher plaque EPA content is associated with a reduced number of foam cells and T cells, less inflammation and increased stability.
Disclosure: I am long AMRN.