title: Potential benefits of eicosapentaenoic acid on atherosclerotic plaques.
abstract: Residual cardiovascular (CV) risk remains in some patients despite optimized statin therapy and may necessitate add-on therapy to reduce this risk. Eicosapentaenoic acid (EPA), an omega-3 polyunsaturated fatty acid, lowers plasma triglyceride levels without raising low-density lipoprotein cholesterol levels and has potential beneficial effects on atherosclerotic plaques. Animal studies have shown that EPA reduces levels of pro-inflammatory cytokines and chemokines. In clinical trials utilizing a wide spectrum of plaque imaging modalities, EPA has shown beneficial effects on plaque characteristics. Studies of patients with coronary artery disease receiving statin therapy suggest that EPA may decrease plaque vulnerability and prevent plaque progression. EPA also decreased pentraxin-3 and macrophage accumulation. A large, randomized, Japanese study reported that EPA plus a statin resulted in a 19% relative reduction in major coronary events at 5years versus a statin alone in patients with hypercholesterolemia (P=0.011). Icosapent ethyl, a high-purity prescription form of EPA ethyl ester, has been shown to reduce triglyceride levels and markers of atherosclerotic inflammation. Results of an ongoing CV outcomes study will further define the potential clinical benefits of icosapent ethyl in reducing CV risk in high-risk patients receiving statin therapy.
authors.affiliation: California Cardiovascular Institute, 7061 N. Whitney, Suite 101, Fresno, CA 93720, United States. Electronic address: jr4nelson@yahoo.com.
authors.forename: J R
authors.initials: JR
authors.lastname: Nelson
authors.affiliation: Mountain Heart, 2000 South Thompson Street, Flagstaff, AZ 86001, United States.
authors.forename: O
authors.initials: O
authors.lastname: Wani
authors.affiliation: Intermountain Heart Institute, 5121 South Cottonwood Street, Murray, UT 84157, United States.
authors.forename: H T
authors.initials: HT
authors.lastname: May
authors.affiliation: Los Angeles Biomedical Research Institute at Harbor-UCLA, 1124 West Carson Street, Torrance, CA 90502, United States.
authors.forename: M
authors.initials: M
authors.lastname: Budoff
mesh_terms: D000818:Animals; D001158:Arteries / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D003952:Diagnostic Imaging / Q000379:methods; D004359:Drug Therapy, Combination; D015118:Eicosapentaenoic Acid / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D008055:Lipids; D015118:Eicosapentaenoic Acid
keywords: Atherosclerosis; Atherosclerotic plaque; Eicosapentaenoic acid; Eicosapentaenoic acid ethyl ester; Omega-3 fatty acids