title: Relation of fish oil supplementation to markers of atherothrombotic risk in patients with cardiovascular disease not receiving lipid-lowering therapy.
abstract: Fish oil supplementation (FOS) is known to have cardiovascular benefits. However, the effects of FOS on thrombosis are incompletely understood. We sought to determine if the use of FOS is associated with lower indices of atherothrombotic risk in patients with suspected coronary artery disease (sCAD). This is a subgroup analysis of consecutive patients with sCAD (n=600) enrolled in the Multi-Analyte, Thrombogenic, and Genetic Markers of Atherosclerosis study. Patients on FOS were compared with patients not on FOS. Lipid profile was determined by vertical density gradient ultracentrifugation (n=520), eicosapentaenoic acid+docosahexaenoic acid was measured by gas chromatography (n=437), and AtherOx testing was performed by immunoassay (n=343). Thromboelastography (n=419), ADP- and collagen-induced platelet aggregation (n=137), and urinary 11-dehydrothromboxane B2 levels (n=259) were performed immediately before elective coronary angiography. In the total population, FOS was associated with higher eicosapentaenoic acid+docosahexaenoic acid content (p<0.001), lower triglycerides (p=0.04), total very low-density lipoprotein cholesterol (p=0.002), intermediate-density lipoprotein cholesterol (p=0.02), and AtherOx levels (p=0.02) but not in patients on lipid-lowering therapy. Patients not on lipid-lowering therapy taking FOS had lower very low-density lipoprotein cholesterol, intermediate-density lipoprotein cholesterol, remnant lipoproteins, triglycerides, low-density lipoprotein cholesterol, AtherOx levels, collagen-induced platelet aggregation, thrombin-induced platelet-fibrin clot strength, and shear elasticity (p<0.03 for all). In clopidogrel-treated patients, there was no difference in ADP-induced aggregation between FOS groups. Patients on FOS had lower urinary 11-dehydrothromboxane B2 levels regardless of lipid-lowering therapy (p<0.04). In conclusion, the findings of this study support the potential benefit of FOS for atherothrombotic risk reduction in sCAD with the greatest benefit in patients not receiving lipid-lowering therapy. Future prospective studies to compare FOS with lipid-lowering therapy and to assess the independent effects of FOS on thrombogenicity are needed.
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Franzese
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland.
authors.forename: Kevin P
authors.initials: KP
authors.lastname: Bliden
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland.
authors.forename: Martin G
authors.initials: MG
authors.lastname: Gesheff
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland.
authors.forename: Shachi
authors.initials: S
authors.lastname: Pandya
authors.affiliation: Department of Chemistry, Indiana University South Bend, South Bend, Indiana.
authors.forename: Kirk E
authors.initials: KE
authors.lastname: Guyer
authors.affiliation: Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
authors.forename: Anand
authors.initials: A
authors.lastname: Singla
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland.
authors.forename: Udaya S
authors.initials: US
authors.lastname: Tantry
authors.affiliation: Department of Preventive Cardiology, CGH Medical Center, Sterling, Illinois; Clinical Family and Community Medicine, University of Illinois College of Medicine, Peoria, Illinois.
authors.forename: Peter P
authors.initials: PP
authors.lastname: Toth
authors.affiliation: Sinai Center for Thrombosis Research, Sinai Hospital, Baltimore, Maryland. Electronic address: pgurbel@lifebridgehealth.org.
authors.forename: Paul A
authors.initials: PA
authors.lastname: Gurbel
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood* / Q000628:therapy / Q000652:urine; D019587:Dietary Supplements; D004281:Docosahexaenoic Acids / Q000097:blood; D015118:Eicosapentaenoic Acid / Q000097:blood; D005260:Female; D005395:Fish Oils / Q000627:therapeutic use*; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013916:Thrombelastography; D013927:Thrombosis / Q000209:etiology / Q000378:metabolism*; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D005395:Fish Oils; D008074:Lipoproteins; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D013929:Thromboxane B2; C049235:11-dehydro-thromboxane B2; D002784:Cholesterol; D015118:Eicosapentaenoic Acid