One year of omega 3 polyunsaturated fatty acid supplementation does not reduce circulating prothrombotic microvesicles in elderly subjects after suffering a myocardial infarction.

Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullevål, 0450, Oslo, Norway; Department of Endocrinology and Nutrition, August Pi i Sunyer Biomedical Research Institute - IDIBAPS, Hospital Clínic of Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain; Faculty of Medicine, University of Oslo, 0372, Oslo, Norway. Electronic address: gchiva@clinic.cat. Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital Ullevål, 0450, Oslo, Norway; Faculty of Medicine, University of Oslo, 0372, Oslo, Norway. Department of Cardiology, Aalborg University Hospital, Denmark. Cardiovascular Program ICCC, Institut de Recerca Hospital Santa Creu i Sant Pau-IIB Sant Pau, Barcelona, Spain; Centro de Investigación Biomédica en Red Cardiovascular (CIBERCV), Instituto de Salud Carlos III (ISCIII), Madrid, Spain.

Clinical nutrition (Edinburgh, Scotland). 2021;(12):5674-5677
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Abstract

BACKGROUND & AIMS Circulating microvesicles (cMV) are both effectors and biomarkers of cardiovascular disease (CVD), and the effects of omega 3 polyunsaturated fatty acids (n3 PUFA) in MV shedding are not yet well known. Therefore, we aimed to investigate the effects of long-term n3 PUFA supplementation on cMV release from cells of the vascular compartment in elderly subjects at very high risk of CVD. METHODS We included 156 elderly patients 2-8 weeks after suffering an acute myocardial infarction from the OMEMI cohort. Subjects were randomly allocated to receive 930 mg EPA + 660 mg DHA (n3 PUFA intervention) or corn oil (56% linoleic acid, 32% oleic acid, 10% palmitic acid) used as placebo daily for two years. At inclusion and after one-year follow-up, prothrombotic [annexin V (AV)+] cMV derived from blood and vascular cells were phenotyped by flow cytometry. RESULTS No differences were observed in the levels of cMV between the randomized groups at inclusion in the study. After one-year follow-up, total AV+, platelet-derived CD61+/AV+, and endothelial-derived CD31+/AV+ and CD31+/CD42b-/AV+ cMV increased significantly in both groups. In the n3 PUFA supplemented group, platelet-derived CD62P+/AV+, CD42b+/AV+ and CD31+/CD42b+/AV+; leukocyte-derived CD62L+/AV+, CD45+/AV+, and CD11b+/AV+, as well as endothelial derived CD146+/AV+, CD62E+/AV+, and CD309+/AV+ cMV also increased significantly. No significant differences were however, observed in the changes of cMV levels between groups. CONCLUSION In elderly Norwegians who have suffered a recent acute myocardial infarction and treated as per guidelines, long-term supplementation with 1.8 g/day n3 PUFA does not modulate prothrombotic MV release from blood and vascular cells. REGISTRATION URL: https://www.clinicaltrials.gov; Unique identifier: NCT01841944.

Methodological quality

Publication Type : Randomized Controlled Trial

Metadata

MeSH terms : Myocardial Infarction