Abstract

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. We included 156 elderly patients 2-8 weeks after suffering an acute myocardial infarction from the OMEMI cohort. Subjects were randomly allocated to receive 930mg EPA+660mg 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. 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. In elderly Norwegians who have suffered a recent acute myocardial infarction and treated as per guidelines, long-term supplementation with 1.8g/day n3 PUFA does not modulate prothrombotic MV release from blood and vascular cells. URL: https://www.clinicaltrials.gov; Unique identifier: NCT01841944.

Highlights

  • Circulating microvesicles are a subset of large extracellular vesicles originated by cell membrane budding and released to the bloodstream by almost all cell types

  • Considering that Circulating microvesicles (cMV) exposing phosphatidylserine are prothrombotic, and the potential antithrombotic effects of n6 PUFA in the intervention (n3 PUFA), we aimed to evaluate the effects of long-term n3 PUFA supplementation on prothrombotic cMV release from cells of the vascular compartment in elderly subjects with a recent acute myocardial infarction (AMI), and thereby at very high risk of cardiovascular disease (CVD)

  • No significant differences were observed in changes in any cMV phenotype between n3 PUFA and the placebo after oneyear of intervention

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Summary

Introduction

Circulating microvesicles (cMV) are a subset of large extracellular vesicles originated by cell membrane budding and released to the bloodstream by almost all cell types. 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. At inclusion and after one-year follow-up, prothrombotic [annexin V (AV)þ] cMV derived from blood and vascular cells were phenotyped by flow cytometry. After one-year follow-up, total AVþ, platelet-derived CD61þ/AVþ, and endothelial-derived CD31þ/AVþ and CD31þ/CD42bÀ/AVþ cMV increased significantly in both groups. In the n3 PUFA supplemented group, platelet-derived CD62Pþ/AVþ, CD42bþ/AVþ and CD31þ/CD42bþ/AVþ; leukocytederived CD62Lþ/AVþ, CD45þ/AVþ, and CD11bþ/AVþ, as well as endothelial derived CD146þ/AVþ, CD62Eþ/AVþ, and CD309þ/AVþ cMV increased significantly. 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.

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