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Updated: May 30, 2026

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
Published on: November 22, 2024
Dose-dependent decrease of platelet activation and tissue factor by omega-3 polyunsaturated fatty acids in patients
Deddo Moertl1, Rudolf Berger, Alexandra Hammer
1Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. deddo.moertl@meduniwien.ac.at
Insights
Omega-3 polyunsaturated fatty acids (n3-PUFA) reduce platelet activation and tissue factor (TF) in chronic heart failure (CHF) patients. Higher doses also offer anti-inflammatory benefits, improving outcomes in severe CHF.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Chronic heart failure (CHF) involves neuroendocrine and inflammatory pathways, promoting a prothrombotic state.
- Omega-3 polyunsaturated fatty acids (n3-PUFA) show mortality benefits in CHF, but mechanisms are unclear.
- Investigating n3-PUFA's impact on platelet activation and thrombogenesis in severe CHF is crucial.
Purpose of the Study:
- To investigate the effects of n3-PUFA on platelet activation and thrombogenesis markers in severe CHF patients.
- To determine the dose-dependent effects of n3-PUFA on these markers.
Main Methods:
- Thirty-six patients with severe non-ischaemic CHF received 1g/day or 4 g/day n3-PUFA, or placebo for 12 weeks.
- Whole-blood flow cytometry assessed monocyte-platelet aggregates (CD14+/CD42b+) and monocytic tissue factor (TF).
- Plasma levels of P-selectin, sCD40L, fibrinogen, prothrombin fragment F1.2, TF, and inflammatory markers were measured.
Main Results:
- n3-PUFA significantly reduced monocyte-platelet aggregates dose-dependently.
- 4 g/day n3-PUFA decreased P-selectin and prothrombin fragment F1.2, and reduced plasma TF and TF+-monocytes dose-dependently.
- Higher n3-PUFA dosage showed anti-inflammatory effects, reducing hs interleukin-6 and hsTNF-alpha.
Conclusions:
- n3-PUFA treatment in severe CHF patients leads to a dose-dependent decrease in platelet activation and tissue factor.
- Higher n3-PUFA dosages provide anti-inflammatory effects, potentially contributing to observed clinical benefits.
- These findings elucidate mechanisms for n3-PUFA's efficacy in managing severe chronic heart failure.
Abstract:
Chronic heart failure (CHF) is characterised by activation of neuroendocrine and inflammatory pathways, and both are linked to a prothrombotic state. Treatment with omega-3 polyunsaturated fatty acids (n3-PUFA) showed significant benefits including mortality reduction in CHF, but exact mechanisms of action are still unclear. We investigated the effects of n3-PUFA on markers of platelet activation and thrombogenesis in patients with severe CHF. Thirty-six patients with non-ischaemic CHF (LVEF<35%, NYHA class>2) under optimised therapy were randomised to supplementation with 1g/day or 4 g/day n3-PUFA, or placebo for 12 weeks. Using whole-blood flow cytometry, monocyte-platelet aggregates characterised by CD14+/CD42b+ co-expression and monocytic tissue factor (TF) were determined. Plasma levels of P-selectin, sCD40L, fibrinogen, prothrombin fragment F1.2, TF and pro-inflammatory markers (high sensitive[hs] interleukin-6, hsCRP, hsTNF-alpha, monocyte chemotactic protein-1) were measured by immunoassay. Supplementation with 1g/day and 4 g/day n3-PUFA but not placebo significantly reduced monocyte-platelet aggregates in a dose-dependent manner (p for trend = 0.02 across the groups). A dose of 4 g/day but not 1g/day n3-PUFA significantly decreased P-selectin (p = 0.03). Plasma TF decreased dose-dependently upon n3-PUFA supplementation (p for trend = 0.02), paralleled by a significant decrease of TF+-monocytes (p for trend = 0.01). The amount of 4 g/day n3-PUFA exhibited modest anti-inflammatory effects with a significant reduction of hs interleukin-6 (p<0.01) and a trend-wise reduction of hsTNF-alpha (p = 0.09). No changes were seen for sCD40L, fibrinogen, hsCRP and monocyte chemotactic protein-1, while F1.2 was decreased by 4 g/day n3-PUFA (P = 0.03). In patients with severe non-ischaemic CHF, treatment with n3-PUFA leads to a dose-dependent decrease of platelet activation and TF. Higher dosage exhibits also anti-inflammatory effects.
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