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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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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

Thrombosis and Haemostasis
|July 30, 2011
PubMed
Summary

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.

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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.