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Postprandial triglycerides and blood coagulation.

A Silveira1

  • 1Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Institutet, Karolinska Hospital, Stockholm, Sweden. angela.silveira@ks.se

Experimental and Clinical Endocrinology & Diabetes : Official Journal, German Society of Endocrinology [And] German Diabetes Association
|July 17, 2001
PubMed
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Post-meal high triglycerides can create a procoagulant state, increasing risks for coronary heart disease through elevated factor VIIa and PAI-1 levels, impacting blood clotting and fibrinolysis.

Area of Science:

  • Cardiovascular Science
  • Hemostasis and Thrombosis

Background:

  • The postprandial state, following meals, occupies a significant portion of daily life.
  • Postprandial triglyceridemia is linked to increased risk of coronary heart disease (CHD).
  • Disturbances in blood coagulation and fibrinolysis, particularly elevated activated factor VII (VIIa) and plasminogen activator inhibitor-1 (PAI-1), characterize this state.

Purpose of the Study:

  • To investigate the role of postprandial triglyceridemia in hemostatic system disturbances.
  • To explore the connection between hypertriglyceridemia and coronary heart disease (CHD).
  • To elucidate the mechanisms linking elevated factor VIIa and PAI-1 to thrombotic events.

Main Methods:

  • Analysis of plasma levels of activated factor VII (VIIa) and plasminogen activator inhibitor-1 (PAI-1) in the postprandial state.

Related Experiment Videos

  • Correlation of factor VII coagulant activity (VIIc) with serum lipid concentrations.
  • In vivo studies using coagulation factor-deficient patients to determine the role of factor IX.

    • Main Results:

    • Elevated plasma levels of VIIa and PAI-1 are observed during postprandial triglyceridemia, indicating a procoagulant state.
    • Factor VII coagulant activity (VIIc) is an independent predictor of myocardial infarction and fatal coronary events.
    • Postprandial activation of factor VII is lipolysis-dependent, primarily mediated by VLDL, and requires factor IX.

    Conclusions:

    • Disturbances in the hemostatic system during postprandial triglyceridemia, specifically elevated VIIa and PAI-1, may partly explain the link between hypertriglyceridemia and CHD.
    • Increased VIIa generation in the postprandial state heightens the potential for thrombin production upon plaque rupture.
    • Elevated PAI-1 levels postprandially enhance the risk of thrombotic occlusion following atherosclerotic plaque rupture.