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Related Experiment Videos

Decrease in factor VII coagulant activity during percutaneous transluminal coronary angioplasty by heparin-mediated

M Mukherjee1, M F Scully, V V Kakkar

  • 1Thrombosis Research Institute, Chelsea, London, UK.

Thrombosis and Haemostasis
|April 1, 1997
PubMed
Summary
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Heparin reduces factor VII coagulant activity (FVII:C) by approximately 30% after coronary angioplasty. This effect appears linked to decreased triglyceride levels, suggesting heparin

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biochemistry

Background:

  • Heparin is a widely used anticoagulant.
  • The extrinsic pathway of coagulation is initiated by tissue factor and factor VII.
  • The relationship between lipids and coagulation factors requires further investigation.

Purpose of the Study:

  • To investigate the effect of heparin on factor VII coagulant activity (FVII:C) and factor VIIa antigen (FVIIa:Ag).
  • To explore the potential role of triglycerides in modulating FVII:C levels.
  • To assess heparin's indirect antithrombotic potential via lipid modulation.

Main Methods:

  • Measurement of FVII:C and FVIIa:Ag in ten patients before and up to 6 hours after heparin administration during percutaneous transluminal coronary angioplasty (PTCA).

Related Experiment Videos

  • Monitoring of triglyceride levels and tissue factor antigen.
  • Statistical analysis to determine significant changes.

    • Main Results:

    • A significant and sustained decrease (approx. 30%) in FVII:C was observed post-heparin.
    • No significant change in FVIIa:Ag or tissue factor antigen levels.
    • A concurrent significant reduction in triglyceride levels, likely due to heparin-induced lipase activity.
    • The decrease in FVII:C correlated with the decrease in triglycerides.

    Conclusions:

    • Heparin administration leads to a significant reduction in FVII:C, independent of FVIIa:Ag levels.
    • Findings suggest a lipid (triglyceride) dependence of FVII:C.
    • Heparin may exert an indirect antithrombotic effect by limiting lipid-dependent coagulation activation.