Thromb Haemost 2002; 87(03): 477-482
DOI: 10.1055/s-0037-1613028
Review Article
Schattauer GmbH

Factor VII Activation, Apolipoprotein A-I and Reverse Cholesterol Transport: Possible Relevance for Postprandial Lipaemia

Authors

  • G. J. Miller

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • C. J. Cooke

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • M. N. Nanjee

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • D. J. Howarth

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • J. A. Cooper

    1   MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK
  • I. P. Stepanova

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
  • J. H. Morrissey

    3   Department of Biochemistry, University of Illinois College of Medicine, Urbana, IL, USA
  • N. E. Miller

    2   Department of Cardiovascular Biochemistry, St Bartholomew’s and Royal London School of Medicine and Dentistry, London, UK
Further Information

Publication History

Received 24 July 2001

Accepted after resubmission 05 December 2001

Publication Date:
14 December 2017 (online)

Preview

Summary

Postprandial lipaemia is associated with activation of factor VII (FVII) and efflux of cholesterol from tissues to nascent plasma high density lipoproteins (HDL) containing apolipoprotein A-I (apo A-I). To determine whether FVII activation and cholesterol efflux occur together in other situations, the responses to intravenous infusion of HDL-like apo A-I/phosphatidylcholine discs were measured in 10 healthy men. Disc infusion (40 mg apo A-I/kg body weight) over 4 h was followed by increases in HDL cholesteryl ester and plasma apo A-I (p <0.0001). Significant activation of FVII was apparent during infusion in fasting subjects (p = 0.03), activated FVII averaging 123% of baseline value by 12 h (p <0.0001). Plasma thrombin-antithrombin (TAT) complex increased to 156% of baseline level by 12 h (p >0.05) but individual responses differed considerably. Peak TAT post-infusion was associated inversely with peak HDL triglyceride concentration (p = 0.004). The coagulation responses to disc-infusion may be due to transfer of phosphatidylserine to cell surfaces during cholesterol efflux.