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

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
› Author Affiliations
Further Information

Publication History

Received 24 July 2001

Accepted after resubmission 05 December 2001

Publication Date:
14 December 2017 (online)

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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.