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Thromb Haemost 1992; 67(05): 503-506
DOI: 10.1055/s-0038-1648481
Original Articles
Schattauer GmbH Stuttgart

Gemfibrozil Reduces Plasma Prothrombin Fragment F1+2 Concentration, a Marker of Coagulability, in Patients with Coronary Heart Disease

H C Wilkes
1   MRC Epidemiology and Medical Care Unit, Northwick Park Hospital, Harrow, UK
,
T W Meade
1   MRC Epidemiology and Medical Care Unit, Northwick Park Hospital, Harrow, UK
,
S Barzega
2   Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts, USA
,
A J Foley
1   MRC Epidemiology and Medical Care Unit, Northwick Park Hospital, Harrow, UK
,
L O Hughes
4   The Department of Cardiology, Northwick Park Hospital, Harrow, UK
,
K A Bauer
2   Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts, USA
,
R D Rosenberg
2   Charles A. Dana Research Institute and Harvard-Thorndike Laboratory, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts, USA
3   Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA
,
G J Miller
1   MRC Epidemiology and Medical Care Unit, Northwick Park Hospital, Harrow, UK
› Author Affiliations
Further Information

Publication History

Received 11 September 1991

Accepted after revision 08 November 1991

Publication Date:
03 July 2018 (online)

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Summary

The effects of gemfibrozil on several indices of haemostatic activity were explored in male patients with coronary heart disease (CHD). Sixty-three of 71 patients completed a crossover study in which gemfibrozil 1,200 mg/day and matching placebo were each taken in randomised order for 2 months in a doubleblind manner, separated by a 2-month washout period. Serum cholesterol decreased by an average (95% confidence interval) of 12 (9 to 15)% and non-fasting triglyceride concentration by 43 (34 to 51)% during active treatment. Plasma prothrombin fragment Fi + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase. Factor VII coagulant activity (VIIC) and antigen concentration, and fibrinopeptide A concentration were not influenced by gemfibrozil in the group overall. However, the VIIC response appeared to be dependent upon the untreated cholesterol level. Hypercholesterolaemic men (cholesterol >6.5 mmol/1) experienced a significant reduction in VIIC averaging 6% of standard during active therapy. Other effects of gemfibrozil were a 5 (2 to 9)% increase in plasma fibrinogen by a gravimetric method, an 11 (8 to 13)% increase in platelet count, and a 6 (2 to 10)% reduction in white cell count. The reduced incidence of CHD following gemfibrozil therapy in hyperlipidaemic patients may arise in part through a reduction in procoagulant activity and thus the risk of an occlusive coronary thrombosis.

 

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