The
platelet factor 4 (PF4) mobilisation properties of
low molecular weight heparin (
Fraxiparine,
Sanofi Winthrop, France) in young survivors of
myocardial infarction (YSMI) and healthy volunteers have been investigated. The study group consisted of 42 YSMI less than 44 years old, all of them with angiographically proven occlusive
coronary artery disease, studied 6 to 24 months after the acute event. The control group was composed of 30 healthy men of similar age. Subjects from the study and control groups were allocated to the following subgroups: those receiving 60 or 120 IU/kg b.w. of standard
heparin (Polfa Kutno, Poland) and those receiving 60, 120 or 180 IC anti-Xa U/kg b.w. of
low molecular weight heparin (
Fraxiparine,
Sanofi Winthrop, France) as a single
intravenous injection. Additionally, in five YSMI patients the influence of prolonged
aspirin administration (0.3g daily for more than 30 days) on the
Fraxiparine mobilsable pool of PF4 and
beta-thromboglobulin (beta-TG) concentration in the plasma was determined after injection of 180 IC anti-Xa U/kg b.w. of the
drug. The PF 4 and beta-TG concentration in the plasma was evaluated using
enzyme immunoassay methods before
heparin or
Fraxiparine intravenous injection and 2, 5, 10, 20, 30 and 60 min after. In both, the control and YSMI groups baseline PF4 levels were found to be normal. Moreover, similar marked dose-dependent increases of PF4 concentration in the plasma measured after 60 and 120 IU/kg b.w. of
heparin as well as after 60 and 120 IC anti-Xa U/kg b.w. of
Fraxiparine was found. The administration of 120 IU/kg b.w. of
heparin resulted in a reduced rise in plasma PF 4 in YSMI as compared to healthy controls. The same phenomenon was observed when 180 IC anti-Xa U/kg b. w. of
Fraxiparine was injected intravenously. In YSMI treatment with
aspirin had no influence on the
Fraxiparine mobilisable pool of PF 4 or the beta-TG concentration in the plasma. These results suggest that mobilisable pool of
platelet factor 4 in young survivors of
myocardial infarction derives from the "nonplatelet pool" and that reduction of
heparin- or
Fraxiparine-releasable pool of PF4 may reflect an impaired endothelium function, probably due to
atherosclerosis.