LOW-MOLECULAR-WEIGHT HEPARIN AND THE HEPARIN MOBILIZABLE POOL OF PLATELET-FACTOR-4 ARE REDUCED IN YOUNG SURVIVORS OF MYOCARDIAL-INFARCTION

The platelet factor 4 (PF4) mobilisation properties of low molecular w eight heparin (Fraxiparine, Sanofi Winthrop, France) in young survivor s of myocardial infarction (YSMI) and healthy volunteers have been inv estigated. The study group consisted of 42 YSMI less than 44 years old , all of them with angiographically proven occlusive coronary artery d isease, studied 6 to 24 months alter the acute event. The control grou p was composed of 30 healthy men of similar age. Subjects from the stu dy and control groups were allocated to the following subgroups : thos e receiving 60 or 120 IU/kg b.w. of standard heparin (Polfa Kutno, Pol and) and those receiving 60, 120 or 180 IC anti-Xa U/kg b.w. of low mo lecular weight heparin (Fraxiparine, Sanofi Winthrop, France) as a sin gle intravenous injection. Additionally, in five YSMI patients the inf luence of prolonged aspirin administration (0.3g daily for more than 3 0 days) on the Fraxiparine mobilisable pool of PF4 and beta-thromboglo bulin (beta-TG) concentration in the plasma was determined after injec tion of 180 IC anti-Xa U/kg b.w. of the drug. The PF 4 and beta-TG con centration in the plasma was evaluated using enzyme immunoassay method s before heparin or Fraxiparine intravenous injection and 2, 5, 10, 20 , 30 and 60 min after. In both, the control and YSMI groups baseline P F4 levels were found to be normal. Moreover, similar marked dose-depen dent increases of PF4 concentration in the plasma measured after 60 an d 120 IU/kg b.w. of heparin as well as after 60 and 120 IC anti-Xa U/k g 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 compar ed to healthy controls. The same phenomenon was observed when 180 IC a nti-Xa U/kg b.w. of Fraxiparine was injected intravenously. In YSMI tr eatment with aspirin had no influence on the Fraxiparine mobilisable p ool 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 tha t reduction of heparin- or Fraxiparine-releasable pool of PF4 may refl ect an impaired endothelium function, probably due to atherosclerosis.