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Isotopic platelet survival time (PST), platelet count, adhesiveness, aggregation, PF4 release and coagulation parameters were examined in 23 patients with prosthetic heart valves (6 mitral, 10 aortic and 7 mitroaortic Starr Edwards or Bjork valves) treated with or without suloctidil.The patients were distributed in 2 comparative groups : the treated group with 11 patients with VKA (nicoumalone) and suloctidil (600 mg/day) and the control group with 12 patients with VKA alone. The biological parameters were performed before (the 10th postop. day) and 6 weeks after treatment with or without suloctidil.Before treatment were : PST shortened, platelet adhesiveness and aggregation normal and PF4 release, factors I, VIII-C, VIII-R-Ag increased in both groups.After treatment, PST returned to normal in the treated group, but remained unchanged or was more decreased in the control group. Platelet adhesiveness and aggregation were unchanged in both groups. PF4 release was reduced in the treated group and unchanged in the control group. Platelet count, factors I, VIII-C, VIII-R-Ag returned to the preoperative values in both groups.Two severe thromboembolic complications appeared in the control group, none in the treated group.

Heparin cofactor activity is measured with the amidolytic method according to 0degard (1975) during in vitro coagulation and during bleeding.Heparin cofactor activity decreases differently during coagulation process of PRP or PFP. It is suggested this is due to heparin neutralization by PF4 and/or to thrombin formation. Antithrombin III level is not modified.During bleeding, the same phenomenon is observed when the amount of heparin in the buffer is low enough. Decrease in heparin cofactor activity is already observed on a sample collected less than 90 seconds after the puncture, before any detectable thrombin formation.Decrease in heparin cofactor activity during bleeding is studied in pathological conditions. It is more marked in some hypercoagulable states.

HNA is measured in several pathological conditions by a biological assay.PFP, platelets and serun are compared.In PFP, HNA/ml is high in thrombocytosis, in acute DIC and in some thrombotic states; it is normal in most cases of thrombocytopenia. When expressed as units/109 platelets, PFP’s HNA is low in thrombocytopenia from hepatic origin.HNA/ml of PFP decreases during treatment with suloctidil; these last results are related to platelet survival time.Serum HNA, more than platelet HNA, reflects the antiheparin capacity of the blood and could be used to estimate the minimal amount of heparin required in therapy.