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Isolation of what is probably the main thrombin inhibitor antithrombin III (At-III) made the preparation of specific antisera for immunochemical analysis possible. When immunoelectrophoresis of At III against anti At III and anti whole human serum was performed a single precipitation arc was formed in the alpha 2-globulin region. When thrombin was added the apparent concentration of At III decreased. Serum concentration of At III is probably influenced by sex hormones since women of childbearing age have lower serum concentrations of At III. They are further decreased by oral contraceptive implying a relationship between the low At III levels and the tendency to thrombosis in women using oral contraceptives.

Objective. The aim of the present study was to determine the risk of major haemorrhagic complications, stroke and other cardiovascular events, and mortality during long-term anticoagulant therapy (ACT) in patients with cerebrovascular disease not included in any prospective trials. Design. The data were collected retrospectively. Setting. All patients with symptomatic cerebrovascular disease discharged from the Stroke Unit, Aker University Hospital, Oslo, with ACT (warfarin) during 1983 through to 1986 were included. Subjects. The material consists of 161 patients with a mean age of 67.8 (range 40–90) years. The reason for initiating ACT was frequent transient ischaemic attacks (TIAs) in 52 patients, stroke in progression (SIP) in 33 patients, and probable embolic stroke in 76 patients. International normalized ratio (INR) of 4.2–2.8 was aimed at. Main outcome measures. Major haemorrhagic complications, recurrent stroke and survival was determined for the total material, and in the subgroups non-valvular atrial fibrillation (NVAF, n = 49), TIAs, and SIP. Results. The mean duration of ACT was 21.1 (range 0.5–60.2) months with a total of 282.9 patient-years. The rate of major (including fatal) haemorrhagic complications was 4.6% per year, and the rate of fatal haemorrhagic complications was 1.4% per year. The complication rates in the subgroups of patients did not differ significantly from that in the total material. Only two out of the 13 major haemorrhagic complications occurred during the initial 6 months of ACT. No strokes occurred in the TIA subgroup. The rate of recurrent stroke (excluding intracranial haemorrhage) was 3.9% per year for all patients, 4.7% per year for the patients with NVAF, and 4.2% per year for the patients with SIP. Conclusions. The total results suggest a positive net effect of ACT in patients with NVAF and TIAs. Without comparable data, no definite conclusions concerning the effect of ACT on patients with SIP can be drawn. The rate of bleeding complications was similar to that in other studied materials and is not negligible. In patients with SIP and TIAs, ACT beyond 6 months should probably only be continued if aspirin is not tolerated or has proven ineffective in the particular patient.

Failure to lyse multiple small blood clots in the cerebrospinal fluid (CSF) reabsorption pathways may be one of the mechanisms leading to posthaemorrhagic ventricular dilatation (PHVD). It has been suggested that intraventricular administration of streptokinase may resolve PHVD but it is not known whether such treatment produces an increase in fibrin degradation products in the CSF. Ventricular CSF was collected from six infants with PHVD before and during intraventricular treatment with streptokinase 1000 units/h. In all six infants, CSF D dimer increased during streptokinase treatment. Median D dimer before treatment was 1642 micrograms/l and during treatment 5440 micrograms/l (p < 0.05). Undetectable D dimer levels in plasma during streptokinase treatment ruled out the possibility that D dimer had merely diffused into the CSF. This augmentation of local fibrinolysis may have therapeutic potential. There was no evidence of systemic fibrinolysis.

In order to prevent prosthetic valve endocarditis (PVE), the implantation of a new silver-coated sewing ring has been introduced to provide peri- and postoperative protection against microbial infection.A 56-year-old woman with aortic stenosis had elective replacement with a St. Jude Medical mechanical valve fitted with a silver-coated sewing ring (Silzone). The patient developed early PVE, which necessitated reoperation after one month. Despite a second Silzone prosthesis being implanted, the endocarditis recurred. During a third operation an aortic homograft was implanted, and after six months a fourth operation was performed for a pseudoaneurysm at the base of the homograft, in proximity to the anterior mitral valve leaflet.The diagnosis of PVE was confirmed by the presence of continuous fever, transesophageal echocardiography and growth of penicillin-resistant Staphylococcus epidermidis from the valve prosthesis.The implantation of all prosthetic valves is encumbered with a risk of endocarditis. Although silver has bacteriostatic actions, the advantages of silver-coated prostheses in the treatment of this condition have yet to be assessed in clinical trials.

The aim of this study was to measure plasminogen in the cerebrospinal fluid (CSF) of control neonates with no infection or haemorrhage and in infants who had suffered intraventricular haemorrhage (IVH). A chromogenic substrate method was used. The 16 reference infants had a median CSF plasminogen level of 0.74% of that of normal adult plasma (range 0.17-1.1%). The 11 infants with IVH had a median CSF plasminogen level of 0.55% of normal adult plasma (range 0-4.4%). Six of the IVH infants went on to develop permanent hydrocephalus despite the use of intraventricular plasminogen activators. Endogenous fibrinolysis and the potential for fibrinolytic treatment in the CSF may be limited by low concentrations of plasminogen, and administration of recombinant plasminogen may assist attempts to clear intraventricular blood clots.

Tissue factor pathway inhibitor (TFPI) controls activation of blood coagulation while antithrombin (AT) regulates the final stage. Both inhibitors inhibit the intermediate stage of activation. Subnormal levels of TFPI increase the risk of disseminated intravascular coagulation (DIC) in septic conditions, and the risk of occlusive thrombi over damaged vascular intima or fissured arteriosclerotic plaques. The risk of venous thrombosis is increased by subnormal AT or subnormal activity of the protein C system. In contrast, TFPI may be little involved in the control of deep venous thrombosis. Heparin strongly accelerates AT and releases TFPI to the blood. Both these effects may contribute to the antithrombotic effect of heparin. In septic DIC, heparin may contribute little to quench activation of coagulation. Once hereditary deficiency of TFPI is described, its biological role will be better understood.