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The presence of the 20210A allele of the prothrombin gene has recently been shown to be a risk factor of venous thromboembolism, probably mediated through increased prothrombin levels. The aim of the study was to determine the frequency of the prothrombin 20210A allele in 193 consecutive unselected patients with venous thromboembolism and 100 healthy controls and to analyze the clinical profile associated with this new inherited thrombophilic factor. In agreement with previous reports, we found a frequency of 7.3% of heterozygous carriers of the 20210A allele among patients and 1% among controls. We confirm that plasma prothrombin levels are more elevated in the individuals bearing the prothrombin 20210A allele compared with those who do not. We did not find any relationship between the presence of the prothrombin 20210A allele and either a family history of thromboembolism, the rate of recurrences or the age at disease onset. However, the co-inheritance in the same individual of both prothrombin 20210A allele and factor V Leiden was associated with a significantly lower age at disease onset suggesting a synergistic contribution of both abnormalities.

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OBJECTIVES: To assess the prevalence of activated protein C resistance (APC-R) among healthy subjects and thromboembolic patients and to determine the clinical characteristics associated with APC-R. DESIGN: A prospective study. SETTING: One academic medical centre. SUBJECTS: 91 health controls and 126 thromboembolic patients. MEASUREMENTS: Patients and control were genotyped for the factor V Leiden (VaQ506) mutation. The anticoagulant response of the patient's plasma to activated protein C was also determined. RESULTS: The frequency of APC-R was 3.3% among healthy control subjects and 22% among thrombotic patients of whom 18% were heterozygous and 4% were homozygous. The mean age at the first thrombotic event and the severity of thrombotic disease including the proportion of proximal deep vein thrombosis and the frequency of lung embolism were identical among APC-R positive and negative patients. A family history of thromboembolic disease was elicited more frequently in APC-R positive than in APC-R negative patients (57% vs. 22%, P < 0.001). The recurrence rate was higher for APCR-R positive patients (57% vs. 34%, P < 0.05). The percentage of cases with a factor predisposing to thrombosis was very similar in APC-R positive (57%) and negative (68%) patients. CONCLUSIONS: A familial history of thromboembolic disease and recurrences are significantly more frequent among APC-R positive than APC-R negative patients.

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Pregnancy induces several haemostatic perturbations. Some authors described possible acquired activated protein C resistance (APCR) during normal pregnancy. We wanted to test this possibility and to evaluate if this acquired APCR might contribute to the known increased tendency to thrombosis associated with pregnancy. To answer the first hypothesis, we tested APCR with standard and with modified (5) APTT assays; to explore the second one, we chose to test some hypercoagulability and hyperfibrinolysis markers, i.e. fibrinopeptide A (FPA), Fragment 1+2 (F1+2) and D-dimers, and to correlate them with APC-ratio.

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Mesenteric vein thrombosis (MVT) and particularly superior mesenteric vein thrombosis (SMVT) can induce 5 to 15 percent of mesenteric and intestinal infarctions in a small and large bowels. The thrombotic process can be idiopathic or consecutive to inherited or acquired thrombophilic states. The clinical diagnosis of this event remains difficult and requires always specific imaging investigation to treat as soon as possible. Its evolution and mortality rate are quite different than these observed in arterial mesenteric ischemic accident. Medical treatment with thrombolytic, anticoagulant, antiplatelet and antispasmodic agents, initiated promptly after precocious diagnosis is able not only to prevent surgical procedure but also to reduce significantly the mortality and recurrence rate of this venous thrombotic event.

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Deep venous thromboses can be divided into two groups according to their pathogenesis, anatomical features and differing responses to therapy. The first and most frequent consists of so-called simple venous thrombosis while the second group, which is less common, comprises severe or recurrent venous thrombosis characterised by a multifactorial pathogenesis, a mixed thrombus rich in platelets and by an incomplete response to both prophylactic and therapeutic treatment with anticoagulants (heparin or vitamin K antagonist). In a randomized, prospective blind study in patients with severe or recurrent venous thrombosis, which included 6 groups each of 100 patients, co-administration of anticoagulants with various types of antiplatelet agent, either with rheological effects (piracetam, buflomedil, pentoxifylline) or without them (dipyridamole), has shown a beneficial potentiating antithrombotic effect with those drugs possessing rheological effects and the absence of this effect with dipyridamole.

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We describe the case of a 72-year-old man who developed unilateral digital necrosis, four years after diagnosis of chronic myeloid leukemia (CML). The etiology of this paraneoplastic phenomenon appears multiple. The digital necrosis responded well to an aggressive varied treatment. The unusual association of CML with digital necrosis and the etiology of this rare paraneoplastic complication are discussed.

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The efficacy and tolerability of O-(beta-hydroxyethyl)-rutosides (HR) in elderly patients (aged over 65 years) with chronic venous insufficiency or varicose veins was studied in a multicentre, double-blind, randomised, placebo-controlled trial. Of the 104 patients entered into the trial, data from 102 were available for analysis of tolerability and from 86 for efficacy. Treatment was for 6 months, with monthly examinations. Three different dosages were used due to slight differences in the registered dosage in various countries: (1) 250 mg 4 times daily (1 g/day), UK, n = 19 patients; (2) 300 mg 3 times daily (900 mg/day), FRG and Belgium, n = 55, and (3) 300 mg 4 times daily (1,200 mg/day), The Netherlands, n = 30. Each centre had its own placebo control group. The HR-treated group (n = 41) showed a significantly greater reduction in the total symptom score, 5.7 +/- 2.4 to 2.3 +/- 1.8, than in the placebo group, 4.4 +/- 3.0 to 3.0 +/- 2.4 (p < 0.01). Of the 5 studied symptoms there was also a significant (p < 0.05) improvement in leg cramps, heavy legs and restless legs. No significant differences between the two groups were seen for aching pains and paraesthesia. A small reduction was also seen in ankle and calf circumferences, which became significant at the end of the trial (p < 0.05). Pitting oedema of the leg (p < 0.01) and eczema of the leg (p < 0.05) also improved significantly greater than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

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OBJECTIVE: To determine hemostasis variables in type I diabetic patients without clinically demonstrable micro- and macroangiopathy and to relate them to glycemic control. RESEARCH DESIGN AND METHODS: Fifty patients and 50 comparable control subjects were enrolled in this study. The patients were subdivided in two groups, according to their level of HbA1c (group 1, n = 30, HbA1c < or = 8%; group 2, n = 20, HbA1c > 8%). We determined the platelet count, the platelet aggregation in the spontaneous state and in the presence of ADP or collagen, beta-thromboglobulin, platelet factor 4, fibrinogen, von Willebrand factor (factors VIII:C, VIIIR:Ag, and VIIIR:VW), plasma and urinary fibrinopeptide A, euglobulin lysis time, anticoagulant proteins C and S, and plasma viscosity. RESULTS: All coagulation variables were significantly higher in diabetic patients compared with control subjects. Moreover, when the patients were subdivided according to their levels of HbA1c, the hemostatic disturbances appeared significantly more pronounced in the poorly controlled than in the well-controlled subjects. CONCLUSIONS: This study confirms the existence of a state of hypercoagulability in type I diabetes. This hypercoagulability may be related to poor glycemic control. Our study suggests that the hemostasis disturbances precede demonstrable vascular complications.

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Piracetam (Nootropil, CAS 7491-74-9) has been investigated in the treatment of primary and secondary Raynaud's phenomenon in three sequential and complementary studies. The first study in 20 patients with primary Raynaud's phenomenon, utilising clinical and ultrasound examination, capillaroscopy and laboratory tests established a daily dose of 8 g as most effective. The second study in 58 patients (47 primary, 11 secondary) confirmed the therapeutic efficacy of piracetam in both primary and secondary Raynaud's phenomenon. The third study, of crossover design, in 30 patients with severe Raynaud's syndrome, examined various agents given singly or in combination. The results not only confirmed the efficacy of piracetam but in addition allowed comparison of the efficacy of the principal therapeutic agents or regimens used in the treatment of Raynaud's syndrome and the formulation of a list of these therapies in decreasing order of efficacy, thus: piracetam 4 g/d + buflomedil 600 mg/d; piracetam 8 g/d; buflomedil 600 mg/d; piracetam 4 g/d + acetylsalicylic acid 100 mg/d; pentoxifylline 1200 mg/d; calcium antagonists; ketanserin 120 mg/d. The particular efficacy of 8 g piracetam daily in 3 divided doses at 8-hourly intervals can be attributed to its unique dual mode of action; inhibition of platelet function by inhibition of thromboxane A2 synthetase or antagonism of thromboxane A2 and increased formation of prostaglandin I2, together with a rheological effect involving reduction in blood and plasma viscosity through an increase in cell membrane deformability and a reduction of 30-40% in the plasma concentrations of fibrinogen and von Willebrand's factor. In addition, the administration of piracetam appears to be devoided of adverse effects.

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The random administration of four different single oral doses of piracetam (Nootropil, CAS 7491-74-9)--1.6 g, 3.2 g, 4.8 g and 9.6 g--at fixed intervals of 2 weeks to 5 healthy subjects has confirmed and explicited its platelet anti-aggregant and rheological properties after doses of 4.8 g and 9.6 g. The effect on platelet aggregation occurs through inhibition of thromboxane synthetase or anti-thromboxane A2 activity together with a reduction in the plasma level of von Willebrand's factor (F.VIIIR:vW). The rheological effect is related to the action of piracetam on cell membrane deformability (red cells, white cells and platelets) and to its simultaneous effect in reducing by 30-40% plasma levels of fibrinogen and von Willebrand's factor. In addition, it exerts a direct stimulant effect on prostacyclin synthesis in healthy endothelium. These effects are greatest between 1 and 4 h after dosage, and then diminish progressively to disappear between 8 and 12 h after administration. This explains the need to divide the total daily dose into 3 intakes at 8-hourly intervals. This study confirms the presence of four sites of action of piracetam: the vessel wall, platelets, plasma and cell membranes (RBC, WBC), which provide the basis for the potentially important antithrombotic activity of piracetam.

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Patency rates of coronary artery saphenous vein bypass grafts can be as low as 50% in the first year after surgery. Of these occlusions, 70% can be attributed to mural thrombus formation. Improvements in surgical handling techniques and in preservation media have improved patency rates, as has the introduction of perioperative antiplatelet therapy. The authors describe a novel preservation medium consisting of heparinized blood from the patient, papaverine and dipyridamole. This medium enhances prostacyclin production and maintains endothelial integrity in preserved saphenous vein segments.

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The systemic activator activity of 4 streptokinase (SK) regimens (250,000 IU intracoronary, group A; 500,000 IU, group B; 1.5 X 10(6) IU, group C; and 30 U anisoylated plasminogen streptokinase activator complex (APSAC) intravenously, group D) was tested with the fibrin plate technique. One hour after initiation of treatment, the activator activity was highest after APSAC (3.6 +/- 0.9 U), slightly but not significantly less after SK 1.5 X 10(6) IU (3.0 +/- 0.7), and significantly less after SK 500,000 IU (1.6 +/- 0.5) and 250,000 IU (0.6 +/- 0.5), p less than 0.001. After SK, activator activity half-lives were 184 minutes (group B) and 169 minutes (group C), and after APSAC 188 minutes (group D). These were all in agreement with greater than 12 hour duration of changes in other markers of systemic fibrinolysis (euglobulin lysis time) and substrates depletion (fibrinogen, plasminogen, alpha 2 antiplasmin). In extended pilot clinical groups given identical thrombolytic regimens during full anticoagulation with heparin, angiographic coronary patency was found in 83% (35 of 42) after intracoronary SK (group 1), in 73 and 75%, respectively, after 500,000 IU (31 of 43) and 1.5 X 10(6) IU (30 of 40) (group 2 and 3, difference not significant) and 80% (8 of 10) after the 30-U bolus of APSAC (group 4). The overall hemorrhagic risk was 24%, equally distributed among the 4 regimens and mostly (91%) related to catheters. The incidence of bleeding unrelated to vessel puncture was 4%; no deaths occurred. It is concluded that APSAC is the most fibrinolytic regimen but its potential thrombolytic superiority over SK remains to be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

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Between 1969 and 1984, twenty-three patients underwent an emergency pulmonary embolectomy under extracorporeal circulation in the Catholic University of Louvain (UCL), Department of Cardiovascular and Thoracic Surgery. The aim of this paper is to delineate the indications of this procedure. Patients were 23 to 70 years old. Diagnosis of Pulmonary Embolism was made according to clinical signs, ECG and Chest X Ray with Swan-Ganz catheter insertion into the pulmonary artery and the help of pulmonary angiogram if time permitted. The surgical technique is briefly described. Four patients died during the immediate postoperative period and three died later. The sixteen survivors all enjoy a normal life.

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The treatment of the first pulmonary embolic accident in Hospital consist in the administration of anticoagulants. Heparin will be first used intravenously or subcutaneously during 10 to 12 days and will be followed by oral anticoagulants (VKA) during 3 to 12 months. These treatments must be controlled following national or international standardized technics and can be associated with antiplatelet drugs or thrombolytic activators. The most important and frequent complications observed are haemorrhages. They are consecutive to a non conformed administration of the drugs or overdosage bound to a non correct control or drugs interferences or to a misappreciated counterindication. They will be corrected in most of the cases by a simple anticoagulant dosage reduction and exceptionally by the interruption of the therapy with administration of antidotes and plasma substitutes. Other complications are extremely rare and bound to the nature of the drugs used.

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