bluuebunny/crossref_metadata_2025_split huggingface dataset:
PLATELET INTERACTION WITH ARTIFICIAL SURFACES UNDER DEFINED FLOW CONDITIONS: ROLE OF VON WILLEBRAND FACTOR
Authors: Badimon L , Badimon J J , Turitto V , Fuster V 
Published: August 2018

Platelets deposit onto artificial surfaces to form mono or multilayers which under certain conditions lead to gross thrombus formation and eventual failure of graft material. Both hemodynamic and blood related factors determine the interaction of blood cells with prosthetic inplants. The objective of this study has been to ascertain the extent to which vWF plays a role in platelet deposition onto artificial surfaces over a range of shear conditions. Polytetrafluoroethylene (PTFE) vascular graft segments were exposed to blood flow in a tubular perfusion chamber with well characterized rheological conditions. The perfusion chamber with test material was placed within an extracorporeal circuit (carotid artery-jugular vein) in normal swine and swine with inherited homozygous vWD. Platelet deposition was measured by labelling autologous platelets with 111Indium and also by optical morphometry of epoxy embedded specimens. Electron microscopy was performed in selected samples. Studies were performed with heparinized blood (300u/Kg iv) for perfusion times of 1 to 10 minutes. Platelet deposition increased with wall shear rate and with exposure time in the presence of vWF (vWF: 89 ± 11%) but in its absence (vWF: < 3%) platelet deposition was significantly(*) inhibited at high (1690s 1, shown below) but not at low (212s x) shear rate. Results are Platelets x 106 /cm2±lSE.Plasma and platelet vWF play an important role in platelet-deposition and stabilization of thrombus growth on a synthetic biomaterial as we have previously observed on vascular surfaces
RELATIONSHIP BETWEEN HAEMORRHAGIC AND LIPASE-RET EASING PROPERTIES OF HEPARIN AND LMV HEPARIN
Authors: Maggi A , Barrowcliffe T W , Gray E , Donati M B , Merton R E , Pangrazzi I 
Published: August 2018

In a preliminary study, a good correlation (r = 0.97) was noted between the relative abilities of an unfractionated heparin, a LMW heparin, pentosan poly sulphate and dermatan sulphate to prolong the template bleeding time in rabbits and their lipase-releasing potencies. In the present study, we have measured the prolongation of both the template and transection bleeding times in groups of 5 rats given i.v. injections of 0.75 mg/kg of two different unfractionated heparins (UEH), A and B, three different LMW heparins, X, Y and Z, and a heparan sulphate, HS. Lipase release was measured in plasma samples from different groups of 5 rats, using a tritiated triolein method.UFH A had the most haemorrhagic effect, with an approximate doubling of both template and transection bleeding times and was also the most potent lipase-releaser, giving an average lipase level of 1126 mu/ml. UFH B had no significant effect on the template bleeding time, but did prolong the transection time; its lipase releasing potency was 70% of UFH A. IMW heparin X had no effect on template or transection bleeding time and released only 40% lipase compared with UEH A. LMW heparins Y and Z did not affect the template bleeding time but did prolong the transection time; they released more lipase (60%) than LMW heparin X. Correlation coefficients with lipase release were 0.97 for the template bleeding time and 0.69 for the transection bleeding time. HS released only 7% lipase but gave significant prolongations of both bleeding times.These results confirm a strong positive correlation between the haemorrhagic and lipase releasing properties of heparin and LMW heparin, suggesting very similar structural requirements for the two biological activities. This correlation exists also for dermatan sulphate and pentosan polysulphate, but not for the heparan sulphate sample tested.
A COMPARISON OF DERMATAN SULPHATE AND HEPARIN AS ANTITHROMBOTIC DRUGS
Authors: Merton R E , Barrowcliffe T W , Thomas D P 
Published: August 2018

Dermatan sulphate (DS) has been shown to accelerate thrcmbin inhibition by its action on heparin cofactor II (HCII) but has no effect on anti thrombin III (Tollefson et al., 1983). In this study, we have examined the in vitro anticoagulant effect of a purified preparation of DS (free from heparin and heparan sulphate), m comparison with that of unfractionated heparin (UEH). We have also studied the effect of DS and UEH in preventing experimental venous thrombosis in rabbits and in inhibiting thrombin generation, both in vitro and in ex vivo plasma samples.Dermatan had low activity in vitro by APTT and anti-Xa assays (< 5 iu/ mg). When thrombin generation was measured in vitro, 1 μg/ml UEH was sufficient to inhibit thrombin formation. Although 1 μg/ml DS reduced thrombin generation to 40% of control values, there was no further reduction when the concentration of DS was increased to 8 μg/ml.When DS was injected into rabbits (n = 10), a dose of 150 μg/kg inpaired thrombogenesis m a Wessler stasis model. The mean thrombus score was reduced to 25% of the control values, although thrombosis could not be completely prevented, even after an eight-fold increase m dose (1250 μg/kg). When the duration of stasis was extended from 10 to 20 minutes, there was no impairment of thrombosis (mean thrombus score 100%) following 1250 μg/kg of DS. Thrombin generation measured in ex vivo plasma after 150 μg/kg of DS was 72% (s.e.m. 63-81) of that measured in pre-injection plasma. In contrast, 150 μg/kg of heparin prevented thrombosis after both 10 and 20 minutes stasis (mean score 0%) and thrombin generation was reduced to 17% (s.e.m. 12-23) of control values m ex vivo plasma samples.Unlike heparin, DS does not completely abolish thrcmbin generation in vitro and is not as potent as UEH in inhibiting thrombin generation m ex vivo plasma. While DS has demonstrable antithrombotic activity under defined conditions, it is less effective than heparin and increasing doses of DS do not improve antithrombotic effectiveness in this model.
PREGNANCY AND CONGENITAL DEFICIENCY IN ANTITHROMBIN III OR PROTEIN C
Authors: Conard J , Horellou M H , Van Dreden P , Samama M 
Published: August 2018

Pregnancy as well as congenital deficiency in coagulation inhibitors are recognized as predisposing conditions to thrombosis. Thus, in women with a congenital deficiency, the risk of thrombosis associated to pregnancy is expected to be higher than in normal women (incidence of approximately 1°/..). We have investigated this risk in 16 women with congenital Antithrombin III (AT III) deficiency and in 31 with Protein C (PC) deficiency.In the 16 women with AT III deficiency, 30 pregnancies occured 3 of them were interrupted by provoked abortions and a deep vein thrombosis (DVT) or pulmonary embolism were observed in 2 patients after abortion. Of the 27 other pregnancies, in the absence of any anticoagulant treatment, 17 were complicated by thrombosis (62 %), either during pregnancy (n = 8) or in the post-partun period (n = 9).In the group of 31 women with PC deficiency, 82 pregnancies occured : 16 ended with a provoked abortion, followed by a DVT in one case. Out of the 66 other pregnancies, 17 (25 %) were associated with thrombosis, during pregnancy (n = 5) or in the post-partum (n = 12).Thus, pregnancy is a situation at high risk of thrombosis in PC deficient women, and even higher in AT III deficient ones. No standardized anticoagulant prophylaxis being available, various anticoagulant treatments (mainly SC heparin) were given at various doses, started at different moments of pregnancy to 6 AT III and 3 PC deficient women : 3 and O thrombosis occured respectively.In the post-partum, a thrombosis was observed in 1 of 4 AT III and 2 of 4 PC deficient women who received a treatment. Consequently, an efficient treatment remains to be determined.If a pregnancy is unwanted, estroprogestogens are contra-indicated but progestogen only treatments with chlormadinone acetate, levonorgestrel or low dose of norethisterone were given to 4 AT III and 6 PC deficient women who were simultaneously receiving AVK : no recurrence of thrombosis was observed afer 1 to 3 years of treatment.
LONG-TERM MORBIDITY AFTER DEEP VEIN THROMBOSIS (DVT)
Authors: Widmer L K , Widmer M Th , Zemp E , Duckert F , Marbet G , Schmitt H E , Brandenberg E , Voëlin R 
Published: August 2018

5 yr follow-up of 341 patients with special consideration of post-thrombotic syndrome (PTS) and methodolo-cigal difficulties.INTRODUCTIONMethodological difficulties responsable for lacking unité de doctrine: (a) Acute phase: random allocation taking into account DVT of different extent; assessment of effect of treatment (b) Follow-up: drop out definition of parameters of success esp. PTS, comparison of truely comparable groups, limited information about economic aspects.5 yr FOLLOW-UP PTS-INCIDENCE after ANTICOAGULATION (AC) or THROMBOLYSIS (TL)Method: 341 non-randomized, consecutive patients; unilateral DVT documented by initial and control-phlebo-gramm (<14 d) , treated by AC or thrombolytic agents. 226 men, 115 women, 51.9 ± 16 yr at entry. DVT: left 193, right 148; limited 35 %, extended 65 %. Treatment effect by analysis “vein per vein”. Re-examination: “blind technique” by 2 observers; definition of PTS considering corona phlebectatica, cyanosis, edema, cirumference difference, trophic changes; Score > 10= PTSResults:1. Group with unchanged initial and control phlebogrammCorrelation between DVT-extent at entry and PTS-incidence (table). Consequently comparison of AC and TL must be made between subgroups with similar DVT-extent at entry.2. Subgroups with clearance ( + ) vs. non-clearance ( - ):Figures white PTS without ulcera, black leg ulcer
BLEEDING RISK IN INTRAVENOUS THROMBOLYTIC TREATMENT FOR ACUTE MYOCARDIAL INFARCTION
Authors: Acar J , Vahanian A , Conard J , Michel P L , Verdy E , Bouton S , Dorent R 
Published: August 2018

To evaluate the risk of bleeding (B) related to intravenous (IV) thrombolysis (TL) in acute myocardial infarction (AMI), we retrospectively studied 110 patients (pts), age<70. All were treated within 6 hours of onset of pain by streptokinase (SK) : 1.5 M IU IV in 1 hour (n = 54) ; APSAC : 30 mg IV in 5 min (n = 16) ; rt-PA IV:.75 mg/kg in 90 min (n = 30), or rt-PA plus intracoronary (IC) SK (n = 10). Pre TL, heparin (H) was administered to all pts : a 5.000 IU bolus followed by continuous infusion . In 40, aspirin (ASA) : 250 or 500 mg IV, followed by 100 mg/day orally was associated with SK (n = 9), APSAC (n = 5) or rt-PA (n =26). At the end of TL, coronary angiography was performed in 73 pts followed by PTCA in 38.No fatal or neurological B occurred. Blood transfusion (BT) was required in 5 pts (4.5 %) : 4 on day 1 (2 hematomas at catheter site, 1 prolonged B at venous puncture site, and 1 hematemesis) and 1 on day 3 (pericardial haemorrhage needing surgery). Significant B, not requiring BT, occurred in 7 pts (6.3 %). B was often related to catheterization as 4 out 12 severe or significant B were located at the femoral puncture site. Minor ecchymo-sis and hematoma were not taken into account.Severe B only occurred in pts treated with SK either IV (3/ 54) or IC following rt-PA (2/10), but differences with other groups were not statistically significant. The responsability of associated H is difficult to assess since all pts were similarly anticoagulated. The frequency ofB was the same in pts with (3/40) as without ASA (9/70). Fibrinogen (F) (Clauss method) was undetectable at 1-4, 6, 12, 16 hours in respectively 75%, 67%, 45%, 5% of pts with SK, which was never the case with rt-PA. Intensity of defibrination was similar with APSAC or SK.In SK pts the mean duration of severe defibrination (F<.5g/1) was 13.3 t 5.5 hrs in pts without B and 10.3 ± 5.4 hrs in pts with B. It is conceivable, that severe defibrination may contribute to the risk of B, but no relationship was found between the intensity of defibrination or its duration and B.We conclude : 1) TL in AMI is relatively safe if contra-indications are respected 2) B is often located at the catheterization site
THROMBOLYTIC THERAPY IN ACUTE MYOCARDIAL INFARCTION: THE SCOPE IN A DISTRICT GENERAL HOSPITAL
Authors: Murray R G , Jagger J , Davies M K , Littler W A 
Published: August 2018

Despite the interest in thrombolytic therapy in acute’ myocardial infarction, it has been reported.that only a small minority of patients considered for thrombloysis would be suitable. .To determine the demand for such therapy in a District General Hospital, data were collected for patients admitted with chest pain to our Coronary Care Unit over a six month period. Of 197 patients admitted with chest pain 131 patients (67%) were proven to have acute myocardial infarction. Criteria for thrombolytic therapy included presentation within six hours of the onset of symptoms, ST elevation ≥ 0.2 mV in 2 or more ECG leads and age ≤ 70 years. Sixty-seven (51%) of the 131 patients with subsequently proven acute myocardial infarction were eligible for thrombolysis. Criteria for thrombolysis were not fulfilled in 41 patients with acute myocardial infarction; 17 (13%) presented later than six hours, 15 (12%) failed to meet the ECG criteria and 9 (7%) were over 70 years. A further 12 (9%) patients were excluded for cardiogenic shock, patients had peptic ulcers, one patient sustained a recent acute myocardial infarction 2 weeks previously and data from 8 patients were lost.These results suggest that around 50% of patients with acute myocardial infarction and 34% of all patients presenting with chest pain would be suitable for thrombolytic therapy. These data do not support the view that such treatment may only be applicable to a small number of patients with acute myocardial infarction.
REPERFUSION VENTRICULAR FIBRILLATION, CORONARY FLOW AND PHARMACOLOGIC PREVENTION
Authors: Cosin J , Hernándiz A , Caffarena T , Andrés F , Cabadés A , Diago J L 
Published: August 2018

Reperfusion ventricular fibrillation (RVF) might be involved in sudden death. A reliable model for the evaluation of the prevention of RVF does not exist and published results vary greatly. To investigate: a) the relationship between coronary flow and RVF and b) pharmacologic prevention of RVF, two experimental series have been performed.a) Ultrasonic flow-meters were implanted in the circumflex coronary artery (cca) of 19 anaesthatised open chest dogs. In each dogs several occlusion/reperfusion procedures on the cca, were performed. b) Two occlusion/reperfusion procedures of 10' on the cca were performed. In each experience the first reperfusion acted as a control of the drug's effects on the second reperfusion. The procedure was followed in 54 dogs with controls of epicardium and surface ECG, cca blood flow (n = 24) and right and left intraventricular pressures. Phentolamine (0.30 mg/kg), Quinidine (8 mg/kg), Nifedipine (0.16 mg/kg), Verapamil (0.25 mg/kg), Dipyridamole (0.40 mg/kg), were injected intravenously.After removing the obstruction, increases in coronary flow were produced, reaching a mean maximum of 218.1% over the basal flow (p < 0.001). The RVF's appeared between 2 and 16 seconds (9.4 ± 6.8 secs) after the beginning of reperfusion, when coronary perfusion had reached 73% above the basal flow (pt 0.001) and had not reached the theoretical maximum flow. The speed of the reperfusion was no a determinating factor of the arrythmia.Only Dipyridamole significantly prevented the incidence of RVF in the second reperfusion in regards to the first (p <. 0.01). Dipyridamole produced a greater increase in basal flow (128.4% ± 70.7) and reperfusion flow (360.5% ± 131).Dipyridamole had a preventive effect of experimental RVF. This action may be a consequence of its effects on coronary flow.
THE ROLE OF VARIOUS HAEMOSTASIS PARAMETERS IN MONITORING FIBRINOLYSIS WITH PRO-UROKINASE/STREPTOKINASE IN TREATMENT OF MYOCARDIAL INFARCTION
Authors: Keller F , Schanzenbächer P , Dati F , Huber J , kochsiek K 
Published: August 2018

The new drug pro-urokinase, a proenzyme of urokinase (scu-PA), seems to have advantages in comparison with other fibrinolytic agents. Properties like higher fibrin specifity, non-systemic activity and lower antigenity may lead to a lower rate of complications. In a pilot study 10 patients with acute myocardial infarction have been treated under angiographical control with pro-urokinase (3-9 millions IU) by i.v. application. In case of no perfusion a further administration of streptokinase was carried on. The blood samples were obtained at therapy begin and after 5, 10, 30, 60 and 120 minutes. The therapy monitoring was performed by determination of established haemostasis parameters, like fibrinogen, fibrin(ogen)-split products (FSP), a2-antiplasmin. Plasminogen and batroxobin-time. Furthermore, the diagnostic relevance of new laboratory tests for fibrinolysis, D-Dimer and thrombin-anti thrombin Ill-complex (TAT) has been investigated considering some typical follow-ups. D-Dimer were determined by latex agglutination test and TAT by enzyme immunoassay.Generally the application of pro-urokinase in contrast to streptokinase results in minimal changes of the classic fibrinolysis parameters like fibrinogen, FSP, batroxobin-time etc. demonstrating no systemic lysis. The appearance of plasmic degradation products of cross-linked fibrin (D-Dimer) is a specific indi-cater of the release of thrombotic material. Other non-specific degradation products (fibrinogenolysis) were detected by the measurement of FSP. In some cases in which perfusion ocurred an increase of TAT followed by a rapid decrease was observed. This indicates a higher thromboplastic activity which may originate from the infarcted area producing TAT complex formation.
REDUCTION OF EARLY MORTALITY AND OF CARDIAC RUPTURE IN ACUTE TRANSMURAL MYOCARDIAL INFARCTION BY INTRAVENOUS STREPTOKINASE
Authors: Figueras J , Cortadellas J , Monasterio Y 
Published: August 2018

Patients (Pts)≤ 70 years old with a first transmural AMI of ≤ 4h (164±55 min) were randomized to receive (Group I,GI n=105) or not (GII, n=102) i.v. streptokinase (SK, 840.000U in lh).Contrc ST segment elevation and at lh and 24h after admission were comparable in both groups. Coronary arteriography performed within 15 days showed a recanalization rate of 64% in GI and of 27% in GII (p<0.001)but an incidence of severe stenosis (≥90<100%) higher in GI (46 vs 22%, p<0.01).Recanalized Pts presented an earlier peak of MB creatin kinase in GI (12 vs 16h p<0.01) as well as in GII (15 vs 21h, p<0.002). The incidence of pericarditis was lower in GI (14 vs 35%, p<0.001). Although hospital mortality was comparable in the 2 groups (GI,8% vs GII,11%), early mortality, <5 days, was lower in GI (2 vs 10%, p<0.02). Sudden electromechanical dissociation was the mechanism of death in 12% of patients from GI and in 77% of those from GII and it was associated with left ventricular free wall rupture in each of the 5 autopsied cases but in none of the 5 autopsied cases who died without electromechanical dissociation During a follow-up of 20±11 months (1-36) , mortality an incidence of angina was similar in both groups but reinfarction rate was higher in GI (16 vs 1%, p<0.05).It is concluded that: 1) In contrast with the changes in ST .segment, an early MB creatin kinase peak is a reliable marker of reperfusion; 2) i.v. SK lowers the incidence of pericarditis and of early mortality reducing the incidence of cardiac rupture; and 3) It is conceivable that early treatment of critical residual stenosis will reduce in hospital mortality and reinfarction in these Pts.
EVALUATION OF OPTIMUM STREPTOKINASE DOSAGE IN SYSTEMIC THROMBOLYTIC THERAPY FOR ACUTE MYOCARDIAL INFARCTION: A RANDOMIZED TRIAL
Authors: Balnave K , Moriarty A J , Nelson S D 
Published: August 2018

The aim of this ongoing study is to determine whether or not there is a difference in terms of efficacy between lower dose and higher dose streptokinase (STK) regimens used in the systemic thrombolytic therapy of acute myocardial infarction. Acute infarction patients are randomized to low dose (600,000 I.U.) or high dose (1,500,000 I.U.) STK delivered over 30 minutes. To date 52 cases have been serially paired and analysed statistically by the method of sequential analysis. One response taken to be of primary importance as an indirect indicator of clot lysis in assessment of treatment is the time to onset of recession of the ST segment towards the isoelectric baseline on the ECG.Another response is the ratio of fibrinogen/fibrin degradation products formed per unit of plasma fibrinogen. This is a direct measurement of plasmin activity. Treatment preference per low dose/high dose pairing is plotted in Figures 1 and 2 respectively for each response. No chart entry is made where there is no marked preference. In both instances, though statistical significance (p < 0.05) has not yet been reached, the trend is strongly in favour of low dose STK or, at a minimum, no difference between the doses. Not least, this has economic implications also.
COMPARATIVE FIBRINOLYTIC ACTIVITY AND THROMBOLYTIC EFFICACY OF APSAC WITH VARIOUS REGIMENS OF STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION
Authors: Col J , Col-De Beys Ch , Lavenne-Pardonge E , Moriau M , Renkin J 
Published: August 2018

Fibrinolytic activity of APSAC (anisoylated plasminogen-strep-tokinase activator complex) 30 U intravenous bolus (n = 10) was compared with intravenous (IV) streptokinase (SK). 1.500.000 IU (n = 14), SK 500.000 IU (n = 6), and intracoronary SK 250.000 IU (n = 20) given for acute myocardial infarction ≤; 4 hours) and following pretreatment with heparin (10.000 IU bolus).Plasminogen activator levels (fibrin plate) were highest for ASPAC group and correlated with the dosages of SK*. Levels also directly correlated to the duration of the activity (> 10 mm2), from 3 hours for SK 250.000 IU up to 18 hours for APSAC*.Plasmin activity (fibrin plate) raised acutely with all regimens and was maintained (> 5 mm2) during 3 hours (SK 250.000 IU), 12 hours (SK 500.000 IU), 16 hours (SK 1.500.000 IU) and 18 hours (APSAC). Reductions of plasminogen, α2 antiplasmin and fibrinogen (Clauss) were found accordingly most depressed after APSAC and significantly less after SK 250.000 IU (p < 0.05).The thrombolytic efficacy was judged on the patency rate assessed from post interventional (4 hours) angiogram in larger groups treated with intracoronary SK 250.000 IU : 28/35 (80 %), IV SK 500.000 IU : 29/41 (72 %), IV SK 1.500.000 : 18/25 (72 %), APSAC : 8/10 (80 %).To conclude, fibrinolytic activity of APSAC was best compared to the intensity and duration of IV SK 1.500.000 IU. Its thrombolytic efficacy appears to be in the range of the other regimens.* p < 0.01 rank test