Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heparin is a parenteral antithrombotic agent with efficacy in the treatment and prevention of venous thromboembolic disease and in preinfarctional angina. Accumulating evidence also suggests that heparin is useful in the prevention of coronary artery reocclusion after thrombolytic therapy for acute myocardial infarction, and in the prevention of left ventricular mural thrombosis after anterior wall myocardial infarction. Heparin appears to offer only marginal benefit in reducing mortality when given in combination with thrombolytic therapy and aspirin for acute myocardial infarction. When used for prevention of venous thromboembolism in moderate risk patients, heparin should be given subcutaneously in a dose of 5000 U every 12 hours for 5 to 7 days or until the patient is ambulatory. In higher risk patients, such as those undergoing total hip replacement, heparin should be given subcutaneously every 12 hours in a dose to prolong the activated partial thromboplastin time (aPTT) by 4 to 5 seconds into the upper normal range. When used to treat active venous thromboembolism or the peri-infarctional state, heparin should be given by intravenous infusion with loading and maintenance doses to consistently prolong the aPTT to between 1.5- and 2.5-fold the control value (mean of laboratory's normal range). If constant intravenous infusion is not possible, the drug should be given subcutaneously every 12 hours to consistently prolong the aPTT between 1.5 and 2.5 times control. This regimen is also recommended in pregnant women with venous thromboembolic disease or mechanical heart valves.
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PMID:Heparin therapy. Regimens and treatment considerations. 128 May 66

The effectiveness of intracoronary (IC) recombinant thromboplastin activator (rt-PA) was prospectively evaluated in seven patients with unstable angina and complex angiographic lesions or intracoronary filling defects (ICFD). There were four men and three women, with a mean age of 60 years. Three patients had multivessel disease and all patients had rest angina; none had evolving myocardial infarction. All patients were pretreated with aspirin and were given heparin. IC rt-PA was infused at the rate of 1 mg/min to a total of 50 mg, and angiographic changes were observed every 15 minutes. At 50 minutes, angiographic improvement was seen in two patients (28%), one of whom had complete and one of whom had partial resolution of ICFD. In two patients (28%) there was no change in the lesion, and three patients (42%) had worsening of the lesion appearance. In two of the latter, paradoxical closure was observed at the end of the infusion, and was treated successfully with ad hoc emergency angioplasty. This pilot study suggests that IC rt-PA at the dosage used may have variable effects on complex coronary lesions associated with unstable angina, and this may be of relevance in further trials evaluating IC thrombolysis in unstable coronary ischemic syndromes.
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PMID:Intracoronary recombinant tissue-type plasminogen activator in unstable angina: a pilot angiographic study. 190 73

This report describes studies on the activation of coagulation factor VII (FVII) and the inhibition of the extrinsic coagulation pathway in acute ischaemic heart disease. FVII and the inhibitor of the tissue thromboplastin-FVII complex, called extrinsic pathway inhibitor (EPI), were determined in plasma from 68 patients and compared to findings in 37 normal individuals. The mean FVII amidolytic activity, the mean FVII clotting activity, as well as the FVII clotting/FVII amidolytic ratio were not significantly different in the patient groups as compared to the controls. The fraction of FVII clotting activity that is sensitive to phospholipase C, 'the FVII-phospholipid complex', was 8% in controls, 19% (P less than 0.05) in patients with acute myocardial infarction, 15% (n.s.) in angina pectoris and 13% (n.s.) in heart failure/arrhythmia patients. The 'FVII-phospholipid complex' was highly significantly correlated to triglycerides in plasma in patients with acute myocardial infarction (r = 0.88, P less than 0.001) and angina pectoris (r = 0.89, P less than 0.001). The mean EPI levels were significantly increased in patients with acute myocardial infarction (132%), angina pectoris (134%), and heart failure (150%) as compared to the control population (110%). The FVII clotting/EPI ratio was significantly decreased both in patients with acute myocardial infarction and heart failure, whereas the FVII amidolytic/EPI ratio was significantly decreased only in the heart failure group. Apparently, in patients with acute ischaemic heart disease, a moderate increase in the procoagulant activity is accompanied by a marked increase in the anticoagulant activity of the extrinsic coagulation pathway, suggesting a balanced activation system.
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PMID:Factor VII and extrinsic pathway inhibitor in acute coronary disease. 278 54

Between September 1985 and April 1987, 110 consecutive patients who had successful coronary angioplasty were included in a randomised prospective controlled evaluation of the effects of warfarin on restenosis. The warfarin (n = 56) and the control (n = 54) groups were not different in terms of age, sex, previous coronary bypass surgery or coronary balloon angioplasty, severity of symptoms, and frequency of multivessel disease or of total coronary occlusions. Warfarin was started on the day of the procedure and the dosage was adjusted to maintain the thromboplastin international normalised ratio greater than or equal to 2.5. One hundred and five (96%) of the patients were given verapamil and other antianginal drugs were prescribed as needed. Low molecular weight dextran and heparin were given during the procedure and heparin was continued for 24 hours in all patients. One hundred and eight (98%) of patients were followed up clinically after a median of five months (range 1-20). Eighty five (77%) had follow up angiography at five months. In the warfarin group symptoms improved in 46 (85%) patients by at least 1 angina class and 31 (57%) were symptom free; the exercise test remained positive in 20 (36%) patients and the angiographic restenosis rate was 25% per lesion and 29% per patient. There were no major bleeding complications. In the control group 46 (85%) patients were improved by at least 1 angina class and 31 (57%) were symptom free; the exercise test was positive in 11 (21%) patients and the angiographic restenosis rate was 33% per lesion and 37% per patient. Although the incidence of angiographic restenosis tended to be lower with warfarin, none of these differences was significant. These data suggest that the combination of verapamil and warfarin, in the absence of aspirin, is not significantly better than verapamil alone in preventing symptom recurrence or angiographic restenosis after coronary angioplasty.
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PMID:Lack of effect of warfarin on the restenosis rate or on clinical outcome after balloon coronary angioplasty. 297 49

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.
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PMID:Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis. 325 21

75 patients with atherosclerosis divided into five disease groups (previous myocardial infarction and cerebral thrombosis, angina pectoris, transient ischemic attacks, arteriosclerosis obliterans) were studied and compared to 20 healthy subjects. Antithrombin III (AT III) concentration was determined by single radial immunodiffusion; AT III and factor Xa-inhibitor (Xa-I) activities were measured by amidolytic methods. No significant difference was found in any group of patients as compared to normal controls by all the methods. A positive correlation was found between AT III concentration and AT III activity, AT III concentration and Xa-I activity, AT III activity and Xa-I activity. Results are discussed in relation to the literature data.
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PMID:Antithrombin III and factor Xa inhibitor in atherosclerosis. 661 88

Ischemic electrocardiographic changes were recorded within 2 hours of admission using a 12-lead electrocardiographic continuous monitor with a 20-second scanning interval and an alarm mode for asymptomatic events. Blood samples were obtained at admission and at the moment of asymptomatic events (group A). In the other patients who did not develop ischemia, a second blood sample was taken 12 hours later (group B). We determined prothrombin time, activated partial thromboplastin time, clotting factor VIII activity, tissue plasminogen activator activity, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation product, and thrombin-antithrombin III complexes. There was a statistically significant difference between group A and B patients when the basal samples were analyzed for thrombin-antithrombin III (p = 0.046) and d-Dimer (p = 0.005). Prothrombin fragment 1 + 2 were significantly reduced, and d-Dimer was elevated when basal blood samples were compared with the second sample in patients who developed silent events (p = 0.008 and 0.055, respectively). A plasma concentration of thrombin-antithrombin III complex was also significantly decreased when sample 2 was compared with the basal blood sample (p = 0.039). Five recurrent episodes of angina and 2 nonfatal infarctions occurred, and 4 urgent revascularization procedures were performed in group A. In group B, there was only 1 nonfatal infarction (p = 0.01). The results of the present study suggest that a time-dependent thrombotic process is detectable in the blood stream as a cyclic movement. Further studies are needed to determine if some other factors, such as intensive shear stress in the vessel wall, may activate plaque instability during asymptomatic episodes.
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PMID:Time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstable angina pectoris. 761 Nov 44

Intravenous heparin has been used in the control of myocardial ischaemia in patients with unstable angina. We set out to assess the efficacy of subcutaneous heparin in reducing myocardial ischaemia in patients with unstable angina. 343 of 399 patients with unstable angina were monitored for 24 h and 108 were refractory to conventional antianginal treatment and were entered into a randomised multicentre trial. 37 patients were assigned to heparin infusion (partial thromboplastin time 1.5-2 times baseline), 35 to subcutaneous heparin (adjusted dose with partial thromboplastin time 1.5-2 times baseline), and 36 to aspirin (325 mg daily). All had additional conventional antianginal therapy. After the run-in patients were monitored for 3 days. The primary endpoint was reduced myocardial ischaemia assessed by the number of anginal attacks, silent ischaemic episodes, and duration of ischaemia per day. At 1 week and 1 month we accounted for anginal attacks and other clinical events (myocardial infarction, revascularisation procedures, and death). Aspirin did not significantly affect the incidence of myocardial ischaemia. On the first 3 days, infused and subcutaneous heparin significantly decreased the frequency of angina (on average by 91% and 86%, respectively), episodes of silent ischaemia (by 56% and 46%), and the overall duration of ischaemia (66% and 61%) versus run-in day and aspirin (p < 0.001 for all variables). The favourable effects of heparin therapy remained evident during follow-up. Only minor bleeding complications occurred. Subcutaneous heparin is effective in the control of myocardial ischaemia in patients with unstable angina.
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PMID:Randomised comparison of subcutaneous heparin, intravenous heparin, and aspirin in unstable angina. Studio Epoorine Sottocutanea nell'Angina Instobile (SESAIR) Refrattorie Group. 761 18

UAP is a frequent manifestation of ischaemic heart disease; it is intermediary between stable angina and myocardial infarction and sudden death resp. The hospitalization mortality is 5%, approximately 15% of the patients with UAP develop myocardial infarction. The aim of UAP treatment is: 1. prevention of ischaemic episodes, 2. prevention of infarction and 3. control or elimination of risk factors, to improve the long-term prognosis in these patients. As antianginal drugs in UAP as a routine calcium antagonists, beta-blockers and nitrates are used. A very important part in the treatment of UAP is played by antithrombotic and thrombolytic treatment as in this disease rupture or fissure of plaques and subsequent thrombus formation is important. Non-occlusive thrombi are present in 80% in UAP, while in infarctions they are present in 21%. Rupture of an atherosclerotic plaque leads to thrombocyte activation, release of tissue thromboplastin and activation of the coagulation system aspirin inhibits platelet function and thus reduces thromboxane A2 formation. Heparin affects the coagulation process in UAP, reduces the number of anginal attacks and protects from the development of infarction. Treatment of UAP with streptokinase and rt-PA has no great advantages, when compared with heparin. Surgical treatment of UAP has somewhat better results than conservative treatment. Coronary angioplasty is an ideal solution in UAP when one or two arteries are damaged.
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PMID:[The present status of treatment of unstable angina pectoris]. 807 49

There is evidence that intravenous nitrates which are frequently used in acute coronary syndromes may interfere with the anticoagulant effect of heparin. We compared the effect of two different nitrate preparations on the activated partial thromboplastin time (APTT), anti-thrombin III activity (AT III) and plasma heparin levels in patients (n = 50) undergoing routine percutaneous transluminal coronary angioplasty (PTCA) for stable angina. Patients were randomized to either: (1) intravenous heparin and nitroglycerin (GTN); or (2) intravenous heparin and isosorbide dinitrate. The APTT, plasma heparin concentration and AT III activity were measured before PTCA and at 2 and 4 hours after commencement of infusions. Both groups received identical doses of heparin. Group 1 patients received a constant dose of 16.6 micrograms/minute of GTN, and group 2 patients received 33.3 micrograms/minute of isosorbide dinitrate. At 4 hours the median APTT ratio was significantly lower in group 1 compared with group 2 (2.6 versus 4.5) (P < 0.05) as was the plasma heparin concentration (0.18 U/ml versus 0.32 U/ml (P < 0.05). However, no significant difference in APTT ratios or plasma heparin concentrations were noted at any of the other sample times. AT III activity was not significantly different between the groups at any sample time. Within-group analysis showed significantly lower APTT ratio and heparin concentrations at 4 hours compared with the respective 2 hour values. These results would suggest that there is a potential impairment of anticoagulation with low-dose intravenous nitroglycerin and to a lesser extent with low-dose isosorbide dinitrate. Early and frequent monitoring may therefore be appropriate when intravenous nitrates and heparin are used in combination.
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PMID:The effect of different nitrate preparations on plasma heparin concentrations and the activated partial thromboplastin time. 817 Aug 77


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