Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Controversy continues about the oxygenator preferable for cardiopulmonary bypass (CPB). This prospective study was undertaken in 52 patients undergoing coronary bypass surgery. Oxygenators were alternated each case between model Q-100, Bentley Laboratories Inc, Irvine, Calif, and Travenol Membrane Oxygenator (TMO), Travenol Laboratories Inc, Deerfield, Ill. The Q-100 group required higher CPB O2 flows, but PO2 levels during CPB were similar for both groups. Heparin sodium dosage and activated clotting, bleeding, prothrombin, and partial thromboplastin times were identical in both groups. Blood loss and platelet reduction after CPB were also similar. Postoperative complications in the Q-100 group included one myocardial infarction, and one neurological problem. The TMO group had no myocardial infarction and one neurological problem. The membrane oxygenator took nine minutes longer to set up and was $63 more expensive to purchase. Blood trauma during CPB was less with the membrane oxygenator (lower plasma hemoglobin level), but we conclude that both oxygenators performing adequately during clinical use in open heart surgery.
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PMID:Membrane vs bubble oxygenators: a prospective study of 52 patients. 49 30

The activated partial thromboplastin time is compared with the corresponding prothrombin ratio in 6378 samples of platelet-poor plasma from 446 patients treated for a total of more than 4500 patient/months with oral anticoagulatnts. A relative decrease in the activated partial thromboplastin time following deep vein thrombosis is described, which tends to become less obvious during the first year of treatment and is greater in older patients. Although this relative decrease is also found in patients treated after cerebrovascular accidents, it is not found in patients treated after myocardial infarction or in patients with mitral valve disease treated prophylactically with long-term oral anticoagulants. It is though possible that these changes following deep vein thrombosis might be useful in helping to determine the duration of oral anticoagulant treatment.
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PMID:The efficacy of long-term oral anticoagulant therapy and its laboratory assessment. 112 47

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 extent and time course of changes in selected procoagulant and anticoagulant factors were investigated in 19 patients undergoing elective abdominal aortic surgery. The coagulation factors were measured preoperatively, and on days two, four, and six postoperatively. It was found that there were no significant changes outside the normal range in prothrombin time, partial thromboplastin time, or thrombin clotting time. However, there were large increases in the procoagulants, fibrinogen, factor VIII coagulant, factor VIIIRag/von Willebrand factor, and in alpha 1-antitrypsin. Over the same time there were marked decreases in the naturally occurring anticoagulants, protein C and antithrombin III, and in alpha 2-macroglobulin. These changes implied that the patients were "hypercoagulable" in the postoperative period. The maximum changes in the procoagulants occurred on either postoperative day two or day four. The maximum changes in the natural anticoagulants occurred on postoperative day two. There were no significant changes in factor V, factor X, alpha 2-antiplasmin, or platelet aggregability. The timing of the changes coincided with a period of high risk of perioperative myocardial infarction in this group of patients. Thus, it is possible that postoperative hypercoagulability contributes to the development of coronary artery thrombosis and myocardial infarction following abdominal aortic surgery.
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PMID:Postoperative changes in coagulant and anticoagulant factors following abdominal aortic surgery. 128 42

The stimulation of platelets, activation of the coagulation cascade, release of platelet-derived vasoconstrictors, and endothelial dysfunction all contribute to the thrombotic vascular occlusion that results in myocardial infarction. Despite the importance of platelets in the initiation of this process, they are activated by multiple endogenous mediators. Thus, one might anticipate that redundancy in the system would confound the efficacy of antiplatelet drugs that were mediator-specific. The success of aspirin in clinical trials is likely to reflect the role of thromboxane A2 (TxA2) as an amplification signal for other platelet agonists. Activated platelets provide a substrate for assembly of the prothrombinase complex and both heparin and warfarin also reduce the mortality due to thrombotic vascular disease. The relative efficacy of these compounds versus aspirin and the safety of their combination, particularly in the setting of therapeutic thrombolysis, are under investigation. Novel antiplatelet agents, particularly those directed against the glycoprotein 11b/111a complex, are more potent than aspirin in animal models. Similarly, direct thrombin inhibitors seem superior to heparin. Whether such compounds can be administered safely in effective doses to humans is under study. It is hoped that the success of aspirin does not impede the clinical evaluation of theoretically more attractive antithrombotic drugs.
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PMID:Antiplatelet and anticoagulant drugs in coronary vascular disease. 134 4

Having previously shown in the Heparin Aspirin Reperfusion Trial that the empiric use of early intravenous heparin after recombinant tissue-type plasminogen activator (rt-PA) is an important component in the overall treatment strategy, we examine in this report the specific relation between the degree of prolongation of activated partial thromboplastin time and coronary artery patency. To evaluate the hypothesis that arterial patency after administration of rt-PA for acute myocardial infarction is sustained by effective anticoagulation, activated partial thromboplastin time of heparin recipients was determined 8 and 12 h after the start of thrombolysis. Mean activated partial thromboplastin time was higher among patients with an open infarct-related artery than in those with a closed artery (81 +/- 4 vs. 54 +/- 9 s, p less than 0.02). Only 45% of patients with values less than 45 s at both 8 and 12 h had Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 in the infarct-related artery at 18 h. In contrast, 88% of patients with activated partial thromboplastin time greater than 45 s and 95% of those with values greater than 60 s had an open infarct-related artery at 18 h (p = 0.003 and 0.0006, respectively). Among patients with an initially patent infarct-related artery who underwent repeat angiography at 7 days, activated partial thromboplastin time was similar in those with a persistently patent artery and those with late reocclusion. Excessive anticoagulation did not appear to increase hemorrhagic risk except that access site-related hemorrhage was more common in patients with activated partial thromboplastin time greater than 100 s at 8 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin-induced prolongation of partial thromboplastin time after thrombolysis: relation to coronary artery patency. HART Investigators. 160 35

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

A young man who had suffered several episodes of deep-vein thrombosis of the legs since the age of 20 had a myocardial infarction at the age of 33, at which time both a prolonged partial thromboplastin time (PTT), compatible with a lupus anticoagulant (LA), and decreased fibrinolytic capacity (FC) were found. His sister presented with deep-vein thrombosis of a leg and subsequent pulmonary embolism when she was 18 years old. She had a miscarriage three years later and developed a hemolytic-uremic syndrome at the age of 35. The PT and FC were normal. Laboratory investigations of the parents revealed positive antinuclear antibodies in the mother's serum but no anomaly in the father. This study suggests a familial tendency to develop autoimmune disorders associated with LA and thromboembolic complications related to decreased FC.
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PMID:Different clinical presentations of a lupus anticoagulant in the same family. 190 97

Stent implantation in native coronary arteries may be complicated by acute thrombosis, despite the use of stringent anticoagulation. Thrombotic occlusion of stented venous grafts may occur less frequently, possibly because of the larger caliber of these grafts. We report our experience with 46 stents (Wallstent, Medinvent, Lausanne, Switzerland) implanted in 35 lesions of 24 consecutive patients (mean age 64 years, range 43 to 75). Two overlapping stents were implanted in seven patients, and three overlapping stents were positioned in two. After implantation, activated partial thromboplastin time was maintained at two to three times the control level by intravenous administration of heparin (160 to 550 mg daily) until thrombotest values were reduced 5% to 10% by acenocoumarol. Impending thrombotic occlusion was recognized in two suboptimally anticoagulated patients: patient A after implantation of four stents and patient B after anticoagulation therapy was discontinued because of acute upper gastrointestinal bleeding. Coronary artery bypass grafting was performed successfully in both patients. A third patient had a myocardial infarction on day 7 after stent implantation, in spite of adequate anticoagulation and optimal medical drug therapy. It is concluded that stringent anticoagulation therapy appears mandatory to maintain graft patency after stent implantation.
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PMID:The importance of adequate anticoagulation to prevent early thrombosis after stenting of stenosed venous bypass grafts. 201 71

We investigated whether clinical and laboratory variables can predict perfusion status after t-PA administration, by using the data from 138 patients who received t-PA during the Thrombolysis in Myocardial Infarction (TIMI) I study. All clinical and laboratory variables that were collected at baseline or during perfusion for TIMI I were evaluated by the current study. Via stepwise discriminant analysis, 7 variables were closely associated with perfusion status at 90 minutes (listed in the order of their discriminant effect): baseline grade of stenosis in the infarct-related coronary artery, whether nausea was present during the infusion, baseline aspartate aminotransferase (SGOT) concentration, whether arrhythmias were present during the infusion, baseline fibrinogen concentration, baseline partial thromboplastin time, and baseline diastolic blood pressure. Baseline severity of stenosis and the likelihood of there being reperfusion were inversely related. Eighty-four percent of patients with adequate perfusion after 90 minutes of t-PA infusion were classified correctly, but only 50% of those without perfusion at 90 minutes were classified correctly. In addition, since 70% of the TIMI I patients, on average, did achieve perfusion, the use of these 7 variables added little predictive information. Our findings suggest that 1) there is as yet no practical way to predict reperfusion after t-PA therapy and 2) the severity of coronary stenoses, if known ahead of time, should be considered when selecting patients for thrombolytic therapy.
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PMID:Prediction of coronary artery reperfusion after tissue plasminogen activator infusion. 211 85


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