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)

Fibrinolysis may be impaired in coronary heart disease patients. 20 coronary heart disease patients and 10 control subjects were examined for tissue-plasminogen activator activity, tissue-plasminogen activator antigen, fast tissue-plasminogen activator inhibitor and other fibrinolytic and haemostatic parameters including antigenic and functional protein C. Both patient and control groups were similar in age and smoking habits. All of these patients had a myocardial infarction between 1-3 months before this study. Assays were evaluated before and after an exercise test. Prothrombin time, activated partial thromboplastin time, protein C, plasminogen, alpha 2-antiplasmin, fibrinogen/fibrin degradation products and contact-activated fibrinolysis were similar before and after exercise in both groups. Fibrinolytic activity assayed by the euglobulin lysis time and fibrin-plate lysis methods was decreased in the patient group as compared with the control group but the difference was not significant. In basal conditions, tissue-plasminogen activator activity was defective in 50% of the coronary heart disease patients (p less than 0.01) and after exercise this percentage rose to 77% (p less than 0.01). However, tissue-plasminogen activator antigen in the coronary heart disease group was similar to that of the control group, both before and after exercise. The activity of the tissue-plasminogen activator inhibitor was persistently increased in coronary heart disease though this increase was not statistically significant. It is concluded that in coronary heart disease patients there is a defective fibrinolytic activity probably due to an increase in tissue-plasminogen activator inhibitor.
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PMID:Reduced fibrinolytic activity in coronary heart disease in basal conditions and after exercise. 408 14

Thirteen patients with less than 5 hours of the onset of symptoms of acute myocardial infarction underwent selective coronary angiography. Ten of them had angiographic signs of coronary thrombosis. In these ten patients 15 mgs of an acylated streptokinase-plasminogen complex (BRL 26921 Beecham Farmaceuticals) were administered intravenously. Total angiographic recanalization was observed in 7 patients. The coronary arteries involved were the left anterior descending in 4 cases and the right coronary artery in 3. In 8 out of the 10 patients significant diminution of injury pattern in EKG was registered, however in all of them the necrosis pattern supervened. Prolongation of the thrombin and thromboplastin times, as well as an important fibrinogen disminution were documented in all instances. There were not complications related to the administration of the drug. An increase of muscle enzimes was documented in all cases. The follow-up was uneventfull with excellent results in all the patients. This study proves that with IV trombolitic therapy coronary recanalization can be achieved in the mayority of the patients; however there is no question that myocardial infarction finally ocurred. We speculate about the possibility of avoiding infarction by the administration of the drug within the first hour after the onset of the symptoms.
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PMID:[Coronary thrombolysis in acute myocardial infarction. Initial experience with an intravenous thrombolytic agent]. 637 17

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

Systematic blood coagulation analyses were conducted in 32 severely hypertensive patients treated with the angiotensin converting enzyme inhibitor captopril. Two hours after the first captopril dose, fibrin monomer complexes had already increased. This rise was even more distinct after 26 h and 1 week. Tests after 6 and 12 months of therapy showed a regression of fibrin monomer complexes to pretreatment values. In several patients with a marked increase in fibrin monomer complexes, the partial thromboplastin time (PTT) became shorter and antiplasmin activity increased. The most pronounced increase in fibrin monomer complexes was seen in patients with a rapid and excessive blood pressure reduction. The concentration of fibrin monomer complexes also rose in 15 healthy normotensive subjects, after a single oral dose of captopril (25 mg). Additionally, the PTT was shortened and antiplasmin significantly rose. An inhibition of fibrinolysis by captopril could be demonstrated by the effect on fibrin plates and thrombus weight after streptokinase. Out of 58 patients with severe hypertension and atherosclerosis treated with captopril, 7 patients suffered vascular complications during antihypertensive therapy: myocardial infarction (n = 2), coronary insufficiency (1), cerebral ischemia (1), renal insufficiency (3). These ischemic lesions may be partly explained by the alterations of coagulation and fibrinolysis under captopril therapy.
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PMID:Effects of the converting enzyme inhibitor captopril on blood coagulation and fibrinolysis in man. 675 Feb 21

Serial coagulation studies were obtained in 25 patients treated with intracoronary streptokinase infusion for myocardial infarction (23 patients) or coronary insufficiency (two patients) to determine the frequency of systemic fibrinolytic activity. Clotting studies were obtained before and after infusion and at 4-hour intervals until normalization. Intracoronary thrombolysis was successful in 20 of 23 patients (87%) with myocardial infarction. Streptokinase dosage in this study was 201,000 +/- 74,000 IU (+/- SD). Systemic fibrinolytic activity, defined as greater than 70% reduction of fibrinogen using a functional assay (Claus method), occurred in 22 of 25 patients (88%) and was present at a mean streptokinase dosage of 119,000 +/- 52,000 IU. Fibrinogen in the total population decreased from 342 +/- 80 to 87 +/- 94 mg% (p less than 0.0001). In patients with systemic effect, the mean fibrinogen level after infusion was 17% of baseline, increased to 43% at 24 hours, and returned to normal at 30 hours. Plasminogen decreased to 7% of baseline activity after infusion (p less than 0.0001), was 44% of baseline at 24 hours, and returned to normal at 48 hours. Intraprocedural sampling during infusion showed reduction of fibrinogen by 25% after 30,000 IU (p less than 0.0005) and by 71% at 120,000 IU (p less than 0.0001); plasminogen decreased by 50% after 30,000 IU (p less than 0.0001) and by 84% at 120,000 IU (p less than 0.0001). Prothrombin time increased from 11.5 +/- 0.8 seconds to 22.0 +/- 7.8 seconds after infusion (p less than 0.0001) and returned to normal at a mean of 18 +/- 11 hours after infusion. Partial thromboplastin time was markedly prolonged (greater than 100 seconds) after infusion, returned to less than or equal to 2 times control at 5 +/- 2 hours, and returned to normal at 9 +/- 4 hours after infusion. Fibrinogen degradation products were less than 10 micrograms/ml before infusion, increased to greater than 40 micrograms/ml after infusion, and remained greater than 40 micrograms/ml in 40% of patients at 24 hours after infusion. These data indicate that systemic fibrinolytic activity occurs in a high percentage of patients with "low-dose" intracoronary streptokinase infusion and that coagulation variables may be altered for 24-48 hours after infusion.
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PMID:Fibrinolytic effects of intracoronary streptokinase administration in patients with acute myocardial infarction and coronary insufficiency. 683 67

Nonsurgical recanalization of the occluded coronary artery has been performed in patients with evolving myocardial infarction since the late 1970s by intracoronary administration of thrombolytic agents at the ostium of the occluded artery or directly to the site of occlusion. The authors review the basic concepts underlying intracoronary thrombolysis, the method applied at their institution and the clinical results. Reperfusion of totally occluded arteries or termination of the ischemic state in subtotally occluded arteries was achieved in 71 (87.7%) of 81 patients. Reocclusion occurred in four patients, in three of these at a time when anticoagulation became temporarily ineffective, emphasizing the need for uninterrupted anticoagulation with a partial thromboplastin time longer than 80 seconds. Thallium scintigraphic studies before and after reperfusion showed a decrease in defect, indicating myocardial salvage, in the successful cases but not in failures or untreated control subjects. A decrease in thallium-201 defect was followed by improvement of regional wall motion and usually also left ventricular ejection fraction. Three of the patients with an unsuccessful result and one patient with a successful result died. Bypass surgery was performed electively in 18 patients because of multiple vessel involvement. Intracoronary thrombolysis appears to be a relatively safe and promising procedure. A large controlled study will be needed for definitive assessment of its role in the management of acute myocardial infarction.
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PMID:Nonsurgical reperfusion in evolving myocardial infarction. 683 64

In a perspective blind study of 147 survivors of myocardial infarction, the 13 patients who had definite recurrent infarction during 38.1 +/- 7.2 months (minimum, 34 months) of follow-up had higher plasma fibrinogen levels (334.4 +/- 13.1 mg/dl vs 291.5 +/- 4.7 mg/dl; P = 0.0055), and higher maximum rate of fibrin growth (generation of turbidity) when measuring prothrombin time (PT Vmax, 7.76 +/- 0.31 units vs 6.48 +/- 0.11 units; P = 0.0003), thrombin time (TT Vmax, 5.24 +/- 0.32 units vs 4.22 +/- 0.11 units; P = 0.0002), and activated partial thromboplastin time (APTT Vmax, 7.47 +/- 0.29 units vs 6.20 +/- 0.10 units; P = 0.0001) than patients who did not have reinfarction. Eleven of the 13 reinfarctions occurred among the quartile (37 patients) with the highest PT Vmax, while only two reinfarctions occurred among the remaining 110 patients (risk ratio, 16.5). The quartile with highest APTT Vmax included nine reinfarctions (risk ratio, 6.7), and the quartiles with the most fibrinogen and largest TT Vmax included eight of the 13 reinfarctions (risk ratio, 4.8). Significant associations (P = 0.018 to 0.005, risk ratios, 2.5 to 4.8) of reinfarction with the values of Vmax corrected for fibrinogen were also found. These findings support recent evidence that hemostatic function contributes to the pathogenesis of the complications of coronary artery disease.
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PMID:Association of recurrent myocardial infarction with hemostatic factors: a prospective study. 707 76

This retrospective analysis reviewed 183 patients with acute myocardial infarction who were given front-loaded recombinant tissue-type plasminogen activator (rt-PA) and r-hirudin (HBW 023) in 1 of 4 dose groups (bolus dose of 0.07, 0.1, 0.2, or 0.4 mg/kg, followed by an infusion of 0.05, 0.06, 0.1, or 0.15 mg/kg/hour over 48 hours). Activated partial thromboplastin time (aPTT) levels were determined at baseline and at 4, 8, 12, 16, 20, 24, 32, 40, and 48 hours. Of the 178 patients with r-hirudin treatment for > or = 12 hours, anticoagulation was optimal in 55.1% (all aPTTs > 2 x baseline), suboptimal in 33.7% (lowest aPTT > 1.5 but < 2 x baseline), and inadequate in 11.2% (> or = 1 aPTT but < 1.5 x baseline). Optimal anticoagulation was observed more frequently in the higher dose groups (dose 1, 15%; dose 2, 44.4%; dose 3, 63.4%; dose 4, 73.4%; p for trend < 0.0001). Patency (according to Thrombolysis in Myocardial Infarction trial grade 2 or 3) of the infarct artery after 36 to 48 hours was higher in the group with optimal anticoagulation compared with those with suboptimal or inadequate anticoagulation: 97.9%, 88.4%, and 85%, respectively (p = 0.03 optimal vs suboptimal or inadequate anticoagulation). In conclusion, r-hirudin in a dose of 0.1 or 0.15 mg/kg/hour achieves an optimal anticoagulation in about 63% or 74% of patients, which is associated with an enhanced patency 24 to 48 hours after rt-PA. A subsequent study revealed that this effective anticoagulation may be accompanied by an increased risk of severe bleeding complications after thrombolysis.
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PMID:Frequency of "optimal anticoagulation" for acute myocardial infarction after thrombolysis with front-loaded recombinant tissue-type plasminogen activator and conjunctive therapy with recombinant hirudin (HBW 023). ALKK Study Group. 748 79

Recombinant hirudins are currently under investigation for use in myocardial infarction and unstable angina. In this study the influence of piroxicam on the pharmacodynamics and pharmacokinetics of a recombinant hirudin preparation (CGP 39393) administered intravenously was determined. Twelve healthy, male volunteers received piroxicam 10 mg and matching placebo once daily for 12 days according to a double-blind, randomised cross-over design. On the 12th day, the dose of piroxicam was followed by a 6-hour infusion of hirudin 0.1 mg.kg-1.h-1. Plasma concentrations and urinary excretion of hirudin and repeated measurements of the activated partial thromboplastin time (APTT), bleeding time and platelet adhesion index were assessed up to 24 h after the start of the infusion. The maximum APTT was 83 s (placebo) and 84 s (piroxicam), 3 to 4 h after the start of the infusion, and was comparable on both study days. The AUD0-24 (APTT) came to 913 s.h.kg-1 under placebo and it was slightly increased to 1,017 s.h.kg-1 after piroxicam; the 95%- confidence interval according to MOSES ranged from 0.97 to 1.24, and the point estimator was 1.10. Bleeding time was significantly prolonged from 290 s under placebo to 345 s under piroxicam before the start of the infusion of hirudin. No further prolongation was found during or after the infusion. No change was observed in the platelet adhesion index. Responsiveness parameters according to a sigmoidal Emax-model were obtained from the hirudin-plasma concentration/effect (i.e. APTT-prolongation)-curves after placebo and piroxicam.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of piroxicam coadministration on pharmacodynamic parameters and the plasma concentration/effect relationship of recombinant hirudin (CGP 39393). 758 48

For four decades, warfarin has been used extensively to treat thromboembolic disorders. Major advances in monitoring have been achieved through recognition of thromboplastin variability and implementation of the international normalized ratio (INR). Recommended INR ranges have shifted to lower intensity, and new clinical information has led to the potential for increased use of warfarin to prevent venous thromboembolism, to treat patients with prosthetic heart valves, to prevent stroke in patients with atrial fibrillation, and to prevent death and recurrent events after myocardial infarction. Optimal management of the patient who requires a drug that has a narrow therapeutic index, such as warfarin, remains challenging. Strategies to enhance patient outcomes with these drugs attempt to improve the risk-benefit ratio of such therapies, which requires optimizing the agent's effectiveness, improving its safety profile, or both.
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PMID:Oral anticoagulation: improving the risk-benefit ratio. 765 May 6


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