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:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A discrete fall in the ACT (activated coagulation time) has been observed in patients with known activation of the coagulation cascade. Injury to the coronary artery resulting in thrombin activation, whether spontaneous as in the case of acute myocardial infarction or planned as with percutaneous transluminal coronary angioplasty (PTCA), may therefore be reflected in a change in ACT values. We reviewed the records of patients undergoing PTCA at St. Luke's Episcopal Hospital/Texas Heart Institute from January 1990 through December 1992 for information regarding ACT values and clinical events. A total of 469 patients, whose record contained adequate information for study inclusion, were divided into four separate groups: acute myocardial infarction (group I, n = 62), unstable angina with heparin therapy that was withdrawn at least 4 hr prior to PTCA (group II, n = 102), unstable angina with heparin therapy continued until the time of PTCA (group III, n = 154), and stable angina undergoing elective PTCA (group IV, n = 151). Heparin was discontinued 12-15 hr after the procedure in all but group I where anticoagulation was often maintained up to 72 hr. ACT values were measured prior to the PTCA procedure (baseline), after the initial heparin bolus of 10,000 U (postheparin) and approximately 12-18 hr after the procedure (heparin withdrawal).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activated clotting times in acute coronary syndromes and percutaneous transluminal coronary angioplasty. 772 56

The current study was designed to investigate the number and affinity of platelet thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptors in patients with unstable angina and, if any, the role played by the increased thrombin formation that is a common finding in these patients. Measurements taken during active unstable angina but not those taken during inactive angina showed an increase number (p < 0.001), without changes in affinity, of platelet TxA2/PGH2 receptors, evaluated as the binding capacity of iodine 125-PTA-OH, a stable TxA2 analogue. Moreover patients with active angina had higher plasma concentrations of fibrinopeptide A (FPA) (p < 0.0001), which were significantly related to the number of platelet TxA2/PGH2 receptors (r = 0.76; p < 0.01). Heparin infusion but not aspirin treatment promptly normalized the number of TxA2/PGH2 receptors and significantly reduced plasma FPA concentrations. In an in-vitro study thrombin in a concentration similar to that found in vivo significantly increased the number of platelet TxA2/PGH2 receptors (p < 0.01), whereas heparin did not affect TxA2/PGH2 receptors. These results have important therapeutic implications and indicate the preferential use of heparin rather than aspirin during the acute phase of unstable angina.
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PMID:Increased number of thromboxane A2-prostaglandin H2 platelet receptors in active unstable angina and causative role of enhanced thrombin formation. 773 75

To characterize the extent of early activation of the hemostatic system following angioplasty, we obtained blood samples from the involved coronary artery of 11 stable angina patients during the procedure and measured sensitive markers of thrombin formation (fibrinopeptide A, prothrombin fragment 1.2, and soluble fibrin) and of platelet activation (beta-thromboglobulin). Levels of hemostatic markers in venous blood obtained from 14 young individuals with low pretest probability for coronary artery disease were not significantly different from levels in venous blood or intracoronary samples obtained prior to angioplasty. Also, there was no translesional (proximal and distal to the lesion) gradient in any of the hemostatic markers before or after angioplasty in samples obtained between 18 and 21 min from the onset of the first balloon inflation. Furthermore, no significant difference was noted between angioplasty and postangioplasty intracoronary concentrations. We conclude that intracoronary hemostatic activation does not occur in the majority of patients during and immediately following coronary angioplasty when high doses of heparin and aspirin are administered.
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PMID:Markers of hemostatic activation in affected coronary arteries during angioplasty. 790 72

Acute coronary syndromes are accompanied by exaggerated vasoconstriction. Since thrombin induces production of the potent vasoconstrictor endothelin-1, we used immunohistochemistry on coronary atherosclerotic specimens from 30 consecutive patients. Endothelin-1-like immunoreactivity was present in 5 of 9 (55%) lesions from patients with stable angina, in 6 of 7 (86%) from crescendo angina, and in all 14 from angina at rest. Endothelin-1 immunoreactivity was most common in areas with a positive Prussian-blue reaction indicative of previous intraplaque haemorrhage. Tissue endothelin-1-like immunoreactivity might contribute to the exaggerated coronary vasoconstriction.
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PMID:Increased tissue endothelin immunoreactivity in atherosclerotic lesions associated with acute coronary syndromes. 796 78

Despite developments in percutaneous transluminal coronary angioplasty, the success of this treatment method remains clouded by early and late reocclusion. Increased experience, advances in technology, and the introduction of adjunctive devices have contributed to a higher procedural success rate (90% to 95%) and to a lower complication rate (4% to 5%), in spite of the expanded indications for angioplasty. Late renarrowing of the treated coronary artery, in combination with recurrence of angina pectoris, occurs in 15% to 40% of angioplasty patients. Several multicenter randomized trials of pharmaceutical agents have been conducted or are in progress, in an effort to diminish the rate of late reocclusion. No major breakthrough has been reported, although a clear progression has been made in the understanding of the restenosis phenomenon. It is evident that thrombin plays a detrimental role in the vascular wall injury resulting from angioplasty procedures. Current pharmacologic research concentrates on direct inhibition of prothrombin conversion and thrombus formation. Animal experimental work in this field is encouraging, and the results of clinical trials will elucidate important questions about the safety, efficacy, and immuno-allergic potential of modern antithrombotic medication.
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PMID:Thrombin and antithrombotic therapy in interventional cardiology. 806 38

We measured various coagulable factors and molecular markers in plasma and serum in the disease group including DIC, DIC suspect, thrombosis, acute myocardial infarction, angina pectoris, sepsis, malignant tumor and type II diabetes and the healthy subject group, and surmised the intravascular coagulative-fibrinolytic activity in each disease group compared with the healthy group. Additionally we selected parameters useful for early detection of the pre-thrombotic state and hypercoagulable state. As a result, of the parameters for the coagulative system, those considered useful were the assay of soluble fibrin monomer complexes using the synthetic substrate (FM.Oita), assay of soluble fibrin monomer complexes using HPLC(SFMC.Oita) and thrombin-anti-thrombin III complex (TAT) in this order. Of the parameters for the fibrinolytic system, those considered useful were FDP assay using ELISA (FDP.Oita) and plasmin-alpha 2 plasmin inhibitor complex (PIC). This FDP.Oita had a considerably high detection sensitivity compared with the FDP assay (Diayatron Co.) using the latex photometric immunoassay which has been commercially available. When measurement was made with plasma and serum in the subject disease group as the sample by the high sensitivity assays mentioned above, it was made clear that both the coagulative activity and fibrinolytic activity are increased, albeit with some differences in intensity, in all the disease groups compared with the healthy group. In order for the hypercoagulable state and pre-thrombotic state to be detected, it is important to know the balance between the coagulative activity and fibrinolytic activity. According to the results of the present experiment, a significant directly proportional correlation was recognized between FM.Oita and FDP.Oita and between TAT and FDP.Oita. Therefore, examination of these ratios will be a more detailed indicator of coagulative-fibrinolytic activity than the TAT/PIC ratio, PAI-1/TPA ratio and ATIII/alpha 2 PI ratio hitherto in use. If useful molecular markers such as FM.Oita are measured over time in various cases and these data are compiled and analyzed statistically, it will not be long before the criteria for the hypercoagulable state and pre-thrombotic state are established.
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PMID:[Molecular marker for detecting hypercoagulable state]. 810 79

Intracoronary thrombus formation has been thought to play an important role in the genesis of acute myocardial infarction an unstable angina. To examine whether the coagulation and fibrinolytic systems are altered in such ischemic heart diseases, the plasma levels of fibrinopeptide A (FPA) and plasminogen activator (PAI) were measured. The plasma level of FPA was increased in patients with variant angina as compared with those with stable exertional angina and there was a significant circadian variation in the plasma level of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina. The plasma FPA level increased in patients with coronary spastic angina after the ischemic attack induced by hyperventilation. Furthermore, FPA was released into the coronary circulation after the anginal attack induced by intracoronary injection of acetylcholine. These findings suggest that the coronary artery spasm may induce thrombin generation and trigger thrombus formation in the coronary artery. On the other hand, the plasma level of PAI activity was higher in patients with unstable angina and coronary spastic angina than in those with stable exertional angina. Moreover, the PAI activity in patients with unstable angina decreased to the level in patients with stable exertional angina after the stabilization of their symptoms by drugs. Our findings suggest that the increased plasma PAI activity may reduce fibrinolytic activity and attenuate removal of the thrombus and may ultimately lead to acute myocardial infarction in some patients with unstable angina and coronary spastic angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blood coagulation and fibrinolysis in ischemic heart disease]. 810 82

Plasma levels of the prothrombin activation fragment 1 + 2 (F 1 + 2) and of thrombin antithrombin III complexes (TAT) were determined in 225 patients with angina pectoris undergoing coronary angiography. Oral anticoagulant therapy was associated with a marked reduction in mean F1 + 2 (0.63 vs 1.62 nmol/l, p < 0.0001) and TAT levels (1.65 vs 2.23 micrograms/l, p < 0.0001). Omitting patients on oral anticoagulants, TAT values showed a positive association with patients' age (r = 0.18; p = 0.01) and were slightly higher in patients with a history of myocardial infarction than in those without (2.47 vs 2.11 micrograms/l; p = 0.06). Both F1 + 2 and TAT levels were increased in patients with angiographically verified coronary atherosclerosis as compared to patients with angina and angiographically normal coronaries (F1 + 2: 1.76 vs 1.36 nmol/l, TAT: 2.35 vs 2.00 micrograms/l; p-values after adjusting for age, sex and past history of myocardial infarction 0.06 and 0.11 respectively). However, no graded relationship between F1 + 2 or TAT values and severity of atherosclerosis was observed. This study provides suggestive evidence that a procoagulant state exists in patients with angina pectoris and coronary atherosclerosis. Its relevance in predicting coronary ischaemic events needs to be studied prospectively.
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PMID:Prothrombin activation fragment 1 + 2 and thrombin antithrombin III complexes in patients with angina pectoris: relation to the presence and severity of coronary atherosclerosis. 811 78

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

Nitroglycerin provides an external source of nitric oxide which stimulates guanylate cyclase and produces vasodilatation and inhibition of platelet function. The antithrombotic effects of intravenous nitroglycerin were recently documented in various experimental models and in patients with unstable angina. This protocol was designed to evaluate whether these effects could also be detected with transdermal nitroglycerin in patients with stable angina. In a randomized, double-blind, controlled parallel trial, 22 patients received transdermal nitroglycerin, 0.6 mg/hour (11 patients), or placebo (11 patients). Platelet aggregation to adenosine diphosphate (ADP) and to thrombin was measured in whole blood. Thrombus formation was assessed on porcine aortic media exposed to the patient's venous blood for 3 minutes at shear rates of 2,546 and 754 s-1. Platelet aggregation to ADP decreased from 7.7 +/- 0.8 to 5.3 +/- 0.8 ohms (p < 0.05) with nitroglycerin, and to thrombin from 15.6 +/- 1.2 to 12 +/- 1.2 ohms (p < 0.05). Thrombus size at the high-shear rate decreased from 2.8 +/- 0.7 to 1.0 +/- 0.3 microns 2 (p < 0.05), and at the low-shear rate from 2.5 +/- 0.5 to 1.0 +/- 0.2 microns 2 (p < 0.05). Placebo had no significant effect on platelet aggregation and platelet thrombus deposition. These parameters were all reduced by > or = 20% in 8 patients taking nitroglycerin but only in 3 patients taking placebo (p < 0.05). Transdermal nitroglycerin significantly inhibits platelet aggregation and mural thrombus formation in patients with angina pectoris.
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PMID:Antithrombotic properties of transdermal nitroglycerin in stable angina pectoris. 819 30


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