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)

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.
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PMID:[A case of unstable angina pectoris associated with an active phase of polymyositis]. 158 49

Unstable angina is a clinical syndrome of recurrent myocardial ischemia. In some cases, this reflects episodic platelet activation and coronary thrombosis. Thus, the biosynthesis of thromboxane A2, which is largely derived from activated platelets, is increased, often coincident with chest pain. The major role of platelets in unstable angina may influence the response to plasminogen activators. Platelets increase the resistance of thrombi to lysis, by inducing clot retraction and cross-linking and by releasing inhibitors. Thus, coronary thrombi in unstable angina may be resistant to lysis. Furthermore, both t-PA and streptokinase cause platelet activation and thrombin formation in vivo, possibly via plasmin. Plasmin can activate platelets and factor V directly. These prothrombotic effects of plasminogen activators may limit their activity in unstable angina. At the very least, their therapeutic efficacy may be highly dependent on the coadministration of potent antiplatelet agents and anticoagulants.
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PMID:Platelet activation in the pathogenesis of unstable angina: importance in determining the response to plasminogen activators. 189 67

To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.
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PMID:Fibrinopeptide A is released into the coronary circulation after coronary spasm. 214 92

Twenty-two patients were infused with 240,000 units streptokinase during a 60-minute period into the ostium of the infarct-related coronary artery (IC), and 23 patients were infused with 1,500,000 units streptokinase intravenously (IV) over 45 minutes; all infusions occurred within 12 hours of the patients' onset of chest pain. Thereafter, heparin was infused for 10 days. Serial coagulation and fibrinolytic parameters were studied over 46 to 72 hours after the streptokinase infusion. A generalized fibrinolytic state was produced in both groups as evidenced by a fall in fibrinogen and plasminogen levels, prolongation of thrombin and reptilase clotting times, a rise in fibrinogen degradation products, and a shortening of the euglobulin lysis time. Recovery to preinfusion levels was similar in both groups of patients. Hemorrhagic complications requiring blood replacement occurred in 7/23 (30%) treated IC, and 4/23 (17%) in the IV group.
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PMID:Coagulation and fibrinolytic changes in evolving acute myocardial infarction treated by high-dose, brief-duration intracoronary or intravenous streptokinase. 230 Dec 85

Chemical pleurodesis induced with fibrin glue (fibrinogen 1.0 g, thrombin 500 mu, 2% CaCl2 10 ml, tranexamic acid 10 ml) was performed in 6 cases with spontaneous pneumothorax in whom surgery was not indicated because of various reasons, such as low pulmonary function or old age. These cases were complicated with left pneumonectomy, bilateral emphysema, pulmonary tuberculosis and interstitial pneumonia. In all cases, favorable results were obtained and there was no recurrence. As side effects, only transient low grade fever and slight chest pain were observed with no liver damage or pleural thickening. These results suggest that chemical pleurodesis induced with fibrin glue is very useful in the treatment of inoperable spontaneous pneumothorax.
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PMID:[Chemical pleurodesis induced with fibrin glue in the treatment of inoperable spontaneous pneumothorax]. 261 97

To evaluate efficacy and tolerability of the systemic infusion of 1,500,000 streptokinase units in 30', we treated 26 consecutive patients with acute myocardial infarction within 3 hours of the onset of chest pain. They were 23 men and 3 women, mean age was 59 +/- 8 years. None of them had a history of previous myocardial infarction. From clinical and electrocardiographic data, as well as from creatine kinase curves, we assumed myocardial reperfusion in 19 patients (73%). Within 30' after infusion, thrombin time increased to more than 300" in 25/26 patients (96%). Streptokinase induced hypotension (which we defined as a decrease in systolic blood pressure of more than 30 mmHg) in 13 patients (50%), and in 5 of them (19%) systolic blood pressure fell below 90 mmHg. Hypotension was counteracted by adopting the Trendelenburg position in 7 patients, and by an intravenous infusion of atropine in 5. In the remaining patient, streptokinase infusion was slowed down. Due to these interventions, a non-significant decrease in systolic blood pressure was observed from 129 +/- 26 to 112 +/- 20 mmHg at the end of the infusion. Streptokinase-induced hypotension was not predicted either by clinical, or electrocardiographic, or chest X-ray film data, or laboratory findings. No other side-effects occurred. Hence, the infusion of 1,500,000 streptokinase units in 30' in the acute phase of myocardial infarction is active, and well tolerated. It must be emphasized, however, that during the infusion, hypotension occurs frequently and unpredictably, sometimes reaching alarm levels. This makes the monitoring of systolic blood pressure imperative during streptokinase infusion.
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PMID:[On the possibility of accelerating thrombolytic therapy in the acute phase of myocardial infarction: efficacy of and tolerance to the infusion of 1.5 million units of streptokinase in 30 minutes]. 274 15

Fibrinopeptide A (FPA) levels were determined in 40 consecutive patients admitted to the coronary care unit with a typical history of chest pain: in 24 of them a diagnosis of acute myocardial infarction (AMI) and in 16 a diagnosis of angina was made. Seven of the patients with AMI suffered from recurrent episodes of early post-infarctional angina. FPA levels were determined in each patient on admission and every 4 h for 48 h. On admission in patients with both angina and AMI the FPA levels were significantly higher than in normal controls; these levels were higher in patients with AMI than in those with angina, but this difference was not significant. In patients with angina the values decreased progressively after 12 h to baseline values, while in those with AMI the high levels of FPA persisted throughout the 48-hour observation period. In many instances, particularly after 24 h, the differences between the two groups were statistically significant. In patients with early post-infarctional angina the episode of angor was preceded by or corresponded to a new great elevation of FPA levels. These data suggest that the thrombin generation is higher and more prolonged in patients with AMI than in those with angina; the determination of FPA levels, which are an index of 'in vivo' thrombin generation, can be useful to follow the clinical course of ischaemic heart disease.
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PMID:Fibrinopeptide A levels in patients with acute ischaemic heart disease. 274 31

Plasma levels of beta-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet release and thrombin generation respectively, were measured in 48 patients within 3 days of admission to hospital for acute chest pain. Twenty-one patients had a confirmed myocardial infarction (MI); 15 had unstable angina without infarction; and 12 had chest pain due to noncardiac causes. FPA and BTG were also measured in 23 control hospital patients of similar age. Mean plasma BTG levels were not significantly different in the 4 groups. Mean plasma FPA levels were significantly higher in all 3 groups with acute chest pain when compared to the control subjects (p less than 0.01), but there were no significant differences between the 3 groups. Increased FPA levels in patients with acute chest pain are not specific for myocardial infarction, nor for ischaemic chest pain.
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PMID:Plasma fibrinopeptide A and beta-thromboglobulin in patients with chest pain. 619 51

Platelet scintigraphy with radioactive indium-111 may be used both to identify and to reflect the activity of thrombin in vivo in man. Forty-one patients with acute myocardial infarction were studied for active left ventricular thrombosis by platelet scintigraphy and followed until in-hospital death, discharge, or same-admission cardiac surgery for evidence of systemic embolization. A total of 4.7 +/- 2.4 X 10(9) platelets (mean +/- 1 SD) labelled with 381 mu Ci +/- 51 mu Ci of indium-111 was injected intravenously at 91 +/- 88 hours following the onset of chest pain. Patients were imaged in multiple views on the day of and three to four days after injection of the platelet suspension. Group 1 (n = 29) had transmural myocardial infarctions, of which 21 were anterior (peak total level of creatine phosphokinase [CPK], 2,272 +/- 2,026 IU; mean +/- 1 SD) and eight were inferior (CPK level, 1,673 +/- 589 IU). Group 2 (n = 12) had subendocardial myocardial infarctions (CPK level 799 +/- 751 IU). Those with subendocardial and transmural inferior myocardial infarctions had neither left ventricular thrombosis nor emboli. Ten (48 percent) of 21 with anterior transmural myocardial infarctions had left ventricular thrombosis by platelet scintigraphy. Three with and one without such thrombosis by scintigraphy had acute neurologic episodes. In the group with anterior myocardial infarctions, seven of ten patients with and four of 11 without left ventricular thrombosis received heparin subcutaneously (chi 2 = 1.22 [Yates correction]; p greater than 0.30). We conclude that platelet scintigraphy may be used to monitor antiplatelet and anticoagulant therapy in patients with anterior transmural myocardial infarctions who are at risk for left ventricular thrombosis and systemic embolization.
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PMID:Detection of active left ventricular thrombosis during acute myocardial infarction using indium-111 platelet scintigraphy. 673 89

A considerable number of tests were carried out comparing 33 patients with acute myocardial infarction (MI), 13 patients with chest pain (CP) and 47 controls. There was some evidence that the plasma platelet factor 4 (PF4) was different in the three groups. The heparin neutralizing activity (HNA) of platelet poor plasma was increased in the MI patients relative to the controls and the intra-platelet HNA was decreased. Malondialdehyde (MDA) formation by platelets maximally stimulated by thrombin was decreased in MI whilst the plasma 5-hydroxyindoles (5HIs) in MI was greatly increased. The acute phase proteins alpha 1 acid glycoprotein and fibrinogen were significantly raised in MI. The results in the CP group were intermediate between the MI and the controls. These findings define more precisely the changes in acute MI and are relevant to the concept of exhausted platelets.
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PMID:Platelet function in acute myocardial infarction patients compared with controls. 745 98


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