Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary thrombolysis reduces morbidity and mortality in patients with acute myocardial infarction, however, the exact effects of thrombolytic agents on the status of intrinsic hemostases are not fully understood. In the present study, we examined serial changes in plasma thrombin and protein C activities of 6 patients with acute myocardial infarction treated with urokinase. Fibrinolysis occurred immediately after urokinase injection with an increase in the plasma thrombin-antithrombin III complex, suggesting a subsequent procoagulant state due to thrombin generation. Correspondent increases in plasma protein C activity were observed, however, protein S levels did not change at all. Our findings suggest that urokinase administration for coronary thrombolysis not only causes fibrinolysis, but also induces thrombin activity, which may be antagonized by augmented intrinsic protein C activity.
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PMID:Augmented plasma protein C activity after coronary thrombolysis with urokinase in patients with acute myocardial infarction. 138 46

A 29-year-old man with congenital protein C deficiency and acute myocardial infarction is reported. Four hours after the onset of chest pain, he was treated intravenously with tissue-type plasminogen activator. Subsequent coronary angiography revealed only slight stenosis of the left anterior descending coronary artery without any atherosclerosis. The propositus, his brother, and his mother, showed low levels of both protein C activity and antigen, while plasma thrombomodulin levels were normal. His grandfather had died from acute myocardial infarction at 38 years of age. We investigated several other risk factors for arterial thrombosis, including factor VII, fibrinogen, heparin cofactor II, lipoprotein (a), and anticardiolipin antibodies. No other haemostatic abnormalities apart from factor VII hyperactivity were detected in this family. To study the effects of protein C and factor VII on procoagulant activity, prothrombin time was measured after the addition of activated protein C and factor VII to protein C-deficient plasma. The prothrombin time ratio decreased along with an increase in the factor VII level. It also decreased with a decrease in the activated protein C level. These findings indicated that the procoagulant activity of factor VII was enhanced by low protein C levels, suggesting that concomitant factor VII hyperactivity may cause acute myocardial infarction in patients with protein C deficiency.
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PMID:Congenital protein C deficiency and myocardial infarction:concomitant factor VII hyperactivity may play a role in the onset of arterial thrombosis. 144 May 17

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.
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PMID:Biological risk factors for sudden death in patients with coronary artery disease and without heart failure. 156 56

The haemostatic parameters were studied within 14 days of acute myocardial infarction (AMI) in 103 patients randomly allocated into a group receiving low-dose heparin or into a group treated without anticoagulants. Patients with isotopic evidence of deep vein thrombosis were excluded from the analysis. An important formation of thrombin-antithrombin III complex (TAT) in the plasma was detected in the early stage of the disease. It was accompanied by an activation of plasma intrinsic fibrinolysis (IF), an elevation of fibrinogen and its degradation products (FDP) and a reduction of extrinsic plasma fibrinolytic activity (EF) together with normal levels of factor X, antithrombin III (AT III), protein C and alpha-2-antiplasmin. Sequentially studies periods of the disease revealed a diminution of TAT complex concentration in the plasma on the seventh day of AMI together with a rise of the both plasma fibrinolytic activities (IF, EF) as well as an elevation of fibrinogen and its degradation products, returning to the initial values on the 14 day of AMI. In the patients treated with heparin the augmentation of TAT complex in the plasma was prolonged until the fifth day of AMI. Moreover, heparin administration was connected with significantly higher levels of AT III and protein C along with a lower concentration of factor X and FDP on the seventh day of the disease. The fluctuation of fibrinolytic activities (IF, EF) in the plasma was heparin-independent. The present results indicate that low-dose heparin treatment modulates the plasmatic fluctuation of TAT complex as well as factor X, AT III and protein C levels in patients with acute myocardial infarction.
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PMID:Fluctuation of thrombin-antithrombin III complex in patients with acute myocardial infarction: influence of low-dose heparin administration. 169 24

Thrombolytic treatment of acute myocardial infarction proved to be able to restore infarct artery patency and to decrease hospital mortality. The number of bleeding complications have remained at an acceptably low level, however some thromboembolic complications occurring during the first week following thrombolytic therapy have been recently observed. Signs of increased in vivo platelet activation (by measuring beta-thromboglobulin and thromboxane metabolite levels) and endothelial damage (Willebrand-factor estimations) could have been detected in our patients treated with brief high dose intravenous streptokinase, altogether with diminished antithrombin III and protein C antigen levels and activity. Intravenous streptokinase treatment of acute myocardial infarction might be able to cause thrombotic haemostatic alterations, which require meticulous haemostasis monitoring and early, correct antithrombiotic therapy.
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PMID:[Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct]. 220 24

The study was carried out of 53 patients with acute myocardial infarction receiving no anticoagulant treatment. Changes were traced in certain indices of the blood clotting system and fibrinolysis in plasma in the first 14 days of the disease, with particular attention given to patients in whom during the hospitalization signs of deep vein thrombosis in the lower extremities appeared or a positive result was obtained of the test with 125I-fibrinogen. In a group of 9 patients with deep vein thrombosis developing during the observation, on the first day of myocardial infarction shortening of the kaolin-cephalin clotting time and considerable rise of the level of fibrinogen-fibrin (FDP) degradation products were noted in serum, and on the 14th day raised fibrinogen level and reduced exogenous fibrinolytic activity of the plasma were noted. Increased level of fibrinogen and FDP and exogenous and endogenous plasma fibrinolytic activity observed on the 7th day of the disease were not related to the development of thrombotic complications. The thrombin clotting time, platelet count, factor X level, protein C concentration and antithrombin III activity in the plasma were not significantly changed during myocardial infarction. The obtained results suggest a limited usefulness of the basic tests of the clotting and fibrinolytic systems for early diagnosis of deep vein thrombosis in acute myocardial infarction.
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PMID:[Assessment of hemostasis in patients with myocardial infarction complicated by deep venous thrombosis]. 227 86

Acute myocardial infarction was observed in two patients receiving standard intravenous doses of 5-fluorouracil (5-FU)-based chemotherapy. Therefore, the authors prospectively assessed the thrombogenicity of this agent by studying ten patients, six with head and neck cancer and four with gastrointestinal malignancies, receiving 5-FU (1 g/m2/day) as a constant intravenous infusion over a 4-day or 5-day period. The six patients with head and neck cancer also received a single dose of 100 mg/m2 of cisplatin on day 1. Blood samples were obtained preinfusion, 24 hours into the infusion, and postinfusion. Samples were assayed for fibrinopeptide A (FpA) by enzyme-linked immunoassay, for protein C activity (PCa) using a chromogenic substrate (Spectrozyme PCa), and protein C (PCag) and free protein S antigen (PSag) by electroimmunoassay. No patient experienced a thrombotic event. A significant increase was observed in FpA levels during the infusion which returned toward baseline at the conclusion of the infusion. After infusion of 5-FU, the PCa value was significantly lower than the PCag (37 +/- 17 versus 69 +/- 24%; P less than 0.002). No effect on protein S was observed. The changes in the patients receiving 5-FU alone were comparable to those who also received CDDP. The authors conclude that during the infusion of 5-FU, the rise in FpA activation and reduction in PCa as compared to PCag are compatible with activation of coagulation.
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PMID:Thrombogenicity of intravenous 5-fluorouracil alone or in combination with cisplatin. 229 59

In a longitudinal study the plasma levels of antithrombin-III, alpha 2-macroglobulin, alpha 2-antiplasmin, histidine-rich glycoprotein, and protein C were followed in two groups of patients with acute myocardial infarction (AMI), one with and one without deep vein thrombosis (DVT). None of the sequentially studied periods revealed significant differences between the two groups of patients. However, small but consistently higher levels of histidine-rich glycoprotein in patients with DVT suggested the existence among patients submitted for myocardial infarction of a subgroup with increased thrombophilic potential. It was concluded that the inhibitors studied are of little value as possible indicators of the presence of DVT at early stages of the disease when clinical signs are absent and when antithrombotic prophylaxis should preferably be initiated.
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PMID:On the significance of antithrombin-III, alpha 2-macroglobulin, alpha 2-antiplasmin, histidine-rich glycoprotein, and protein C in patients with acute myocardial infarction and deep vein thrombosis. 241 53

Plasma thrombin-antithrombin III complex (TAT), FDP-D-dimer, activated protein C (APC)-protein C inhibitor (PCI) complex, and tissue type plasminogen activator (t-PA), PA inhibitor-1 (PAI-I) were significantly increased in patients with acute myocardial infarction (AMI) at onset. These patients exhibited a hypercoagulable state and protein C activation at onset. The plasma PCI level at onset of AMI was within the normal range, but was significantly decreased after percutaneous transluminal coronary angioplasty (PTCA). After PTCA, plasma t-PA, FDP-D-dimer, and plasmin-alpha 2-plasmin inhibitor were increased but APC-PCI complex and TAT were not. The decrease in PCI after PTCA may have been caused by the activation of fibrinolysis. PCI may play an important role in the inhibition of fibrinolysis in stimulated or damaged endothelial cells. These findings suggest that the protein C pathway plays an important role in the onset of AMI and after PTCA.
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PMID:Decreased protein C inhibitor after percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction. 774 Nov 29

Protein C has an important role in the regulatory mechanisms of coagulation and fibrinolysis. In patients with heterozygous protein C deficiency, there is an increased risk for thromboembolic disease, especially in the venous system. We describe a patient with protein C deficiency presenting with an acute myocardial infarction (AMI). Direct sequence analysis of the whole protein C gene detected a single base mutation at exon 7; 157 [Arg(CGA) to stop codon (TGA): 6182 C to T]. Thus, the patient was suspected to have a deficiency of the protein C heavy chain molecule, resulting in both a low protein C antigen and activity level. The mutation was also found in the propositus' son and was confirmed by differential termination of the primer extension (DTPE).
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PMID:Protein C deficiency found in a patient with acute myocardial infarction: a single base mutation 157 Arg (CGA) to stop codon (TGA). 789 31


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