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)

Controversy currently exists regarding the use of diltiazem in the treatment of acute myocardial infarction (AMI). due to conflicting results from clinical trials and animal studies. The purpose of this project was to evaluate the changes in the hemostatic profile during AMI following low dose intracoronary diltiazem infusion. Fourteen Yorkshire swine underwent thoracotomy and 50 min LAD occlusion, followed by 3 h of reperfusion. The first group (n = 8) received 2.5 mg of diltiazem intracoronary at a rate of 5.6 micrograms kg min-1 at the onset of reperfusion. The second group (n = 6) received 0.9% saline intracoronary at the onset of reperfusion and served as the control. The dynamics of plasma antithrombin-III (AT-III), Protein C, total Protein S, fibronectin, endothelin-1 (ET-1), and the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1a) were determined at baseline, then twice during occlusion and finally three times during reperfusion. Diltiazem infusion resulted in diminished ET-1 (34.5%), fibronectin (23.2%), and TxB2 (35.6%); and elevated Protein C (29.3%) when compared with controls. We conclude that intracoronary diltiazem favorable influences hemostasis during AMI in swine. The cardioprotective effects of diltiazem during AMI may be related to the improved hemostatic profile and the reduced incidence of thrombotic complications in such patients.
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PMID:Effects of intracoronary diltiazem on certain hemostatic parameters during acute myocardial infarction in swine. 929 28

To investigate the possibility that activated protein C (APC) resistance due to the factor V could be an important predisposing factor in acute myocardial infarction (AMI), we have retrospectively examined the prevalence of APC resistance with protein C, protein S and antithrombin III deficiency and antiphospholipid antibody syndrome in AMI patients (< or = 50 years) admitted to our hospital over the past 7 years. Forty-seven patients were enrolled in the study. We divided the patients into two groups, warfarin group (group A) and a non-warfarin group (group B). APC resistance is defined as when the APC ratio is below or equal to the cut-off value 2. APC resistance was not detected in either group. The prevalence of an APC ratio below or equal to 2.5 was 16.7% (1 case) in group A and 24.4% (10 cases) in group B. The prevalence of protein C deficiency was 5.0% (2 cases) in group B. Two cases (5.0%) in group B had protein S deficiency. Antithrombin III deficiency was not detected in either group. The prevalence of antiphospholipid antibody syndrome measured by APTT was 40.4% (19 cases). We compared the AMI patients with 97 healthy volunteers (< or = 50 years old) without any thromboembolic events or bleeding tendency in their past history. No significant difference were found between these groups and the volunteers. APC resistance is a major cause of venous thromboembolism in Europe and the United States, while in Japan it is believed to be a minor cause of arterial thromboembolism.
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PMID:Prevalence of activated protein C resistance in acute myocardial infarction in Japan. 948 29

Thrombolytic therapy in acute myocardial infarction fails to re-establish coronary blood flow in a significant number of patients. One reason for this may be haemostatic imbalance. We investigated whether coagulation factor VII antigen (FVIIag), fibrinogen and protein C were related to reperfusion. Plasma from 45 patients was drawn before treatment and reperfusion assessed by means of continuous, on-line, vector-ECG analysis. Among the 17 patients with no reperfusion, FVIIag levels were significantly higher than among the 28 with signs of reperfusion (560 vs. 410 microg/l median, p = 0.006). Protein C levels where higher in the group with successful reperfusion (1.10 vs. 1.01 U/ml median, p = 0.03), whereas no difference was seen in fibrinogen levels. The findings were not influenced by plasma-triglycerides, body-mass index, age or time between onset of chest pain and thrombolytic therapy. The results suggest that FVII is of importance for the formation as well as resolution of coronary clots.
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PMID:Failure of thrombolytic therapy in patients with myocardial infarction is associated with high plasma levels of factor VII antigen. 960 23

A 35 year old woman presented with acute myocardial infarction without any of the usual risk factors: she had never smoked; she had normal blood pressure; she did not have diabetes; plasma concentrations of total cholesterol and high and low density lipoprotein cholesterol, fibrinogen, homocysteine, and Lp(a) lipoprotein were normal. She was not taking oral contraceptives or any other medication. Coronary angiography showed occlusion of the left anterior descending coronary artery but no evidence of arteriosclerosis. Medical history disclosed a previous leg vein thrombosis with pulmonary embolism. Coagulation analysis revealed protein C deficiency. The recognition of protein C deficiency as a risk factor for myocardial infarction is important as anticoagulation prevents further thrombotic events, whereas inhibitors of platelet aggregation are ineffective.
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PMID:Recurring myocardial infarction in a 35 year old woman. 1002 61

Recurrent venous thrombotic and thromboembolic disease, once thought to be an uncommon entity, is increasingly being recognized. Etiologies of recurrent deep venous thrombosis usually include elements of Virchow's triad. Venous stasis (e.g., immobilization, congestive heart failure, acute myocardial infarction, obesity), hypercoagulability (e.g., malignancy, inflammatory bowel disease, hyperhomocysteinemia, protein C resistance, antithrombin III, protein C or S deficiency) and endothelial trauma (e.g., surgical trauma, venous trauma, in-dwelling venous instrumentation) are risk factors. Diagnosis is dependent on objective testing, including venography duplex Doppler (color) ultrasonography and impedance plethysmography. Treatment is usually started with heparin or low-molecular-weight heparin and advanced to warfarin (adjusted to international normalized ratio). Prophylaxis may continue using low-molecular-weight heparin, warfarin, venacaval interruption (Greenfield filter), or concomitant use of the platelet-active agent indobufen and graduated compression stockings.
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PMID:Clinical therapeutic conference: recurrent venous thrombotic and thromboembolic disease. 1009 38

Hereditary protein C deficiency is associated with a predisposition to venous thrombosis. It is not clear whether the deficiency is involved in arterial occlusion. In the present study, we screened for protein C amidolytic activity in patients admitted to the National Cardiovascular Center Hospital, and we identified among them 43 probands and 51 relatives with heterozygous protein C deficiency. Among them, 34 patients with heterozygous protein C deficiency had manifested 45 episodes of arterial occlusive disease. Venous thrombotic diseases were less common. In the examination of whether protein C deficiency hastens arterial occlusion, we found a significant difference (p =0.02) in the age at onset of acute myocardial infarction between the patients with protein C deficiency (n=10; 49.4+/-14.8 years) and a group of patients with normal protein C levels (n=42; 60.5+/-10.6 years). Acute myocardial infarction occurred before 40 years of age in a significantly greater proportion of the patients with protein C deficiency (3:10, 30%) as compared with the controls (2:42, 5%) (chi2=5.9, p=0.015). At the onset of atherothrombotic cerebral infarction the patients with protein C deficiency were significantly (p=0.022) younger (n= 11; 57.4+/-12.8 years) than those with normal protein C levels (n=48; 64.6+/-10.1 years). Venous thrombosis was the most frequent clinical manifestation (21 of 31 episodes) in the patients with antithrombin III deficiency (n=26; 68% of the total), who were admitted to our hospital. Thus, our study suggests that congenital protein C deficiency contributes to earlier onset of arterial occlusive diseases, especially acute myocardial infarction, in Japanese subjects.
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PMID:Analysis of 45 episodes of arterial occlusive disease in Japanese patients with congenital protein C deficiency. 1023 Aug 91

Protein C is one of the most important antithrombotic components. After activation by the thrombin-thrombomodulin complex on endothelial cells, activated protein C (APC) inactivates factors Va and VIIIa, which leads to the inhibition of thrombin formation. We examined the association of plasma levels of APC with the responsiveness to coronary thrombolytic therapy of the infarct-related coronary artery in patients with acute myocardial infarction (AMI). Plasma levels of APC, thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor (PAI) activity were measured in 32 consecutive AMI patients who underwent coronary angiography followed by thrombolytic therapy, and compared to the measurements in 23 control subjects. On admission, APC levels (ng/mL) were significantly elevated in patients with AMI, as compared with controls (2.5+/-0.4 vs. 1.2+/-0.2, 1.3+/-0.2, respectively, p<0.01). At discharge, plasma levels in AMI patients decline to values not significantly different from those in controls. (1.2+/-0.2, 1.3+/-0.2, respectively). TAT levels (ng/mL) were different among the groups in a fashion similar to that of APC (14.1+/-3.1 on admission vs. 3.3+/-0.4 at discharge, 1.8+/-0.1 in the control subjects, respectively, p<0.01). PAI activity levels (IU/mL) were higher on admission than at discharge and higher than the control subjects (19.7+/-1.8 vs. 10.5+/-1.0, 5.4 +/- 0.7, respectively, p<0.01). Thirty-two patients with AMI were classified into two groups according to the results of thrombolysis: the success group (24 patients) and the failure group (eight patients). APC levels were higher in the failure group than in the success group (5.1+/-0.7 vs. 1.6+/-0.2, p<0.01). TAT levels were also higher in the failure group than in the success group (30.8+/-9.6 vs. 8.6+/-1.7, p<0.01). PAI activity levels (IU/mL) were lower in the failure group than in the success group (13.5+/-3.1 vs. 21.7+/-2.1, p<0.05). There were correlations between APC and TAT levels both on admission (r=0.75, p<0.0001) and at discharge (r=0.71, p<0.0001). Elevated APC was thought to correlate with increased thrombin generation in patients with AMI. This study demonstrated that there was a significant relation between plasma APC level and the responsiveness to thrombolytic therapy of the infarct artery. This study may also indicate that increased thrombin generation is a cause of the resistance to thrombolytic therapy.
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PMID:Association of plasma levels of activated protein C with recanalization of the infarct-related coronary artery after thrombolytic therapy in acute myocardial infarction. 1040 85

Persistent coagulation activity after an acute myocardial infarction may increase the risk of reinfarction. We prospectively investigated the effects on plasma coagulation of a low, fixed dose of warfarin in combination with aspirin after myocardial infarction. We also evaluated the influence of coagulation activity on clinical outcome. Plasma samples from 97 patients, randomised to 1.25 mg of warfarin daily in combination with 75 mg of aspirin or aspirin alone were drawn 4 days, 1 month, and 6 months after myocardial infarction. Patients receiving warfarin had a greater reduction in factor VII coagulation activity (FVII:C) after 6 months: 0.18 vs. 0.06 U/mL,(95% CI, 0.02-0.22), whereas no differences were seen in levels of protein C, protein S, or prothrombin fragment 1+2. In the acute phase, the level of free protein S was lower than after 6 months in both groups: 25.6 vs. 28.8% (95% CI, 4.19--2.35). Cardiovascular mortality, reinfarction, and stroke were evaluated after 4 years (median). In a survival analysis, every 0.1 U/mL increase in the level of FVII:C1 month after myocardial infarction was associated with an 15% increase in risk of cardiovascular events (95% C1, 1.01-1.30). Warfarin at 1.25 mg daily reduces FVII:C but not systemic thrombin generation measured as prothrombin fragment 1 +2. Low levels of the anticoagulant protein S may contribute to a procoagulant state.
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PMID:Changes in levels of factor VII and protein S after acute myocardial infarction: effects of low-dose warfarin. 1058 63

The genetic defect of coagulation factor V known as factor V Leiden produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thromboembolism. The data on arterial thrombosis associated with APC resistance are still not clearly defined. We conducted a study in patients presenting with acute myocardial infarction (MI) to assess whether factor V Leiden increases the risk of arterial thrombosis. We studied 109 patients who had a diagnosis of acute MI (69 males and 40 females, aged 25-91 years), and 112 controls. The study population was identified by characteristic ECG changes and elevation of serum CK-MB, whereas the control subjects were anonymous healthy blood donors with no known history of coronary artery disease. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. Heterozygous factor V Leiden mutation was found in 9 of 109 (8%) MI patients and 5 of 112 (4%) control subjects (P =.42). In conclusion, this study shows no evidence of an association between factor V Leiden and acute MI.
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PMID:Incidence of factor V Leiden in patients with acute myocardial infarction. 1059 Jan 88

Alterations in various hemostatic factor have been identified as risk factors for survival after acute myocardial infarction (AMI). However, these clinical data are primarily limited to observations made during the postinfarct stage. We assessed the effects of 50 minutes of left anterior descending artery occlusion on several hemostatic factors and analyzed their changes with outcome in 18 Yorkshire swine. Blood samples were obtained from the systemic circulation at base-line and at 25 and 50 minutes of occlusion. Platelet aggregability and plasma antithrombin-III protein C, protein S, fibronectin, endothelin-1, as well as the metabolites of thromboxane and prostacyclin were measured. Of the 18 swine, 7 survived the infarct and 11 animals developed fatal ventricular fibrillation. Both groups demonstrated significant decreases in platelet aggregation, and a decline in plasma protein S when compared with baseline. Thromboxane, prostacyclin, and ondothelin-1 plasma concentrations were also markedly reduced at the end of occlusion. There were significant changes in antithrombin-III, protein C, and fibronectin levels between surviving animals and those that died of ventricular fibrillation. Acute coronary artery occlusion is associated with substantial changes in the hemostatic factors in swine. Plasma levels of fibronectin, antithrombin-111, and protein C differed between survivors and nonsurvivors and thus might serve as predictors of mortality due to fatal ventricular fibrillation during AMI. The mechanisms of these changes during the acute phase of AMI are unclear. Immediately AMI prognosis may be related to hemostatic changes not only after thrombolysis or spontaneous reperfusion, but also during the occlusion phase as well.
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PMID:Survival in Acute Myocardial Infarction Induced by Coronary Ligation: Prognostic Relevance of Certain Hemostatic Factors During the Occlusion Phase. 1060 47


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