Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In view of the association between pre-eclampsia and disseminated intravascular coagulation, three patients presenting with severe pre-eclampsia before the 28th week of pregnancy were treated with heparin. In all three patients, there was deterioration of hypertension and proteinuria that necessitated the withdrawal of treatment after five to six days. During treatment, serum and urinary fibrinolytic degradation products (FDPs) continued to rise or remained unaltered, plasminogen levels showed a steady fall, and the platelet count remained at a reduced level. These data suggest that heparin was an ineffective form of treatment and did not prevent the intravascular fibrin deposition associated with severe pre-eclampsia.
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PMID:Failure of heparin therapy to affect the clinical course of severe pre-eclampsia. 118 91

The study of the fibrinolytic system and the activity of interleukin 1 and 2 in 75 patients with various cardial manifestations of atherosclerosis (angina of effort, angina decubitus, arrhythmia, symptomatic hypertension) revealed a decrease in the activity of plasminogen--a blood activator--in patients with angina of effort, angina decubitus and cardiac arrhythmias. In those with atherosclerotic hypertension the activatory activity was in the normal limits. A decrease in the activity of interleukin 1 and 2 was noted in all those examined.
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PMID:[Fibrinolysis, interleukins and coronary atherosclerosis]. 150 14

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

Increased cholesterol levels above 200 mg/dl, LDL levels above 130 mg/dl and total cholesterol/HDL ratio above 4.5 in males and above 5.0 in females are recognized as indicators of increased risk of atherosclerosis. Risk associated to increased triglyceride levels (above 200 mg/dl) must be judged in relation to associated factors such as family history of coronary heart disease, presence of remnants (type III hyperlipidemia), presence of Lp(a), increased levels of Apo B, reduced levels of HDL2 or Apo A1. VLDL and chylomicron remnants and Lp(a) have an atherogenic power in vitro 2 to 4 times that of LDL. There is a correlation between hypertriglyceridemia and reduced HDL2 and Apo A1 levels. Hypertriglyceridemia is frequently associated to other risk factors like diabetes, obesity, hyperinsulinism, and high blood pressure. Finally, VLDL may elevate levels of plasma plasminogen inhibitor. Thus, hypertriglyceridemia should be investigated when, evaluating risk of atherosclerosis.
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PMID:[Cholesterol and triglycerides in atherosclerosis: epidemiologic and physiopathologic considerations]. 184

The percentage of patients with acute myocardial infarction (AMI) who were eligible for thrombolytic therapy was evaluated prospectively, with analysis of the causes for exclusion, in 857 patients with AMI hospitalized in the Chaim Sheba Medical Center, Tel-Hashomer, in 1988. Thrombolytic therapy was given to 127 patients (14.8%); 99 patients were treated with tissue plasminogen activating factor and 28 patients received streptokinase. Three hundred and sixty patients (42.0%) were rejected because of age (greater than 72 years). Other reasons for exclusion were duration of pain lasting for more than 4 h (28.5%), unknown time of onset of the chest pain (9.7%), absence of ST elevation on admission ECG (8.1%), systemic hypertension (4.4%), and presence of severe congestive heart failure upon admission (10.1%). Restricting thrombolytic therapy only to patients less than 72 years old with chest pain duration of 4 h limits the impact of this treatment on the general welfare of patients with AMI. By raising the age limit and extending the time interval between pain onset and treatment initiation, adding newer indications, and enhancing public awareness for early arrival to hospital, the benefit of thrombolytic therapy may be made available to more patients with AMI.
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PMID:Incidence of and reasons for excluding patients with acute myocardial infarction from thrombolytic therapy. 190 38

Seventy-one healthy subjects, aged 20 to 60, 19 males and 52 females, body mass index (BMI) 19 to 40, were enrolled in the study. None of them were smokers, or affected by hyperlipidemia, arterial hypertension or impaired glucose tolerance. We measured plasminogen activators inhibitor (PAI) activity, C-peptide levels, plasma fibrinolytic activity. We found a correlation between BMI and plasma fibrinolytic activity (r = -0.382, p less than 0.005), between BMI and PAI (r = 0.353, p less than 0.005), between BMI and C-peptide (r = 0.694, p less than 0.001) and between PAI and C-peptide (r = 0.404, p less than 0.02). Our data show a correlation between obesity and low fibrinolytic activity, probably due to high PAI levels. In obesity impaired fibrinolytic activity, maybe linked to hyperinsulinemia, could induce thrombophilic state.
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PMID:[Relations between overweight, thrombophilia and cardiovascular risk]. 211 69

In this study, blood coagulation and fibrinolytic parameters were measured in maternal blood and fetal umbilical cord blood in 200 normal pregnant women and in 46 with severe toxemia of pregnancy (Toxemia), and the relationships between fetal growth and concentrations protein C (PC), antithrombin-III (AT-III) and alpha 2-plasmin inhibitor (alpha 2-PI) were studied. 1. Significant increases in fibrin degradation products (FDP) and in plasminogen (Plg), AT-III and PC were found in maternal blood of Toxemia. A significant increase in AT-III and a decrease in alpha 2-PI and PC were observed in cord blood from these patients. 2. The platelet count (Pl) tended to be low in patients with Toxemia complicated by fetal growth retardation (IUGR). 3. Pl and fibrinogen (Fib) tended to be high in Toxemia complicated by normal fetal growth. 4. PC increased from early pregnancy, and a further increase was observed in the puerperium. 5. The PC concentration correlated with the AT-III but not with the alpha 2-PI concentration in maternal blood. 6. PC in cord blood was lower than that in maternal blood, and was correlated with AT-III and alpha 2-PI. 7. In patients with Toxemia, PC was reduced in both maternal and cord blood, and this correlated with AT-III as well as alpha 2-PI in maternal blood. 8. PC was low in Toxemia complicated by hypertension and proteinuria. These results suggest the involvement of FDP, AT-III, PC and Plg in the pathogenesis of Toxemia, and that the Pl, Fib, FDP and alpha 2-PI concentrations are related to fetal growth. Therefore, the PC and AT-III concentrations appeared to be a useful index for the blood coagulation and fibrinolysis in pregnant women and appeared to be important factors in the degree of Toxemia and IUGR.
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PMID:[Blood coagulation and fibrinolytic studies in patients with toxemia of pregnancy]. 227 12

Pulmonary embolism can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

This study prospectively evaluates hypercoagulable states in patients under 51 years of age undergoing lower extremity revascularization for ischemia and assesses early outcome after operation. Twenty patients whose ages range from 23 to 50 years (mean 40.8 years) were identified prospectively who underwent lower extremity revascularization and evaluation of hypercoagulability. Fifteen patients were male (75%), 10 were black (50%), six had hypertension (30%), and four were diabetic (20%). All but two were cigarette smokers (90%). Seven aortoiliac procedures and 13 infrainguinal procedures were performed. Six patients had one or more abnormalities of regulatory proteins (protein S deficiency, four; protein C deficiency, three; presence of lupus-like anticoagulant, three; plasminogen deficiency, two). Eight of 17 patients in whom platelet aggregation profiles were obtained showed increased reactivity (47%). Only 4 of 17 patients (24%) were normal when tested for all parameters. Arterial or graft thrombosis developed in four of the 20 patients within 30 days after operation. Hypercoagulability was found in all four patients whose revascularizations failed. A high incidence of hypercoagulable states was found in patients under 51 years of age with lower limb ischemia requiring revascularization. Hypercoagulability may have contributed to early postoperative thrombosis of the vascular procedure.
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PMID:Hypercoagulable states and lower limb ischemia in young adults. 252 8

The accepted correct procedure for treating occlusive arterial diseases includes surgical disobstruction, CL as well as PTA. Combined non-surgical strategies are effective in about 60% of these patients. However, a high risk of rethrombosis despite from the prophylaxis with anticoagulants like heparin or antiplatelet drugs like ASA is proven, especially in patients with multi-segmental stenosis as well as in patients with extensive narrowing of the arteries. In these cases primary lesions (endangitis obliterans) or secondary lesions of the endothelium cause local depletion of plasminogen in the endothelium. Independent of the method used for reopening the vessel in these patients, a significant progression of the vessel disease and a high rethrombosis rate during longterm follow-up is observed. These results lead us to apply plasminogen locally to decrease the rate of rethrombosis. In patients suffering from stage III-IV (La Fontaine) including patients with multi-segmental stenosis as well as extended narrowing of the artery, PTA in combination with CL was performed. The catheter was placed as near as possible to the thrombus. In some cases the 'fibrinolyticum' could be injected directly into the thrombus. In these cases a bolus of 4,000 U/ml was locally infused, otherwise 1.0-1.5 million U urokinase per 24 hrs. were locally infused with heparin. In 28% (22 patients) no sufficient clinical response occurred using this combined therapy and plasminogen was applied locally. The following criteria supported our decision to include the patients in this study: 1. Insufficient response occurring after 12-24 hrs. of local infusion. 2. Following 6 bolus injections no reopening of the vessel occured within 60 minutes or the clinical response was insufficient due to rethrombosis. 3. Insufficient effects of lysis therapy after 2 hours and contraindication for a systemic fibrinolytic therapy (e.g. hypertension, age, etc.). 1,000 U plasminogen per ml were infused locally or 2,000 U up to 5,000 U plasminogen (in 5 to 10 ml 0.9% saline) were infused slowly (2-4 minutes infusion time) into the catheter in these patients 10 minutes after unsuccessful treatment with local urokinase therapy. Five minutes after administering plasminogen local intraarterial fibrinolytic therapy with urokinase was continued. No severe side effects due to this therapy were observed, although some patients suffered from acute pains in the peripheral segments of the arteries occurring immediately after infusion of plasminogen. In 16 of 22 patients a complete recanalization occurred and in 3 patients a satisfying clinical improvement was observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effectiveness of intraarterial plasminogen application in combination with percutaneous transluminal angioplasty (PTA) or catheter assisted lysis (CL) in patients with chronic peripheral occlusive disease of the lower limbs (POL). 296 85


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