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)

Although cardiovascular mortality has decreased in recent years, it is still largely due to coronary disease: 1 out of 5 men and 1 out of 17 women are affected by that disease before the age of 60. Among the risk factors involved are lipid disturbances, themselves divided into three factors: LDL-cholesterol, triglycerides and HDL-cholesterol. A plasma LDL-cholesterol level above 150 units is a high risk factor. Triglyceride levels higher than 1.50 g/l, associated with HDL levels lower than 40 mg/dl constitute a new entity, a genetic disease associated with a special fragment on chromosome 11, characterized by high risk low HDL levels (below 40). Another risk factor, even in elderly people, is arterial hypertension. Cigarette smoking, lack of physical activity, diabetes and mental stress remain important factors, whereas obesity has become a separate factor. Finally, such factors as ECG abnormalities, plasma uric acide or plasminogen levels, familial context, etc., may be taken into consideration. All dietetic and therapeutic measures aimed at lowering the cholesterol level show a 2-3 p. 100 fall in the incidence of coronary disease for each 1 p. 100 reduction of blood cholesterol. A new programme, similar to those used in screening for high blood pressure subjects, will be set up in the U.S.A. to identify people with a blood cholesterol level higher than 2.40 g/l, treat them and bring that figure down below 2.00 g/l. The management of arterial hypertension is still based on treatments which do not increase blood cholesterol or increase HDL. They include alpha-blockers, beta-2 agonists and blockers of intracellular contractility. They have the additional advantage of improving capillary perfusion.
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PMID:[Framingham 36 years later]. 311 92

In eight male patients with normal liver and kidney function fibrinolytic components were measured in arterial blood and in renal and hepatic vein blood, obtained during catheterization for analysis of hypertension. Blood samples were collected simultaneously from veins und corresponding arteries before and 5 minutes after the completion of intravenous injection of desmopressin (DDAVP), 0.4 micrograms/kg body weight over a 10 minute period. DDAVP induced a rise in t-PA antigen and activity, and in von Willebrand factor, accompanied by a decrease in free PA-inhibitor level. We failed to detect a significant rise in plasma urokinase activity. The concentrations of fibrinogen, plasminogen, alpha 2-antiplasmin, antithrombin III and coeruloplasmin did not change either. Renal production of t-PA under basal conditions was inferred from a negative arterio-venous (A-V) difference in t-PA-activity and in t-PA-antigen levels but this could not be confirmed by orthogonal regression analysis of the same data. A-V differences of other fibrinolytic factors were negligible. In the hepatic vessels a significant positive A-V difference of t-PA-activity and of t-PA-antigen levels was a uniform finding. After DDAVP, when plasma levels were elevated, the mean A-V difference was proportionally higher, consistent with a constant fractional elimination rate. Free PA-inhibitor was virtually absent from arterial blood after DDAVP, but appeared in hepatic vein blood, indicating either production of the inhibitor by the liver or dissociation of a circulating complex of t-PA and its inhibitor in the liver. The blood levels of the other investigated components did not show any change upon passage through the liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and hepatic handling of endogenous tissue-type plasminogen activator (t-PA) and its inhibitor in man. 314 78

Epidemiological studies of oral contraceptives pertaining to premenopausal women are briefly reviewed. Therapeutic considerations are noted. The clinical effects of aging and hormone replacement therapy are indicated in terms of metabolism, the endometrium, and bone mass. The pharmacological advantages and consequences of nonhormonal and hormonal contraception are explored. For aging women over 40, there is a need for relief of menopausal symptoms, contraception, and reduction of risks for atherosclerosis, hypertension, coronary heart disease, endometrial carcinoma, breast cancer, and osteoporosis. With the availability and use of low estrogen products, women over 40 can insure tissue support and prevent bone loss as long as the therapy is instituted within 3 years of the last menses. Over-40 women who drink and smoke should not use oral contraceptives. Sterilization does not satisfy longterm hormonal needs, and has other reported menstrual side effects. The dose and duration regimen of hormonal therapy must be carefully considered due to the effects on the endometrium., the coagulation system, the liver, lipids, and bone. Combination estrogen and progestogen is necessary, but consideration must be given to existing levels of endogenous hormones. Lipid patterns may change due to hormone replacement or as a result of aging and contribute to coronary heart disease. Hormone replacement can reverse the atherogenic pattern of increased low density lipoprotein levels and decreased high density lipoprotein levels; a chart gives the effects on lipids and coagulation from various estrogen or estrogen plus progestogen products. For the estrogen-deficient menopausal woman, high estrogen can decrease antithrombin III plasminogen and alpha-antitrypsin antigen levels. Lower dose progestogens are recommended. Studies of dose and effects on bone mass are reviewed and vaginal rings and transdermal steroid patches, triphasic formulations, and new progestational agents such as 19-nortestosterone derivatives are described. Newer low dose formulations are needed for the aging woman, as well as further research on what product best suits the variability of women aged 40-50
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PMID:Contraception for the perimenopausal patient. 330 20

Fibrinogenolysis induced by thrombolytics exposes the risk of haemorrhagic complications. The efficacy is proved for pulmonary emboli of recent origin. The aim of this study is to research into the effect of local administration of low dose urokinase in six patients aged 40 (+/- 16 years) and presenting with old emboli (10 +/- 4 days). The initial clinic picture was serious with shock (2 cases), hypoxaemia (6 cases), pulmonary arterial hypertension (mean 40 +/- 8 mmHg) and a Miller index of 58 (+/- 8%). Mechanical ventilation was necessary four times. Urokinase was administered in situ using a Swan Ganz catheter, with 1,000 units per Kg per hour for six hours followed in sequence with 30 microkatals per hour of plasminogen for two hours. This eight hourly rotating sequence was followed for at least 72 hours. Six patients were cured with an end of treatment (5 +/- 2 days) improvement in their hypoxaemia of 22%, a fall of 47% of the pulmonary arterial pressure and a rise of 71% in the Miller index. The fibrinogenesis fell by 11% and the thrombolytics could not blamed for any side-effect. The sequence urokinase-plasminogen in low dose administered locally may represent an alternative treatment for severe and long standing pulmonary emboli in patients with a risk of haemorrhage.
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PMID:[Value of thrombolysis in situ without general fibrinogenolysis in pulmonary embolisms of more than 5 days duration]. 344 74

The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, alpha 2-antiplasmin and alpha 2-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.
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PMID:Fibrinolytic behavior in long-standing branch retinal vein occlusion. 369 97

Fibrinogen, fibrinogen-related antigen (FR-antigen), and components of the fibrinolytic enzyme system were measured in patients with essential hypertension, renal disease with and without hypertension, and normal subjects. Essential hypertension was associated with a decrease in plasminogen activator and an increase in FR-antigen. In renal disease these changes were accompanied by increases in plasminogen activation inhibitor, alpha(2)-macroglobulin, alpha(1)-antitrypsin, and fibrinogen.
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PMID:The fibrinolytic enzyme system in hypertension. 471 59

A highly-standardized plate method was used to study fibrinolytic profiles in 14 patients with essential hypertension and 245 normotensive healthy control subjects. Compared with the normotensive group, the group with essential hypertension showed a defect in fibrinolysis, as evidenced by a significant increase in the mean level of inhibitor of plasminogen activation, and a subset of the hypertensive patients also showed a significant decrease in the mean level of vascular plasminogen activator. There were no significant differences between the two groups in relation to plasma fibrinogen level, total fibrinolytic activity and plasmin inhibitor. The alterations in inhibitor of plasminogen activation and vascular plasminogen activator in the patients with essential hypertension may reflect a defect in the fibrin-clearing mechanism and, perhaps, contribute to the vascular complications of hypertension.
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PMID:Abnormalities of fibrinolysis in essential hypertension. 624 55

By activating plasminogen into plasmin, which in turn dissolves fibrin, fibrinolytic agents can dissolve pathologic thrombi. Streptokinase, a fibrinolytic agent derived from group C beta-hemolytic streptococci, is antigenic and can elicit allergic reactions. Urikinase, a fibrinolytic agent obtained by purification from human urine or from human fetal kidney cell culture, is not antigenic, and for this reason can be used repeatedly, if needed, whereas streptokinase cannot be used for retreatment within six months of a course of therapy. Either agent can be introduced into the circulation systemically (intravenously) or locally (via catheter). The indications for systemic therapy include deep-vein thrombosis, pulmonary embolism, and arterial thrombosis and embolism. The indications for local therapy include acute myocardial infarction, arterial thrombosis and embolism, and the clearing of occluded arteriovenous cannulae and access shunts. Contraindications include an actively bleeding lesion, a vascular intracranial disorder, or uncontrolled hypertension; relative contraindications include pregnancy; a recent wound, fracture, surgery, or deep closed biopsy; or a general contraindication to anticoagulation, such as coagulopathy, uremia, or severe liver disease. During thrombolytic therapy, invasive procedures, intramuscular injections, and the use of other anticoagulant or antiplatelet agents should be avoided. Measurement of fibrinogen levels, the titer of fibrin/fibrinogen degradation product, or thrombin time can be used to monitor therapy.
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PMID:Fibrinolysis and its current usage. 634 82

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62

To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.
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PMID:Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris. 761 16


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