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)

The relationship between coffee consumption and acute myocardial infarction (AMI) was analyzed using data from a case-control study conducted in 1988 to 1989 within the framework of the GISSI-2 trial on streptokinase versus alteplase and heparin versus no heparin in the treatment of AMI. A total of 801 male patients with AMI and 792 control subjects who were hospitalized in several Italian regions for diseases unrelated to known or potential risk factors for cardiovascular diseases were included. Compared with coffee nondrinkers, the multivariate relative risks (RRs), after allowance for age, education, body mass index, smoking habits, alcohol consumption, family history of AMI, cholesterol level, history of diabetes, and hypertension, were 0.8 (95% confidence interval (CI), 0.5 to 1.2) for consumption of one cup/d, 1.3 (95% CI, 0.9 to 2.0) for two cups/d, 1.8 (95% CI, 1.1 to 2.7) for three cups, 2.5 (95% CI, 1.5 to 4.1) for four cups, and 2.6 (95% CI, 1.6 to 4.2) for five cups or more. The trend in risk with dose was statistically significant (P < 0.001). Duration of coffee consumption was not associated with the risk of AMI. The RRs for daily coffee consumption were elevated across strata of various covariates, including age, smoking habits, cholesterol level, diabetes, and hypertension, with a particularly elevated (although not significantly heterogeneous) estimate in patients younger than 50 years (RR, 5.7; 95% CI, 3.0 to 10.9 for four or more cups/d). The RR in patients who drank four or more cups of coffee per day and were current smokers was 8.1 (95% CI, 5.1 to 13.0), suggesting an unfavorable effect on the combination of cigarette smoking and high coffee intake on the risk of AMI.
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PMID:Coffee consumption and risk of acute myocardial infarction in Italian males. GISSI-EFRIM. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto, Epidemiologia dei Fattori di Rischio del'Infarto Miocardico. 792 6

The relationship between physical activity and acute myocardial infarction (AMI) was examined in a case-control study conducted in Italy in 1988 to 1989 within the framework of the GISSI-2 trial of streptokinase versus alteplase and heparin versus no heparin in the treatment of AMI. A total of 916 case patients admitted to coronary care units from various Italian regions for AMI were interviewed. Control subjects were 1106 patients admitted to the same network of hospitals for a broad spectrum of acute diseases not related to known or potential risk factors for myocardial infarction. Among various types of physical activity (occupational activity, walking, stair climbing, and sport and leisure-time physical activity), occupational physical exercise emerged as the most protective. Multivariate odds ratios (ORs) were 1.4 (95% confidence interval (CI), 1.0 to 2.0) and 1.6 (95% CI, 1.2 to 2.1) for the two lowest levels of occupational physical activity. The trends of increasing risk with decreasing activity were consistent, although less strong, when other types of activity were considered. The protection conveyed by occupational physical activity was similar across various strata of sex, age, education, smoking habits, and diabetes, and was not explained by serum cholesterol, body weight, or hypertension. This study therefore confirms that low physical activity is an indicator of subsequent risk of AMI.
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PMID:Physical activity and the risk of acute myocardial infarction. GISSI-EFRIM Investigators. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto-Epidemiologia dei Fattori di Rischio dell'Infarto Miocardico. 792 13

The first generation high-dose ( 80 mcg estrogen) oral contraceptives (OCs) were associated with an increased risk of deep venous thrombosis (DVT). So manufacturers removed the high-dose OCs and first replaced them with OCs with 50 mcg estrogen, resulting in a lower incidence of thromboembolic events (40 vs. 20/100,000 users). When they introduced an even lower dose OC (30 mcg estrogen), the incidence fell further (about 8/100,000 users). Yet, women using the lowest-dose OCs still have DVT more often than do control women. Life-style, age, and smoking may be confounding factors, however. It is not clear whether loss of endogenous ovarian steroid production or the effects of the orally administered contraceptive steroids cause significant changes in hemostatic factors (antithrombin III, protein S, protein C, plasminogen, tissue-type plasminogen activator, plasminogen activator inhibitor 1, histidine-rich glycoprotein, and VII, VIII, X, XII coagulation factors) during OC use. These changes tend to be within normal ranges. There is some doubt that these changes have any clinical significance. In nonsmokers, increased activity of anticoagulant factors and fibrinolytic factors counteract the effects on coagulation factors. Progestin-only OCs appear to affect hemostasis but have not increased the risk of thrombosis. There are considerable differences between people in pharmacokinetics and pharmacodynamics of contraceptive steroids. These differences may account for the increased risk of thromboembolic events in some people. Further research should identify methods of individualizing the dose of contraceptive steroids for a single patient. It should also explore the close interrelationship between hemostasis and lipid metabolism, carbohydrate metabolism, and hypertension in the development of cardiovascular disease in OC users. Providers should discourage women with a past history of DVT from using hormonal contraception.
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PMID:Coagulation and anticoagulation effects of contraceptive steroids. 817 1

Pregnancy is associated with depressed fibrinolysis as judged from the decreased fibrinolytic response to venous occlusion. In order to elucidate if this decreased response is due to an increase in plasminogen activator inhibitors 1 and 2 (PAI-1, PAI-2), and/or to decreased release of tissue-type plasminogen activator (t-PA) antigen during venous occlusion, 36 women (18 women with normal pregnancy and 18 with gestational hypertension without proteinuria) were followed during pregnancy and puerperium. In each women a 20 min venous occlusion was performed in the second and in the third trimester of pregnancy and 3 days after delivery. The increase in t-PA antigen after venous occlusion relative to basal value was in the second trimester of pregnancy on average 3.7 fold, in the third trimester 4.4 fold, and so not reduced compared to non-pregnant women (3.7 fold increase). After delivery the increase in t-PA antigen was significantly enhanced (8.5 fold, p < 0.005). The fibrinolytic response to venous occlusion measured by euglobulin and t-PA activity was significantly decreased in the third trimester compared to non-pregnant values (both p < 0.005) and returned to somewhat higher (euglobulin clot lysis) or significantly higher (t-PA activity, p < 0.01) values 3 days after delivery. Decreased euglobulin and t-PA activity after venous occlusion in the third trimester coincided with significant increases in basal PAI activity, PAI-1 antigen and PAI-2 antigen (2.9, 2.5 and > 30 fold increase relative to non-pregnant values, respectively, all p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue-type plasminogen activator after venous occlusion in pregnancy and puerperium. 825 54

Arterial hypertension (HTN) increases the risk of cerebral coronary, and other vascular complications that frequently involve platelet activation and blood coagulation. Several key proteins in the blood coagulation, fibrinolytic and inhibitory systems were studied in 29 men with HTN (aged 45 +/- 3 yr) and 15 normal men of the same age. Plasma levels of high-molecular-weight kininogen and factors XII, IX, VII, X, II, and XIII, as well as von Willebrand factor (vWF), fibrinogen, fibronectin, alpha 2-antiplasmin, tissue-plasminogen activator, D-dimer, platelet factor-4, and protein C were measured by the use of appropriate functional and immunologic assays before and after a cardiopulmonary exercise stress test. The concentrations of vWF, alpha 2-antiplasmin, and D-dimer were significantly (P < 0.02) higher in the HTN group as compared with the control group. The exercise stress test resulted in significant rises in the plasma vWF, alpha 2-antiplasmin, and tissue-plasminogen activator levels in the two groups. The concentrations of vWF and D-dimer were related to diastolic blood pressure (r = 0.44 and 0.40, respectively; P < 0.02). Levels of vWF also were related to left ventricular mass index and left ventricular posterior wall and septal thickness (r = 0.34, 0.43, and 0.34, respectively; P < 0.05). The constellation of these findings suggests a low-grade fibrin formation and degradation, the magnitude of which is related to the diastolic blood pressure. The observed abnormalities can potentially contribute to the cardiovascular complications of untreated HTN.
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PMID:Coagulation and inhibitory and fibrinolytic proteins in essential hypertension. 840 86

Cardiovascular risk factors associated with hypertension include alterations in arterial compliance and an increased tendency to thrombosis. In this study we examined the relationship between arterial compliance and endothelial derived components of the hemostatic system: von Willebrand factor (vWF) and tissue plasminogen activator (t-PA). Ten males (4 normal and 6 untreated hypertensives, 41 +/- 12 years) were studied. Compliance of proximal (large vessel) and distal (small vessel) arteries was measured by intraarterial pulse wave analysis; left ventricular wall thickness by echocardiography; and vWF and t-PA by immunoassay of plasma obtained before and immediately after maximum treadmill exercise. Baseline t-PA and vWF correlated inversely with distal compliance (r = -0.74, p = 0.01; r = -0.56, p = 0.09). Exercise strengthened the relationship between vWF and both distal compliance (r = -0.56 to r = -0.86) and proximal compliance (r = -0.44 to r = -0.70). Moreover, post-exercise levels of vWF and t-PA were each significantly related to left ventricular posterior wall and septal thickness. Of note, these protein concentrations correlated more strongly with arterial compliance and left ventricular wall thickness than with blood pressure. Thus, arterial compliance and left ventricular wall thickness appear to be more powerful than blood pressure as predictors of the endothelial release of vWF and t-PA in response to exercise. These findings indicate that some of the key cardiac and arterial characteristics of hypertension might be linked to increased endothelial reactivity to hemodynamic stress.
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PMID:The relationship of arterial compliance with endothelial-derived proteins of the hemostatic system. 844 90

Comparative study was performed on the Heart-Qi Deficiency and Blood Stasis type (HQDBS) of hypertensive patients treated with Qigong. The results showed that the clinical symptoms alleviated, cardiac morphology and function, hemorheology and erythrocyte deformity were improved. After one year of practicing Qigong, plasma histofibrinogen activation inhibitor (PAI) and VIII factor related antigen (VIII R: Ag) levels decreased, while plasma tissue fibrinolytic activator (t-PA) and anti-thrombogen III (AT-III) levels increased. Capillary blood velocity of nailfold microcirculation raised from 0.2940 +/- 0.0206 mm/s to 0.3045 +/- 0.0236 mm/s, the diameter and length of afferent limb tended to increase. The above data indicated that Qigong could benefit HQDBS. This might be the mechanism by which HQDBS type of hypertension was treated.
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PMID:[Effect of qigong on heart-qi deficiency and blood stasis type of hypertension and its mechanism]. 858 Jun 89

The fibrinolytic system is thought to be impaired in older hypertensive adults, thus contributing to the elevated risk of atherothrombosis, stroke, and acute myocardial infarction in this population. However, studies that have examined the fibrinolytic system in hypertensive individuals have failed to control for the confounding effects of other metabolic risk factors, making it difficult for one to determine the independent effect of hypertension on the fibrinolytic system. The purpose of the present study was to test the hypothesis that the fibrinolytic system is not impaired in older sedentary hypertensive men when the confounding effects of cardiovascular disease, diabetes, and dyslipidemia are controlled. Plasma concentrations of tissue-type plasminogen activator antigen and activity as well as plasminogen activator inhibitor-1 antigen and activity were measured under resting conditions in 12 hypertensive (69.4 +/- 1.4 years) and 11 normotensive 65.2 +/- 1.3 years) older men. The hypertensive and normotensive subjects had similar anthropometric and metabolic characteristics. There were no significant differences between the hypertensive and normotensive men in tissue-type plasminogen antigen (7.3 +/- 0.5 versus 6.1 +/- 0.6 ng/mL) and activity (1.8 +/- 0.3 versus 1.7 +/- 0.2 IU/mL) or plasminogen activator inhibitor-1 antigen (14.1 +/- 2.3 versus 10.8 +/- 2.2 ng/mL) and activity (17.4 +/- 1.2 versus 17.5 +/- 1.8 arbitrary units [AU]/mL) levels. In addition, the molar concentration ratio of active tissue type plasminogen activator to active plasminogen activator inhibitor-1 did not differ between the hypertensive (1:9.7 +/- 2.3) mmol/L) and normotensive (1:10.5 +/- 2.2 mmol/L) subjects, indicative of no impairment in fibrinolytic potential in either group. These results support the hypothesis that hypertension does not directly result in impaired fibrinolytic function in older adults. Furthermore, our findings suggest that abnormalities in fibrinolytic function in older hypertensive men are likely due to the primary effects of other metabolic disorders that usually accompany hypertension, such as hyperinsulinemia and dyslipidemia.
Hypertension 1996 May
PMID:The fibrinolytic system is not impaired in older men with hypertension. 862 Nov 96

Over 200 risk factors for cardiovascular disease (CVD) have now been identified. Among these, the three most important are (1) abnormal lipids, including the fact that there are more than 15 types of cholesterol-containing lipoproteins and four different types of triglyceride-rich particles, some of which are very atherogenic, (2) high blood pressure, and (3) cigarette smoking. In addition, many other factors including diabetes, haemostatic factors such as fibrinogen, factor VII, plasminogen activator inhibitors, and new factors such as apolipoprotein E4 and homocysteine, are known to increase the risk of developing clinical CVD. A low risk for CVD requires that these various factors are present in the circulation in the correct proportions. Two simple tests for determining plasma lipid levels can be used to identify those individuals with an atherogenic lipid profile and who are, therefore, at increased risk for CVD. Firstly, the ratio of total cholesterol to high density cholesterol (HDL cholesterol) should be determined, followed by measurement of plasma triglyceride concentrations. This will allow differentiation of whether the low density lipoproteins (LDL), HDL cholesterol or triglyceride-rich particles such as the small dense beta-very low density lipoproteins (VLDL) are the major cause for concern. Once identified, those individuals with a high lipid risk profile should be treated before, rather than after, experiencing coronary heart disease (CHD).
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PMID:Lipids, risk factors and ischaemic heart disease. 883 10

The plasmid pMK16 containing-SV40 replicated origin defective gene was efficiently introduced into early-passage human umbilical vein endothelial cells (HUVEC) using positively charged liposomes. The resulting cell line acquired an almost infinite lifespan, was morphologically unchanged, expressed SV40-antigen, and coexpressed von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), angiotensin conversion enzyme (ACE), and endothelin converting enzyme (ECE). In addition, these are the first immortalized human endothelial cells, to our knowledge, that biosynthesized and secreted interleukins (IL-1 beta and IL-6) in both a constitutive and regulated fashion and endothelin-1 (ET-1), the most potent vasoactive peptide, which has been suggested to be implicated in the pathogenesis of hypertension. Interestingly enough, both of the immortalized cells and the early-passage HUVEC from which the immortalized cells were obtained biosynthesized and secreted the same levels of ET-1 suggesting full maintenance of its biosynthetic pathway including the presence of active ECE, which cleaves big endothelin-1 (big-ET-1) to ET-1 and regulation factors. Moreover, the immortalized cells retained the ability to express the functional specific amino acid Na(+)-independent system Y+ transporter, which mediates L-arginine transport into endothelial cells from which endothelium-derived relaxing factor (EDRF, nitric oxide) is formed via the action of nitric oxide-synthase. Obtaining these immortalized human endothelial cells without alteration of the differentiated characteristics constitutes a useful model: (a) to study ET-1 secretion, gene regulation, and human ECE, which may be an important therapeutic target in disease conditions in which ET-1 is to be implicated; (b) to study L-arginine transport, which is a key step in the formation of EDRF; (c) to study IL-1 beta and IL-6 secretions, and gene regulations; (d) to substitute large quantities of HUVEC; and, finally, (e) to reproduce, starting with different primary endothelial cells both from human and animal origin.
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PMID:Establishment of permanent human endothelial cells achieved by transfection with SV40 large T antigen that retain typical phenotypical and functional characteristics. 883 14


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