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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that the hypercoagulable state in hypertension is significantly altered by anti-hypertensive therapy, we conducted a pilot prospective randomised double-blind trial of 40 untreated hypertensive patients (30 males, mean age 59 years) who were treated with either enalapril (10-20 mg per day) or losartan (50-100 mg per day) for 8 weeks. Thrombogenicity was assessed by measurement of plasma fibrinogen, soluble P-selectin (an index of platelet activation), plasminogen activator inhibitor 1 (PAI-1, an index of fibrinolysis) and von Willebrand factor (an index of endothelial dysfunction). Baseline von Willebrand factor alone was significantly higher in untreated hypertensive patients compared to controls (P<0.001). Following 8 weeks treatment with enalapril (mean dose 17 mg/day) or losartan (mean dose 77 mg/day), there was a significant reduction in mean blood pressure from 169+/-11/94+/-8 mmHg (baseline) to 147+/-14/84+/-7 mmHg (post-treatment) (P<0.001). However, there were no statistically significant changes in the levels of haemostatic markers (von Willebrand factor, fibrinogen, s-Psel and PAI-1). Our pilot study confirms previous observations of endothelial dysfunction in hypertensives. However, plasma fibrinogen and indices of platelet activation, fibrinolysis or endothelial dysfunction were not significantly affected by antihypertensive treatment with enalapril or losartan, despite satisfactory blood pressure control.
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PMID:Effect of antihypertensive therapy using enalapril or losartan on haemostatic markers in essential hypertension: a pilot prospective randomised double-blind parallel group trial. 1137 27

Endothelial cells are a rich source of a variety of vasoactive substances, which either cause vasodilation or vasoconstriction. Important endothelium-derived vasodilators are prostacyclin, bradykinin, nitric oxide and endothelium-derived hyperpolarizing factor. In particular, nitric oxide inhibits cellular growth and migration. In concert with prostacyclin. nitric oxide exerts potent anti-atherogenic and thromboresistant properties by preventing platelet aggregation and cell adhesion. Endothelium-derived contracting factors include the 21 amino acid peptide endothelin (ET). vasoconstrictor prostanoids such as thromboxane A2 and prostaglandin H2, as well as free radicals and components of the renin angiotensin system. In hypertension, elevated blood pressure transmits into cardiovascular disease by causing endothelial dysfunction. Hence, modem therapeutic strategies in human hypertension focus on preserving or restoring endothelial integrity. Angiotensin converting enzyme (ACE) inhibitors are a primary candidate for that concept as they inhibit the circulating and local renin angiotensin system. Angiotensin converting enzyme is an endothelial enzyme which converts angiotensin-I (A-I) into angiotensin-II (A-II). This effect of the ACE inhibitor prevents direct effects of angiotensin-II such as vasoconstriction and proliferation in the vessel wall but also prevents activation of the ET system and of plasminogen activator inhibitor. Furthermore, inhibition of ACE prolongs the half-life of bradykinin and stabilizes bradykinin receptors linked to the formation of nitric oxide and prostacyclin. In isolated arteries ACE inhibitors prevent the contractions induced by angiotensin II and enhance relaxation induced by bradykinin. Chronic treatment of experimental hypertension with ACE inhibitors normalizes endothelium-dependent relaxation to acetylcholine and other agonists. In addition, the dilator effects of exogenous nitric oxide donors are enhanced, at least in certain models of hypertension. In humans with essential hypertension ACE inhibitors augment endothelium-dependent relaxation to bradykinin, while those to acetylcholine remain unaffected, at least in the time frame of the published studies, i.e. 3-6 months. In patients with coronary artery disease, however, paradoxical vasoconstriction to acetylcholine is markedly reduced after 6 months of ACE inhibition. After myocardial infarction ACE inhibitors reduce the development of overt heart failure, the occurrence of reinfarction and cardiovascular death in hypertensive patients. These effects have also been demonstrated in a subgroup analysis of the SOLVD (Studies of Left Ventricular Dysfunction) trial. Thus, in summary, ACE inhibitors are an important class of drugs providing cardiovascular protection in patients with increased cardiovascular risk.
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PMID:Vascular protective effects of angiotensin converting enzyme inhibitors and their relation to clinical events. 1139 75

While the blood vessels are exposed to high pressures in hypertension, the main complications of hypertension (stroke and myocardial infarction) are paradoxically thrombotic rather than haemorrhagic. To investigate abnormalities of haemorheology (plasma viscosity, fibrinogen), endothelial dysfunction (von Willebrand factor), platelet activation (soluble P-selectin) and thrombogenesis (plasminogen activator inhibitor and fibrin D-dimer) in stroke and the effects of concurrent hypertension, we studied 86 consecutive patients (58 male, 28 female) aged < 75 years (mean age +/- SD, 64.2 +/- 9.2 years) with acute stroke (ictus < 12 h). Baseline blood tests on admission were compared with 46 'hospital controls' (patients with uncomplicated essential hypertension; mean age +/- SD, 65.9 +/- 3.8 years) and 24 healthy normotensive controls (mean age +/- SD, 65 +/- 14.0 years). Further comparisons were made between stroke patients with hypertension (systolic blood pressure > 160 mmHg and/or diastolic > 90 mmHg) on admission and those without hypertension. Mean plasma viscosity (one-way analysis of variance, P = 0.026) and fibrinogen levels (P = 0.016) were significantly higher in stroke patients and hospital controls, when compared with healthy controls. The von Willebrand factor, plasminogen activator inhibitor soluble P-selectin and fibrin D-dimer levels were highest in the acute stroke patients, intermediate in hospital controls and lowest in healthy controls (all P < or = 0.001). There were no significant differences in measured indices of haemorheology, endothelial dysfunction and thrombogenesis between the three stroke pathological subtypes (ischaemic/thrombotic, haemorrhagic or transient ischaemic attack). There were also no significant differences in the measured parameters for stroke patients with or without systolic blood pressure > 160 mmHg or diastolic blood pressures > 90 mmHg using clinical (manual) readings or mean daytime or night-time ambulatory blood pressure monitoring recordings. There were no statistically significant differences between the measured parameters on admission and at 3 months follow-up in 26 patients (all P = not significant). Plasma viscosity was significantly correlated with mean daytime systolic blood pressure (r = 0.314, P = 0.021) and mean night-time systolic blood pressure (r = 0.309, P = 0.025). This study of hypertension and haemostasis in acute stroke has demonstrated clear abnormalities of haemorheology, endothelial dysfunction, platelet activation and thrombogenesis, which do not appear to be affected by the height of the blood pressure or the presence of hypertension. This is despite the known hypercoagulable state found in hypertension and the relationship of haemostatic abnormalities to vascular complications.
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PMID:Abnormal haemorheology, endothelial function and thrombogenesis in relation to hypertension in acute (ictus < 12 h) stroke patients: the West Birmingham Stroke Project. 1146 15

Although the incidence of strokes is not maximal during sleeping hours, several lines of evidence make it probable that sleep in combination with breathing disorders like snoring and obstructive apneas are risk factors for ischemic strokes: the natural history of snoring and obstructive sleep apnea shows a higher incidence of strokes than in undisturbed sleep, the prevalence of snoring and sleep apneas in stroke patients is by far higher than in non-stroke patients; odds-ratios of stroke are higher in snorers and apneic patients than in normals, although the correction for confounders seems never perfect. The analysis of potential pathomechanisms linking sleep disordered breathing to strokes is another approach to the main topic: snoring and sleep apnea induce hypertension and arrhythmia, the carotid intima-media-thickness is increased, carotid atheromas are more common among apneics than among normals, the flow in the A. cerebri media is as well altered as the reaction to angiotensine II, noradrensine, isoproterenol and bradykinin. Homocysteine is increased, plasminogen activator inhibitor type 1 is inhibited and platelets are activated leading to an increased risk of thrombosis. There are no studies showing the effectiveness of treatment with nasal continuous positive airway pressure (nCPAP) on the rehabilitation of apneic stroke patients, but the outcome of non-apneic stroke patients is better than that of apneic stroke patients.
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PMID:Sleep and stroke. 1192 38

The present study was designed to test the hypothesis that markers of a hypercoagulable state predict subsequent cardiovascular events in hypertensives. To do this, we performed a prospective follow-up analysis of 178 patients (86 male; mean age, 54 years (standard deviation, 15); mean blood pressure, 188/103 mmHg) recruited from a hypertension clinic in a city-centre teaching hospital serving a multi-ethnic population. The main outcome measures were clinical and echocardiographic details, and laboratory markers of thrombosis and haemostasis (fibrinogen, fibrin D-dimer, plasminogen activator inhibitor, soluble P-selectin, von Willebrand factor, and viscosity) that were measured at baseline. After a mean follow-up of 45 months (interquartile range, 37-54), 30 subjects experienced one of a number of endpoints that included death or adverse cardiovascular event. These patients were older (P<0.001) and had significantly higher plasma von Willebrand factor (P=0.015) and fibrin D-dimer levels (P=0.005) compared with those 148 who were free of endpoints at follow-up. There were no statistically significant differences in mean blood pressure, other measured parameters, and the left ventricular mass index between the groups. Using univariate 'time to event' analysis, only high (> or = median) baseline systolic blood pressures were associated with a shortened event-free survival (log rank test, P= 0.0078). We conclude that hypertensive patients who experienced a new cardiovascular event were much older and had more endothelial dysfunction and thrombogenesis than those who were free of complications. However, only high baseline systolic blood pressures were associated with a shortened event-free survival.
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PMID:Baseline abnormalities of endothelial function and thrombogenesis in relation to prognosis in essential hypertension. 1199 65

Retinal vein occlusion (RVO) is a relatively common disease that is often associated with a variety of systemic disorders including arterial hypertension, diabetes mellitus, dyslipidemia, and systemic vasculitis. There are various types of RVO, categorized on the basis of the site of occlusion and on the type of consequent vascular damage. Central retinal vein occlusion (CRVO) is the most frequently occurring and clinically relevant type of RVO. In addition to the well-known classical risk factors, new hemostasis-related ones have been investigated in patients affected by CRVO. The data concerning a number of parameters remain contradictory; yet, high levels of type 1 plasminogen activator inhibitor (PAI-1) and hyperhomocysteinemia appear to play a significant role in the pathogenesis of this disease. Although based on a limited number of studies, this new knowledge could eventually provide important indications regarding prognosis and therapeutic strategies.
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PMID:Cardiovascular and thrombophilic risk factors for central retinal vein occlusion. 1202 Jun 23

Early diagnosis and therapy of the underlying insulin resistance of heritable polycystic ovary syndrome (PCOS), often manifested at menarche, facilitate the reduction and/or reversal of the reproductive and metabolic morbidity of PCOS, as well as reduce the risk factors for cardiovascular disease. PCOS is characterised by oligoamenorrhoea, clinical and biochemical hyperandrogenism, infertility, recurrent miscarriage, insulin resistance, hyperinsulinaemia, gestational diabetes, impaired glucose tolerance, Type 2 diabetes, morbid obesity, hypertension, hypofibrinolysis, hypertriglyceridaemia, low levels of high density lipoprotein-cholesterol and a sevenfold risk increase in cardiovascular disease. Insulin sensitising-lowering agents reduce insulin resistance and hyperinsulinaemia, reverse PCOS endocrinopathy and ameliorate the reproductive, metabolic and cardiovascular morbidity of the disorder. The largest literature on the subject discusses metformin. Improved pregnancy outcomes in women with PCOS receiving metformin may be attributed to its ability to reduce insulin resistance, hyperinsulinaemia and hypofibrinolytic plasminogen activator inhibitor activity by the enhancement of folliculogenesis and improvement of oocyte quality.
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PMID:Treatment of polycystic ovary syndrome with insulin-lowering agents. 1215 Jun 95

The role of angiotensin II (AII) and angiotensin IV (AIV) as inducers of PAI-1 expression during hypertension was studied in vivo. A 2-week infusion of AII (300 ng/kg/min) via an osmotic pump increased systolic blood pressure (171 +/- 2 vs. 138 +/- 6 mm Hg), urinary protein excretion (32 +/- 6 vs. 14 +/- 2 mg/day), and renal (2.2 +/- 0.5 vs. 1.0 +/- 0.1) and cardiac (1.8 +/- 0.3 vs. 1.0 +/- 0.1) gene expression of plasminogen activator inhibitor 1 (PAI-1). AIV infusion did not affect any of the above with the exception of PAI-1 gene expression which was increased in the left ventricles (1.7 +/- 0.3 vs. 1.0 +/- 0.1). AII-infused rats displayed a decreased creatinine clearance (538 +/- 75 vs. 898 +/- 96 ml/min) and hypertrophic left ventricles (0.275 +/- 0.006 vs. 0.220 +/- 0.011 g/100 g). Our results demonstrate that AII but not AIV infusion is associated with increased renal PAI-1 gene expression.
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PMID:Effects of angiotensins II and IV on blood pressure, renal function, and PAI-1 expression in the heart and kidney of the rat. 1216 62

A clustering of risk factors, including elevated triglycerides, decreased high-density lipoprotein cholesterol, hyperinsulinemia, and hypertension often are observed in patients who are insulin resistant. Insulin resistance has been found to play a critical role in the development of cardiovascular disease, particularly in patients with type 2 diabetes. Patients with insulin resistance have an increase in small, dense low-density lipoprotein (LDL) cholesterol, which is more atherogenic than large, buoyant LDL cholesterol. In the context of insulin resistance, insulin has reduced effects on the phosphatidylinositol 3 kinase (PI3K) pathway, whereas mitogen-activated protein kinase activity is maintained. The result is an exaggeration of the mitogenic actions of insulin leading to vascular smooth muscle proliferation and elevated plasminogen activator inhibitor (PAI)-1. Notably, nitric oxide-mediated vasodilation also is impaired, further contributing to atherogenicity. In addition, hyperinsulinemia further contributes to cardiovascular risk by promoting thrombosis. Patients who are insulin resistant have decreased fibrinolysis, as indicated by increased levels of PAI-1. Studies have shown that enhancing insulin sensitivity with insulin sensitizers, such as thiazolidinediones, may improve insulin resistance and limit the development of adverse cardiovascular consequences.
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PMID:Current concepts in insulin resistance, type 2 diabetes mellitus, and the metabolic syndrome. 1223 Oct 75

Levels of fibrinogen, von Willebrand factor, d-dimer, antithrombin III, protein C, plasminogen, and plasminogen activator inhibitor were measured in 62 men and 37 women with ischemic heart disease before and after 20-min venous occlusion. Women compared with men had higher baseline levels of fibrinogen (4.046-/+0.1785 and 3.584-/+0.1591 g/l, respectively, p=0.021), von Willebrand factor (122.1-/+9.31 and 99.5-/+6.16%, respectively, p=0.035), plasminogen activator inhibitor (4.8-/+0.31 and 2.9-/+0.27 IU/l, respectively, p=0.009). Levels of antithrombin III, protein C, and plasminogen in women were higher than in men both at baseline (108.5-/+1.65 and 100.7-/+1.60 %, p=0.001; 129.1-/+2.91 and 107.2-/+3.79%, p=0.001; 113.6-/+2.13 and 104.1-/+1.89%; p=0.001, respectively) and after venous occlusion. There were no gender differences in dynamics of parameters of hemostasis during venous occlusion. Multifactorial regression analysis showed that gender was independently (of age, duration of hypertension, smoking, body mass index, and total cholesterol level) related to only antithrombin III and protein C levels.
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PMID:[Gender differences in the state of the system of hemostasis in patients with ischemic heart disease]. 1249 45


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