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 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

The aim of this study was to determine differences in atherothrombotic risk factors in South Asian subjects with a history of ischaemic stroke and South Asian subjects free from personal and family history of clinically detectable stroke. Eighty South Asian patients with ischaemic stroke (confirmed on cranial computerised scan) and 80 South Asian controls with similar age and gender distributions were recruited at random. The frequency of hypertension (P=<0.0001), myocardial infarction (P=0.003) and diabetes mellitus (<0.0001) were significantly higher in stroke patients. Stroke patients had lower high-density lipoprotein cholesterol (0.95 vs. 1.1 mmol/l, P=<0.0001), higher plasma glucose (8.1 vs. 6.6 mmol/l, P=0.01) and trendwise higher HBA(1C) (6.4 vs. 6.0%, P=0.09). There was no difference in insulin levels but insulin resistance was significantly higher in stroke patients (3.75 vs. 2.66, P=0.01). Stroke patients showed elevated levels of fibrinogen (3.78 vs. 3.41 mg/dl, P=0.02), von Willebrand factor (1.78 vs. 1.50 IU/ml, P=0.006) and tissue plasminogen activator (12.8 vs. 11.3 ng/ml, P=0.04), but the differences did not persist after adjustment for glucose, triglycerides, HDL, WHR, and BMI. Higher levels of fibrinogen, von Willebrand factor and t-PA in South Asian stroke patients disappeared after adjustment for features of insulin resistance syndrome but persisted after adjustment for presence of diabetes, confirming that these changes are essentially dependant on features of insulin resistance syndrome. A prospective study would be required to elucidate the role of thrombotic risk factors in South Asians with ischaemic stroke.
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PMID:Increased fibrinogen, von Willebrand factor and tissue plasminogen activator levels in insulin resistant South Asian patients with ischaemic stroke. 1205 85

Malignant hypertension (MHT) is a rare and severe form of hypertension characterised by arteriolar necrosis and severe vascular damage, leading to stroke, myocardial infarction and death. We hypothesised that in addition to endothelial damage, MHT may be associated with increased oxidative stress. Lipid hydroperoxides (LHP, an index of oxidative damage) and plasma von Willebrand factor (vWf, an index of endothelial damage/dysfunction) were measured in 16 patients with MHT and compared with 16 non-malignant essential hypertensives and 32 normotensive controls. vWf was greater in MHT (mean 117 iU/dL) than in non-malignant hypertensives (97 iU/dL) or normotensive controls (100 iU/dL) (ANOVA P = 0.017). However, although LHP were greater in MHT (mean 10.6 micromol/L) than in normotensives (4.5 micromol/L, P < 0.001), the levels in MHT were similar to those in non-malignant hypertension (12.3 micromol/L). In conclusion endothelial damage (raised vWf) was more evident in MHT compared with both normotensive controls and with non-malignant hypertension, whilst oxidative stress (raised LHP) was increased to a similar extent in both hypertension groups when compared with normotensive controls. These observations raise the possibility abnormal oxidative stress is probably not the mechanism responsible for the endothelial damage seen in malignant phase hypertension.
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PMID:Oxidative stress in malignant and non-malignant phase hypertension. 1208 94

To investigate the relationship between soluble markers of platelet, endothelial and rheological function, and target organ damage and their response to intensified management in a population of middle-age hypertensive patients at high risk of cardiovascular complications, we studied 382 consecutive patients (308 men; mean age, 63 years, SD 8) along with 60 normotensive controls free of cardiovascular disease. Patients were divided into those with target organ damage (TOD; n=107) and those free of end-organ damage. Plasma levels of soluble P-selectin (sP-sel), a marker of platelet activation, and von Willebrand factor (vWF), an index of endothelial damage/dysfunction (both enzyme-linked immunosorbent assay), and the rheological indices fibrinogen, plasma viscosity, hematocrit, platelet, and white cell count were measured. In 53 patients, variables were further measured after 6 months of intensified cardiovascular risk management. Patients with TOD had significantly higher vWF, 137 (SD 33) versus 125 (SD 33) IU/dL (P=0.002,) and a greater proportion of smokers, 31% versus 16% (P=0.002). There were no statistically significant differences in plasma viscosity, fibrinogen, hematocrit, white blood cell count, platelet count, or sP-sel between the 2 subgroups. In multivariate analysis, vWF was a significant independent predictor for TOD. After 6 months of intensified management in 53 patients who entered the trial, there were significant reductions in systolic blood pressure, total cholesterol, hematocrit, plasma viscosity, sP-sel, and vWF (all P<0.01) but no significant change in fibrinogen. In conclusion, there is a relationship between TOD and endothelial damage/dysfunction in hypertension. Intensified management results in improvements in hemorheology, endothelial and platelet function.
Hypertension 2002 Jul
PMID:Von Willebrand factor, soluble P-selectin, and target organ damage in hypertension: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT). 1210 39

The aim of the study was to examine whether the circulating cell adhesion molecules, von Willebrand factor (vWf) and endothelin-1, are elevated in patients with essential hypertension with no other risk factors for atherosclerosis and thus may serve as a markers of endothelial dysfunction in uncomplicated hypertension. Furthermore, the effect of treatment with the ACE inhibitor, quinapril, on levels of endothelial dysfunction markers were studied. The levels of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], E-selectin, P-selectin), von Willebrand factor (vWf) and endothelin-1 were measured in patients with hypertension without any other risk factors of atherosclerosis before and after treatment with quinapril (n = 22) and in normotensive controls (n = 22). Compared with normotensive subjects, the hypertensive patients had significantly higher levels of ICAM-1 (238 vs 208 ng/ml, P = 0.02), vWf (119 vs 105 IU/dl, P < 0.05) and endothelin-1 (5.76 vs 5.14 fmol/ml, P < 0.05). Three-month treatment of hypertensive patients with quinapril led to a significant decrease in the levels of endothelin-1 (5.76 vs 5.28 fmol/ml, P < 0.01). We did not observe significant changes in the levels of adhesion molecules and vWf after ACE inhibitor treatment, although a trend toward a decrease was apparent with all these parameters. Patients with uncomplicated hypertension with no other risk factors of atherosclerosis had significantly elevated levels of ICAM-1, vWf, and endothelin-1. Our data suggest that these factors may serve as markers of endothelial damage even in uncomplicated hypertension. In hypertensive patients, treatment with the ACE inhibitor quinapril resulted in a significant decrease in endothelin-1 levels. These findings indicate a beneficial effect of ACE inhibitors on endothelial dysfunction in hypertensive patients.
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PMID:Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors. 1214 57

Separate reports have identified differences in plasma levels of the endothelial markers soluble E-selectin, von Willebrand factor (vWf) and soluble thrombomodulin in each of the major modifiable risk factors for atherosclerosis (smoking, hypertension and hypercholesterolaemia), and abnormal levels of some plasma markers predict various adverse cardiovascular events. However, it is unclear whether there is an increasing effect on the endothelium with a worsening risk-factor profile. We measured the three endothelial cell markers by enzyme-linked immunosorbent assay in the plasma of 200 subjects (mean age, 54 years; 58% men) free of the symptoms and clinical signs of atherosclerosis. Levels of the markers were then correlated with the Framingham coronary heart disease (CHD) and cerebrovascular disease (CVD) scores to help determine which (if any) may be useful as good laboratory predictors of future cardiovascular events in prospective epidemiological studies. vWf correlated with CHD (r(s) = 0.269, < 0.001) and CVD risk (r(s) = 0.331, P < 0.001), but soluble E-selectin correlated only with CHD risk (r(s) = 0.163, P = 0.021). We conclude that, of the three specific endothelial markers, vWf correlates most closely with the Framingham risk-factor prediction scores and therefore may be the better plasma endothelial marker of the future development of an atherothrombotic event.
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PMID:Relationship between plasma markers of endothelial cell integrity and the Framingham cardiovascular disease risk-factor scores in apparently healthy individuals. 1269 60

By promoting atherosclerosis and thrombosis, a blood-clotting diathesis could contribute to excess cardiovascular morbidity and mortality in patients with systemic hypertension and/or obstructive sleep apnoea. Since psychological states affect haemostatic activity, we wondered about the contribution of behavioural factors to a hypercoagulable state in subjects with increased risk of cardiovascular disease. To tease apart the potential additive nature of cardiovascular disease risk, we examined four patient groups - hypertensives and normotensives, with and without sleep apnoea. The procoagulant molecules thrombin-antithrombin III complex, fibrin D-dimer and von Willebrand factor antigen were measured in 88 subjects (mean age 47 years; range 32-64 years) who underwent full polysomnography. Subjects completed the Center for Epidemiological Studies - Depression (CES-D) Scale, the Cook-Medley (CM) Hostility Scale, and the Profile of Mood States (POMS). Sleep apnoea, hypertension status, age, body mass index and psychological variables (CES-D, CM Stress, and POMS Vigour-Activity) together explained 29% of the variance in D-dimer, a marker of fibrin turnover ( r (2)=0.29, P =0.001). CES-D, CM Stress and POMS Vigour-Activity explained 17% of this variance even after controlling for sleep apnoea, hypertension status, age and body mass index (Delta r (2)=0.17, P =0.001). Thrombin-antithrombin III complex and von Willebrand factor were not significantly related to psychological variables, but this may reflect limited statistical power. Thus psychological factors are independently associated with D-dimer and explain as much of its variance as do traditional correlates (hypertension, sleep apnoea, age and body mass index). These results may provide a rationale for linking behavioural aspects with cardiovascular events.
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PMID:Independent contribution of psychological factors to fibrin turnover in subjects with sleep apnoea and/or systemic hypertension. 1224 29

Von Willebrand disease (VWD) type 1 is reported to be common but frequently is difficult to diagnose. Many people have nonspecific mild bleeding symptoms, von Willebrand factor (VWF) levels display low heritability, and low VWF levels (15% to 50% of normal) are weak risk factors for bleeding. Therefore, bleeding and low VWF levels often associate by chance. Even with stringent diagnostic criteria based on a triad of bleeding symptoms, a low VWF level, and a positive family history, the prevalence of "false-positive" VWD type 1 is comparable to the published prevalence of the disease. Consequently, many patients diagnosed with VWD type 1 do not have a specific hemorrhagic disease at all, which limits the utility of the diagnosis. This unfortunate reality is a consequence of trying to force patients into binary categories of "diseased" or "healthy" that are incompatible with the continuous biologic context in which VWF functions. The problem may be avoided by substituting an empirical epidemiologic approach like that applied to other modest risk factors for disease such as elevated cholesterol and high blood pressure. Such a risk management strategy could be generalized to include other hemorrhagic and thrombotic risk factors.
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PMID:Von Willebrand disease type 1: a diagnosis in search of a disease. 1241 Dec 89

The objective of the investigation was to assess whether circulating adhesion molecules, von Willebrand factor (vWf) and endothelin-1 are elevated in patients with mild uncomplicated essential hypertension without further risk factors of atherosclerosis and whether they could serve as indicators of endothelial dysfunction in this form of hypertension. Furthermore the authors investigated the effect of ACE inhibitor treatment (ACEI), quinapril, on the level of these markers of endothelial dysfunction. The level of adhesion molecules [intercellular cytoadhesion molecule-1 (ICAM-1), E-selectin, P-selectin], von Willebrand s factor (vWf) and endothelin-1 were assessed in patients with mild essential hypertension without further cardiovascular risk factors or clinical manifestations of atherosclerosis before and after quinapril treatment (n = 25) and compared with normotensive controls (n = 29). The results of the examinations provided evidence that contrary to controls the hypertensive subjects had significantly higher ICAM-1 levels (237.8 vs. 207.8 ng/ml, P = 0.02) vWf (118 vs. 106 IU/dl, p < 0.05) and endothelin-1 (5.81 vs. 5.15 fmol/ml, p < 0.05). Three-month treatment of hypertensive patients with ACEI led to a significant drop of endothelin-1 levels (5.81 vs. 5.26 fmol/ml, p = 0.01). The authors proved also an unequivocal declining trend of other cytoadhesion molecules and vWf after ACEI treatment, the changes however were not statistically significant. From the investigation it may be concluded that also patients with uncomplicated essential hypertension without other cardiovascular risk factors or clinical manifestations of atherosclerosis have significantly elevated plasma levels of ICAM-1, vWf and endothelin-1. Higher concentrations of these factors suggest endothelial dysfunction already in mild forms of essential hypertension without further risk factors or cardiovascular complications. A significant drop of endothelin-1 and declining trend of the other investigated indicators suggest that ACEI treatment can favourably influence endothelial dysfunction in hypertensive patients also independently on reduction of the BP.
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PMID:[Is mild essential hypertension without obvious organ complications and risk factors associated with increased levels of circulating markers of endothelial dysfunction? Effect of ACE inhibitor therapy]. 1242 1

A hypercoagulable state might contribute to increased atherothrombotic risk in hypertension. The sympathetic nervous system is hyperactive in hypertension, and it regulates hemostatic function. We investigated the effect of nonspecific beta-adrenergic stimulation (isoproterenol) and blockade (propranolol) on clotting diathesis in hypertension. Fifteen hypertensive and 21 normotensive subjects underwent isoproterenol infusion in two sequential, fixed-order doses of 20 and then 40 ng. kg(-1). min(-1) for 15 min/dose. Thirteen subjects were double-blind studied after receiving placebo or propranolol (100 mg/day) for 5 days each. In hypertensive subjects, isoproterenol elicited a dose-dependent increase in plasma von Willebrand factor (vWF) antigen [F(2,34) = 5.02; P = 0.032] and a decrease in D-dimer [F(2,34) = 4.57; P = 0.040], whereas soluble tissue factor remained unchanged. Propranolol completely abolished the increase in vWF elicited by isoproterenol [F(1,12) = 10.25; P = 0.008] but had no significant effect on tissue factor and D-dimer. In hypertension, vWF is readily released from endothelial cells by beta-adrenergic stimulation, which might contribute to increased cardiovascular risk. However, beta-adrenergic stimulation alone may not be sufficient to trigger fibrin formation in vivo.
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PMID:Effects of nonspecific beta-adrenergic stimulation and blockade on blood coagulation in hypertension. 1248 65


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