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)

Left ventricular hypertrophy in systemic arterial hypertension is associated with an increased risk of morbidity and mortality due to cardiovascular disease. Therefore, the diagnosis of left ventricular hypertrophy is clinically important. In current clinical practice, echocardiography is the method of choice for diagnosing left ventricular hypertrophy. This review describes current, clinically applied techniques of measuring left ventricular mass using M-mode and two-dimensional echocardiography. Using M-mode techniques, left ventricular hypertrophy is usually present when myocardial mass estimates exceed 150 g/m2 in males and 120 g/m2 in females. Using two-dimensional echocardiography, upper limits of normal have been described to be slightly lower (102 g/m2 in males and 88 g/m2 in females). In serial clinical two-dimensional echocardiographic studies, image acquisition and quantitation predominantly determine total variability in left ventricular mass estimates. Using any single technician and any single reader, left ventricular mass estimates in normal subjects may vary by 35 g (standard deviation) between serial studies. Strategies to reduce the magnitude of this variability include increasing the number of technicians and readers acquiring and analyzing a single study.
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PMID:Diagnosis of left ventricular hypertrophy by echocardiography. 138 99

Glucocorticoid (GC) excess (Cushing's syndrome) is associated with hypertension in at least 70% of patients (in our series 89/130), independently of the subtype (pituitary or adrenal) and the duration, but not of the age of the patients. Cardiovascular damage is quite frequent in hypertensives, but is sometimes also present in normotensives. The mortality of patients with Cushing's syndrome is four times that of the general population when matched for age and sex, and much of this excess mortality is caused by cardiovascular disease. Hypertension remits in most of the patients after successful treatment, but may persist in some. Hypertension also occurs in 20% of patients treated with GC orally. The type of hypertension is independent of salt uptake, can not be controlled by spironolactone but is inhibited by a GC antagonist such as RU486. Experimentally-induced hypertension with oral cortisol (F) is associated with a rise in cardiac output, a fall in calculated total peripheral resistance, an increased forearm vascular responsiveness to exogenous norepinephrine, but no change in overall sympathetic tone, or in norepinephrine reuptake. The increased pressor responsiveness is probably due to local postsynaptic effector mechanisms in the resistance vessels, which could be important in phasic increases in neuronally mediated constrictor responses. Both in patients with Cushing's syndrome and in those on chronic GC treatment, the circadian blood pressure variations are absent or reversed. This may contribute to the deleterious effects of the GC excess on blood vessels. The vascular effects of the GC may be mediated by the activation of specific cardiovascular receptors, by modulating vascular transport systems, or by altered catecholamine or prostaglandin metabolism. GC may also act as mineralocorticoids (MC): in fact type 1 MC receptors are unable, in vitro, to distinguish between aldosterone and cortisol. The specificity-conferring mechanism of typical target organs for MC (e.g. kidney)--is thought to be due to the action of local 11-beta-hydroxysteroid dehydrogenase, which converts F to biologically inactive cortisone (E). When the activity of the enzyme is impaired (syndrome of apparent MC excess, liquorice or carbenoxolone administration), F acts as a MC and MC-hypertension with hypokalemia occurs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glucocorticoid-dependent hypertension. 139 Feb 89

In 1989, we sent a medical follow-up questionnaire to 2,728 members of 98 Utah families originally screened from 1980 to 1983 in the Cardiovascular Genetics Research Clinic. The response rate was 69.9%. Of 1,134 nondiabetic individuals initially age 18 or older who returned the questionnaire, 10 were found to be newly diagnosed with diabetes. The incidence of diabetes was higher among individuals who were found at baseline to have central obesity, lipid abnormalities, especially increased triglyceride levels, and hypertension. Family histories of coronary heart disease and diabetes were not related to the development of diabetes. Our findings that cardiovascular disease risk factors predict the development of diabetes in this relatively young, Caucasian population are consistent with the results of studies from several different populations.
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PMID:Risk factors for cardiovascular disease predict the development of diabetes among Utah families. 139 Nov 41

Microalbuminuria is diagnosed when the UAER is greater than 20 but less than 200 micrograms/min. The prevalence of microalbuminuria among diabetic patients is 15-20%. Persistent microalbuminuria in diabetic patients is a risk marker not only of renal disease, but also of proliferative retinopathy and cardiovascular morbidity and mortality. Even among nondiabetic individuals, those with microalbuminuria tend to have an increased cardiovascular morbidity. The established cardiovascular risk factors, such as smoking, elevated plasma cholesterol, fibrinogen, and hypertension, are seen more frequently in diabetic patients with persistent microalbuminuria than in normoalbuminuric diabetic patients of similar age, sex, and diabetes duration. However, these risk factors cannot by themselves explain the cardiovascular overmortality in these patients. In addition, insulin resistance or genetic disposition to hypertension or cardiovascular disease fails to be the missing link. Accumulating evidence suggests a common pathogenetic mechanism for microalbuminuria and premature atherosclerosis (i.e., qualitative alterations of the extracellular matrix, including decreased density and sulfation of HS-PG). Decreased density of HS in the glomeruli may lead to albuminuria and mesangial proliferation. In the intima of large vessel walls, decreased density and/or sulfation of HS may enhance several of the processes involved in premature atherosclerosis. Diabetes affects the composition and structure of the extracellular matrix in many ways and leads to decreased density and sulfation of HS-PG by several mechanisms. Genetic differences in the sulfation of HS and/or genetic defects in the coordinated biosynthesis of HS-PG might contribute to decreased concentration and sulfation of HS-PG in susceptible individuals. It is hoped that susceptibility genes can be identified soon, thereby making prevention of severe late diabetic complications more successful.
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PMID:Microalbuminuria. Implications for micro- and macrovascular disease. 139 15

Diabetes mellitus has become the leading cause of ESRF in the United States. Patients with diabetic nephropathy suffer high cardiovascular morbidity and mortality. Because only 40% of diabetic patients eventually develop diabetic kidney disease, it may be possible to devise primary prevention measures targeted at the subset of patients at risk. Recently, a predisposition to hypertension, a family history of diabetic nephropathy, and a family history of CVD disease each have been associated independently with the development of diabetic renal complication in IDDM. Risk factors for macrovascular damage, including raised arterial BP, dyslipidemia, and insulin resistance, can be detected early in the course of progression to diabetic nephropathy. These risk indicators recently have been shown to be already present at the stage of normoalbuminuria in those patients who eventually will progress to microalbuminuria. Treatment of established renal disease can only delay the onset of ESRF, and lowering of microalbuminuria has been shown to retard the onset of persistent proteinuria. However, no study to date has demonstrated prevention of renal disease in these patients. The ultimate aim should, therefore, be the prevention of the transition from normoalbuminuria to microalbuminuria in individuals who are at higher risk of diabetic renal disease and CVD.
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PMID:Diabetic nephropathy. Future avenue. 139 18

Data on the evolution and prognostic implications of left ventricular hypertrophy (LVH) determined by ECG, chest X-ray and echocardiogram in the Framingham Study are reviewed. Echocardiographic examination provides the most sensitive and specific measure of left ventricular hypertrophy, providing a quantitative evaluation of the anatomical condition. Chest X-ray evaluation is also more sensitive than the ECG, but less specific than the echocardiogram. When ECG-LVH is present, X-ray and echocardiographic LVH are often found; but, when negative, the ECG clearly does not exclude anatomical LVH. The incidence of each variety of LVH increases with age, weight and blood pressure. Although it may also appear following coronary heart disease (CHD), valvular deformity and congenital cardiac defects, the former are the major determinants of LVH in the general population. Each contributes independently to the occurrence of LVH. LVH has emerged as a powerful non-invasive indicator of increased vulnerability to the occurrence of major cardiovascular disease outcomes in hypertension. It appears that X-ray and echocardiographic LVH measure anatomical hypertrophy, whereas the ECG variety is also indicative of ischaemic myocardial involvement when repolarization abnormality is present. Hypertension clearly predisposes to both anatomical and ECG-LVH which cannot be taken as an incidental compensatory feature since at any blood pressure those with ECG-LVH, X-ray or echo LVH are distinctly more prone to cardiovascular sequelae. ECG-LVH carries a greater risk than anatomical (X-ray) LVH. ECG-LVH with repolarization abnormality is more dangerous than that with voltage alone. The latter appears to reflect chiefly the severity and duration of accompanying hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular hypertrophy as a risk factor in arterial hypertension. 139 65

Epidemiological studies have demonstrated that, compared with the population as a whole, there is increased cardiovascular morbidity and mortality among lower socio-economic groups. To explore determinants of the increased risk within this group, a prospective 6.5 year investigation of a cohort of 416 middle-aged (40.8 +/- 9.6 years) male blue-collar workers was undertaken. In addition to established somatic and behavioural risk factors, psychosocial influences that measured chronic occupational stress in terms of an imbalance between high effort and low reward were assessed. Multivariate logistic regression analysis shows that hypertension (odds ratio (o.r.) 3.85; 95% CI 1.59-9.34), left ventricular hypertrophy (o.r. 3.62; 95% CI 1.06-12.37), hyperlipidaemia (o.r. 2.55; 95% CI 1.08-6.00), status inconsistency (measuring low reward at work) (o.r. 2.86; 95% CI 1.04-7.80) and 'immersion' (measuring high intrinsic effort at work) (o.r. 3.57; 95% CI 1.22-10.47) independently contribute to the prediction of fatal or non-fatal cardiovascular events (acute myocardial infarction, stroke). Expected probabilities of cardiovascular events are clearly elevated if the combined effects of left ventricular hypertrophy and psychosocial risks are analysed. In conclusion, increased incidence of cardiovascular disease among lower socio-economic groups is explained by a co-manifestation of established risk factors including left ventricular hypertrophy (by ECG) and psychosocial factors measuring chronic stress at work.
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PMID:The role of hypertension, left ventricular hypertrophy and psychosocial risks in cardiovascular disease: prospective evidence from blue-collar men. 139 66

Health hazards associated with the use of smokeless tobacco were evaluated in a cross-sectional study of 97,586 Swedish construction workers undergoing health examinations in 1971-74. All users of smokeless tobacco only (5014 subjects) and all exclusive smokers of > or = 15 cigarettes daily (8823 subjects) were compared with all non-users of any tobacco (23,885). Both smokeless tobacco users and smokers showed higher prevalences of circulatory and respiratory disorders. Hypertension was most common in smokeless tobacco users. In the 45- to 56-years age group, the odds ratio for a diastolic blood pressure of > 90 mmHg was 1.8 (95% CI, 1.5-2.1), and for a systolic blood pressure > 160 mmHg, 1.7 (95% CI, 1.3-2.1). Smokers showed the lowest prevalence of hypertension. Disability pensions due to cardiovascular disease were nearly 50% more frequent in both smokeless tobacco users and smokers. These findings indicate that an increased cardiovascular risk is also associated with the use of smokeless tobacco.
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PMID:Use of smokeless tobacco: blood pressure elevation and other health hazards found in a large-scale population survey. 140 36

DETERMINANTS OF BLOOD RHEOLOGY: Blood flow depends on driving pressure and a resistance factor, the latter being related to geometrical hindrance and to the intrinsic viscosity of the blood. Since whole blood is non-Newtonian in nature, blood viscosity is strongly dependent on shear conditions. Low-shear areas occur in cardiovascular disease, and therefore the interaction between blood viscosity and flow conditions may affect vascular disorders. Increased shear stress secondary to increased viscosity may produce endothelial activation and release of endothelium-derived relaxing factors, leading to flow-dependent vasodilation. All the determinants of blood rheology, including plasma protein and erythrocyte factors may be altered in patients with arterial hypertension. BLOOD RHEOLOGY IN HYPERTENSION: A hyperviscosity state is created which is associated with an unfavourable prognosis, since it is correlated with blood pressure levels and the severity and complications of the disease including left ventricular hypertrophy. The mechanisms of haemorheological abnormalities in hypertension are still unclear. It is not known whether blood rheology is an independent variable in patients with hypertension or whether it is a covariable with other established indices of heterogeneity. However, many aetiopathological changes identified in hypertensive disease may contribute to the observed changes in blood rheology. Haemorheological changes in hypertension, through complex interactions with platelet activation and endothelial function, may contribute to the development of thrombosis and atherosclerosis. Moreover, in acute and chronic ischaemia and other conditions where compensatory mechanisms such as collateral formation and vasodilation are limited, rheological factors may become important determinants of blood flow and tissue oxygenation. TREATMENT EFFECTS: Many antihypertensive agents have direct or indirect potential effects on haemorheological variables. However, to date, most studies that have investigated the effects of therapy on rheological variables have not been performed in clinically relevant situations. Controlled studies that monitor both the acute and longterm effects of antihypertensive drugs on relevant haemorheological variables are required to show whether specific therapeutic approaches can correct abnormalities in blood rheology.
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PMID:Blood rheology in arterial hypertension. 140 36

The incidence of end-stage renal disease is increasing and this results in an enhanced requirement of renal replacement therapy facilities. This brings about a significant burden on health care budgets and makes strategies that slow down or even prevent deterioration of the renal function mandatory. Although large scale randomized, controlled and prospective clinical trials on the effect of blood pressure control on the course of renal function are lacking, there is circumstantial evidence from animal, epidemiological and clinical studies to state that treatment of hypertension to blood pressure values well within the normal range is most important to ameliorate the downhill course of renal function in patients with chronic renal failure. Moreover, treatment of hypertension is critical to reduce morbidity and mortality of cardiovascular disease in these patients, who have an increased risk for such events. Low-protein diets, if possible with ketoacid supplement, are advocated to slow down the deterioration of renal function. However, based on the results of recent studies, low-protein diets may only have a moderate effect in patients with diabetic nephropathy and, possibly, in patients with chronic glomerulonephritis. The possibility of influencing renal ammoniagenesis by protein restriction or calcium carbonate administration, and an attenuation of alternative complement pathway activation and tubulo-interstitial injury, are challenging. Finally, in animal studies it has been found that abnormalities in serum lipid profile contribute to the progression of chronic renal failure, which may be prevented by pharmacological treatment of hyperlipidemia. Studies in humans concerning this subject are lacking at this moment, but treatment of hyperlipidemia is proper to reduce cardiovascular events.
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PMID:Clinical strategies for arresting progression of renal disease. 140 61


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