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

The prevalence of glucose intolerance and diabetic complications was determined in second-generation Japanese-American (Nisei) women and compared to previously obtained results in Nisei men. A volunteer study sample of 191 Nisei women 45-74 years old was enrolled from a study population of 1489 Nisei women born 1913-1942, raised and educated in the U.S., and residing in King County, Washington. The enrolled sample included 72 with normal glucose tolerance, 67 with impaired glucose tolerance (IGT), and 52 with non-insulin-dependent diabetes. A random sample was also drawn from the study population to form a reference sample of 157 women. Based upon observations in the reference and enrolled samples, an estimated 16% of Nisei women in the study population have diabetes and 40% IGT. These rates compare to 20% diabetes and 36% IGT previously estimated for Nisei men 45-74 years old. The prevalence of cardiovascular disease (hypertension, peripheral vascular disease, and/or coronary heart disease) was highest among diabetic women, lowest in those with normal glucose tolerance, and intermediate in women with IGT. In comparison to diabetic men, there was a significantly lower frequency of neuropathy, peripheral vascular disease, and coronary heart disease in diabetic women. However, hypertension occurred equally often in both. Thus Japanese-American men and women 45-74 yr old have a similar prevalence of glucose intolerance, although less severe in women, and complications, except for hypertension, are reduced in women.
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PMID:Glucose intolerance and diabetic complications among Japanese-American women. 177 9

Hyperandrogenism and lipid metabolism were shown to be related intimately. Any discussion of the nature of their relationship must include other clinical and metabolic variables such as hyperinsulinemia and UBO. Despite the many correlations among each of these factors, the appropriate sequence in the pathogenesis of these conditions has not been defined. Do conditions that result in insulin resistance (e.g., genetic defects, insulin receptor antibodies, and obesity) also lead to the development of hyperandrogenemia by direct or indirect ovarian stimulation by insulin? Does hyperandrogenism of ovarian or adrenal origin cause abnormal upper body fat distribution, in turn leading to lipid abnormalities and insulin resistance? Regardless of the issue of mechanism of causality, women with hyperandrogenism are thought to be at greater risk for cardiovascular morbidity and mortality than their normoandrogenic counterparts. These women often are obese, hypertensive, and sedentary; ingest diets high in saturated fats; and have glucose intolerance and/or insulin resistance. All these abnormalities are well known independent risk factors for the development of lipid abnormalities and cardiovascular disease. Whether hyperandrogenism is a secondary consequence of any of these or whether it is an independent contributor to lipid aberrations requires future study. Treatment strategies for hyperandrogenic women, however, should not only be directed toward alleviation of the cosmetic problem of hirsutism but also toward the prevention and treatment of cardiovascular morbidity using modalities aimed at eradicating hyperinsulinemia, hypertension, and dyslipidemia. These modalities should include modifications in diet, exercise, and weight in addition to pharmacologic and/or surgical manipulation. Weight reduction will reduce many cardiovascular risk factors. Obesity is easier to target because of the many risk factors that result in it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipid metabolism and hyperandrogenism. 177 28

The incidence of impaired glucose tolerance, the relation of blood glucose levels to the prevalence of risk factors for coronary heart disease (CHD) and to myocardial infarction morbidity and mortality were studied over 15 years among males aged 45-59 years, excluding patients with diabetes mellitus. The data analysis was made in quintils of glucose levels. Impaired glucose tolerance was detected in 20.6% of the males. In the fifth versus the first quintil, there was an increase in the prevalence of systolic and diastolic arterial hypertension (p less than 0.001), obesity (p less than 0.001), low physical activity and hypercholesterolemia (p less than 0.05). As compared with the first, the fifth quintil showed higher total mortality rates and higher myocardial infarction morbidity and cardiovascular disease and CHD morbidity rates. But for age, and major risk factors, the risk for CHD, total and cardiovascular mortality increase at low and high blood glucose concentrations.
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PMID:[Disorders of glucose tolerance and ischemic heart disease]. 177 10

A group of 293 middle-aged subjects with a parental history of hypertension was compared with 210 middle-aged subjects without this history. The adjusted odds ratio for hypertension (WHO-criteria) was 2.0 with parental hypertension - independent of obesity, physical leisure time activity, age and sex. Comparatively in all 503 participants, the independent odds ratio for hypertension was 3.3 with obesity. Analysis of variance in all participants disclosed that blood pressure was independently related to three predictors, parental hypertension (p less than 0.05), body mass index (p less than 0.001), and 2-h blood glucose (p less than 0.001). Additional analysis of variance in all subjects, to estimate if these three predictors were interrelated, disclosed that parental hypertension was not related to either 2-h glucose or body mass index. A clear association was seen between 2-h glucose and body mass index (p less than 0.001). This was underlined in a separate analysis of the 88 hypertensives, among which 25% had impaired glucose tolerance (WHO-criteria). In conclusion, own obesity (environment) had about 1.5 times stronger influence on hypertension than parental hypertension (heredity). Parental hypertension seemed to have a separate influence on the blood pressure. Body mass index and 2-h glucose seemed to have partly separate, and partly interrelated, influences on the blood pressure.
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PMID:Influences of familial and environmental factors on hypertension. 181 84

Hypertension is a major contributor to cardiovascular morbidity and mortality, increasing risk threefold. It predisposes to every clinical manifestation of coronary heart disease, now the most common and lethal outcome. It is as relevant a risk factor in the elderly as in the young. Risk is proportional to the degree of blood pressure elevation without a discernible critical value. Cardiovascular sequelae do not derive chiefly from the diastolic component, and isolated systolic hypertension confers increased risk at all ages. Hypertension tends to cluster with other cardiovascular risk factors, which must be taken into account in evaluating the risk and in choosing treatment. The excess cardiovascular risk in hypertension is concentrated in those with an increased total/high density lipoprotein cholesterol ratio, glucose intolerance, cigarette smoking, elevated fibrinogen, and electrocardiogram abnormalities. Left ventricular hypertrophy (LVH) is a common feature of hypertension and an ominous harbinger of cardiovascular sequellae. Electrocardiographic evidence of LVH, when manifested by repolarization abnormalities and voltage elevations, is particularly hazardous, reflecting not only anatomical hypertrophy but also ischemia. Electrocardiogram-LVH adds to cardiovascular risk associated with X ray or echocardiographic evidence of anatomical LVH. Because of a tendency to ventricular ectopy, LVH is associated with increased risk of sudden death. Electrocardiogram-LVH can be corrected or avoided by control of hypertension and weight reduction. The efficacy of correcting LVH remains to be demonstrated but benefits seem likely.
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PMID:Hypertension, hypertrophy, and the occurrence of cardiovascular disease. 183 77

The frequent association of sleep apnea syndrome and essential hypertension led to think of sleep apnea as an etiology of hypertension, especially as a good correlation has been found between the severity of both diseases. Moreover, treating the apnea syndrome results in a decrease of blood pressure. The aim of our study is to depict the outlines of a severe hypertensive individual with sleep apnea by comparing 9 men primarily referred to the hypertension clinic with refractory hypertension and finally found to have sleep apnea (study group) to 23 men whose diagnosis of sleep apnea was made in the pulmonary unit (controls). Fifteen of these were hypertensives. Mean age of the study group was 47 +/- 7 years vs 60 +/- 11. Controls were less overweighted: BMI = 33 +/- 6 kg/m3 vs 39 +/- 5. Mean blood pressure was 171 +/- 16/107 +/- 4 mmHg in the study group vs 157 +/- 19/92 +/- 12 mmHg in controls. Prevalence of glucose metabolism disorders was significantly greater in the study group: 6 patients with maturity onset diabetes and 3 with proven glucose intolerance, vs respectively 4 and 6 controls. Triglycerides were elevated in both groups whereas mean cholesterol was slightly above normal values. Six patients of the study group could have an echocardiogram which showed left ventricular hypertrophy (mean left ventricular mass index = 206 +/- 31 g/m2 after the Penn convention).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Should arterial hypertension in sleep apnea syndrome be stressed?]. 183 55

Left ventricular hypertrophy (LVH) is one of the less common but ominous risk factors for coronary disease, stroke and cardiac failure. The chief determinants of LVH, aside from age, are elevated blood pressure, obesity, stature and glucose intolerance. Cardiac valve disease and chronic heart disease (CHD) also cause LVH. Downward trends in the prevalence of LVH over four decades indicate that LVH is preventable, and this has coincided with improved hypertension control. When evidence of LVH disappears, the risk of all-cause, cardiovascular and CHD mortality is substantially reduced. Cardiovascular events occur incrementally in relation to left ventricular mass with no discernible critical value identifying pathological hypertrophy. LVH as evidenced by electrocardiogram (ECG-LVH), manifested by repolarization abnormality as well as increased voltage, was a lethal finding; with 5 years, 33% of men and 21% of women were dead. ECG-LVH was associated with ventricular ectopy and a sudden death risk comparable to that of CHD or cardiac failure. ECG-LVH was associated with a 3-15-fold increase of cardiovascular events with greatest risk ratios for cardiac failure and stroke. However, CHD is the predominant clinical sequel. No other risk factor approaches LVH in potency. Anatomical (echocardiographic or X-ray) LVH and ECG-LVH each independently contribute to the risk of cardiovascular disease, and having both confers a greater risk than having either alone. LVH is a clinical finding which should be taken seriously and corrected as soon as detected. It should not be regarded as an innocuous adaptive process, augmenting cardiac function.
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PMID:Left ventricular hypertrophy as a risk factor: the Framingham experience. 183 65

Several previous studies have suggested that hypertension is associated with altered sodium transport across the cell membrane. The aim of the present study was to study the skeletal muscle Na:K ratio in relation to blood pressure and glucose tolerance in obese and non-obese men. Muscle biopsies were taken from the femoral vastus lateralis muscle in men aged 52 +/- 5 years and the electrolytes were analyzed. Ten obese men with impaired glucose tolerance and hypertension, 10 obese normotensive controls, 10 lean men with hypertension and 10 lean normotensive controls participated in the study. Higher insulin levels were found in both hypertensive groups compared with the respective normotensive groups. Increased muscle Na:K ratio was found in obesity (P less than 0.01) and this was further enhanced when combined with hypertension and impaired glucose tolerance (P less than 0.001). However, hypertension in lean individuals was not associated with an increased muscle Na:K ratio. These data suggest that the increased muscle Na:K ratio in obese subjects and those with impaired glucose tolerance is not solely due to insulin resistance and hyperinsulinemia. Furthermore, the data clearly suggest that there is no important general perturbation of the Na-K pump in hypertension per se.
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PMID:The skeletal muscle Na:K ratio is not increased in hypertension: evidence for the importance of obesity and glucose intolerance. 184 62

The association of obesity with hypertension has been amply demonstrated in cross-sectional, longitudinal, and dietary-intervention studies, but the mechanisms remain enigmatic. Both conditions are independently characterized by similar metabolic alterations, i.e., glucose intolerance, dyslipoproteinemia, elevated serum uric acid, and inadequate Na+ transport. Obesity, hypertension, and these metabolic alterations are associated with hyperinsulinemia/insulin resistance. The degree of these alterations is lowest in lean hypertensives, intermediate in obese normotensives, and greatest in obese hypertensives, but mortality risk is highest in lean hypertensives. This apparent discrepancy may be related to the divergent hemodynamic characteristics, possibly indicating different etiology, of lean and obese hypertensives, i.e., contracted blood volume, increased total vascular peripheral resistance, and normal sympathetic drive in the former, expanded blood volume, normal peripheral resistance, and increased sympathetic drive in the latter. Current knowledge suggests that the interrelationships of obesity and hypertension with the metabolic alterations could be mediated by high carbohydrate and fat consumption and low physical activity, resulting in obesity and separate pathways in hyperinsulinemia and increased sympathetic drive, leading to a double vicious cycle. In one, hyperinsulinemia and the consequent insulin resistance would compound one another. In the second, the increasing hyperinsulinemia would increasingly stimulate the sympathetic nervous system. This double vicious cycle could result in increasing hemodynamic and metabolic derangements causing hypertension, diabetes, and atherosclerotic cardiovascular disease (ASCVD). The association of lean hypertension with ASCVD may be through other mechanisms, e.g., hemodynamic forces on the vascular endothelium.
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PMID:Hyperinsulinemia or increased sympathetic drive as links for obesity and hypertension. 186 20

The evaluation of lipometabolic disorders is presented within the framework of epidemiological and pathophysiological findings. Insurance medicine can base its risk assessment practices on the recommendations of American and European consensus conferences. The upper normal value for total cholesterol is in the vicinity of 200 mg/dl. The atherogenic risk of an elevated total cholesterol level can be further defined by determining the LDL and HDL cholesterol. The LDL cholesterol level should not exceed 160 mg/dl and the HDL level should not be lower than 35 mg/dl for men and 45 mg/dl for women. The quotients from the total/HDL cholesterol levels (normal value less than 6) and the LDL/HDL levels (normal value less than 4) can be used for differentiated risk assessment. Triglyceride levels exceeding 200 mg/dl are primarily to be taken into consideration as a risk indicator if there is a simultaneous reduction of HDL cholesterol. Additional parameters, such as nicotine abuse, hypertension, a family history of cardiovascular disease, impaired glucose tolerance, male sex, obesity and the existence of peripheral vascular disorders are also to be included in the risk profile. Determining additional lipometabolic substances is only of relevance to insurance medicine in individual cases.
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PMID:[Disorders of lipid metabolism and insurance medicine practice]. 187 45


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