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

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37

Mounting data support a causal connection between high-normal fibrinogen levels and atherosclerotic cardiovascular disease. There is clearly a thrombogenic component to atherosclerosis and the onset of clinical manifestations. This offers the possibility to better identify high-risk candidates and also to protect them by reducing blood fibrinogen concentration or blocking its action. The relationship of antecedent fibrinogen to the subsequent development of cardiovascular disease is examined, based on 18 years of surveillance of a cohort of 1274 men and women aged 47 to 79 years who participated in the Framingham Study. The association with the development of peripheral arterial disease and cardiac failure is now examined in addition to previously studied relationships to coronary heart disease and stroke. In men and women, there is a significant age-adjusted relationship of fibrinogen level to coronary heart disease and to cardiovascular disease in general. In women, a significant relationship to cardiac failure and peripheral arterial disease, but not to stroke, was also found. These data on women are unique as they are not available elsewhere. Age-adjusted cardiovascular, all-cause, and coronary heart disease mortality were all related to fibrinogen in both sexes. In men, fibrinogen impact was the greatest for stroke and the least for peripheral arterial disease. For women, the impact on coronary heart disease was greatest. The absolute risk for an elevated fibrinogen level was greatest for coronary heart disease in both sexes. Average fibrinogen values are higher in women and in persons with other risk factors, including hypertension, cigarette smoking, diabetes, obesity, and elevated hematocrit. However, there is an independent contribution of fibrinogen to cardiovascular disease in general and coronary disease in particular, on adjustment for coexistent risk factors. Fibrinogen enhances the risk of cardiovascular disease in hypertensives, diabetics, and cigarette smokers. About half the cardiovascular risk of cigarette smoking appears due to the higher fibrinogen values. Now, five prospective studies document the excess incidence of cardiovascular events in persons with elevated fibrinogen levels within the "normal range." Each standard deviation increase in fibrinogen is associated with a 30% increment of coronary heart disease in men and a 40% increase in women. Fibrinogen should be added to the list of major cardiovascular risk factors. Trials of intervention to lower fibrinogen in high-risk coronary candidates are needed.
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PMID:Update on fibrinogen as a cardiovascular risk factor. 134 96

When adipose tissue enlarges in obesity, as the result of an imbalance between caloric intake and caloric expenditure, many changes occur in the cellular components of the adipose mass. A combination of increased cell size and number underlies the accretion of the adipose mass, however, only a reduction in cell size is possible with weight loss. Several metabolic abnormalities accompany obesity--most important--hyperinsulinemia, hyperlipidemia, insulin resistance, and carbohydrate intolerance. Clinical consequences of obesity include hypertension, venous insufficiency, gallbladder disease, osteoarthritis, pulmonary and cardiovascular insufficiency, diabetes, and atherosclerotic cardiovascular disease, and all are dependent on the severity and duration of the obesity. Once established, obesity is difficult to correct because of the development of many adaptive mechanisms by which obesity defends itself.
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PMID:Cellular, metabolic, and clinical consequences of adipose mass enlargement in obesity. 180 21

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

Epidemiologic research indicates that glucose intolerance and hypertension are interrelated phenomena, each powerfully predisposing to atherosclerotic cardiovascular disease. Both diabetic and hypertensive patients have greater amounts of atherogenic risk factors, including dyslipidemia, hyperuricemia, elevated fibrinogen, and left ventricular hypertrophy. Diabetic persons have an increased prevalence of hypertension (50%), and glucose intolerance is more common in hypertension (15% to 18%). Both share a strong relationship to excess weight, but the excess of hypertension in diabetic persons occurs in both lean and obese subjects. Diabetes doubles the risk of hypertension associated with overweight. The risk of coronary disease, stroke, and peripheral arterial disease increases with increasing blood pressure to the same degree in diabetic persons as in nondiabetic persons, but at any level of blood pressure, diabetic persons have a doubled risk of these outcomes. Both diabetic and hypertensive patients are particularly prone to silent or unrecognized myocardial infarctions. Greater efforts at primary prevention of both hypertension and diabetes are clearly needed, including efforts at weight control, exercise, limitation of salt intake, and control of blood lipid levels. In either diabetic or hypertensive candidates for cardiovascular disease, optimization of the chances of avoiding sequelae requires a comprehensive multifactorial approach. Prevention requires more than normalization of either the blood sugar or blood pressure. Rational preventive measures must also include weight reduction, a fat-modified diet, cessation of smoking cigarettes, raising high-density lipoprotein, lowering low-density lipoprotein, and reduction of fibrinogen. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol tend to coexist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of impaired glucose tolerance and hypertension. 200 55

Diabetes mellitus is commonly associated with systolic/diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive control subjects, a heightened plasma insulin response to a glucose challenge is consistently found. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the insulin/glucose-clamp technique, in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: Na+ retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth muscle cells. Physiological maneuvers, such as calorie restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; evidence indicates that these maneuvers can also lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia are also associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate-density and low-density lipoproteins, both of which are atherogenic. Last, insulin, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of various growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including non-insulin-dependent diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. 204 34

The nocturnal decline of blood pressure (BP) is not observed in autonomic dysfunction (after cardiac transplantation and in patients with diabetic neuropathy) or in patients with atherosclerotic cardiovascular disease. This study evaluated if smoking prematurely alters the blood pressure during the night and if the cumulative risk of hypertension and smoking may additionally alter this nocturnal profile. Three different groups of subjects were studied. In each subject systolic and diastolic BP was recorded, for 24 hours at 15 min intervals, by automatic non-invasive monitoring. Group 1 consisted of 14 normotensive nonsmokers (with a mean age 50, range 38 to 54 years); Group 2 consisted of 14 normotensive heavy smokers (with a mean age 48, range 37 to 52); Group 3 consisted of 14 heavy smokers with mild or moderate hypertension and with left ventricular hypertrophy (with a mean age 51, range 39 to 54 years). We have evaluated particularly the average systolic and diastolic BP during 3 hours of the day and 3 hours of the night, the latter selected from midnight to 3.00 am, when the patients were asleep, and the former selected from 3.00 pm to 6.00 pm when they were engaged in social activities in the hospital. The statistical analysis showed that in normotensive heavy smokers (and in hypertensive smokers) the normal nocturnal decline of BP is not present. This physiologic fall in arterial pressure was normally observed in the group of normotensive nonsmokers. The absence of nocturnal decline of BP may be related to the reduced arterial distensibility secondary to smoking damage and may represent an important and early marker of this vascular alteration.
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PMID:[Importance of the determination of blood pressure profile in the diagnosis of atherosclerotic cardiovascular disease]. 209 30

Screening for dyslipoproteinemias should be undertaken in all individuals older than 20 years of age at least once every 5 years. The initial screening, as recommended by the Adult Treatment Guidelines Panel of the National Cholesterol Education Program, is to determine the concentration of total blood cholesterol. This initial determination can be made on blood obtained in the nonfasting state. Further evaluation of the patient's lipoprotein concentrations is dependent upon the presence of other cardiovascular risk factors. in the absence of definite coronary heart disease, hypertension, diabetes mellitus, a family history of coronary artery disease, cigarette smoking, or severe obesity, the patient with a total blood cholesterol concentration less than 200 mg/dL requires no specific instruction and should have a repeated screening performed within 5 years. Patients with blood cholesterol concentrations greater than 200 mg/dL should have their lipoprotein profiles determined if they have atherosclerotic cardiovascular disease or two other cardiovascular disease risk factors. The lipoprotein profile includes the determination of fasting cholesterol and triglyceride and HDL cholesterol concentrations. From these values, the LDL cholesterol concentration can be calculated. This LDL cholesterol concentration is central in selecting the appropriate therapy. HDL cholesterol concentrations may be useful in evaluating patients with ischemic heart disease. Concentrations of HDL cholesterol less than 35 mg/dL are associated with increased risk for coronary artery disease. Although there is currently no convincing evidence that support the specific treatment of depressed HDL cholesterol concentrations, therapy directed to modulating lipoprotein metabolism in patients with heart disease and low HDL concentrations may be of benefit. Patients with recurrent abdominal pain, pancreatitis, and eruptive xanthomatosis frequently have fasting hypertriglyceridemia concentrations exceeding 1000 mg/dL. These patients should be identified in order to effectively reduce their triglyceride concentrations, which can prevent these complications.
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PMID:Detection and evaluation of dyslipoproteinemia. 219 76

Cholesterol crystal embolization (CCE) frequently presents with nonspecific manifestations that mimic other systemic diseases. The authors reviewed 221 cases of histologically proven CCE in the English literature to define the clinical, laboratory, and pathologic characteristics of this disorder. CCE affected predominantly elderly males (mean age sixty-six) with a frequent history of hypertension (61%), atherosclerotic cardiovascular disease (44%), renal failure (34%), and aortic aneurysms (25%) at presentation. At least one possible predisposing factor was present in 31% and included operative and radiological vascular procedures and the use of anticoagulants. Cutaneous findings (34%) and renal failure (50%) were two of the most common clinical findings throughout the course of CCE. The nonspecific signs and symptoms included: fever (7%), weight loss (7%), myalgias (4%), and headache (3%). Premortem diagnoses were established in 31% of patients most commonly by biopsy of the muscle, skin, and kidney. Mortality was high (81%) and was most commonly due to multifactorial, cardiac, and renal etiologies. The authors conclude that CCE should be strongly considered in elderly patients with atherosclerotic vascular disease who have the onset of renal insufficiency and cutaneous manifestations. CCE may be confirmed by a skin or muscle biopsy.
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PMID:Cholesterol crystal embolization: a review of 221 cases in the English literature. 331 Jul 42

Within a 2 month period 131 Ethiopian immigrants were admitted for treatment at a general hospital in Jerusalem. There were 52 patients with malaria, 13 with typhoid fever, 24 with pneumonia, seven with tuberculosis, nine with shigella and 11 with campylobacter. Over three-quarters of these patients were anaemic. In the majority of cases anaemia was normocytic and was most probably secondary to malaria and other intercurrent infections. The prevalence of diffuse non-toxic goitre was 7% in children and 19% in adults with a male to female ratio of 4:13. A positive rapid plasma reagin (RPR) test was found in 4% of sera tested and a positive HBsAg in 13%. IgG antibodies to HBc antigen were found in 75% of subjects. All patients with infectious diseases responded to therapy and, despite their poor condition at arrival, there were no fatalities and no late sequelae. The high HBsAg carrier state calls attention to the risk of vertical transmission by infected mothers and underlines the need for active immunization of infants at risk. The high prevalence of untreated tuberculosis and malaria poses a potential public health hazard, but with the current systematic screening of this population leading to identification and effective treatment of affected subjects, chances for the practical eradication of malaria and tuberculosis are excellent. Finally, the large scale transfer of a population from rural Africa to a modern and largely urban society presents a unique opportunity for a prospective study of the impact of environment on the emergence of diseases which plague modern society such as diabetes, atherosclerotic cardiovascular disease, hypertension and cancer.
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PMID:Medical problems in Ethiopian refugees airlifted to Israel: experience in 131 patients admitted to a general hospital. 346 61


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