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The paper presents the evolution of the levels of smoking, hypercholesterolemia, essential hypertension and obesity in the course of a prophylactic action carried out for 15 years (1971-1986) in a group of 5000 males aged 40-60 years. In the group still available after 15 years of follow up consisting of 2000 subjects, a decrease was obtained in the number of smokers, from 22.3% to 5.6% of hypercholesterolemia from 31.3% to 23.7%. The cumulated incidence of essential hypertension has increased from 15.5% to 36.7% and of obesity from 12.6% to 14.4%. At the same time the incidence of angina pectoris and myocardial infarction increased from 1.1% to 5.3%. For comparison are presented data obtained in a similar control group.
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PMID:Evolution of ischemic heart disease risk factors in "The Bucharest Multifactorial Preventive Trial of Coronary Heart Disease" after 15-year follow-up. 209 93

Hypertension that occurs before the age of 60 years is strongly aggregated in families, mostly due to genetic factors with weaker contributions from a shared family environment. Hypertension is probably a heterogeneous collection of overlapping subsets of pathophysiological mechanisms, such as dyslipidemia, obesity, hyperinsulinemia and cation metabolism. Highly heritable traits such as sodium-lithium countertransport, urinary kallikrein excretion and a body fat pattern index show evidence of major gene segregation in families with hypertension. They are thought to be intermediate phenotypes in the chain of pathophysiological events leading from specific genes to the distant phenotype of hypertension. They provide evidence of measurable contributions from single gene traits to the susceptibility to hypertension. Genetic linkage studies have suggested that other specific loci (e.g. histocompatibility leukocyte antigen, blood group MN and the haptoglobin protein) contribute to the susceptibility to hypertension. DNA sequencing has shown a point mutation for lipoprotein lipase that conveys susceptibility to lipid abnormalities, and possibly also hypertension, as seen in families with dyslipidemic hypertension. Further application of these approaches, especially in families that include multiple siblings with hypertension, shows promise of a true understanding of how the combined effects of a few specific genes, the polygenic background and selected environmental factors can lead to essential hypertension. This understanding should foster better tailored and more effective approaches to the prevention, diagnosis and treatment of hypertension.
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PMID:Multigenic human hypertension: evidence for subtypes and hope for haplotypes. 209 95

When one is faced with the problem of essential hypertension it is prudent to pay attention to lifestyle factors, especially alcohol, smoking and obesity. Modification of salt intake in the diet is a simple measure. Drug therapy will need to be long-term therapy and ease of treatment is important, which means that drugs given once a day or at most twice a day should be used. Diuretics and beta-blockers are inexpensive and well proven but have many side-effects. Newer agents may have fewer side-effects but are more expensive. The choice will be an individual one.
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PMID:Essential hypertension--investigations and management. 209 50

To elucidate the impact of increased afterload during physical and mental stress on myocardial hypertrophy, a homogeneous population of 73 patients with untreated mild-to-moderate essential hypertension were enrolled in the current study. Left ventricular mass and cross-sectional area, both determined by 2-D guided M-mode echocardiography, were related to blood pressure measured at rest as well as during various stress situations. Left ventricular mass and cross-sectional area correlated with systolic pressure at work site (r = 0.28 and r = 0.23 respectively, P less than .05) and systolic pressure at complete rest (r = 0.35 and r = 0.33, P less than .01). Neither the response in blood pressure to mental arithmetic or a bicycle exercise test performed in the laboratory, nor blood pressure during both stress tests were significantly related to the degree of left ventricular hypertrophy. In addition, patients with a hyperreactive response to mental arithmetic or to the physical stress test did not disclose a greater left ventricular mass than normoreactors. Examining the hemodynamic response pattern during mental arithmetic, we found that patients with vasoconstriction during mental stress had a greater left ventricular mass than individuals with vasodilation during mental stress (244 +/- 73 v 204 +/- 53 g, P less than .05), but this was due to the impact of obesity on left ventricular mass (analysis of covariance: F = 2.1, P = NS). Thus, blood pressure at work site and at rest, but not blood pressure during mental or physical stress, nor the response of blood pressure to both stress tests, was linked to the degree of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of hemodynamic reaction during stress to left ventricular hypertrophy in essential hypertension. 214 Jun 89

The sensitivity of tissue to insulin is of physiological, pathophysiological and therapeutic relevance. The quantity of insulin and the response to insulin are paramount complementary factors in the regulation of glucose metabolism, and may, at least under certain pathophysiological conditions, also affect cardiovascular function. Hypertension has a high prevalence among subjects with decreased insulin sensitivity and/or hyperinsulinaemia due to obesity, impaired glucose tolerance, non-insulin-dependent diabetes mellitus, and certain other conditions. There is evidence that, even in the absence of obesity or diabetes mellitus, essential hypertension tends to be associated with insulin resistance. The latter elicits a compensatory increase in insulin secretion. Hyperinsulinaemia also occurs in diabetes type 1 as a consequence of insulin treatment. Considering the acute effects of insulin on sympathetic nervous activity, transmembranous cation transport, renal sodium reabsorption, cellular proliferation and lipid metabolism, insulin resistance and/or hyperinsulinaemia may possibly contribute to the genesis of essential, obesity-associated and diabetes-associated hypertension, and may also promote dyslipidaemia in these disorders.
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PMID:Insulin, insulin sensitivity and hypertension. 216 83

It is now well recognized that insulin resistance and/or hyperinsulinemia are characteristic of a number of common human disease states including obesity, non-insulin dependent diabetes mellitus (NIDDM), essential hypertension, and atherosclerotic cardiovascular disease. More recent evidence suggests that impaired insulin action and elevated levels of circulating insulin may also be present in a substantial proportion of apparently healthy nonobese individuals. Considerable attention is now being focused on the potential long term adverse consequences of elevated circulating insulin levels. In particular, the frequent concurrence of these clinical disorders of carbohydrate metabolism, lipid metabolism, and vascular disease has led to the hypothesis that insulin resistance and the ensuing hyperinsulinemia may be a common pathophysiologic factor in the etiology of these disease states. In this review, we will examine the evidence for this hypothesis with particular attention to the adverse effects of chronic hyperinsulinemia.
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PMID:Hyperinsulinemia and its sequelae. 220 24

Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Blood pressure lowering treatment should therefore be metabolically neutral in order to avoid aggravation of this risk factor syndrome. Clinical studies applying CE-inhibitors in type II diabetes are critically reviewed under this aspect. The majority of the available studies in type II diabetes report a reduction of insulin resistance and a marginal improvement of metabolic control. The order of magnitude in HbA1 reduction is nearly 10% of the glycosylated haemoglobin, reduction of fasting and postprandial blood glucose approximates 1 mmol/l. From a more extended view, considering essential hypertension as insulin resistant and thus possibly "prediabetic" state, this marginal metabolic effect gets further support from recent studies in essential hypertension consistently reporting an improvement of metabolic parameters of similar magnitude. This might become a central argument in the discussion about individualized and metabolically neutral antihypertensive treatment in essential hypertension.
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PMID:Clinical studies with CE-inhibitors in diabetes. 220 31

Using the criteria of weight(g)/height(cm)2 greater than or equal to 2.26 as cut off point, 292 (7.56%) of the 3,861 school children in the age group 5-15 years were identified as obese. The mean blood pressure levels, both systolic and diastolic, were found to be significantly higher in the obese subjects compared to the controls (p less than 0.001). Further, 10 (3.4%) of the 292 obese subjects were detected to have sustained elevations in BP levels (BP greater than mean + 2 SD for age-sex) on monthly follow-up for 6 months. On the contrary, persistent hypertension was detected in only six (0.16%) of the 3,569 controls. None of these hypertensive children had any symptoms attributable to raised blood pressures and all had only mild elevations in BP levels. Baseline investigations, carried out in 9/16 subjects, failed to document any underlying cause for hypertension. Serum cholesterol levels, however, were elevated in six subjects. This suggests a close association between childhood obesity and essential hypertension.
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PMID:Childhood obesity and hypertension. 181 68

Hypertension and diabetes mellitus are chronic medical conditions that frequently coexist. In the United States, it is estimated that 10 million persons suffer from diabetes mellitus, 60 million from hypertension, and 3 million from the combination of the two. There may be a causal relationship between hypertension and diabetes. Obesity may be a precipitating factor for both hypertension and non-insulin-dependent diabetes mellitus. Those with insulin-dependent diabetes mellitus generally become hypertensive only with the onset of nephropathy. Glucose tolerance, insulin resistance, and hyperinsulinemia frequently occur with essential hypertension and may be aggravated by hypertension therapy, especially with diuretics and beta-blockers. Hyperinsulinemia may be an important common factor promoting sodium retention, sympathetic nervous system stimulation, and inhibition of the sodium pump. The Working Group on Hypertension in Diabetes has outlined a flexible modified version of the stepped-care approach to the treatment of hypertension in diabetes. Management is complex because diabetes is associated with autonomic neuropathy, sexual dysfunction, hyperlipidemia, and fluid and electrolyte disorders. All these problems can be exacerbated by antihypertensive treatment. Nonpharmacologic measures, which address weight reduction and sodium restriction, are logical, but aggressive antihypertensive medication is invariably necessary. Diuretics and/or beta-blockers were the mainstay of treatment until the introduction of angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers. These newer agents have no deleterious effects on carbohydrate metabolism and are generally better tolerated. Antihypertensive therapy may slow the rate of deterioration in diabetic nephropathy. This was first shown with diuretics, beta-blockers, and hydralazine and more recently with ACE inhibitors, which provide effective blood pressure control and a significant drop in albuminuria without affecting the glomerular filtration rate adversely. ACE inhibition may also lead to increased insulin sensitivity and glucose disposal rate. Long-term trials are needed to assess the effects of these new agents on the treatment of hypertension in the diabetic population.
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PMID:Diabetes mellitus and hypertension. 222 Jul 97

Insulin resistance, independent of obesity or non-insulin-dependent diabetes mellitus, has been demonstrated to be associated with high blood pressure. To determine if insulin resistance could be an antecedent to hypertension in a high-risk population, we studied normotensive (112 +/- 12/70 +/- 10 mm Hg) and borderline hypertensive (135 +/- 8/85 +/- 5 mm Hg) lean young black men (22-26 years old) with the euglycemic hyperinsulinemic clamp technique. All subjects had clinically normal oral glucose tolerance. Body mass index and percent adipose mass were the same in both groups. Fasting plasma insulin concentration was significantly higher in the borderline hypertensive group (p less than 0.01). Insulin-directed exogenous glucose metabolism at the same degree of steady-state hyperinsulinemia was significantly lower in the borderline hypertensive group (5.98 +/- 2.22 versus 8.22 +/- 1.96 mg/kg/min; p less than 0.01). For the total population, a significant inverse correlation existed between the glucose infusion rate and systolic blood pressure (p less than 0.01). These data indicate that there is a relation between insulin-mediated glucose uptake and blood pressure. Furthermore, in this high-risk population insulin resistance may precede the onset of established essential hypertension.
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PMID:Insulin resistance and blood pressure in young black men. 224 37


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