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

Cardiovascular disease constitutes an expanding problem in the elderly because of the increasing size of the aged population. Atherosclerosis, hypertension, and diabetes are responsible for the predonderance of cardiovascular disease, which causes 70% of all deaths beyond age 75. Coronary heart disease (CHD) is the most common and most lethal cardiovascular event in both sexes, exacting a large toll in disability and deteriorated quality of life in old age. Unrecognized myocardial infarctions are especially common and are as serious as symptomatic infarctions. beyond age 65, women are as vulnerable to cardiovascular death as men. The predisposing modifiable risk factors for coronary disease, stroke, peripheral arterial disease, and cardiac failure are similar in young and old and in men and women. These include hypertension, dyslipidemia, impaired glucose tolerance, physical indolence, and cigarette smoking. An attenuated risk ratio for some risk factors is offset by a greater incidence of cardiovascular events in advanced age so that the attributable risk and the potential benefit of treatment rise with age. Because the major risk factors predict CHD as efficiently in the elderly as in the young, and the decline in cardiovascular mortality has included the elderly, preventive efforts in the elderly may have substantial potential benefit. At advanced age, total cholesterol levels are considerably higher in women than in men. Some 10 million elderly, two-thirds of whom are women, may require investigation and treatment for elevated lipid levels, as determined by National Heart, Lung, and Blood Institute (NHLBI) guidelines. Because of the preponderance of women in the elderly population, trials of the efficacy of correcting risk factors in general, and lipids in particular, should include women.
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PMID:Demographics of the prevalence, incidence, and management of coronary heart disease in the elderly and in women. 134 64

Hypertension can no longer be regarded as a single entity; it frequently coexists with other powerful coronary risk factors such as left ventricular hypertrophy (LVH), lipid and clotting disorders, obesity, and insulin resistance/impaired glucose tolerance.
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PMID:Hypertension--interaction with other coronary heart disease risk factors. 134 67

The incidence of hypertension and coronary artery disease among diabetic patients is approximately two to three times greater than in nondiabetics. Recent evidence suggests that even moderately elevated blood pressure levels may result in diabetic complications involving the eyes or kidneys. However, treatment of diabetic patients with antihypertensive drugs may have a deleterious metabolic effect. Previous studies have suggested that calcium antagonists may reduce insulin secretion and therefore impair glucose tolerance. This has not been substantiated clinically; in general, it would appear that calcium antagonists have a minimal hyperglycemic effect. To establish whether interruption of excitation-contraction coupling in arterial smooth muscle and altered stimulus-secretion coupling occur at pharmacologically equivalent doses of calcium antagonist, the effect of nicardipine on insulin output and vascular resistance was studied in the isolated perfused rat pancreas and in eight hypertensive patients with impaired glucose tolerance during oral glucose tolerance testing (OGTT). Baseline insulin output in vitro was 86 +/- 22 ng/min at 8.0 mM glucose and 2.5 mM calcium. Application of 10 nM nicardipine reduced insulin output to 86% of baseline, whereas output was reduced to 16% by 1 microM nicardipine and to 6% by 10 mM nicardipine. Changes in duodenopancreatic outflow indicated maximal vasodilation of the pancreas at all three concentrations of nicardipine (10 nM-10 mM). In vivo nicardipine 30 mg t.i.d. for 2 weeks reduced systolic blood pressure from 168 +/- 2 mm Hg to 136 +/- 4 mm Hg (p < 0.001) and diastolic blood pressure from 96 +/- 3 mm Hg to 78 +/- 2 mm Hg (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effects of calcium antagonists in hypertensive diabetics. 136 2

Twenty-five middle-aged subjects with impaired glucose tolerance (IGT) were analysed 5 years later, showing normal glucose tolerance in 28% and persistent glucose deterioration in 72%. Body mass index (strongly) and 2-h glucose levels were clinically useful predictors, in the newly detected IGT-subjects, of persistent glucose deterioration (IGT or NIDDM) 5 years later. The frequency of hypertension was 36% in the newly-detected IGT subjects. Five years later this frequency increased to 54% in the persistently hyperglycaemic group, and decreased to none in the normalized group. Predictors of hypertension at the follow-up were baseline blood pressure and parts of the hyperinsulinaemic syndrome, such as serum triglyceride at baseline, BMI and 2-h glucose at the follow-up. Microalbuminuria (greater than 20 mg day-1) was not found at the 5-years follow-up, either if the subjects then had NIDDM, IGT or normal glucose tolerance. ECG abnormalities (ST segment and T wave changes) were two-fold more prevalent in the group with IGT or NIDDM than in the normalized group at the follow-up. Predictors were baseline BMI and incremental BMI. In conclusion, obesity and high 2-h glucose in newly-detected IGT-subjects seemed to predict the persistence of IGT 5 years later. Hypertension, but not microalbuminuria, was frequent when glucose deterioration persisted.
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PMID:What causes impaired glucose tolerance to deteriorate or normalize? 141 Dec 61

The hypothesis of the atherogenic role of endogenous insulin was based on a series of epidemiological studies. Several large-scale prospective studies have demonstrated that diabetes constitutes an independent risk factor for cardiovascular disease. However, neither the duration of diabetes nor the blood glucose level appear to be predictive of the incidence of a cardiovascular accident. More recent prospective studies (Finland, Australia, Paris) in non-diabetic men have shown that hyperinsulinemia, while fasting or after glucose stimulation, constitutes a risk factor for fatal myocardial infarction, but they failed to show whether diabetes or the blood glucose level constituted a risk factor for the disease. Cross-sectional studies have provided similar results. Insulin resistance affects the majority of non-insulin-dependent diabetics and glucose-intolerant patients. It has also been observed in 25 percent of non-obese subjects with a normal glucose tolerance test. Associated hyperinsulinemia prevents the development of diabetes, but diabetes appears when the beta-cell function is altered and can no longer maintain this hyperinsulinemia. However, hyperinsulinemia is not devoid of cardiovascular consequences. Insulin resistance and hyperinsulinemia are also observed in patients with essential hypertension: a correlation between plasma insulin and blood pressure has been reported. These data, together with other experimental arguments, suggest that excessive endogenous insulin may participate in the rise in blood pressure. Furthermore, hypertensive patients have a high risk of coronary heart disease and this risk is not significantly decreased by anti-hypertensive treatments. This is probably related to the presence of other metabolic risk factors associated with insulin resistance: hyperinsulinemia, glucose intolerance, hypertriglyceridemia, decreased HDL cholesterol. These metabolic disorders have been grouped together under the term "syndrome X". All of these risk factors are probably also involved in the development of coronary heart disease in general population. In conclusion, epidemiological studies now suggest that insulin resistance and hyperinsulinemia increase the risk of hypertension and coronary heart disease. A great many experimental studies support this hypothesis. Lastly, it can be proposed that the increased cardiovascular risk in non-insulin-dependent diabetics is related to the fact that they belong to a larger group of insulin-resistant subjects. The management of diabetes, hypertension, and all of the metabolic abnormalities would appear to be the only way of reducing the incidence of cardiovascular disease.
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PMID:[Pathogenic role of hyperinsulinism in macroangiopathy. Epidemiological data]. 143 99

The only drugs which commonly cause diabetes during therapeutic use are the anti-hypertensive vasodilator diazoxide, and corticosteroids in high doses such as those used to palliate intracranial tumours. Thiazide diuretics have in the past been used in higher doses than necessary to treat hypertension, and the lower doses now used probably carry only a slight risk of inducing diabetes. The risk from beta-blockers is also quite small, but there is some evidence that thiazides combined with beta-blockers may be more likely to cause diabetes than either drug alone. The combination is probably best avoided in patients with a family history of non-insulin-dependent diabetes. The effect of the low-oestrogen combined oral contraceptive pill seems to be slight, and it presents a risk only to women who have had gestational diabetes. Bodybuilders who take enormous doses of anabolic-androgens can develop impaired glucose tolerance. Several drugs, including theophylline, aspirin, isoniazid and nalidixic acid can cause transient hyperglycaemia in overdosage, but only streptozotocin, alloxan and the rodenticide Vacor are likely to cause permanent diabetes.
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PMID:Drug-induced diabetes. 144 73

A public health strategy carries more constraints than a high risk strategy because it targets both low risk and high risk individuals; this requires cautious intervention and hence achieves only a modest reduction in risk. Nevertheless, a modest population-wide fall in the concentrations of atherogenic lipoproteins leads to substantial numbers of preventable heart attacks and deaths. Other strategic considerations are to lower non-lipid cardiovascular risks (hypertension, clotting tendency) and to prevent other diet-related disease (such as cancer) through interventions which lower plasma lipids. The major nutritional changes which achieve this are optimising energy balance, reducing total fats and saturated fatty acids and increasing plant foods which are rich sources of unsaturated fatty acids, fibre and antioxidants. Each of these contributes to optimising the low density lipoprotein (LDL) concentration. Antioxidants (vitamins C and E mainly) may inhibit LDL oxidation. The strategy for lowering plasma triglyceride, especially in the context of atherogenic lipoprotein phenotypes, is mainly through energy balance, reduced saturated fat and alcohol. Correcting overweight especially in those with abdominal obesity, may normalise raised plasma triglyceride, low high density lipoprotein (HDL), abnormal LDL and even glucose intolerance and hypertension, which may be associated. The scientific basis for the lipid optimising effects of the different nutrients will be discussed.
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PMID:Optimising plasma lipids: public intervention versus high risk management. 144 40

The insulin resistance syndrome ("syndrome X") consists of hyperinsulinemia, glucose intolerance, dyslipidemia, and hypertension, although the inclusion of hypertension has been challenged. Insulin has biological effects that could produce a hyperdynamic circulation. We therefore postulated that an insulin-induced hyperdynamic circulation is an early feature of the insulin resistance syndrome and that this circulatory abnormality leads to later fixed hypertension. The San Antonio Heart Study cohort, a population-based cohort of 3,301 Mexican Americans and 1,857 non-Hispanic whites, was used to define individuals who were hyperdynamic (pulse pressure and heart rate in the upper quartile of their respective distributions), intermediate, and hypodynamic (pulse pressure and heart rate in the bottom quartile). The characteristics of the insulin resistance syndrome were then examined according to these three hemodynamic categories. We also examined the 8-year incidence of hypertension and of type II diabetes according to these hemodynamic categories. A hyperdynamic circulation was associated with statistically significant increases in body mass index (BMI) (p < 0.001), subscapular-to-triceps skinfold ratio (p = 0.042), triglyceride (p = 0.002), 2-hour glucose (p = 0.002), and fasting and 2-hour insulin (p = 0.019 and 0.006). When hemodynamic status was examined separately in lean (BMI < 27 kg/m2) and obese (BMI > or = 27 kg/m2) individuals, the above effects persisted, although they were somewhat attenuated. The odds ratio for the hyperdynamic state as a predictor of future hypertension was 1.66, although this was not statistically significant (p = 0.304). The odds ratio for predicting future type II diabetes was 3.97, which was statistically significant (p = 0.047).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Dec
PMID:Hyperdynamic circulation and the insulin resistance syndrome ("syndrome X"). 145 96

A clustering of metabolic disturbances has been indicated in hypertension. The distribution of such factors was assessed among hypertensives and normotensives in a general population sample of 644 men aged 67 years. Fasting serum insulin, glucose and triglyceride levels were measured. In this study hypertension was defined as DBP > or = 95 mmHg or present use of antihypertensives. Impaired glucose tolerance (IGT) or diabetes mellitus, hyperinsulinaemia (> or = 20 mU l-1) and hypertriglyceridaemia (> or = 2.3 mmol l-1) were defined as metabolic disturbances. When all these disturbances were present simultaneously a complete 'metabolic syndrome' was considered to be present. Hypertension was found in 185 (29%) men, IGT in 15%, diabetes mellitus in 11%, hyperinsulinaemia in 18% and hypertriglyceridaemia in 19%. Among hypertensives, 11 (6%) men had a 'metabolic syndrome', compared to 12 (3%) men in the normotensive group (P = 0.039). At least one metabolic disturbance was present in 109 (59%) of the hypertensive men, and in 173 (38%) of the normotensive men (P < 0.001). The prevalence rates of metabolic disturbances did not differ significantly between lean (BMI < 26 kg m-2) and obese (BMI > or = 26 kg m-2) hypertensives. Only hypertriglyceridaemia was more frequent in obese than in lean hypertensives (20% vs. 37%, P = 0.015). The 'metabolic syndrome' was found in 6% of all hypertensives, which was twice as common as in the normotensive population. The 'metabolic syndrome' was uncommon in both lean and obese hypertensives (5% vs. 7%, NS). These findings indicate that hypertension and metabolic disturbances may have a common underlying cause, at least in some individuals.
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PMID:Metabolic disturbances in hypertension: results from the population study 'men born in 1913'. 145 22

The authors summarize the principles of the therapeutic approach to the 5H syndrome [1. hyperinsulinism, 2. hyperglycaemia (NIDDM), 3. hyperlipoproteinaemia (obesity), 4. hypertension, 5. hirsutism], in particular its two components, i.e. NIDDM and arterial hypertension. The authors found that early treatment of hyperinsulinism, e.g. already in the stage of impaired glucose tolerance or NIDDM with oral antidiabetics, their disproportionate increase with regard to the blood sugar level and glycosylated haemoglobin without making "hygienic" provisions (radical weight reduction; increased physical activity to the maximum possible individual level; energy restricted diet in particular as regards carbohydrates and fat) does not prevent progression of the components of the 5H syndrome to the clinical stage. In treatment of arterial hypertension associated with 5H syndrome non-selective beta-blockers and thiazide diuretics are unsuitable because they worsen the HPLP and enhance insulin resistance. Suitable preparations are combinations of ACE-inhibitors, calcium antagonists, selective beta-blockers in particular with ISA and beta-blockers with a partial selective sympathomimetic activity (devalol and celiprolol). Hygienic provisions must be started in childhood, or when hyperinsulinism is detected.
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PMID:[How should we implement the basic principles of treatment of type 2 diabetes mellitus from the aspect of the hormono-metabolic syndrome X (5H)?]. 145 53


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