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

The relationships between body fatness, adipose tissue distribution, plasma glucose, insulin levels, lipoprotein levels, and resting blood pressure were studied in 81 men aged 36.0 +/- 3.3 years (mean +/- s.d.) (body mass index (BMI): 27.4 +/- 3.8 kg/m2, percentage body fat: 26.4 +/- 6.6%). Systolic and diastolic blood pressures (BP) were significantly associated with the BMI (r = 0.31, r = 0.33, P < 0.01), the waist circumference (r = 0.33, r = 0.27; P < 0.01) as well as with adipose tissue areas measured by computerized tomography (CT) (0.27 < or = r < or = 0.36, P < 0.01). Furthermore, the relative accumulation of subcutaneous abdominal fat, as estimated by the ratio of abdominal to femoral adipose tissue areas measured by CT, was positively correlated with systolic and diastolic BP (P < 0.01). Fasting plasma insulin level (r = 0.30, P < 0.01) as well as the insulin area measured during an oral glucose tolerance test (0.34 < or = r < or = 0.37, P < 0.01) were significantly correlated with blood pressure. Systolic and diastolic BP were significantly associated with HDL2-cholesterol (C) as well as with the HDL2-C/HDL3-C ratio (-0.24 < or = r < or = -0.34), whereas triglycerides (r = 0.23) and the HDL-C/C ratio (r = -0.23) were significantly correlated with diastolic BP only (P < 0.05). Multivariate analysis indicated that the insulin area was the most important variable associated with blood pressure and that this association was independent of total body fatness and regional adipose tissue distribution. Plasma insulin levels explained 14% and 11% of the variance observed in the systolic and diastolic blood pressures respectively. These results suggest that most of the association between abdominal obesity and high blood pressure is mediated by the hyperinsulinemia and/or the related insulin resistant state.
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PMID:Relation of abdominal obesity to hyperinsulinemia and high blood pressure in men. 133 43

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes. 145 17

Possible factors predisposing to peripheral vascular disease (PVD) in hypertensive subjects with Type 2 diabetes mellitus were studied. Details of age, sex, duration of diabetes, blood pressure, and smoking habit were recorded in 180 subjects of either White, West Indian Black or Asian ethnic origin. Glycosylated haemoglobin, fasting serum total cholesterol, total high density lipoprotein (HDL), HDL2, low density lipoprotein (LDL-cholesterol), and triglycerides were measured in all subjects. Peripheral vascular disease was defined as an ankle/brachial systolic pressure < 1.0 as measured by the Doppler technique. Multivariate analysis was performed and the following factors were identified as being strongly associated with the presence of PVD with a statistical significance of p < 0.001; LDL-cholesterol, total HDL-cholesterol, age, male sex, diet or oral hypoglycaemic therapy, diastolic blood pressure, and of p < 0.003; systolic blood pressure. When blood pressure was excluded from the analysis the other factors retained their predictive value. We conclude that hypertension and dyslipidaemia are important risk factors for peripheral vascular disease in Type 2 diabetes mellitus.
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PMID:Risk factors for peripheral vascular disease in hypertensive subjects with type 2 diabetes mellitus. 147 34

The predictors of premature coronary atherosclerosis were examined in 203 patients (99 men aged less than or equal to 50 years, and 104 women aged less than or equal to 60 years) undergoing elective diagnostic coronary arteriography. Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. In men, age (p less than 0.05), smoking (p less than 0.05), and plasma triglyceride (p less than 0.02) and apoA-1 (p less than 0.05) levels were independently associated with CAD. In women, smoking (p less than 0.001) and plasma apoB levels (p less than 0.04) were the strongest variables independently associated with CAD. It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors.
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PMID:Comparison of the plasma levels of apolipoproteins B and A-1, and other risk factors in men and women with premature coronary artery disease. 156 71

Forty-five patients with mild hypertension were treated for 2 months with either metoprolol or pindolol in a randomized, blind, crossover study. The effects of metoprolol (100-300 mg/day) and pindolol (5-15 mg/day) on triglyceride (TG), cholesterol (C), high-density lipoprotein cholesterol (HDL-C), and HDL subfraction (HDL2-C and HDL3-C) levels were compared in males and females separately. Pindolol and metoprolol significantly elevated (10% above baseline level) the plasma TG level in both males and females. After metoprolol treatment, the HDL-C level remained unchanged in both sexes; however, a shift was found between HDL2-C and HDL3-C:HDL2-C decreased and a concomitant elevation in HDL3-C was observed. Pindolol significantly decreased total C, HDL-C, and HDL2-C levels in males. A similar trend (although the changes were not significant) was found in females. The results demonstrate the role of beta blockers in the inhibition of TG-rich lipoprotein elimination. These findings suggest that during long-term administration of metoprolol and pindolol, risks and benefits from beta-blocker therapy must be carefully considered. Continuous monitoring of lipid profiles is suggested during this treatment in order to avoid the potential worsening effect of beta blockers on risk factors of ischemic heart disease.
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PMID:Effect of metoprolol and pindolol monotherapy on plasma lipid- and lipoprotein-cholesterol levels (including the HDL subclasses) in mild hypertensive males and females. 169 13

The purpose of this study was to investigate the effect of carvedilol on serum lipids in patients with mild-to-moderate essential hypertension. Twenty-one patients with blood pressure greater than or equal to 160/95 mm Hg after a 4-week placebo run-in period were initially given 10 mg of carvedilol once daily. The dose was increased to 20 mg after 4 weeks if the target blood pressure was not achieved. The duration of treatment was 12 weeks. After 12 weeks of administration, blood pressure and the pulse rate (PR) declined significantly (blood pressure from 173/105 to 142/91 mm Hg, p less than 0.001; PR from 74 to 67 beats/min, p less than 0.001); however, serum lipids [total cholesterol, triglycerides, low-density lipoprotein, high-density lipoprotein (HDL), HDL2, and HDL3], lipoprotein fraction (alpha, pre-beta, and beta), apoprotein fraction (A-I, A-II, CII, CIII, and E), and atherogenic index [(total cholesterol - HDL cholesterol) divided by HDL cholesterol] were not altered significantly. There were no side effects reported during the trial. From these results, it can be concluded that carvedilol has no adverse effect on the coronary risk profile as reflected by lipid measurements, and is an efficacious, safe, well-tolerated antihypertensive drug in patients with mild-to-moderate hypertension.
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PMID:Effects of carvedilol on serum lipids in patients with essential hypertension. 172 79

Recent reports of risk factors for and survival of patients with diabetic retinopathy do not include exudative maculopathy as a separate entity. We therefore studied a group of hypertensive Type II diabetic subjects with exudative maculopathy (n = 26) compared to a carefully matched hypertensive diabetic comparison group without retinopathy (n = 26) over seven years. Diabetic maculopathy patients had higher mean diastolic blood pressure (101.6 +/- 14 versus 94.8 +/- 10 mmHg, p less than 0.05), serum cholesterol (6.65 +/- 2.2 versus 5.9 +/- 1.31 mmol/l), HDL2 subfraction levels (0.46 +/- 0.23 versus 0.32 +/- 0.18 mmol/l) and a higher prevalence of hyperlipidaemia (54% versus 35%) compared to the comparison group. After seven years, the maculopathy group showed a strikingly higher prevalence of renal failure and nephrotic syndrome (42% versus 8%, p less than 0.05) and of macroproteinuria (58% versus 15%, p less than 0.01) compared to the comparison group. Mortality and cardiovascular disease event rate was 12% and 38% in the maculopathy and 15% and 31% respectively in the comparison group. We conclude that although mortality is not significantly higher in diabetics with exudative maculopathy, proteinuria, renal failure and nephrotic syndrome may be associated features on long term follow-up. Hypertension and hypercholesterolaemia may also be risk factors in the development of diabetic maculopathy.
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PMID:Long-term follow-up of and underlying medical conditions in patients with diabetic exudative maculopathy. 180 Jan 69

In order to explore the pathogenic risk factors or protective factors of cerebral thrombosis, 1:1 matched case control study was done in 110 cases diagnosed by computerized tomography (CT). Both cases and controls were selected from several provincial and municipal hospitals in Jinan, Shandong Province, China. Every case was matched with one control on sex, race, age, occupation, residential area, educational level and economic status. 31 factors were analysed and 9 risk or protective factors were found by univariate analysis and multiple stepwise regression. Using the same 9 factors as independent variables, conditional logistic regression was performed and 4 factors were confirmed as pathogenic risk factors or protective factor of cerebral thrombosis (alpha = 0.01). They are high blood pressure (beta = 3.46, OR = 7.57), abdominal skinfold thickness (beta = 3.21, OR = 3.77), familial aggregation of stroke (beta = 2.25, OR = 12.64) and high level HDL2-C (beta = -2.99, OR = 0.16). Moreover, reliability of collective data and control o: bias were evaluated and discussed.
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PMID:[Case control study on risk factors of cerebral thrombosis]. 181 95

The beneficial effects of combined estrogen-progestin-containing oral contraceptives (OCs) include prevention of pregnancy (less than 1 failure out of 100 regular users); the prevention of ectopic pregnancy; the reduction of preeclampsia (2.4 times lower risk compared with barrier methods); and reduction of pelvic inflammation to about one-half. The effects on menstruation include the reduction of sideropenic anemia (by lowering the incidence and duration of menstruation, OCs reduce the loss of iron to 50% or to as much as 33%); dysmenorrhea by 40% (symptoms receded in 90% of users); and premenstrual syndrome by 30%. OCs exert a favorable effect on menstrual epilepsy; reduce sports-related accidents in the premenstrual and menstrual periods; and reduce intermenstrual bleeding. The protection from cancer includes the lowering of endometrial cancer risk (every 2 years of use reduces the risk by 38%, 12 years of use by 70%, and the beneficial effects last 3-15 years); reduction of the risk of the ovarian cancer (already 3-6 months of use reduces the risk by 30%, and more than 5 years by 50% in women under 50 years of age with a longterm effect of 10 years or more, which drops sharply in women over 60 who are mostly at risk). Among other beneficial effects, they reduce benign mastopathy by 50-75%; reduce the risk of follicular ovarian cysts to 50% and the risk of corpus luteal ovarian cysts to 1/5; and they lessen bone loss which favorably affects osteoporosis. Low-dose OCs minimize the well-known risks of thrombotic and cerebrovascular accidents, myocardial infarction, hypertension, altered carbohydrate metabolism, gallbladder diseases, and liver cancer. A new OC with 30 mcg of ethinyl estradiol was tested with daily doses of 150 mcg of desogestrel. The high density lipoprotein (HDL) either increased or did not change with desogestrel: the HDL2 subfraction that protects from atherosclerosis did not change, and probably the HDL3 raised the HDL level.
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PMID:[Favorable effects of oral estrogen-progestin contraception]. 181 41

Increased cholesterol levels above 200 mg/dl, LDL levels above 130 mg/dl and total cholesterol/HDL ratio above 4.5 in males and above 5.0 in females are recognized as indicators of increased risk of atherosclerosis. Risk associated to increased triglyceride levels (above 200 mg/dl) must be judged in relation to associated factors such as family history of coronary heart disease, presence of remnants (type III hyperlipidemia), presence of Lp(a), increased levels of Apo B, reduced levels of HDL2 or Apo A1. VLDL and chylomicron remnants and Lp(a) have an atherogenic power in vitro 2 to 4 times that of LDL. There is a correlation between hypertriglyceridemia and reduced HDL2 and Apo A1 levels. Hypertriglyceridemia is frequently associated to other risk factors like diabetes, obesity, hyperinsulinism, and high blood pressure. Finally, VLDL may elevate levels of plasma plasminogen inhibitor. Thus, hypertriglyceridemia should be investigated when, evaluating risk of atherosclerosis.
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PMID:[Cholesterol and triglycerides in atherosclerosis: epidemiologic and physiopathologic considerations]. 184


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