Quality of life during treatment of hypertensive patients with diuretics.
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Biomedical subjects
Publications and source records attributed to R Van Hoof.
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With the use of a linear model, the relation between urinary sodium and blood pressure has been reported to be positive, non-significant, or negative. The hypothesis that this relationship is more complex than linear was investigated in two different study populations, which were independently recruited and examined by different observers. In 1,071 men randomly selected from the general population and in an unrelated sample of 1,209 military men, systolic and diastolic blood pressure were correlated with urinary sodium following a model, which included both the linear and quadratic terms of urinary sodium. In both groups of men, these second order models, adjusted for age and body mass index, provided a better fit (P less than 0.05) than the relationships with only the linear term of urinary sodium. The quadratic models explained from 0.35 to 1.10% of the blood pressure variance. Third order models, which in addition included the cubic term of urinary sodium, did not further improve the correlations between systolic and diastolic blood pressure and urinary sodium in men. In 1,010 women drawn from the general population and in 499 military women, neither the first nor the second order correlations between systolic and diastolic blood pressure and urinary sodium were statistically significant. In conclusion, the present results, reproducible in two different study populations, suggest that a second order model is more appropriate than a simple linear correlation to describe the weak relationship between blood pressure and urinary sodium in men. However, recommendations for the prevention of hypertension must not be changed, until the present findings are confirmed by intervention studies.
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In hypertensive patients as well as in normal subjects urapidil has a hypotensive action. This is mainly mediated by a peripheral alpha 1-adrenoceptor blockade with a decrease in systemic vascular resistance; in addition, during acute animal experiments a centrally mediated hypotensive action was demonstrated, possibly by 5-hydroxytryptamine1A (5-HT1A)-receptor stimulation. Studies in humans showed an increase in cardiac output, which was not always significant; it did result either from an increased heart rate or an increased stroke volume. Acute changes in pulmonary hemodynamics after administration of urapidil were most pronounced in patients with pulmonary hypertension: pulmonary artery pressure and pulmonary vascular resistance decreased significantly and pulmonary capillary wedge pressure decreased nonsignificantly. A small reduction in pulmonary artery pressure and capillary wedge pressure were seen in patients with congestive heart failure and in patients in whom acute blood pressure elevation developed after coronary bypass surgery. In patients with essential hypertension forearm, renal and splanchnic flow were shown to increase and vascular resistance to decrease significantly after acute intravenous doses of urapidil. The hemodynamic changes during chronic therapy are largely unknown, except for systemic vascular resistance which remains decreased.
The effect of 4 months of physical training on resting, exercise and 24-hour blood pressure (BP) was studied using a randomized crossover design in 26 healthy, sedentary men, with an average age of 39 +/- 10 (standard deviation) years. Peak oxygen uptake increased by 14% (p less than 0.001) and the physical working capacity at a heart rate of 130 beats/min by 25% (p less than 0.001). The heart rate was reduced by 7 beats/min at night (p less than 0.01) and by 6 beats/min during the day (p less than 0.001). Training-induced changes of BP varied according to measuring conditions. A decrease in BP at rest while sitting in the morning in the laboratory was significant for diastolic (-5 mm Hg, p less than 0.01) but not for systolic BP. During exercise, systolic BP was significantly lower after training, when measured at the same submaximal workloads. However, when workload was expressed as a percentage of peak oxygen uptake, systolic BP was not different before and after training. When measured during 24 hours, the training-induced change in BP was not significant at night either for systolic or diastolic BP. During the day the decrease in diastolic BP was significant (-5 mm Hg, p less than 0.001), but the change in systolic BP was not.
Angiotensin-converting enzyme inhibitors are gaining acceptance as safe and effective agents for treatment of hypertension. Addressed in this review of the available literature are the questions whether they are effective in lowering blood pressure in the elderly, whether their effects are age-related, and what effects, if any, do they have on morbidity and mortality in geriatric hypertension.
Using pulse rate and urinary sodium as indices of sympathetic tone and salt intake, respectively, we investigated whether both an increased sympathetic activity and a high salt consumption are needed to increase blood pressure in the population at large. A random population sample of 2081 subjects with a minimum age of 18 years was stratified by tertiles of pulse rate. In subjects with a slow and in those with a fast pulse rate, a significant curvilinear relation between blood pressure and urinary sodium was found, while in the middle pulse rate third the correlation was not significant. A significant interaction between pulse rate and urinary sodium indicated that, when urinary sodium increased from 160 to 300 mmol/24 h, both systolic and diastolic pressure rose in subjects with a fast pulse rate, but declined in those with a slow pulse rate. In conclusion, our results suggest that a high salt intake is associated with an elevated blood pressure in subjects with a high sympathetic tone, but with a decreased pressure in individuals with a low sympathetic activity.
The erythrocyte 2,3-diphosphoglycerate concentration (2,3-DPG) and the activity of red cell hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase and glutathione reductase were studied in 27 normal volunteers before and after 2 and 4 months of physical endurance training. The 4 months of training increased maximal oxygen uptake and physical working capacity (PWC130) by 16% (p less than 0.001) and 29% (p less than 0.001) respectively. Resting heart rate was decreased (p less than 0.001) by 11 beats.min-1. With 2 months of training the erythrocyte 2,3-DPG concentration increased by 9% (p less than 0.001); with 4 months training the increase was only 4% (p less than 0.05). The training-induced increase in red cell 2,3-DPG was not accompanied by enhanced activity of erythrocyte hexokinase, pyruvate kinase, glucose-6 phosphate dehydrogenase or glutathione reductase. It is concluded that the rise in red cell 2,3-DPG induced by physical endurance training is not due to activation of red cell glycolytic enzymes or the enzymes involved in the pentose-phosphate cycle.
The effect of endurance training on plasma lipoproteins was investigated in 27 healthy sedentary men between the ages of 20 and 55 years. During the first 4 months of the study, 13 of them (group A) participated in a training program (3 hours/wk), whereas the others served as control subjects (group B). At the end of this period the control subjects also underwent a 4-month training program. In both groups the training significantly increased physical working capacity at a heart rate of 130 bpm (PWC130), whereas it decreased the resting heart rate (p less than 0.05). Concomitantly with this improvement in cardiorespiratory fitness, a significant increase in the high-density lipoprotein (HDL) cholesterol concentration was observed (p less than 0.01); this was due to an increase in both HDL2 beta and HDL2 alpha + 3 cholesterol concentrations. The plasma total and HDL-apoprotein AI and apoprotein AII concentrations were not significantly affected by the training. Significant decreases in plasma triglyceride (p less than 0.05), very-low-density lipoprotein cholesterol (p less than 0.05), and low-density lipoprotein (LDL) cholesterol (p less than 0.001) concentrations were also observed, but only in group B, which showed a much greater increase in PWC130 at the end of the training period than group A; the decrease in the LDL cholesterol concentration in this group was accompanied by a slight decrease in the LDL-apoprotein B concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
Results on total and cause-specific mortality from various randomized intervention trials on antihypertensive drug treatment in elderly hypertensives are reviewed, compared and pooled. Mortality from all causes tended to decrease in all trials, but this decrease was not statistically significant in any of the trials separately, nor when all results were pooled. When the results of all the trials were combined, there was a significant overall decrease in cardiovascular mortality of 28%. This decrease in cardiovascular mortality was mainly related to a significant reduction in cerebrovascular mortality of 41%. Mortality from coronary heart disease also tended to decrease by 28%, but statistical significance was not reached.
The effect of physical endurance training on the plasma renin-angiotensin-aldosterone system was studied in 27 normal sedentary volunteers aged between 20 and 55 years, using a randomized two-period cross-over study design. After 4 months of training (2.5 h/week), peak oxygen uptake and physical working capacity at a heart rate of 130 beats/min were increased by 16% (P less than 0.01) and 29% (P less than 0.001) respectively, whereas resting heart rate was decreased by 15% (P less than 0.001). The plasma noradrenaline concentration and haematocrit were both decreased (P less than 0.01) after training. For the total group of subjects, the small decreases in plasma renin activity (PRA) and in the plasma concentrations of angiotensin-I, angiotensin-II and aldosterone were not statistically significant. However, the change in PRA during the training period was negatively correlated with the increase in physical working capacity (r = -0.49, P less than 0.01), suggesting that PRA decreased only in those subjects with the greatest increase in exercise capacity. Also, the change in plasma aldosterone during training was negatively related to the rise in physical working capacity (r = -0.57, P less than 0.01). Furthermore, the changes in plasma angiotensin-I (r = 0.75), angiotensin-II (r = 0.49) and aldosterone (r = 0.43) during the training period correlated positively with the change in PRA. It is concluded that physical endurance training, leading to a substantial gain of physical working capacity, suppresses the plasma renin-angiotensin-aldosterone system in normal man.
Cross-sectional studies have demonstrated in the past that endurance-trained persons are characterised by a less atherogenic lipid profile than their sedentary counterparts: the former have clearly higher HDL-cholesterol and lower serum triglyceride concentrations than the latter, and also their LDL-cholesterol and total cholesterol concentrations are slightly lower. In a longitudinal intervention study in previously sedentary men, the effect of moderate short term physical training on the serum lipid profile was investigated. 30 healthy male volunteers were trained for 16 weeks, 3 hours weekly. After training their physical working capacity was increased on average by 29%. This was accompanied by an increment in the HDL-cholesterol fraction of 26%; the relative increase was greater for HDL2-(+32%) than for HDL3-cholesterol(+24%). VLDL-cholesterol was reduced by 21% at the end of the training period. On average, plasma total cholesterol, total triglycerides and LDL-cholesterol were not significantly changed at the end of the training period. Negative associations were, however, found between the training-induced increase in exercise capacity and the concomitant changes in plasma triglycerides and LDL-cholesterol. In conclusion, these longitudinal observations show that short term moderate endurance training improves the serum lipid profile in previously sedentary men.
The intracellular concentrations and transmembrane fluxes of Na+ and K+ in erythrocytes, and plasma lipids were investigated in 30 middle-aged volunteers, before and after physical training. During the first 4 months of the study, half of the subjects (group A) were subjected to a training programme (3 h/week), while the others (group B) served as controls. At the end of the control period the group B subjects also underwent a period of training. At the end of the training, in both experimental groups, the intra-erythrocyte Na+ concentration was decreased (P less than 0.001); the magnitude of this decrease was related to the increase achieved in physical working capacity (r = -0.44; P less than 0.05). After training the activity of the erythrocyte Na+-Li+ counter-transport system was decreased (P less than 0.001) in both groups, whereas Na+,K+ cotransport activity was increased (P less than 0.001). The training intervention did not affect erythrocyte ouabain-sensitive 86Rb uptake, or the calculated rate constant for ouabain-sensitive Na+ efflux. Furthermore, the plasma concentrations of high density lipoproteins (HDL)2- and HDL3-cholesterol (P less than 0.001) markedly increased in both groups during the training period. However, these changes were not significantly correlated with the observed training-induced changes in erythrocyte transmembrane cationic fluxes. It is concluded that physical training decreases intra-erythrocyte Na+ concentration. No significant associations between training-induced changes in plasma lipids and erythrocyte sodium balance could be demonstrated.
The different intervention trials in elderly hypertensive subjects are compatible with the hypothesis that antihypertensive drug treatment decreases cardiovascular mortality, mainly by a reduction of cerebrovascular mortality. Antihypertensive drug treatment in elderly hypertensive subjects also leads to a decrease in fatal and nonfatal cardiovascular and cerebrovascular events. It has not yet been proven whether antihypertensive drug treatment should be recommended for symptomless patients with isolated systolic hypertension and for patients with uncomplicated hypertension above the age of 80 years.
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An impressive number of patients has been followed in intervention trials, some of them carefully designed and executed. The different intervention trials in hypertensives are compatible with the hypothesis that hypotensive drug treatment can decrease cardiovascular mortality mainly by decreasing cerebrovascular mortality. A decrease in fatal and non-fatal cardiovascular event rate is mainly due to the decrease in cerebrovascular events. On the basis of these trials the expert committee of the WHO and ISH recommend first general hygienic measures. When the blood pressure remains above 100 mm Hg after 3 months or above 95 mm Hg after 6 months follow-up, hypotensive drugs should be considered. It is not established whether the hypotensive drug treatment is advisable in: --symptomless patients with isolated systolic hypertension, --hypertensive patients above age 80. Sudden reduction in blood pressure should be avoided but whether a progressive reduction of the systolic blood pressure below 140 mm Hg and a diastolic blood pressure below 85 mm Hg is dangerous or advantageous remains to be established.
Angiotensin-converting enzyme inhibitors are gaining acceptance as safe and effective agents for treatment of hypertension. Data on their use specifically in elderly hypertensives, however, are limited. Addressed in this review of the available literature are the questions whether they are effective hypotensives in the elderly, whether their effects are age-related, and what effects, if any, do they have on morbidity and mortality in geriatric hypertension.
A consecutive series of 14 708 coronary arteriograms, performed between 1 April 1975 and 1 August 1983 was examined for the presence of coronary artery fistulas. The incidence was 0.13. There was 1 traumatic and 19 congenital cases. All fistulas were small and of little haemodynamic significance. No symptoms or complications could be ascribed to these fistulas. In the large majority no continuous or other murmurs suggested their presence. The large majority arose from the proximal anterior descending artery and emptied in the pulmonary artery. Surgical treatment for these fistulas is not indicated.