Hypertension, antihypertensive medication use, and risk of renal cell carcinoma.
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To investigate whether diuretic medication use increases risk of renal cell carcinoma (RCC), the authors conducted a case-control study of health maintenance organization members in western Washington State. Cases (n = 238) diagnosed between January 1980 and June 1995 were compared with controls (n = 616) selected from health maintenance organization membership files. The computerized health maintenance organization pharmacy database provided information on medications prescribed after March 1977. Additional exposure information was collected from medical records. For women, use of diuretics was associated with increased risk of RCC (odds ratio (OR) = 1.8, 95% confidence interval (CI) 1.0-3.1), but the association was not independent of a diagnosis of hypertension (adjusted for hypertension, OR = 1.1, 95% CI 0.5-2.1). Similarly, nondiuretic antihypertensive use was associated with increased risk, but only when unadjusted for hypertension. For men, neither diuretic nor nondiuretic antihypertensive use was associated with risk of RCC. A diagnosis of hypertension was clearly associated with RCC risk for women (OR = 2.5, 95% CI 1.2-5.1), but not men (OR = 1.3, 95% CI 0.7-2.5). High systolic and diastolic blood pressures were associated with increased risk in both sexes. These results do not support the hypothesis that use of diuretic medication increases RCC risk; they are more consistent with an association between RCC and high blood pressure. (+info)
Effect of long-term exercise training on regional myocardial perfusion changes in patients with coronary artery disease.
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The cardiac rehabilitation of patients with coronary artery disease (CAD) promotes exercise tolerance, improves left ventricular function, and decreases the heart rate and systolic blood pressure at the same load intensity. Several studies have shown that cardiac rehabilitation improves myocardial perfusion in CAD patients. However, the long-term (> or = 1 year) effect of cardiac rehabilitation on myocardial perfusion is still controversial. The effect of long-term exercise training on myocardial perfusion in CAD patients was assessed using thallium-201 (201Tl) exercise studies at a baseline (4 months after the onset of CAD) and at a 1-year or more follow-up in 58 patients with stable CAD. The subjects had been divided into a training group (n=35) participating in supervised exercise 2 times per week for the follow-up period, and the control group (n=23). There was an improvement in the myocardial perfusion on stress 201Tl scintigraphy in 20 of the 35 (57.1%) trained patients and in 3 of the 23 (13.0%) of the control patients (p<0.001). The number of 201Tl stress myocardial perfusion defect segments was significantly decreased after the cardiac rehabilitation training (231 to 153 segments), but showed no change in the control group (158 to 156 segments) (p<0.01). In spite of no significant differences in the number of involved coronary arteries, it improved (12/17 patients: 70.6%) more in the patients who had trained for more than 2 years compared to the patients who had trained for less than 2 years. The exercise tolerance increased in 25 of the 35 training group patients (71.4%), and in only 3 of the 23 control group patients (13.0%). The peak double products increased from 20,131+/-6,010 to 28,370+/-5,600 (p<0.01) in the training group, and showed no change in the control group (20,567+/-5,112 to 20,964+/-7,728 (NS)). The results indicated that the long-term physical training increased exercise tolerance and the double products of CAD patients. In addition, the training resulted in improved cardiac perfusion as evidenced by 201Tl scintigraphy. The findings suggest that exercise training is an advisable and effective treatment for patients with CAD. (+info)
Relationship between brain atrophy estimated by a longitudinal computed tomography study and blood pressure control in patients with essential hypertension.
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To evaluate the relationship between blood pressure control and the progression of brain atrophy in the elderly, patients with essential hypertension and brain atrophy were longitudinally evaluated using computerized tomography (CT). The study evaluated 48 patients with essential hypertension aged 46-78 years, and 30 sex- and age-matched normotensive control subjects. The extent of brain atrophy as determined by caudate head index (CHI), the inverse cella media index (iCMI), and Evans' ratio (ER) was estimated twice at an interval of 5-9 years (mean, 6.9 years). The mean annual increases in CHI (deltaCHI), iCMI (delta iCMI), and ER (deltaER) were evaluated. Mean blood volume in the common carotid artery (BF) and the decrease in BF per year (deltaBF) were also determined. The deltaCHI, delta iCMI, and deltaER increased with age in the hypertensive subjects as well as the control group across all age groups evaluated. The deltaCHI, delta iCMI, and deltaER were significantly greater in the patients with essential hypertension in their 50 s as compared with the controls. In patients with essential hypertension aged 65 years or older, the deltaCHI, delta iCMI, and deltaER were significantly lower in the group in whom the blood pressure was controlled within the range of borderline hypertension than the groups in which it was controlled in the range of normal or mild hypertension. In the younger patients under the age of 65 with essential hypertension, blood pressure control did not affect the deltaCHI, delta iCMI, and deltaER. The deltaCHI, delta iCMI, and deltaER were significantly correlated with deltaBF in both groups. These findings indicate that control of systolic blood pressure within the range of borderline hypertension may delay the progression of brain atrophy in elderly patients with essential hypertension. (+info)
Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis.
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Adhesion molecules on the endothelial cell membrane play an important role in the pathogenesis of atherosclerosis. Levels of soluble forms of cell adhesion molecules are reportedly elevated in patients with peripheral artery vessel disease and in patients with an atherosclerotic aorta. The present study investigated the association of serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular adhesion molecule 1 (sICAM-1), and soluble P-selectin (sP-selectin) with coronary heart disease (CHD) and the extent of coronary atherosclerosis, and examined the influence of serum levels of lipids, lipoproteins and apolipoproteins (apo) in subjects with (n=52, M/F:43/9) and without (controls, n=40, M/F:25/15) angiographically proven coronary atherosclerosis. After controlling for age and gender, levels of sVCAM-1 (least squares mean +/- std error: 565+/-36 ng/ml vs 540+/-41 ng/ml, ns), sICAM-1 (261+/-17ng/ml vs 247+/-19ng/ml, ns), and sP-selectin (142+/-8ng/ml vs 149+/-10 ng/ml, ns) in patients with coronary atherosclerosis were not different from those in controls, as assessed by an analysis of covariance. After also adjusting for body mass index, hypertension, diabetes mellitus, and smoking by a multiple logistic function analysis, the association of sVCAM-1, sICAM-1, and sP-selectin with CHD was still not significant. Levels of sVCAM-1, sICAM-1, and sP-selectin were also not related to the extent of coronary atherosclerosis as judged by the number of stenosed vessels. However, inverse (p<0.05) relationships were observed between sVCAMs and serum levels of HDL3-cholesterol, apo A-II, and lipoprotein containing apo A-I and A-II, between sICAMs and levels of apo A-II and Lp A-I/A-II (Lp A-I/A-II), and between sP-selectin and lipoprotein containing only apo A-I. In conclusion, serum levels of soluble VCAM-1, ICAM-1, and P-selectin were not related to CHD or the extent of coronary atherosclerosis, but were inversely related to serum levels of high-density lipoprotein-related lipoproteins. (+info)
Role of phosphatidylinositol 3-kinase in angiotensin II regulation of norepinephrine neuromodulation in brain neurons of the spontaneously hypertensive rat.
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Chronic stimulation of norepinephrine (NE) neuromodulation by angiotensin II (Ang II) involves activation of the Ras-Raf-MAP kinase signal transduction pathway in Wistar Kyoto (WKY) rat brain neurons. This pathway is only partially responsible for this heightened action of Ang II in the spontaneously hypertensive rat (SHR) brain neurons. In this study, we demonstrate that the MAP kinase-independent signaling pathway in the SHR neuron involves activation of PI3-kinase and protein kinase B (PKB/Akt). Ang II stimulated PI3-kinase activity in both WKY and SHR brain neurons and was accompanied by its translocation from the cytoplasmic to the nuclear compartment. Although the magnitude of stimulation by Ang II was comparable, the stimulation was more persistent in the SHR neuron compared with the WKY rat neuron. Inhibition of PI3-kinase had no significant effect in the WKY rat neuron. However, it caused a 40-50% attenuation of the Ang II-induced increase in norepinephrine transporter (NET) and tyrosine hydroxylase (TH) mRNAs and [3H]-NE uptake in the SHR neuron. In contrast, inhibition of MAP kinase completely attenuated Ang II stimulation of NET and TH mRNA levels in the WKY rat neuron, whereas it caused only a 45% decrease in the SHR neuron. However, an additive attenuation was observed when both kinases of the SHR neurons were inhibited. Ang II also stimulated PKB/Akt activity in both WKY and SHR neurons. This stimulation was 30% higher and lasted longer in the SHR neuron compared with the WKY rat neuron. In conclusion, these observations demonstrate an exclusive involvement of PI3-kinase-PKB-dependent signaling pathway in a heightened NE neuromodulatory action of Ang II in the SHR neuron. Thus, this study offers an excellent potential for the development of new therapies for the treatment of centrally mediated hypertension. (+info)
Hypertension treatment and the prevention of coronary heart disease in the elderly.
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Both isolated systolic hypertension (>140 mm Hg/<90 mm Hg) and systolic/diastolic hypertension (>140 mm Hg/>90 mm Hg) are major risk factors for cardiovascular disease in the elderly. Specific antihypertensive drug therapy is available if lifestyle interventions fail to reduce blood pressure to a normal level. Diuretics and beta blockers both reduce the occurrence of adverse events related to cerebrovascular disease; however, diuretics are more effective in reducing events related to coronary heart disease. Treated patients are less likely to develop severe hypertension or congestive heart failure. In most instances, low-dose diuretic therapy should be used as initial antihypertensive therapy in the elderly. A long-acting dihydropyridine calcium channel blocker may be used as alternative therapy in elderly patients with isolated systolic hypertension. Trials are being conducted to evaluate the long-term effects of angiotensin converting enzyme inhibitors and angiotensin-II receptor blockers in elderly patients with uncomplicated hypertension. (+info)
Discriminant function analysis of factors related to myocardial infarction in male patients on antihypertensive therapy.
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Records of 367 male patients who began attending the Dunedin Hospital Hypertension Clinic between 1959 and 1969 were coded up to the end of 1972. Of these patients, 60 had their first myocardial infarction, or sudden cardiac death without previous evidence of myocardial infarction, while they were attending the clinic. This infarct group was compared with a control group of 120 which was chosen from the remaining patients so that the two groups would be comparable with regard to their age and year of first attendance. A stepwise discriminant function analysis showed that the basal systolic and diastolic pressures measured when patients started attending the clinic were the variables with the most significant difference. Further analysis showed that inclusion of the average casual standing systolic pressure when patients were receiving antihypertensive therapy improved the discrimination between the groups. The average casual standing diastolic pressure during antihypertensive therapy also improved the discrimination, but, curiously enough, with a negative sign in the discriminant function. Quetelet's index of obesity similarly improved the discrimination, obese subjects having less risk of infarction or sudden death. Serum cholesterol, however, was not related to prognosis. (+info)
Haemodynamic adaptation at rest and during exercise to long-term antihypertensive treatment with combination of beta-receptor blocking and vasodilator agent.
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Systemic and pulmonary haemodynamics were studied at rest in the supine and upright position, and during exercise in the sitting position at 75 and 150 Watt, in 13 hypertensive men aged 50-8 +/- 8-7 years before and after 13 months treatment with oral oxprenolol (120 to 160 mg t.i.d.) supplemented by oral hydrallazine (50 to 75 mg t.i.d.) during the last 6 months. Pressures were recorded by means of catheters inserted percutaneously into the pulmonary and brachial artery; cardiac output was determined according to Fick. Treatment resulted in a significant reduction of systemic systolic, diastolic, and mean pressures at rest in the supine position and during exercise, and of systolic pressures in the upright posture. Pulmonary systolic and mean pressures increased slightly at rest in the supine position and during exercise, and no changes occurred at rest in the upright position. The left ventricular filling pressure was unchanged at rest both in the supine and upright position; it increased slightly during exercise. The haemodynamic changes by which systemic pressure was reduced were those typical of beta-adrenergic blockade: reduction of cardiac output resulting from a decrease of both heart rate and stroke volume, while the total systemic vascular resistance was unchanged at rest in the supine position but increased in the upright posture and during exercise. The A-V O2 difference increased remarkably. This long-term observation again suggests that the acute haemodynamic effects of an antihypertensive regimen can be modified during long-term application. It did not give evidence of a readjustment of the vascular resistance occurring, at least not in the upright position and during exercise, as has been suggested for long-term beta-adrenergic blockade. (+info)