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E Bragulat

Publications and source records attributed to E Bragulat.

18 recordsLinked to original sources
PubMed2003

Effect of long-term irbesartan treatment on endothelium-dependent vasodilation in essential hypertensive patients.

Endothelial dysfunction plays a pivotal role in the development of essential hypertension and its complications. The purpose of this study is to assess the effect of antihypertensive treatment with the angiotensin receptor blocker irbesartan on endothelial function in a group of essential hypertensive patients. Thirty-two untreated hypertensives are examined at baseline and at the end of a six-month period of irbesartan treatment. Endothelium-dependent and -independent responses are determined by measuring changes in forearm blood flow (FBF) by strain gauge plethysmography in response to intrarterial infusions of acetylcholine (endothelium-dependent vasodilation [EDV]), sodium nitroprusside (endothelium-independent vasodilation [EIV]), with and without the addition of the nitric oxide (NO) synthase inhibitor L-NMMA. Plasma endothelin, plasma and urinary nitrates and nitrites, and cyclic GMP are measured at baseline and at the end of treatment. Irbesartan promoted a significant increase in EDV (from 433+/-147% to 488+/-75%; P=0.027) and EIV (from 442+/-130% to 495+/-104%; P=0.041). L-NMMA-induced vasoconstriction was significantly enhanced after irbesartan treatment (relative decrease of FBF from 33.4+/-9.5% to 39.5+/-5.6%; P=0.001). Plasma concentrations of endothelin fell significantly after irbesartan treatment (from 5.78+/-1.86 to 4.16+/-1.52 pg/mL; P=0.001). We concluded that long-term irbesartan treatment enhances both endothelium-dependent and -independent vascular vasodilation capacity. In addition to this non-specific effect, irbesartan restores the vasoconstriction capacity of NO synthase inhibitors, suggesting a direct effect on tonic NO release, and decreases endothelin production. These actions may play an important role in the vascular protecting effects of irbesartan.

Adult↗
PubMed2003

Analysis of patient flow in the emergency department and the effect of an extensive reorganisation.

OBJECTIVES: To evaluate the different internal factors influencing patient flow, effectiveness, and overcrowding in the emergency department (ED), as well as the effects of ED reorganisation on these indicators. METHODS: The study compared measurements at regular intervals of three hours of patient arrivals and patient flow between two comparable periods (from 10 February to 2 March) of 1999 and 2000. In between, a structural and staff reorganisation of ED was undertaken. The main reason for each patient remaining in ED was recorded and allocated to one of four groups: (1) factors related to ED itself; (2) factors related to ED-hospital interrelation; (3) factors related to hospital itself; and (4) factors related to neither ED nor hospital. The study measured the number of patients waiting to be seen and the waiting time to be seen as effectiveness markers, as well as the percentage of time that ED was overcrowded, as judged by numerical and functional criteria. RESULTS: Effectiveness of ED was closely related with some ED related and hospital related factors. After the reorganisation, patients who remained in ED because of hospital related or non-ED-non-hospital related factors decreased. ED reorganisation reduced the number of patients waiting to be seen from 5.8 to 2.5 (p<0.001) and waiting time from 87 to 24 minutes (p<0.001). Before the reorganisation, 31% and 48% of the time was considered to be overcrowded in numerical and functional terms respectively. After the reorganisation, these figures were reduced to 8% and 15% respectively (p<0.001 for both). CONCLUSIONS: ED effectiveness and overcrowding are not only determined by external pressure, but also by internal factors. Measurement of patient flow across ED has proved useful in detecting these factors and in being used to plan an ED reorganisation.

Analysis of Variance↗
PubMed2002

Lack of correlation between two methods for the assessment of salt sensitivity in essential hypertension.

The existence of a heterogeneous blood pressure (BP) response to salt intake, a phenomenon known as salt sensitivity, has increasingly become a subject of clinical hypertension research, and has important clinical and prognostic implications. However, two different methodologies are currently used to diagnose salt sensitivity. The aim of the present study was to compare the BP response to intravenous sodium load and depletion on the one hand, and to changes in dietary salt intake on the other, in order to assess salt sensitivity in a group of essential hypertensive patients. Twenty-nine essential hypertensives underwent two different procedures separated by 1 month: a dietary test consisting of a 2-week period of low (20 mmol/day) and high (260 mmol/day) salt intakes, and an intravenous test consisting of a 2 litre saline load over a 4-h period, followed by 1 day of low (20 mmol) salt intake and furosemide (40 mg/8 h orally) administration. BP was registered at the end of every period using 24-h ambulatory BP monitoring. In the whole group of hypertensive patients studied, both low salt intake and furosemide administration significantly (P < 0.01) decreased mean BP. Correlation coefficients of BP changes obtained using the two methodologies were between 0.3 and 0.4. Moreover, coefficients of agreement between the oral and the intravenous tests, using several cut points for BP changes, were systematically below 0.5, thus indicating a misclassification of salt sensitivity greater than 50%, depending on the method used. None of the cut points for BP changes during furosemide administration showed a good combination of sensitivity and specificity compared with changes in response to low dietary salt. The present results indicate that the diagnosis of salt-sensitive hypertension should be based on the BP response to changes in dietary salt intake, while BP response to saline and furosemide administration leads to a systematic misclassification of more than 50% of patients, even using different cutpoints for changes in BP.

Administration, Oral↗
PubMed2001

[Impact in the quality of health care and cost-effectiveness analysis of the reform of an emergency medicine service].

BACKGROUND: To determine the effects that the reform of an emergency department (ED) have on efficacy, health care quality and efficiency. MATERIAL AND METHOD: Reforms consisted of 50% and 34% increases in structural and human resources, respectively. Roles of each ED member were redetermined, new assistance pathways were implemented, and the relationship between ED and the remaining hospital departments was reassessed. As efficacy markers, we determined the number of patients waiting to be attended (Pesp), the waiting time of patients to receive medical assistance (T(esp)),and the total waiting time of patients staying in the ED (T(total)). As health-care quality markers, we determined the percentage of patients leaving ED without having been visited by a physician(IPNV), the percentage of patients who were visited again (IPR),and the percentage of mortality (IPF). We also quantified the number of visits to the ED. All these data were obtained daily over 3 weeks, before (February 1999) and after (February 2000)the reforms. Effectiveness was estimated from the ratio P(total)/T(esp)(E1) and P(total)/P(esp) (E2). Costs were recorded for both periods and a cost-effectiveness analysis was performed to study the efficiency. RESULTS: In 2000, the number of visits increased by +12% (CI 95%: 2% to 22%). Despite this increase, we observed an improvement of most efficacy and health-care quality markers after the ED reforms. E1 increased by 996% (CI 95%: 335% to 1,658%) and E2 increased by 186% (CI 95%: -23%to 395%). Cost-effectiveness analysis showed 70% (CI 95%: 33%to 107%) and 56% (CI 95%: 18% to 94%) increases regarding E1 and E2, respectively, after the reforms. CONCLUSIONS: Providing ED with the necessary resources leads to an objective improvement of its efficacy and health-care quality and, consequently, the service and quality perceived by users improve. Despite the total cost increase after the ED reforms, efficiency also improves.

Cost-Benefit Analysis↗
PubMed2001

Endothelial dysfunction in salt-sensitive essential hypertension.

The aim of this study was to evaluate endothelium-dependent and -independent vasodilation, as well as endothelium biochemical markers, in a group of essential hypertensive patients classified on the basis of salt sensitivity. Changes in forearm blood flow in response to acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA) infusion were determined by means of strain-gauge plethysmography. Moreover, plasma and urinary concentrations of nitrates, cGMP, and endothelin were measured during low (50 mmol/d) and high (250 mmol/d) salt intake. Salt-sensitive hypertension was diagnosed in 26 patients who exhibited a significant increase in 24-hour mean blood pressure assessed by ambulatory blood pressure monitoring after 1 week of high salt intake. Nineteen patients were considered salt resistant. Compared with salt-resistant hypertensives, salt-sensitive patients presented a significant lower (P=0.005) maximal acetylcholine-induced vasodilation (21+/-6.3 versus 28+/-7.5 mL. 100 mL(-1). tissue. min(-1)). On the contrary, maximal sodium nitroprusside-induced vasodilation did not significantly differ between groups (22.4+/-4.5 versus 23.9+/-5.3 mL. 100 mL(-1). tissue. min(-1)). The decrease in maximal acetylcholine-induced vasodilation promoted by the coadministration of L-NMMA was significantly more pronounced in salt-resistant compared with salt-sensitive patients (P=0.003). Finally, high salt intake promoted a significant decrease in 24-hour urinary nitrate excretion in salt-sensitive patients (from 443+/-54 to 312+/-54 micromol/d; P=0.033) compared with salt-resistant hypertensives (from 341+/-50 to 378+/-54 micromol/d). We conclude that salt-sensitive hypertension is associated with endothelial dysfunction characterized by a defective endothelium-dependent vasodilation. Impairment of the L-arginine-nitric oxide pathway may be responsible for this abnormal endothelial response.

Acetylcholine↗
PubMed2001

Molecular basis of salt sensitivity in human hypertension. Evaluation of renin-angiotensin-aldosterone system gene polymorphisms.

We analyzed the association between salt sensitivity in essential hypertension and 8 genetic polymorphisms in 6 genes of the renin-angiotensin aldosterone system. Seventy-one patients with essential hypertension were classified as salt sensitive or salt resistant by means of the 24-hour ambulatory blood pressure (BP) change to high salt intake. The polymorphisms evaluated correspond to the following genes: ACE (I/D), angiotensinogen (M235T), angiotensin II type 1 receptor (A1166C), 11beta-Hydroxysteroid dehydrogenase type 2 (11betaHSD2) (G534A), aldosterone synthase (C-344T and Intron 2 conversion), and the mineralocorticoid receptor (G3514C and A4582C); all were determined using standard polymerase chain reaction methods. Thirty-five patients (49%) were classified as salt sensitive. We analyzed the BP response to high salt intake among genotypes and found a significant association for ACE I/D and 11betaHSD2 G534A polymorphisms. Patients homozygous for the insertion allele of the ACE gene (II) had a significantly higher BP increase with high salt intake than did patients homozygous for the deletion allele (DD). Heterozygous patients (ID) exhibited an intermediate response. The prevalence of salt-sensitive hypertension was also significantly higher (P=0.003) in II (68%) and DI patients (59%) compared with DD hypertensives (19%). With respect to 11betaHSD2 G534A, patients with the GG genotype had a significantly higher systolic BP increase with high salt intake than did GA patients. In addition, plasma renin activity suppression in response to high salt was significantly greater in GA patients than in GG patients. The prevalence of salt-sensitive hypertension was 14.3% in GA patients and 50.8% in GG patients (P=0.067). In conclusion, the I allele of ACE I/D polymorphism is significantly associated to salt-sensitive hypertension. The BP response to high salt intake was different among genotypes of ACE I/D and 11betaHSD G534A, suggesting that these polymorphisms may be potentially useful genetic markers of salt sensitivity.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed2001

Effect of salt intake on endothelium-derived factors in a group of patients with essential hypertension.

The aim of the present study was to evaluate the effects of the level of salt intake on endothelium-derived factors in a group of patients with essential hypertension. A group of 50 patients with essential hypertension who had never been treated for the condition were placed on a low-sodium (50 mmol/day), low-nitrate (400 micromol/day) diet, which was supplemented, in a single-blind fashion, with placebo tablets for the first 7 days and then with NaCl tablets (200 mmol/day) for a further 7 days (total sodium intake 250 mmol/day). At the end of both periods, 24-h ambulatory blood pressure monitoring was performed. In addition, plasma levels and 24-h urinary excretion of nitrites plus nitrates and cGMP were measured, along with plasma levels of endothelin. A high salt intake promoted significant decreases in plasma levels of nitrites plus nitrates (from 41.0+/-2.1 to 32.8+/-1.8 nmol/ml; P<0.001), 24-h urinary nitrate excretion (from 417+/-36 to 334+/-37 micromol/24 h; P=0.045) and plasma endothelin levels (from 5.6+/-0.3 to 4.6+/-0.3 pg/ml; P=0.007). The plasma concentration and 24-h urinary excretion of cGMP were not altered significantly by a high salt intake. We did not find any relationship between endothelium-derived products and 24-h mean blood pressure, at either low or high salt intakes, or between changes induced by the high-salt diet. A high salt intake also induced significant decreases in plasma renin activity, angiotensin II and aldosterone, and a significant increase in atrial natriuretic peptide. We conclude that a high salt intake decreases the plasma concentration and urinary excretion of nitrates and plasma levels of endothelin in patients with essential hypertension, suggesting that the level of salt intake may affect endothelial cell function. However, these alterations are not correlated with changes in blood pressure induced by the high salt intake.

Adult↗
PubMed2000

Genetic variation of the gamma subunit of the epithelial Na+ channel and essential hypertension. Relationship with salt sensitivity.

We evaluated the association of a common polymorphism in gammaENaC, consisting in a C to G transversion in codon 649, with essential hypertension and to the pressor response to salt in whites. Two hundred fifteen essential hypertensive patients, and 137 normotensive controls were genotyped for the gamma649 ENaC polymorphism by polymerase chain reaction method and diagnostic restriction enzyme digestion. The genotype distribution of the gamma649 ENaC polymorphism in the hypertensives, 129 CC (60%) and 86 CG/GG (40%) was not significantly different from that of the control group, 84 CC (61%) and 53 CG/GG (39%) (P = .81). Salt sensitivity was assessed in a group of 48 patients by 24-h mean blood pressure response to changes in salt intake. Nineteen patients were diagnosed as salt sensitive, whereas 29 had salt-resistant hypertension. The gamma649 ENaC genotype distribution in salt-sensitive patients was 12 CC (63%) and 7 CG/GG (37%), not significantly different from the distribution in the salt-resistant group, 19 CC (65%) and 10 CG/GG (35%), P = .87. The changes in systolic, diastolic, and mean blood pressure as measured by ambulatory blood pressure monitoring, and in plasma renin activity and plasma aldosterone induced by high salt diet were not different among the gamma649 ENaC genotypes. In the present study we found no association between the gamma649 ENaC polymorphism and essential hypertension or salt sensitivity. Although these data do not support a major causative role for this polymorphism, we cannot exclude that a functional mutation elsewhere in ENaC might be associated with essential hypertension.

Adult↗
PubMed2000

Prolonged cholestasis after acute paraquat poisoning through skin absorption.

Ingestion of paraquat is the most common cause of fatal pesticide poisoning. Liver involvement in acute paraquat poisoning is self-limited and usually consists of cholestasis. However, long-term hepatic effects after paraquat exposition have not been described up to now, probably because of the high mortality rate of this acute poisoning. We report the case of an agricultural worker who developed persistent cholestasis after an episode of acute paraquat poisoning through skin absorption.

Acute Disease↗
PubMed2000

Renin-angiotensin system genetic polymorphisms and salt sensitivity in essential hypertension.

We evaluated the association between salt-sensitive hypertension and 3 different genetic polymorphisms of the renin-angiotensin system. Fifty patients with essential hypertension were classified as salt sensitive or salt resistant, depending on the presence or absence of a significant increase (P<0.05) in 24-hour ambulatory mean blood pressure (BP) after high salt intake. The insertion/deletion (I/D) angiotensin-converting enzyme (ACE) gene, the M235T angiotensinogen (AGT) gene, and the A1166C angiotensin II type 1 (AT1) receptor gene polymorphisms were determined with the use of standard polymerase chain reaction methods. Twenty-four (48%) patients with significantly increased (P<0.05) 24-hour mean BP with high salt intake (from 107.3+/-9.4 to 114.8+/-10.6 mm Hg) were classified as salt sensitive. In the remaining 26 patients (52%), high salt intake did not significantly modify 24-hour mean BP (from 107.6+/-10 to 107. 8+/-9 mm Hg), and they were classified as having salt-resistant hypertension. We did not find any significant association between either M235T AGT or A1166C AT1 receptor genotypes and the BP response to high salt intake. However, patients with essential hypertension homozygous for the insertion allele of the ACE gene (II) had a significantly higher BP increase with high salt intake (9. 8+/-8.1 mm Hg for systolic BP and 5.2+/-4.2 mm Hg for diastolic BP) than that observed in patients homozygous for the deletion allele (DD) (1.2+/-5.9 mm Hg for systolic BP; P=0.0118 and -0.2+/-4.2 mm Hg for diastolic BP; P=0.0274). Heterozygous patients (ID) exhibited an intermediate response. The prevalence of salt-sensitive hypertension also was significantly higher (P=0.012) in II (67%) and DI patients (62%) compared with DD hypertensives (19%). We conclude that a significant association exists between the I/D polymorphism of the ACE gene and salt-sensitive hypertension. Patients with II and DI genotypes have significantly higher prevalence of salt sensitivity than DD hypertensives.

Adult↗
PubMed2000

Microalbuminuria in essential hypertension: clinical and biochemical profile.

This study aims to evaluate the clinical and biochemical profile associated with the presence of microalbuminuria in a group of essential hypertensive patients referred to a hypertension clinic. A total of 188 non-diabetic, untreated essential hypertensive patients (100 men, 88 women) aged 55.8 +/- 11.7 years are studied. Urinary albumin excretion was determined in two 24-h urine collections. Clinical and biochemical evaluations and 24-h ambulatory blood pressure (BP) monitoring were performed at baseline. Forty-two patients (22.3%) showed an increased urinary albumin excretion rate (20-200 micrograms/min). These patients showed significantly higher values (P < 0.01) for 24-h, daytime and night-time systolic and diastolic BP, compared with essential hypertensives with normal urinary albumin excretion. However, nocturnal reduction in BP did not differ between the groups. Furthermore, patients with microalbuminuria showed significantly higher (P < 0.01) creatinine, serum uric acid and triglycerides, as well as lower high-density lipoprotein (HDL)-cholesterol. In a multiple logistic regression analysis, a 24-h systolic BP > 140 mmHg (odds ratio: 3.19; 95% confidence interval [CI 95%]: 1.44-7.06) and a serum creatinine > 88 mumol/L (odds ratio: 3.08; CI 95%: 1.39-6.84) were the two factors associated independently with increased urinary albumin excretion. We conclude that, in essential hypertensive patients, the presence of microalbuminuria is associated with elevated BP, but not with its circadian pattern. Likewise, microalbuminuria is associated with the degree of renal impairment, and with increased uric acid and triglycerides and decreased HDL-cholesterol.

Adult↗
PubMed1996

Fluid, ionic and hormonal changes induced by high salt intake in salt-sensitive and salt-resistant hypertensive patients.

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin-aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 +/- 35 to 226 +/- 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 +/- 76 to 364 +/- 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 +/- 0.11 to 1.56 +/- 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 +/- 0.08 to 1.12 +/- 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

Aldosterone↗
PubMedDate not supplied

[Absence of an association between the C825T polymorphism of the G-protein beta 3 subunit and salt-sensitivity in essential arterial hypertension].

The genetic functional variant C for T in position 825 of the gene encoding G protein beta 3 subunit, GNB3, has been associated with enhanced G protein activation, cell growth and proliferation. This phenotype is associated with enhanced G protein activation and Na(+)-H+ exchanger activity in cells from hypertensive patients. Salt sensitivity affects approximately 50% of hypertensive patients and constitutes an intermediate phenotype determined in part by genetic factors. An association between enhanced Na(+)-H+ exchanger activity and salt sensitivity has been previously reported. The aim of the present study was to investigate the possible association between the G protein polymorphism and salt sensitivity in patients with essential hypertension. A total of 46 patients were studied and classified according to their blood pressure response to a change in sodium intake from low (20 mmol/day) to high (260 mmol/day) into salt sensitive (SS) (n = 20) and salt resistant (SR) (n = 26). GNB3 polymorphism was determined by PCR of genomic DNA and restriction digestion with BseDI. The genotypes distribution among the SS hypertensives was: 8 CC and 12 CT + TT, whereas in SR was: 10 CC and 16 CT + TT (p = 0,577). 24 h mean blood pressure response to salt in the whole group was not different among the different genotypes: CC 4.1 +/- 5.4 mmHg compared to CT + TT 2.9 +/- 6.3 mmHg (p = 0.51). There were no significant differences in the salt induced changes in plasma renin activity, aldosterone, ANP or noradrenaline among the different genotypes. These results indicate that the GNB3 C825T polymorphism has no major influence on the pressor response to salt in essential hypertension and therefore do not support its usefulness as an early genetic marker of salt sensitivity in this disease.

Adult↗