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A de la Sierra

Publications and source records attributed to A de la Sierra.

At least 19 recordsLinked to original sources
PubMed2004

Comparison of the antihypertensive effects of the fixed dose combination enalapril 10 mg/nitrendipine 20 mg vs losartan 50 mg/hydrochlorothiazide 12.5 mg, assessed by 24-h ambulatory blood pressure monitoring, in essential hypertensive patients.

Fixed combinations of calcium channel blockers and angiotensin converting enzyme inhibitors represent an alternative to diuretic-based combination therapy. The aim of the present study was to compare the antihypertensive efficacy of the combination enalapril 10 mg/nitrendipine 20 mg (E/N) vs losartan 50 mg/hydrochlorothiazide 12.5 mg (L/H), assessed by 24-h ambulatory blood pressure monitoring. This multicentre, double-blind, parallel study included 97 hypertensive patients (office diastolic blood pressure (DBP) 90-109 mmHg and daytime DBP > 85 mmHg). After a 2- to 3-week period of single-blind placebo, they were randomized to receive double-blind treatment with E/N (n = 48) or L/H (n = 49) for a 4-week period. The primary outcome measure was the difference in 24-h DBP reduction between treatments from randomization to the end of the double-blind period. Secondary efficacy variables included differences in 24-h systolic (S) BP reduction, daytime, night-time and office SBP and DBP reduction, proportion of responders and controlled patients, trough-to-peak ratio and smoothness indexes. Safety was assessed by the proportion of patients with adverse events and the detection of laboratory abnormalities. No significant differences were observed in the primary outcome measure. The group receiving E/N tended to show greater reductions in most measures (24 h, daytime and office SBP and DBP) and higher BP control rates, but only the difference in the rate of office SBP control (< 140 mmHg) reached statistical significance (42.2 vs 22.4%; P = 0.048). The trough-to-peak ratios and smoothness indexes were similar in both groups. The incidence of adverse events related to the treatment was 27.1% (95% CI 14.5-39.6%) in E/N-treated patients and 14.3% (95% CI 4.5-45.8%) in the L/H group, but differences were not significant. The kind of event more frequently observed were flushing and headache in E/N, and dizziness and asthenia in L/H; all observed adverse events were mild. We conclude that E/N and L/H have a similar antihypertensive efficacy, assessed by office or ambulatory blood pressure monitoring. E/N achieved a significantly higher office SBP control rate, but this was accompanied by an apparently higher proportion of mild adverse events.

Antihypertensive Agents↗
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

[Effect of anti-hypertensive therapy with irbesartan on the absolute cardiovascular risk].

Blockade of the renin-angiotensin system with angiotensin converting enzyme inhibitors or with angiotensin receptor antagonists confers patients with arterial hypertension (AH) and associated risk factors, target organ lesion or cardiovascular disease with greater protection in morbidity and mortality terms. The objective of the present study was to evaluate the effect of irbesartan, an angiotensin II receptor antagonist, on the absolute cardiovascular risk in a cohort of hypertensive patients with moderate, high, or very high cardiovascular risk. This was a multicenter, prospective, observational, cohort study with 1974 patients (63 11 years; 47% males) with newly diagnosed essential AH or AH non-controlled with anti-hypertensive monotherapy, and moderate to very high cardiovascular risk. Irbesartan therapy at a dosage of 150300 mg was instituted as monotherapy or associated with hydrochlorothiazide, 12.5 mg. The clinical follow-up was 6 months. The evaluated parameters included the absolute cardiovascular risk, measured either quantitatively (Framingham algorithm) or qualitatively (low, moderate, high, and very high risk groups following the WHO/International Hypertension Society guidelines). Irbesartan therapy led to a significant (p = 0.0001) decrease in SBP (from 170.9 18.4 to 138.5 16.5 mmHg) and DBP (from 96.6 11 to 82 9 mmHg). The quantitative absolute cardiovascular risk decreased by 29.8% (from 12.14 8 to 8.65 6.2; p < 0.0001). The percentage of patients with very high cardiovascular risk decreased from 1.52% to 0.51% and that for patients with high cardiovascular risk from 92.77% to 88.32%. The latter patients changed to the moderate risk group. As a result, this moderate risk group increased from 5.71% to 11.17%. The adverse reaction rate was very low as only 2.2% of patients had some adverse reaction. In conclusion, irbesartan as monotherapy or associated with hydrochlorothiazide has been shown to be effective in reducing the absolute cardiovascular risk, which is obtained by a substantial decrease in arterial pressure and a good safety profile on the biochemical parameters. Tolerability was excellent, with a very low rate of adverse reactions.

Angiotensin Receptor Antagonists↗
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

Increased insulin resistance in salt sensitive essential hypertension.

OBJECTIVE: To determine the possible relationship between insulin resistance and salt sensitivity in essential hypertension. DESIGN AND METHODS: We studied 17 non-obese, essential hypertensive patients (24-h blood pressure: 149 +/- 15/94 +/- 5 mm Hg) with normal glucose tolerance. Salt sensitivity was diagnosed in the presence of a significant increase (P < 0.05, more than 4 mm Hg) in 24-h mean blood pressure (MBP) when patients switched from a low-salt intake (50 mmol/day of Na(+)) to a high-salt intake (240 mmol/day of Na(+)), each period lasting 7 days. The insulin sensitivity index was determined by the euglycaemic hyperinsulinaemic clamp. RESULTS: Six patients were classified as salt sensitive (24-h MBP increase: 6.2 +/- 1.1 mm Hg), and 11 as salt resistant (24-h MBP increase: -1.2 +/- 3.8 mm Hg). No significant differences were observed between salt sensitive and salt resistant patients regarding baseline characteristics, fasting serum insulin, fasting serum glucose, glycosylated haemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, uric acid and microalbuminuria. Salt sensitive patients exhibited a reduced insulin sensitivity index compared with salt resistant patients (1.7 +/- 1.1 vs 3.5 +/- 1.2 mg/kg/min; P = 0.009). An inverse relationship (r -0.57; P = 0.016) between the insulin sensitivity index and 24-h MBP increase with high salt intake was found. CONCLUSION: Salt sensitive essential hypertensive patients are more insulin resistant than salt resistant patients when both salt sensitivity and insulin resistance are accurately measured. Indirect measures of both insulin and salt sensitivity and/or the presence of modifying factors, such as obesity or glucose intolerance, may account for differences in previous studies.

Adult↗
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

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

[Relationship between cardiovascular risk profile and anti-hypertensive drug use. GEDEC (Spanish group of cardiovascular studies].

BACKGROUND: Hypertension guidelines emphasize the selection of antihypertensive treatment on the basis of absolute cardiovascular risk. Moreover, compelling and possible indications for each antihypertensive drug class are recommended for patients with other concomitant conditions. The aim of the present study was to analyze the relationship between the cardiovascular risk profile and co-morbid conditions on antihypertensive drug class use. METHODS: This is an observational, multicenter, cross-sectional study performed in 2,850 essential hypertensive patients. Antihypertensive drug treatment has been evaluated on the basis of the presence of other cardiovascular risk factors, target organ damage or cardiovascular diseases, as well as the absolute cardiovascular risk profile. RESULTS: Patients with diabetes were treated more frequently with calcium channel blockers (CCB) and ACE inhibitors. However, the presence of hypercholesterolemia or smoking habit did not influence the use of antihypertensive drug classes. The presence of cerebrovascular disease increased the use of CCB and ACE inhibitors, whereas coronary disease increased the use of CCB and betablockers. The use of diuretics and angiotensin II receptor antagonists was increased in patients with cardiac failure, whereas neither betablockers nor ACE inhibitors were affected by this concomitant disease. Patients with the highest cardiovascular risk received more antihypertensive treatment than those with lower risk, but this was not accompanied by switching from old classes to new ones. CONCLUSION: Cardiovascular risk profile seems to have little influence on the use of antihypertensive drug classes, particularly the presence of hypercholesterolemia or cardiac failure. It seems adequate to emphasize the necessity of an individualization of antihypertensive treatment, based on the presence of concomitant conditions that influence the absolute cardiovascular risk.

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

Lack of association between ACE gene polymorphism and left ventricular hypertrophy in essential hypertension.

The possible association between the insertion/deletion (I/D) polymorphism of the angiotensin I converting enzyme (ACE) gene and left ventricular hypertrophy (LVH) was investigated in a group of essential hypertensive patients. Seventy-one essential hypertensive patients (35 men and 36 women), aged 51 +/- 1 years, were genotyped by PCR for the I/D polymorphism of the ACE gene. Cardiac morphology and function were assessed by means of M-mode echocardiography. The relative frequencies of the three genotypes, DD, DI, and II, were respectively: 24%, 55%, and 21%. Mean values of left ventricular mass index were 145, 144, and 150 g/m2 for DD, DI, and II genotypes, without significant differences among them (P = 0.82). Likewise, the prevalence of LVH (76%, 64%, and 87%) was not significantly different among the three genotypes (P = 0.23). We conclude that the ACE gene I/D polymorphism is not associated with LVH in essential hypertension. Journal of Human Hypertension (2000) 14, 47-49.

Adolescent↗
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↗
PubMed1999

[Relationship between sympathetic activity and response to treatment with atenolol in hypertensive patients. Investigation group of the study of efficiency and tolerance of atenolol in hypertensive patients with increase in the sympathetic activity].

BACKGROUND: Therapeutical response to antihypertensive treatment is poorly predicted by individual clinical or biochemical characteristics. Some preliminary data indicate that therapeutical response to atenolol might depend on physical and/or sympathetic activity. The aim of the present study was to evaluate the blood pressure response to atenolol depending on physical and sympathetic activity. PATIENTS AND METHODS: One thousand one hundred forty hypertensive patients were treated with the beta adrenorecepetor blocker atenolol in an open fashion during 3 months. Before the beginning of the treatment, we evaluated current weekly physical activity (direct interview), as well as sympathetic activity (direct interview and baseline heart rate). RESULTS: Age or physical activity did not correlate with blood pressure response to atenolol. Conversely, hypertensive patients with symptoms suggesting sympathetic overactivity (three or more of the following symptoms: palpitations, anxiety, diaphoresis, headache, tremor or weakness; n = 456), showed a more pronounced decrease in systolic (27.7 [13.4] vs 25.8 [14.3] mmHg; p = 0.0226) and diastolic (17.6 [8.3] vs 15.5 [8.6] mmHg; p = 0.0001) blood pressures (SBP and DBP), with respect to the remaining hypertensive patients (n = 719). Moreover, we found a statistically significant correlation between blood pressure fall with atenolol and baseline heart rate (r = 0.107, P < 0.001 for SBP, and r = 0.142, p < 0.001 for DBP). CONCLUSION: Baseline tachycardia or symptoms suggesting anxiety, emotional tension or sympathetic overactivity are associated with a more pronounced blood pressure fall to antihypertensive treatment with atenolol. These circumstances may play a role when choosing a new antihypertensive therapy.

Adolescent↗
PubMed1999

[Genetic polymorphisms of the renin-angiotensin system and essential hypertension].

BACKGROUND: The renin-angiotensin system (RAS) plays an important role in blood pressure (BP) regulation. A number of RAS polymorphisms have been linked to essential hypertension (EH), but there is uncertainty about this association in other studies. We examined whether the insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene, and the M235T and T174M polymorphisms of the angiotensinogen (AGT) gene are associated with EH in a Spanish sample of hypertensive patients. MATERIAL AND METHODS: We studied 75 patients with EH (BP > 160/100 mmHg), aged 55 (8.5) years, 30 males, systolic BP (SBP) 182 +/- (22.1) mmHg, diastolic BP (DBP) 109 +/- (9.9) mmHg (mean [SD]) and a strong family history of the disease. As a control group, 75 healthy subjects with no family history of cardiovascular disease were studied. The polymorphisms were determined by PCR amplification of genomic DNA, followed by enzyme digestion for the AGT gene polymorphisms. RESULTS: The genotype distribution and the frequencies of the alleles of the three RAS polymorphisms were similar in hypertensive and control subjects. In addition, we did not find any compound effect of the I/D ACE gene and M235T AGT gene polymorphisms on BP levels in hypertensive and control subjects. CONCLUSIONS: In this sample, the contribution of the ACE I/D polymorphism and the AGT M235T and T174M polymorphisms in the development of EH seems to be less important than previously estimated.

Adult↗
PubMed1999

[Calcium pump changes in patients with essential arterial hypertension].

BACKGROUND: Transmembrane Ca2+ fluxes are mediated, at least in part, by the Ca(2+)-dependent ATPase. Thus, genetic or acquired abnormalities of this pump could explain the increase in free cytosolic Ca2+ content that has been observed in essential hypertensive patients. PATIENTS AND METHODS: We carried out a kinetic study of the Ca2+ pump in intact erythrocytes from 49 essential hypertensive patients and 27 normotensive healthy persons. We used Sr2+ as a calcium analogue to measure Ca2+ fluxes dependent of the Ca2+ pump. The intracellular concentrations of Sr2+ and Ca2+ were modified using the A-23187 ionophore in a Ringer isotonic solution. RESULTS: Hypertensive patients showed a significant increase of the maximal efflux rate for Sr2+ (Vmax) with respect to controls (6.6 [2.3] vs 5.2 [1.6] mmol/l cel/h; p = 0.006). Mean values of apparent dissociation constants for intracellular Ca2+ (KCa) were also increased in essential hypertensives (80.36 [53.46] vs 55.25 [15.13] mumol/l cel; p = 0.06). A significant correlation between Vmax and age (r = 0.342; p = 0.016), and serum creatinine (r = 0.446; p = 0.001) was observed. The KCa only correlated with serum creatinine (r = 0.402; p = 0.004). Using the KCa confidence interval of 99% as the higher normal limit, patients were segregated into two subgroups depending on normal KCa values (33 patients, 67.3%) or increased KCa values (16 patients, 32.6%). Age (50.8 [13.5] vs 43 [10.2] years; p = 0.02), serum creatinine (1.13 [0.17] vs 0.95 [0.17] mg/dl; p = 0.001) and serum uric acid (7.27 [3.32] vs 6.14 [1.49] mg/dl; p = 0.04) were higher in patients with increased KCa. Finally, patients with increased KCa also showed increased values of Vmax (9.13 [2.02] vs 5.38 [12.81] mmol/l cel/h; p < 0.0001). CONCLUSIONS: Essential hypertensive patients are heterogeneous regarding ion transport abnormalities, only affecting subgroups of hypertensive patients. We have observed abnormalities of the Ca(2+)-dependent ATPase in 33% of essential hypertensive patients. These patients are older and tend to exhibit higher values of serum creatinine and uric acid.

Adult↗
PubMed1999

Prospective comparison of therapeutical attitudes in hypertensive type 2 diabetic patients uncontrolled on monotherapy. A randomized trial: the EDICTA study.

OBJECTIVE: To compare the anti-hypertensive effect of combination therapy versus a single drug regimen schedule (dose-titration or switching to a different drug class) in type 2 diabetic hypertensive patients with inadequate blood pressure (BP) control on monotherapy. DESIGN: Prospective, randomized, open-fashion, parallel study of two therapeutic strategies during an 8-week period. SETTING: Primary care centers in Spain. PARTICIPANTS: A total of 898 men and women with type 2 diabetes mellitus and hypertension, receiving antihypertensive treatment with one single drug and whose BP was > 140 and/or 90 mmHg. INTERVENTION: Patients were randomized to a fixed combination therapy (verapamil 180 mg plus trandolapril 2 mg; Knoll AG, Ludwigshafen, Germany) or continued on a single drug regimen, either increasing the dose of the current drug or switching to a different drug class. MAIN OUTCOME MEASURE: Absolute BP reduction in the two groups of treatment, and the percentage of normalized patients (< 140/90 mmHg) in each group. RESULTS: The diastolic BP (DBP) decrease (5.6 mmHg) was significantly greater in patients treated with combination therapy, compared to patients on monotherapy (2.9 mmHg). The decrease in systolic BP (SBP) was not significantly different (11.1 versus 10.0 mmHg). In addition, a significantly higher number of patients treated with combination therapy (82% versus 74%) reached diastolic BP normalization (< 90 mmHg). CONCLUSIONS: In type 2 hypertensive patients with uncontrolled BP despite anti-hypertensive monotherapy, the change to combination therapy was more effective in attaining DBP control than any monotherapy schedule (either increasing the dose or switching to another different drug class).

Aged↗
PubMed1999

Effect of alcohol abstinence on blood pressure: assessment by 24-hour ambulatory blood pressure monitoring.

Several studies have shown that cessation of alcohol drinking reduces blood pressure (BP). However, attempts to reproduce these findings by ambulatory BP monitoring (ABPM) have shown inconsistent results. The aim of the present study was to assess the effect of 1 month of proven abstinence from alcohol on the 24-hour BP profile in heavy alcohol drinkers. Forty-two men who were heavy drinkers (>100 g of pure ethanol per day) were consecutively admitted to a general ward for voluntary alcohol detoxification. On the day of admission, they received a total dose of 2 g/kg of ethanol diluted in orange juice in 5 divided doses, and a 24-hour ABPM was performed. A new 24-hour BP monitoring in the same environmental conditions was performed after 1 month of proven alcohol abstinence while the subjects were receiving the same amount of fluid but without the addition of alcohol. After 1 month of proven alcohol abstinence, BP and heart rate (HR) significantly decreased. The reduction was 7.2 mm Hg for 24-hour systolic BP (SBP) (95% CI, 4.5 to 9.9), 6.6 mm Hg for 24-hour diastolic BP (DBP) (95% CI, 4.2 to 9.0), and 7.9 bpm for HR (95% CI, 5.1 to 10.7). The proportion of alcoholic patients considered hypertensive on the basis of 24-hour BP criteria (daytime SBP >/=135 mm Hg or daytime DBP >/=85 mm Hg) fell from 42% during alcohol drinking to 12% after 1 month of complete abstinence. Abstinence did not modify either the long-term BP variability, assessed by SD of 24-hour BP, or its circadian profile. We conclude that abstinence in heavy alcohol drinkers significantly reduces BP assessed by 24-hour ABPM and that this reduction is clinically relevant. These results show that heavy alcohol consumption has an important effect on BP, and thus cessation of alcohol consumption must be recommended as a priority for hypertensive alcohol drinkers.

Adult↗