[Causes and consequences of mild hypertension].
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Humans↗
Biomedical subjects
P Omvik
Publications and source records attributed to P Omvik.
[Consensus on hypertension?].
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Antihypertensive Agents↗
Factors influencing reduction in blood pressure and left ventricular mass in hypertensive type-1 diabetic patients using captopril or doxazosin for 6 months.
The effect of doxazosin versus captopril on blood pressure, albuminuria, and left ventricular mass was studied in 33 hypertensive type-1 diabetic patients randomized to 6 months treatment with captopril (17 patients, mean daily dose 100 mg) or doxazosin (16 patients, mean daily dose 9 mg). Casual and 24-h ambulatory blood pressure (24hBP) were reduced from 163/95 to 144/83 mm Hg and 152/86 to 145/81 mm Hg, respectively, in the captopril group, and from 160/93 to 145/86 mm Hg and 156/86 to 147/79 mm Hg in the doxazosin group (all P < .05). The achieved 24hBP on treatment was positively associated with pretreatment levels of glycosylated hemoglobin (HbA1c) and plasma atrial natriuretic peptide (r = 0.53 and 0.59, respectively, both P < .01). Albuminuria did not change significantly in either group. Left ventricular hypertrophy was present in 13 patients (7 in the captopril and 6 in the doxazosin group). Left ventricular mass was reduced by an average of 27% and 23%, respectively, in these patients (both P < .01), but did not change significantly in patients without left ventricular hypertrophy. The reduction in left ventricular mass was positively associated with the presence of baseline left ventricular hypertrophy and inversely with dietary sodium intake and achieved casual blood pressure on treatment (R2 = 0.59, P < .001). We conclude that doxazosin and captopril used for 6 months are equally effective in reducing blood pressure and left ventricular hypertrophy in hypertensive type-1 diabetic patients; the antihypertensive effect is closely related to glycemic control; and dietary sodium intake and achieved casual blood pressure after treatment are independent determinants of the reduction in left ventricular mass seen in these patients.
Adult↗
Beta-2 adrenoceptor genetic variation is associated with genetic predisposition to essential hypertension: The Bergen Blood Pressure Study.
We tested the hypothesis that genetic variation in the beta-2 adrenoceptor gene is associated with a genetic predisposition to hypertension. Offspring of two hypertensive parents were compared with offspring of two normotensive parents. The subjects were participants of the Bergen Blood Pressure Study, where couples were recruited in 1963 to 1964 and re-examined in 1990. We studied offspring of those couples in which both partners were either hypertensive or normotensive in both examinations. Twenty-three hypertensive and 22 normotensive families met the inclusion criteria. DNA samples from the first born of hypertensive family-history offspring and normotensive family-history offspring were analyzed. We used multiplex sequencing and specifically examined the promoter and the N-terminal portion of the beta-2 adrenoceptor gene. We found four genetic variants: at position -47, a C-->T substitution in the 5' leader cistron causing an Arg-->Cys exchange, at -20, a T-->C substitution, at +46 an A-->G substitution leading to an Arg16-->Gly exchange, and at +79, a C-->G substitution leading to a Gln27-->Glu exchange. The frequency of the Arg16 allele was significantly higher in the hypertensive family-history offspring compared to normotensive family-history offspring (58% vs. 28% P < 0.011). We constructed haplotypes for the four intragenic variants and found significant linkage dysequilibrium. In particular, the 5' leader cistron mutant with the wild type alleles at the other loci was significantly more frequent in offspring of hypertensive parents, compared to offspring of normotensive parents. We also performed a relative risk analysis comparing the Gly/Gly, Arg/Gly, and Arg/Arg alleles, which implicated the Arg-containing allele. Finally, we analyzed the effect of genotype on blood pressure in the offspring. We found a significant step-wise effect for all four polymorphisms examined. Our data suggest that the Arg variant of the Arg-->Gly exchange is associated with parental hypertension and higher blood pressure values in this northern European population.
Adult↗
Factors influencing left ventricular mass in salt sensitive and salt resistant essential hypertensive patients.
UNLABELLED: To investigate whether salt sensitivity is associated with differences in left ventricular mass or geometry, salt sensitivity testing and Doppler echocardiography was performed in 30 essential hypertensive patients (7 women and 23 men) with mean age 43+/-9 years. Salt sensitivity was defined as a 10% increase or more in 24-h blood pressure (24hBP) when going from low to high dietary sodium intake based on a single test. Eight patients were characterized as salt sensitive and 22 as salt resistant. At baseline, there was no difference in casual blood pressure (156/103+/-17/9 vs 158/100+/-18/11 mmHg) or 24hBP (152/ 90+/-25/15 vs 159/89+/-19/8 mmHg), in duration of hypertension (5+/-4 vs 4+/-3 years), daily sodium excretion (144+/-68 vs 171+/-68 mmol), left ventricular mass (LVM) (212+/-45 vs 246+/-52 g) or left ventricular relative wall thickness (RWT) between the salt sensitive and salt resistant groups of patients. In the total study population, increased RWT was found in 17 patients, and increased LVM in 10 patients. In only 10 patients were both these variables normal. Left ventricular geometric pattern did not differ between the salt sensitive and salt resistant groups. LVM and RWT were significantly correlated with 24hBP (r = 0.57 and 0.51, respectively; both p < 0.01). Significant correlation was also found between LVM and casual blood pressure, blood volume, body surface area, serum creatinine and albuminuria (r = 0.53, 0.60, 0.54, 0.54 and 0.43, respectively; all p < 0.01). In multiple regression analysis, 24hBP and blood volume were identified as independent predictors of LVM (R = 0.51, p < 0.001). CONCLUSIONS: increased RWT or LVM is common in both salt sensitive and salt resistant essential hypertensive patients. Salt sensitivity status based on a single test does not influence left ventricular hypertrophy or geometry. Twenty-four-hour blood pressure is related to increased RWT and LVM.
Adult↗
Characteristics of 9194 patients with left ventricular hypertrophy: the LIFE study. Losartan Intervention For Endpoint Reduction in Hypertension.
-Losartan was the first available orally administered selective antagonist of the angiotensin II type 1 receptor developed for the treatment of hypertension. The Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of the beta-blocker atenolol on the reduction of cardiovascular morbidity and mortality. Patients with essential hypertension, aged between 55 and 80 years, and ECG-documented left ventricular hypertrophy (LVH) were included. Altogether, 9223 patients in Scandinavia, the United Kingdom, and the United States were randomized from June 1995 through April 1997, and 9194 remain after exclusion of a study center at which irregularities were discovered. This population of hypertensives (mean systolic/diastolic blood pressure, 174.4/97.8 mm Hg) with LVH comprises women (54.1%) and men, mostly retired from active work (mean age, 66.9 years), with a high prevalence of overweight (mean body mass index, 28.0 kg/m2), diabetes mellitus (12.3%), lipid disorders (18.0%), and symptoms or signs of coronary heart disease (15.1%). There were fewer current smokers (<17%) than in the general population, and approximately 7% were nonwhite. Almost 30% of participants had been untreated for at least 6 months when screened for the study. Only 1557 persons who entered the placebo run-in period of 14 days were excluded, predominantly because of sitting blood pressures above or below the predetermined range of 160-200/95-115 mm Hg and ECG-LVH criteria not met. By application of simple 12-lead ECG criteria for LVH (Cornell voltage QRS duration product formula plus Sokolow-Lyon voltage read by a core laboratory), hypertensive patients with LVH with an average 5-year coronary heart disease risk of 22.3% according to the Framingham score were identified. This population is now being treated (goal, <140/90 mm Hg) in adherence with the protocol for at least 4 years after final enrollment (ie, through April 2001) and until at least 1040 patients suffer myocardial infarction, stroke, or cardiovascular death.
Aged↗
Will the millimetre of mercury be replaced by the kilopascal?
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Blood Pressure Determination↗
Factors influencing LVM in hypertensive type-1 diabetic patients.
Diabetes mellitus is associated with a high prevalence of hypertension and left ventricular hypertrophy (LVH), and a causative relationship with abnormal sodium metabolism in diabetic patients has been suggested. Factors influencing left ventricular mass (LVM) were assessed in 30 hypertensive type-1 diabetic patients, mean age 46 +/- 9 (range 24-67) years, with a mean duration of diabetes and hypertension of 19 +/- 10 and 6 +/- 5 years, respectively. In the total study population, casual blood pressure was 163/94 +/- 24/10 mmHg and 24 h blood pressure was 155/87 +/- 17/8 mmHg. Twenty-four-hour urine samples were obtained to measure daily albumin excretion (0.77 +/- 1.06 g) and dietary sodium intake was assessed as 24 h sodium excretion (173 +/- 77 mmol). Creatinine clearance averaged 1.41 +/- 0.53 ml/s. LVM determined by echocardiography was 221 +/- 74 g (range 104-408 g) and 33% of the patients had LVH. Multiple regression analysis identified dietary sodium intake and plasma atrial natriuretic peptide as independent predictors of LVM (R2 = 0.52, p < 0.001). No significant association was found between LVM and blood pressure or albuminuria. The results propose dietary sodium intake as an important factor in the development of LVH in hypertensive type-1 diabetic patients.
Adult↗
The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study: rationale, design, and methods. The LIFE Study Group.
The treatment of hypertension mainly with diuretics and beta blockers reduces cardiovascular mortality and morbidity, largely due to a decreased incidence of stroke, whereas the beneficial effects of antihypertensive therapy on the occurrence of coronary events have been less than expected from epidemiological studies. Furthermore, treated hypertensive patients still have a higher cardiovascular complication rate, compared with matched normotensives. This is particularly evident in patients with left ventricular hypertrophy (LVH), a major independent risk indicator for cardiovascular disease. In addition to elevating blood pressure, angiotensin II (A-II) exerts an important influence on cardiac structure and function, stimulating cell proliferation and growth. Thus, to further reduce morbidity and mortality when treating hypertensive patients, it may be important to effectively block the effects of A-II. This can be achieved directly at the A-II receptor level by losartan, the first of a new class of antihypertensive agents. It therefore seems pertinent to investigate whether selective A-II receptor blockade with losartan not only lowers blood pressure but also reduces LVH more effectively than current therapy, and thus improves prognosis. The Losartan Intervention For Endpoint reduction (LIFE) in Hypertension study is a double-blind, prospective, parallel group study designed to compare the effects of losartan with those of the beta-blocker atenolol on the reduction of cardiovascular morbidity and mortality in approximately 8,300 hypertensive patients (initial sitting diastolic blood pressure 95 to 115 mm Hg or systolic blood pressure 160 to 200 mm Hg) with electrocardiographically documented LVH. The study, which will continue for at least 4 years and until 1,040 patients experience one primary endpoint, has been designed with a statistical power that will detect a difference of at least 15% between groups in the incidence of combined cardiovascular morbidity and mortality. It is also the first prospective study with adequate power to link reversal of LVH to reduction in major cardiovascular events. The rationale of the study, which will involve more than 800 clinical centers in Scandinavia, the United Kingdom, and the United States, is discussed, and the major features of its design and general organization are described. On April 30, 1997, when inclusion was stopped, 9,218 patients had been randomized.
Adrenergic beta-Antagonists↗
[How does smoking affect blood pressure?].
It has been known for a long time that blood pressure and heart rate increase during smoking. These effects are associated specifically with nicotine. The rise in blood pressure is due both to an increase in cardiac output and in total peripheral vascular resistance. The rise in blood pressure occurs immediately, before any increase in circulating catecholamines. In hypertensives the blood pressure lowering effect of beta-blockers may be diminished by tobacco smoking whereas alpha-receptor blockers on the other hand seem to maintain their antihypertensive efficacy. It is a paradox that while smoking acutely increases blood pressure, some extensive epidemiological studies have shown a slightly lower blood pressure level among smokers than among non-smokers. Because blood pressure may rise after discontinuation of smoking, a smoking cessation programme should not postpone initiation of antihypertensive drug therapy in patients otherwise in need of such treatment.
Blood Pressure↗
[Losartan and the LIFE-study. Antihypertensive treatment with AT1-receptor antagonist].
The renin-angiotensin system, through the effects of angiotensin II, may be involved in the pathogenesis of essential hypertension and associated left ventricular hypertrophy. Treatment with angiotensin-converting enzyme inhibition (ACEI) lowers blood pressure and reduces left ventricular hypertrophy. ACEI, however, may not completely inhibit the production of angiotensin II and its effects, and adverse effects like cough and rise in creatinine have been associated with ACEI and reduced degradation of bradykinin. The first selective antagonist of the angiotensin II-1 (AT1) receptor, losartan, has recently been approved. The LIFE study has been started, in which 8,300 hypertensive patients with left ventricular hypertrophy in Scandinavia and the USA will be randomized to blinded treatment with either atenolol or losartan to compare the effects on cardiovascular morbidity and mortality over a period of five years.
Angiotensin I↗
How smoking affects blood pressure.
The addictive effects of smoking are only partly known, but it is likely that hemodynamic effects of tobacco smoking may contribute to the habituation. It has since long been known that blood pressure and heart rate increase during smoking. These effects are specifically associated with nicotine while the other components of which more than a thousand have been isolated seem to be of minor importance. The rise in blood pressure is due both to an increase in cardiac output and total peripheral vascular resistance. The blood pressure rise appears immediately and occurs before any increase in circulating catecholamines. In hypertensive patients the blood pressure lowering effect of beta-blockers may be partly abolished by tobacco smoking whereas alpha-receptor blockers seem to maintain the antihypertensive efficacy in smokers. It is a paradox that while smoking acutely increases blood pressure, a slightly lower blood pressure level has been found among smokers than nonsmokers in larger epidemiological studies. Because blood pressure may increase after cessation of smoking, a smoke quitting program should not postpone initiation of antihypertensive treatment in patients otherwise in need of such treatment.
Adrenergic alpha-Antagonists↗
Salt sensitivity in hypertensive type-1 diabetes mellitus.
UNLABELLED: As sodium retention has been proposed as a causal factor in the development of hypertension in diabetic patients, a high incidence of salt sensitivity has been suggested. To evaluate the influence of dietary sodium intake on blood pressure, casual and 24-h blood pressure was measured in 30 hypertensive type-1 diabetic patients aged 24-67 (mean 46) years while they were on habitual diet, after 6 days of low-sodium diet (50 mmol/day), and after 6 days of high-sodium diet (250 mmol/day). Nine patients (30%) who increased their 24-h mean blood pressure by more than 10% when going from low- to high-sodium intake were classified as salt sensitive; the others as salt resistant. The salt sensitive group had a significantly lower urinary excretion of dopamine at baseline, and a higher diuresis and a more pronounced decrease in 24-h blood pressure during salt depletion (all p < 0.01). Low-sodium diet reduced casual and 24-h blood pressure by 4% in the total study population compared with 9% in the salt sensitive group (p < 0.01). There was no difference in glomerular filtration rate, filtration fraction, proteinuria or urinary sodium excretion between the groups. CONCLUSIONS: Sodium restriction more effectively reduces blood pressure in the salt sensitive minority of hypertensive type-1 diabetic patients irrespective of renal function. The incidence of salt sensitivity is not increased in hypertensive type-1 diabetic patients compared with essential hypertensive patients.
Adult↗
Comparison of the angiotensin II antagonist losartan with the angiotensin converting enzyme inhibitor enalapril in patients with essential hypertension.
OBJECTIVE: To evaluate the blood pressure lowering efficacy as well as tolerability and safety of the angiotensin II antagonist losartan compared with that of the angiotensin converting enzyme inhibitor enalapril in patients with mild-to-moderate essential hypertension. DESIGN AND METHODS: The study was a multicentre, double-blind, double-dummy, randomized, parallel study. Patients (n = 407) with diastolic blood pressure > or = 95 and < or = 120 mmHg at the end of a 2-week baseline placebo period were randomly allocated to receive either 50 mg losartan once a day or 20 mg enalapril once a day for 12 weeks. Blood pressure, clinical and laboratory safety, specific symptoms including coughing determined using a symptoms questionnaire and metabolic variables were examined at baseline and at weeks 6 and 12. RESULTS: Both losartan and enalapril decreased systolic and diastolic blood pressure from baseline at weeks 6 and 12. Blood pressure changes from baseline at trough (22-26 h after the dose) did not differ between the two groups in the per-protocol analysis. Response to treatment at trough was excellent or good (diastolic blood pressure < 90 mmHg or reduction in diastolic blood pressure of 10 mmHg) in 51 and 53% of the patients in the losartan and enalapril groups, respectively. Enalapril administration increased dry coughing symptoms whereas losartan did not. The incidence of dry coughing was 1.0 and 12.2% as a spontaneously reported discomfort at week 12 and 3.0 and 15.1% as a clinical adverse experience in the losartan and enalapril groups, respectively. The difference from baseline at week 12 in the incidence of dry coughing between the two groups was 14.9% as a specific symptom in the symptoms questionnaire. Losartan reduced serum uric acid concentration, whereas effects on other metabolic parameters did not differ between the groups. CONCLUSIONS: Losartan is an effective and well-tolerated antihypertensive drug showing similar blood-pressure-lowering efficacy to that of enalapril at trough. However, in contrast to enalapril, losartan does not increase the incidence of dry coughing. Thus, the angiotensin II antagonist losartan provides a promising new approach to treatment of hypertension.
Adult↗
The Bergen Blood Pressure Study: prehypertensive changes in cardiac structure and function in offspring of hypertensive families.
Cardiac morphology and function were determined by echocardiography in normotensive offspring of 23 hypertensive and 22 normotensive families. The family histories of hypertension or normotension were based on 27 years' observation of parental blood pressure. Pulsed Doppler and M-mode echocardiography were performed in standard views. Out of the total 109 offspring, 94 participated in the present study (age (mean +/- SD) 36 +/- 7 years). Left ventricular posterior wall thickness was higher in offspring of hypertensive than normotensive families (10.1 +/- 1.7 vs. 9.3 +/- 1.5 mm; p < 0.05). Offspring of hypertensive families had lower transmitral early/late peak flow velocities (p < 0.001) and higher transmitral late peak flow velocities (p < 0.001) than offspring of normotensive families, but the differences between groups became inconsistent after adjustment for confounding variables (including left ventricular structural parameters). On the other hand, the family history of hypertension was consistently associated with increased transmitral early peak flow velocity and increased transmitral acceleration and deceleration slopes p < 0.05), a pattern suggesting increased left ventricular stiffness. Increased posterior wall thickness and diastolic functional changes may indicate cardiac hypertrophy and decreased left ventricular compliance and precede the development of hypertension in offspring of hypertensive families.
Adult↗
Unchanged central hemodynamics after six months of moderate sodium restriction with or without potassium supplement in essential hypertension.
Sodium (Na) restriction and potassium (K) supplementation has been recommended as treatment of essential hypertension but the mechanism by which these may reduce blood pressure (BP) is unknown. We examined if moderately reduced Na intake, combined with a low-Na/high-K salt alternative (Pansalt: NaCl 57%, KCl 28%, MgSO4 12%) as substitute for standard table salt, induced clinically significant BP reduction in hypertensive patients and, if this therapy reduced total peripheral resistance. After a 2-month control period 40 patients aged 21-67 years with mean casual BP 156/103 mmHg were given a salt restricted diet (120 mmol Na/24 h) for 6 months. In addition, they were randomised in a double-blind manner to receive either Pansalt (P-group) or standard NaCl (S-group) as table salt in small amounts. Cardiac output was measured by dye dilution. Daily Na excretion was similarly reduced (20%) in both groups while K excretion was slightly increased in the P-group and reduced in the S-group (difference p < 0.05). No large changes occurred in 24-h ambulatory BP (by Accutracker II) or intraarterial pressure (through a brachial artery catheter) at rest or during exercise while casual BP was reduced (p < 0.05) 13/8 mmHg in the P-group and 8/5 mmHg in the S-group. While cardiac output was slightly reduced at rest and during 50W exercise in the P-group, no significant changes were seen in total peripheral resistance in either group. Thus, moderate reduction in Na intake, with or without addition of K, is not sufficient to induce significant long-term intraarterial or 24-h ambulatory BP changes in essential hypertension. Without BP changes invasively determined central hemodynamics remains remarkably stable over a 6-month period.
Adult↗
Evaluation and quality-of-life assessment of amlodipine and enalapril in patients with hypertension.
In this multicentre, double-blind trial in 461 patients with essential hypertension, amlodipine (5-10 mg once daily) and enalapril (10-40 mg once daily) were compared in terms of quality of life, efficacy and tolerability after 1 year of treatment (part 1). In part 2, 177 patients successfully treated with amlodipine in part 1 continued in an open evaluation of efficacy and safety of antihypertensive treatment with amlodipine for a further 2 years. In part 1, both drugs were similarly effective in lowering blood pressure (BP) (although significantly more enalapril patients required a diuretic) while maintaining quality of life. Apart from class-typical effects, such as oedema for calcium antagonists and cough for angiotensin-converting enzyme inhibitors, both drugs were equally well tolerated, with few adverse effects of clinical significance. Only a few patients (eight amlodipine (4%), nine enalapril (4%)) were withdrawn from the trial because of drug-related adverse events, demonstrating that the tolerability was good. Neutral to slightly beneficial effects were found in blood lipid concentrations after treatment with amlodipine. The BP reduction seen in the amlodipine patients after part 1 was maintained during part 2. Also, blood lipids and safety variables remained virtually constant. It is concluded that, at similar BP reduction, quality of life is equally well maintained on amlodipine and enalapril therapy. Thus, amlodipine compares favourably with enalapril as an effective and well-tolerated anti-hypertensive agent over the first year. Additionally, amlodipine patients evaluated over a 2-year extension maintained good BP control and the drug was well tolerated.
Adult↗
The Bergen blood pressure study: offspring of two hypertensive parents have significantly higher blood pressures than offspring of one hypertensive and one normotensive parent.
OBJECTIVE: To study blood pressure and antihypertensive drug treatment in subjects with contrasting family histories of hypertension. SUBJECTS AND METHODS: We grouped 520 offspring examined in 1990 (mean +/- SD age 36 +/- 7 years) according to their parents' blood pressure screened in 1963-1964 as offspring of two normotensive (systolic/diastolic blood pressure < 135/70 mmHg) parents (group 1); offspring of one hypertensive (> or = 145/95 mmHg) and one normotensive (<135/70 mmHg) parent (group 2); and offspring of two hypertensive (> or = 140/90 mmHg) parents (group 3). Offspring blood pressure was measured with a conventional mercury sphygmomanometer by one observer. The mean of the last two of three seated measurements was used for analyses. Drug treatment was determined by interview. RESULTS: Mean +/- SD blood pressure was lowest in group 1 (121 +/- 12/72 +/- 10 mmHg), intermediate in group 2 (125 +/- 12/76 +/- 9 mmHg) and highest in group 3 (135 +/- 15/85 +/- 11 mmHg), P<0.01 for each. Of the subjects in groups 1, 2 and 3, 1.3, 2.4 and 11.7%, respectively, were taking antihypertensive drugs (P<0.01). CONCLUSIONS: Screening blood pressure in parents has implications for offspring blood pressure almost 30 years later. Offspring of hypertensive parents have higher blood pressure and are given antihypertensive drugs at higher rates than the offspring of normotensive parents. Also, substantial differences were seen between the offspring of one and of two hypertensive parents. Thus, risk associated with a family history of hypertension varies with the definition of the family history. To obtain maximum contrast in the predisposition to high blood pressure, comparative studies in offspring of hypertensive and normotensive families should be based on blood pressure data from both parents.
Adult↗