Search PubMed⌕ Search

Biomedical subjects

R Eggertsen

Publications and source records attributed to R Eggertsen.

At least 37 records · Page 2Linked to original sources
PubMed1991

Swedish Isradipine Study in Hypertension: evaluation of quality of life, safety, and efficacy. SWISH Group.

This was a double-blind multicenter study to compare the efficacy, tolerability and effects on the quality of life with isradipine and atenolol in the treatment of essential hypertension. Of 588 patients entering the 6-week placebo run-in period, 549 were eligible for randomization to receive either isradipine or atenolol for 8 weeks. If, at the end of this period, diastolic blood pressure (DBP) remained greater than 90 mm Hg, then both agents were given in combination for a further 10 weeks. Tolerability and quality of life were assessed repeatedly during the placebo and active-treatment phases. A subgroup of 30 patients were followed by 24-h ambulatory blood pressure monitoring, and their results are now being analyzed. In another subgroup of 26 patients, maximum exercise capacity, as determined by ergometer bicycle-testing, was measured once during placebo and twice during active treatment. At the end of the 24-week study period, both isradipine and atenolol as monotherapy had produced significant decreases in blood pressure. There were no significant differences overall between the compounds in quality-of-life and side-effect profiles, although there was a relative absence of ankle edema and headache with isradipine. Furthermore, patients receiving isradipine had no change in performance on exercise testing whereas patients on atenolol had a significant decrease (p less than 0.01).

Antihypertensive Agents↗
PubMed1989

Additive effect of isradipine in combination with captopril in hypertensive patients.

The effects of combined treatment with the calcium antagonist isradipine and the angiotensin-converting enzyme inhibitor captopril were investigated in a randomized, placebo-controlled parallel-group trial comprising 28 patients with essential hypertension. The average age was 50 years (range, 31 to 65 years). After all patients were given captopril 50 mg twice daily plus placebo for four weeks, they were randomly assigned into groups receiving in addition either placebo or isradipine 1.25 mg twice daily in increasing doses at four-week intervals. During Weeks 20 to 24, the captopril plus placebo group was given hydrochlorothiazide 12.5 mg per day. Blood pressure was measured in the morning, 12 hours after tablet intake. Supine blood pressure was reduced in the captopril plus isradipine group by -8/-6, -14/-9, -16/-8, and -11/-7 mm Hg compared with the placebo group. Changes in diastolic blood pressure were statistically significant at Week 8, whereas changes in systolic blood pressure were statistically significant at Weeks 12, 16, and 20. With the addition of hydrochlorothiazide (Weeks 20 to 24), only supine systolic blood pressure was significantly reduced. One patient was withdrawn from the trial due to a rash. The results indicate that combined treatment with a calcium antagonist and an angiotensin-converting enzyme inhibitor is effective in lowering blood pressure and that the combination is well tolerated during long-term therapy. The combination of captopril and isradipine was more effective than captopril given with a low dose of hydrochlorothiazide.

Adult↗
PubMed1988

Screening for thyroid disease in a primary care unit with a thyroid stimulating hormone assay with a low detection limit.

In a study at a primary care centre in a predominantly rural area of Sweden the records of all patients with established thyroid disease were scrutinised and 2000 consecutive adult patients screened with an immunoenzymometric thyroid stimulating hormone assay. The aims of the study were fourfold: firstly, to assess the total burden of thyroid disease in primary care centres in Sweden; secondly, to assess the efficacy of clinical diagnosis of the disease in unselected populations of patients; thirdly, to assess the efficacy of clinical evaluation of treatment with thyroxine; and, lastly, to see whether a single analysis of the serum thyroid stimulating hormone concentration by recent methods would be enough to identify an abnormality of thyroid function. Of the roughly 17,400 adults in the study community, 111 women and 10 men were being treated for thyroid disease. Screening detected 68 patients (3.5%) not receiving thyroxine who had a serum thyroid stimulating hormone concentration of 0.20 mU/l or less, all of whom were followed up clinically. Fifty of these patients were also studied biochemically during follow up. Only nine of the 68 patients had thyroid disease (three with thyrotoxicosis requiring treatment), no evidence of the disease being found in the remainder. Sixteen patients had spontaneous hypothyroidism requiring treatment, and neither these nor three patients with thyrotoxicosis had been detected at the preceding clinical examination. Of 35 patients in whom thyroid disease was suspected clinically at screening, none had laboratory evidence of thyroid dysfunction. In this series 1.3% of all women in the study community (2.6% of all 50-59 year olds) and 0.1% of the men were being treated for thyroid disease at the primary care centre, roughly 1.0% of adults subjected to screening were found to have thyroid disease requiring treatment, and most patients with a thyroid stimulating hormone concentration of 0.20 mU/l or less did not have thyroid dysfunction. It is concluded that measuring the basal serum thyroid stimulating hormone concentration by present methods is insufficient for the biochemical assessment of thyroid dysfunction in unselected populations.

Cross-Sectional Studies↗
PubMed1988

Diltiazem in hypertensive patients with type II diabetes mellitus.

Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.

Adult↗
PubMed1988

Calcium antagonists combined with beta-blockers or ACE inhibitors in the treatment of hypertension.

During the last few years, there has been a growing awareness that treated hypertensive patients are still at substantially increased risks for cardiovascular morbidity and mortality and that one conceivable explanation for this is that their blood pressure has not been lowered to strictly normotensive levels. To obtain normotensive blood pressures, it may be necessary to skillfully combine antihypertensive drugs much more frequently than has been common so far. In this context, calcium antagonists in combination with beta-blockers are of special interest, since several controlled studies have shown that a combination between a beta-blocker and nifedipine, nitrendipine, isradipine, or felodipine have been remarkably potent as regards their antihypertensive effect. In controlled trials, such combinations have also been shown to be more effective and better tolerated than a combination between a beta-blocker and hydralazine. Marked efficacy has also been noted when a calcium antagonist has been combined with an angiotensin converting enzyme (ACE) inhibitor. So far, most studies have dealt with small numbers of patients and study design has not always been optimal. Results from controlled studies will presumably be ready for presentation in the near future. It can be concluded that combination therapy between calcium antagonists and beta-blockers or ACE inhibitors appear to be markedly effective and well tolerated. This would offer the possibility of reducing elevated arterial pressure to normotensive levels in many hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1987

Hemodynamic effects of loud noise before and after central sympathetic nervous stimulation.

The hemodynamic effects of loud noise after central alpha 2-adrenoceptor stimulation were studied in 13 patients with mild (WHO 1) essential hypertension. The patients were randomized (double-blind) to treatment with either placebo or guanfacine 1-2 mg for four weeks and then crossed over and treated for another four weeks. All patients were exposed to a loud broad-band noise (105 dBA for 30 min) and all were studied both on placebo and guanfacine. Guanfacine significantly reduced the resting blood pressure from 141/92 to 134/88 mmHg (p less than 0.01) as well as heart rate at rest from 63 to 58 beats/min (p less than 0.05). Noise stimulation caused a significant increase in blood pressure and resistance in the placebo-treated group, while cardiac output decreased significantly. Pretreatment for one month with the central alpha 2-adrenoceptor stimulating agent guanfacine did not block the noise-induced pressor response nor the increase in peripheral resistance. A significant decrease in stroke volume was observed and cardiac output also tended to decrease in this group. It could be concluded that loud noise is a potent pressor stimulus which causes vasoconstriction and that the blood pressure response during noise could not be blocked by the centrally acting antihypertensive agent guanfacine. Since noise causes vasoconstriction it also induces an increased tone in the small arteries and, if the noise stimulus is sufficiently strong and repeated for a long time, it might cause structural changes in the resistance vessels and permanent arterial hypertension in humans.

Adrenergic alpha-Agonists↗
PubMed1987

Influence on blood pressure of oestrogen substitution therapy in the menopause.

In a Swedish health centre an analysis was made of the effect on blood pressure of oestrogen substitution therapy in 33 normotensive women in the menopause. Comparisons were made with a control group of 33 normotensive women of the same ages but left without oestrogen therapy. Following three years of therapy with oestrogen alone or in combination with progesterone, there were no significant changes in blood pressure. This was true also when a subgroup consisting of 11 women treated with equinous oestrogens was analysed separately. These results could therefore indicate that chronic treatment with oestrogens in postmenopausal women probably has small effect on the general blood pressure level and that the risk of inducing arterial hypertension must be low.

Aged↗
PubMed1987

Acute and long-term hemodynamic effects of carvedilol, a combined beta-adrenoceptor blocking and precapillary vasodilating agent, in hypertensive patients.

The purpose of these studies was to investigate the hemodynamic effects of carvedilol, a compound with combined properties of nonselective beta-adrenoceptor blockade and precapillary vasodilatation. The acute effects were studied with invasive technique (dye dilution) in 10 patients taking 25 mg orally and noninvasively (forearm plethysmography) in 10 patients taking 25 mg and in 10 patients taking 50 mg orally, all with essential hypertension. Significant reductions of systolic and diastolic blood pressure (p less than 0.05-0.001) were observed in all groups. Total peripheral resistance (TPR) did not change acutely whereas resistance in the forearm was reduced by 16% (p less than 0.05; invasive group). When a comparison with propranolol (80 mg x 2) was made in a randomized double-blind placebo controlled trial in 30 patients, carvedilol acutely reduced blood pressure significantly by 13/6 mg Hg (25 mg) and 17/10 mm Hg (50 mg) in contrast to propranolol. Resistance in the forearm fell significantly with 50 mg carvedilol, whereas propranolol caused a significant rise. After 4 weeks, both compounds had reduced blood pressure significantly. Blood flow was still reduced with propranolol in contrast to the findings with carvedilol. In conclusion, the summary of these studies shows that carvedilol given orally has a useful antihypertensive effect both acutely and during prolonged treatment, and it has an attractive hemodynamic profile, in agreement with the hemodynamic findings in essential hypertension.

Adrenergic beta-Antagonists↗
PubMed1987

Addition of the calcium antagonist PN 200-110 to pindolol markedly augments the antihypertensive effect in essential hypertension.

Several large-scale studies have recently drawn attention to the fact that arterial hypertension frequently is inadequately controlled and that therapeutic alternatives other than the commonly employed stepped-care treatment may be needed in order to obtain normotension. For this reason PN 200-110, a new dihydropyridine calcium antagonist--at two different dose levels (average 3.8 mg b.i.d. or 5.7 mg b.i.d.)--or placebo was added in a double-blind cross-over trial to pindolol, 10 mg per day, in 20 patients with essential hypertension, after an initial 3-week placebo period. Ionized calcium in serum was determined repeatedly during the study. From an initial level of 157/100 mm Hg, PN 200-110 at the first dose level reduced blood pressure by 14/11 mm Hg (p less than 0.01/0.001) and at the second dose level reduced blood pressure by 22/18 mm Hg (p less than 0.001/0.001). The reduction in mean arterial pressure was significantly correlated to age (=0.050, p less than 0.05). There was no significant increase in heart rate, nor were there any significant correlations between ionized calcium and the effect of PN 200-110 nor between the changes in ionized calcium and the changes in blood pressure. Adverse effects were few and mild. One patient had to be withdrawn because of side effects, probably not related to the investigated drugs. Thus, addition of PN 200-110 to hypertensive patients treated with pindolol caused highly significant and clinically relevant further reductions in arterial pressure. The results show that a combination of this kind offers the possibility of good blood pressure control.

Adult↗
PubMed1987

The long-term effect of isradipine in pindolol-treated patients.

The long-term efficacy of isradipine, a new dihydropyridine calcium antagonist with marked vascular selectivity, was evaluated in 17 patients with essential hypertension. All had a supine diastolic blood pressure of greater than 95 mmHg with 10 mg pindolol once daily. After a short-term, double-blind, dose-finding, crossover comparison with addition of isradipine or placebo twice daily, they continued on pindolol and their optimal dose of isradipine in a single-blind, long-term follow-up study. Eighteen patients were recruited but one male patient discontinued treatment after 2 weeks due to ankle oedema and will not be accounted for in the overall evaluation. There were 11 males and six females with a mean age of 56 +/- 10 years. In the short-term study on the optimal dose of isradipine (5.1 mg twice daily) blood pressure was lowered by 24/18 mmHg (P less than 0.001). No change in heart rate was seen despite the substantial drop in blood pressure. In the long-term study the patients were seen for a mean follow-up time of 12.5 months (range 4-17 months). After the longest follow-up time mean arterial pressure was 107.0 +/- 7.4 compared with 120.1 +/- 8.2 mmHg after placebo baseline [delta = 13 mmHg (11%), P less than 0.001, n = 17]. The heart rate was unchanged (delta = 0.2 beats/min, 95% confidence limits -3, +3), and so was ankle circumference (delta = 0.12 cm, 95% confidence interval, -1, +1). On the other hand, mean weight was reduced by 2 kg from 90 kg (P less than 0.05, n = 17).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Hemodynamic effects of combined beta-adrenoceptor blockade and precapillary vasodilatation in hypertension.

Carvedilol (BM14190) is a new compound with combined properties of nonselective beta-adrenoceptor blockade, devoid of ISA, and precapillary vasodilatation. Its acute hemodynamic effects were studied with invasive technique (dye-dilution using Cardio-Green) in 10 patients taking 25 mg orally and noninvasive (fore-arm plethysmography) in 10 patients taking 25 mg and in 10 patients taking 50 mg orally, all with essential hypertension. Significant reductions of systolic and diastolic blood pressures (p less than 0.05 - 0.001) were observed in all groups. TPR did not change acutely whereas resistance in the fore-arm was reduced by 16% (p less than 0.05). When a comparison with propranolol (80 mgx2) was made in a randomized, double-blind placebo controlled trial comprising 30 patients with essential hypertension, carvedilol acutely reduced blood pressure significantly 13/6 mm Hg (25 mg) and 17/10 mm Hg (50 mg) in contrast to propranolol. Resistance in the fore-arm (plethysmography) fell significantly with carvedilol 50 mg whereas propranolol caused a significant rise. After 4 weeks both compounds had reduced blood pressure significantly and to the same extent. Blood flow was still reduced with propranolol in contrast to the findings with carvedilol. We conclude that carvedilol given orally has a useful antihypertensive effect both acutely and during prolonged treatment. It has an attractive hemodynamic profile.

Adrenergic beta-Antagonists↗
PubMed1985

Potentiation of the antihypertensive effect of enalapril by randomized addition of different doses of hydrochlorothiazide.

The purpose of this study was to evaluate the potentiating effect of hydrochlorothiazide (HCTZ) 12.5 or 25 mg once daily when added in a placebo-controlled double-blind randomized study of patients with essential hypertension, whose diastolic blood pressure (DBP) was not adequately controlled (DBP > 90 mmHg) following 6 weeks of single-blind treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril, 20 mg once daily. Forty-eight patients started the first period with enalapril after 4 weeks on placebo. In 13 patients DBP fell to < or = 90 mmHg after enalapril for 6 weeks. In this group supine mean arterial pressure (MAP) was reduced by 13% (P < 0.01). In the patients whose DBP was > 90 mmHg after 6 weeks on enalapril (n = 32) the average supine MAP fell by 9% (P < 0.001). After 3 weeks there was no further drop in blood pressure (BP). Addition of HCTZ to the 32 patients with DBP > 90 mmHg caused a significant further drop in supine BP by 13/7 mmHg with 12.5 mg and by 15/7 mmHg with 25 mg. Seven patients discontinued the study, none due to side effects on enalapril alone. Well-being, assessed with a special questionnaire, was significantly better with enalapril as monotherapy compared with previous treatment, but not different from well-being during the placebo periods. It is concluded that 20 mg enalapril once daily lowered BP effectively and was well tolerated. The maximum BP lowering effect was seen within 3 weeks. Addition of HCTZ caused a significant, and clinically relevant, further drop in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Vasodilators in hypertension--a review with special emphasis on the combined use of vasodilators and beta-adrenoceptor blockers.

This paper presents a review of studies dealing with combined beta-adrenoceptor blockade and vasodilatation in the treatment of hypertension. This therapy can be achieved either through the combined use of conventional beta-adrenoceptor blocking compounds given together with vasodilator drugs or with agents which show multiple action of this kind. From a hemodynamic point of view this therapeutic approach is quite logical since most forms of established hypertension are characterized by increased vascular resistance. It can therefore be concluded that combined beta-adrenoceptor blockade and vasodilation offers a rational and useful treatment of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1984

Haemodynamic effects of loud noise in hypertensive patients treated with combined beta-adrenoceptor blockade and precapillary vasodilatation.

The effects of acute exposure to noise on central and regional (calf and forearm) haemodynamics were studied during placebo therapy and during combined nonselective beta-adrenoceptor blockade and precapillary vasodilatation in 9 patients with essential hypertension. On placebo therapy a loud noise (105 dBA for 10 min) caused a significant increase in diastolic and mean arterial pressure due to vasoconstriction. There was also a significant increase of vascular resistance in the calf. After combined precapillary vasodilatation and non-selective beta-adrenoceptor blockade, the increase in blood pressure during stimulation with noise was not prevented. Thus, systolic as well as diastolic and mean arterial pressures increased significantly. This indicates a temporary resetting of the baroreceptors, allowing a higher level of blood pressure during stimulation with noise. Such a resetting would involve the central nervous system pathways of the baroreflex and this would explain why the peripherally active therapeutic principle--precapillary vasodilatation and beta-adrenoceptor blockade--was unable to inhibit the blood pressure response induced by noise.

Adult↗
PubMed1984

Haemodynamic effects of carvedilol, a new beta-adrenoceptor blocker and precapillary vasodilator in essential hypertension.

Carvedilol (BM 14190) is a new antihypertensive compound which combines beta-adrenoceptor blocking and precapillary vasodilating properties but is devoid of intrinsic sympathomimetic activity. The acute and long-term effects on blood pressure and regional haemodynamics (forearm plethysmography) were studied with carvedilol 25 mg b.i.d. or 50 mg b.i.d. Comparisons were made with propranolol 80 mg b.i.d. in a randomized double-blind placebo controlled trial comprised of 30 patients with essential hypertension. After a four-week placebo period active therapy was given for four weeks. Carvedilol administered acutely reduced blood pressure at both doses, delta 13/6 mmHg (P less than 0.001/P less than 0.01) and 17/10 mmHg (P less than 0.001/P less than 0.01). Resistance in the forearm fell significantly with the higher dose. This was in contrast to propranolol which only reduced heart rate acutely, and as expected caused a rise in forearm resistance. After four weeks both compounds had reduced blood pressure significantly and to the same extent. Blood flow was still significantly reduced with propranolol in contrast to the findings with carvedilol. We conclude that carvedilol given orally has a useful antihypertensive effect both acutely and during prolonged treatment. It is well tolerated and its haemodynamic profile is attractive.

Adrenergic beta-Antagonists↗
PubMed1984

Acute haemodynamic effects of carvedilol (BM 14190), a new combined beta-adrenoceptor blocker and precapillary vasodilating agent, in hypertensive patients.

Carvedilol (BM 14190) is a new compound with combined nonselective beta-adrenoceptor blocking activity, devoid of ISA, and a precapillary vasodilating effect. Its acute haemodynamic effects were studied by invasive techniques in 10 patients given 25 mg carvedilol and noninvasively in 10 patients given 25 mg and in 10 given 50 mg orally. All had essential hypertension. In the invasive study intraarterial blood pressure was measured and cardiac output was determined by the dye-dilution method using Cardio-Green as the indicator. Peripheral haemodynamics in all 30 patients were studied in the forearm using strain gauge plethysmography. Measurements were made at rest before and repeatedly for 90 minutes after oral administration of one capsule of 25 mg or 50 mg carvedilol. Significant reductions in the systolic and diastolic blood pressures (p less than 0.05-0.001) were observed in all groups. Cardiac output showed a small, non-significant decrease from 5.81/min to 5.1 l/min. Total peripheral resistance did not change, whereas resistance in the forearm fell by 16% (p less than 0.05). These findings are different from what would have been expected acutely after administration of a pure beta-adrenoceptor blocking agent. They indicate that carvedilol possesses vasodilating activity in addition to its beta-adrenoceptor blocking effect.

Adrenergic beta-Antagonists↗