PubMed Health⌕ Search

Biomedical subjects

P Lund-Johansen

Publications and source records attributed to P Lund-Johansen.

At least 19 recordsLinked to original sources
PubMed1995

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↗
PubMed1994

The Bergen Blood Pressure Study: inappropriately low levels of circulating atrial natriuretic peptide in offspring of hypertensive families.

Plasma atrial natriuretic peptide (ANP), plasma and 24-h urine catecholamines, plasma renin activity (PRA), and serum aldosterone were studied in offspring of hypertensive and normotensive families [n = 82; age 37 +/- 7 years (mean +/- SD)]. Despite higher age, higher blood pressure, and higher urine excretion of catecholamines--all of which are factors associated with increased ANP levels--the mean basal plasma ANP concentration tended to be lower in offspring of hypertensive than normotensive families. The same pattern was found in all age-tertiles, and the between-group difference was statistically significant in subjects aged 34-39 years (p < 0.01). Also, the family history of hypertension was associated with low ANP levels after covariate adjustment (p < 0.05). The 24-h urine excretion of epinephrine and norepinephrine tended to be higher in offspring of hypertensive than normotensive families while the morning venous plasma levels were similar. The ratio between venous plasma ANP and norepinephrine was lower in offspring of hypertensive than normotensive families (p < 0.05). PRA, serum aldosterone level, and 24-h urine excretion of dopamine did not differ significantly between groups. Inappropriately low basal plasma ANP concentrations and low plasma ANP/norepinephrine ratios may be related to the development of essential hypertension in offspring of hypertensive families.

Adult↗
PubMed1993

Cardiac effects of ACE inhibition.

Hypertension frequently is associated with a number of changes in heart structure and function, such as left ventricular hypertrophy, disturbed diastolic function, and subnormal stroke volume during exercise. Most of these changes probably are related to myocardial fibrosis. Antihypertensive agents reverse the structural and functional changes to different degrees. The hemodynamic changes in central hemodynamics at rest and during exercise were studied before and after angiotensin-converting enzyme (ACE) inhibition in 68 patients with essential hypertension (ranging from severe to moderately severe). In patients with moderately severe hypertension who were administered perindoprilat intravenously, mean arterial pressure was reduced by approximately 17% due to reduction in total peripheral resistance and no changes in heart pump function. Chronic treatment with captopril, enalapril, or lisinopril for 6-12 months induced reduction in blood pressure associated with decreased peripheral resistance. In general, there were only minor changes in cardiac output, stroke volume, and heart rate. Studies from other laboratories have shown that ACE inhibitors reverse left ventricular hypertrophy and improve left ventricular diastolic function. Captopril also appears to improve coronary circulation. The effect of ACE inhibitors on heart structure and function appears promising with regard to cardioprotection during chronic use, but long-term studies are needed to prove that this will occur in clinical practice.

Adult↗
PubMed1992

[Treatment of hypertension in Norway. Indications, therapeutic intensity and economic aspects].

The Norwegian Society of Hypertension held its third scientific meeting in February 1991. One of the issues discussed was when to initiate drug treatment of uncomplicated essential hypertension and what level of blood pressure should be the goal of treatment. The American guidelines suggest that a blood pressure of 140/90 mm Hg or higher should be treated pharmacologically, whereas WHO suggests 160/95 mm Hg. The consensus at the meeting was that, in otherwise healthy subjects without end organ damage, a diastolic blood pressure of 100 mm Hg or more over three to six months should be treated with drugs, and that a safe goal would be around 135-140/85-90 mm Hg.

Drug Costs↗
PubMed1992

Treatment of hypertension in the elderly--what have we learned from the recent trials?

Treatment of hypertension in the elderly has so far mainly been based on clinical judgment and very few large controlled trials. During the last year several large new trials have been published, the so-called STOP-Hypertension, SHEP, and MRC trials. All have shown that drug treatment of hypertension in the elderly (65-85 years) with permanent diastolic hypertension or isolated systolic hypertension reduces stroke incidence. Most patients have needed combined drug treatment with diuretics and beta-blockers. When thiazide diuretics are used, serum potassium should be followed very closely and most likely amiloride should be added to the thiazide therapy, since this was done both in the STOP and the MRC trials. Since many elderly patients with hypertension suffer from other diseases that might represent contraindications to thiazide diuretics or beta-blockers, the choice of drug must be made after careful clinical evaluation. With the newer classes of antihypertensive agents (calcium antagonists, ACE inhibitors and alpha-blockers) side effects are probably seen less often, but long-term data on morbidity and mortality are still lacking.

Aged↗
PubMed1992

Long-term hemodynamic effects of antihypertensive treatment.

The cardinal hemodynamic disorder in established essential hypertension is increased total peripheral resistance. During exercise, the increase in stroke volume of the heart is abnormal. A 20-year follow-up study of the hemodynamics in essential hypertension demonstrated a progressive increase in total peripheral resistance and deterioration of the heart pump function. Long-term treatment with antihypertensive agents modifies the circulatory system in different ways. Vasodilators (angiotensin converting enzyme inhibitors, alpha 1-blockers, and calcium antagonists) all reduce total peripheral resistance, and in general, cardiac output, heart rate, and stroke volume remain unchanged. Calcium antagonists like verapamil and diltiazem reduce the heart rate approximately 10% during exercise, but since stroke volume increases, cardiac output is unchanged. Chronic treatment with conventional beta-blockers induces a permanent reduction in cardiac output and heart rate during exercise. In contrast, carvedilol--a beta 1,beta 2-blocker with alpha 1-blocking activity--prevents the immediate increase in total peripheral resistance during acute beta-blockade. In 19 patients followed by hemodynamic measurements over 6-9 months, blood pressure was well controlled by carvedilol. During exercise, total peripheral resistance decreased 6% (P less than 0.05), and the reductions in heart rate and cardiac index were less than on conventional beta-blockade. Echo-Doppler studies showed a significant reduction in the intraventricular septum of 13%.

Adrenergic beta-Antagonists↗
PubMed1992

Chronic haemodynamic effects of carvedilol in essential hypertension at rest and during exercise.

Nineteen men (mean age 44 years) with essential hypertension, WHO stage I, were studied invasively at rest and during exercise. Blood pressure was recorded intra-arterially (brachial artery), cardiac output by dye dilution method and heart rate by electrocardiography. After initial pre-drug recordings, the patients received 25 mg carvedilol orally and central haemodynamics at rest and during exercise were recorded 1 and 2 h after tablet intake to evaluate the immediate effects of carvedilol. The results indicated a combined beta-blocking and vasodilating effect. After 6-9 months of treatment, supine haemodynamics were recorded 12-24 h after the last dose and then 1 and 2 h after an additional 25 mg dose. During chronic treatment (2 h after last dose at rest supine) mean arterial pressure was reduced by 17% (P less than 0.001) and total peripheral resistance index by 6% (NS) while heart rate and cardiac index were reduced by 12%. Exercise haemodynamics demonstrated a fall in blood pressure of 17% (P less than 0.001). Exercise stroke index increased by 5% (NS), partly compensating for the reduction in heart rate of 17%. Total peripheral resistance index was reduced by 5% (NS). It is concluded that carvedilol is an effective anti-hypertensive agent in a large proportion of patients with essential hypertension. The haemodynamic mode of action reflects an alpha 1-blocking activity, particularly in situations with low sympathetic tone. During exercise the beta 1-blocking activity (demonstrated by the reduction in heart rate) is more prominent.

Administration, Oral↗
PubMed1992

Effects of carvedilol on atrial natriuretic peptide, catecholamines, and hemodynamics in hypertension at rest and during exercise.

Possible counterregulatory neurohumoral and hemodynamic responses to carvedilol (a new vasodilating nonselective beta-receptor blocker) were studied in 19 men with essential hypertension (age range, 34-59 years; mean age, 44 years). Intra-arterial pressure, cardiac output (Cardio-green), heart rate, and the vasoactive peptides norepinephrine, epinephrine, and atrial natriuretic peptide (ANP) were measured at rest supine and sitting and during 100-W bicycle exercise before and 2 h after administration of 25 mg carvedilol. The same protocol was followed after 9 months of chronic carvedilol treatment (mean dose, 52 mg/day). Carvedilol induced both acute and chronic reductions (at rest supine, 11%) in mean arterial pressure, due in part to reduction in cardiac output (5%) and in part to reduction in total peripheral resistance (5%). At rest supine, carvedilol induced a reduction in ANP (27%) that could be viewed as a counterregulatory response to decrease in cardiac output, preventing excessive blood pressure reduction. ANP decreased (18%) when the patient sat up from the supine position and increased (67%) during exercise, but no further change was seen after acute or chronic carvedilol treatment. With the patient in the sitting position, norepinephrine was 110% higher than at rest supine; during 100-W exercise, norepinephrine increased 368%. A further increase (38-86% in the three situations, respectively) was seen after the first dose of carvedilol. Epinephrine showed similar but less marked changes. Neither extracellular fluid volume nor plasma volume (isotope dilution techniques) changed significantly during the study, but the acute blood pressure response to carvedilol was directly related to changes in extracellular fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1992

Long-term haemodynamic effects of amlodipine at rest and during exercise in essential hypertension.

Haemodynamic responses at rest and during exercise were studied in 18 patients with essential hypertension following long-term treatment with amlodipine. Patients underwent a 2-week placebo run-in period followed by a mean duration of 11 months' treatment with amlodipine 5-10 mg (mean dose 9 mg) once daily. Blood pressure was measured intra-arterially, cardiac output by dye dilution and heart rate by electrocardiogram. Amlodipine produced a mean reduction in systolic and diastolic arterial pressure of 27 and 16 mm Hg, respectively, at rest and after exercise. At rest sitting, mean systolic and diastolic arterial pressures were reduced by 16 and 14% (p less than 0.01), respectively, from initial mean values of 182.4/111.2 mm Hg. This reduction in blood pressure was associated with a marked reduction in the total peripheral resistance index of 19% (p less than 0.001). Similar responses were observed at rest supine and during exercise. No significant changes were seen in heart rate. Stroke index showed a small increase at rest and during exercise together with a trend towards an increase in cardiac index after treatment with amlodipine. Ambulatory blood pressure monitoring was carried out in 10 patients after the placebo run-in and at the end of the study. Amlodipine showed effective blood pressure control throughout the 24 h after one daily dose. The incidence of side effects was low (ankle oedema in 2 patients).

Adult↗
PubMed1992

The Bergen Blood Pressure Study: definition of hypertensive and normotensive families based on 27 years' follow-up.

The familial aggregation of hypertension is well documented. However, many studies on the familial predisposition have suffered from insufficient knowledge of parental blood pressure (BP). In the present study, the family history is defined according to parental data from two BP surveys conducted almost 30 years apart. Data from a population screening in Bergen in 1963-64 were linked with information on marital status to define couples with or without a history of hypertension. Within the screened population a total of 344 married couples, 688 individuals, matched defined age and BP criteria. Four hundred and thirty individuals, representing 270 of the 344 families initial included (79%), attended a follow-up examination in 1990. Six hundred and ninety-one offspring were registered. In all families represented at follow-up, parental BP data from the 1963-64 screening were available. In 160 families (noffspring = 393), both parents also attended the follow-up examination in 1990. In 23 families (noffspring = 54) both parents were hypertensive in 1963-64 as well as in 1990. In 22 families (noffspring = 55) both parents were normotensive at both examinations. Thus, a family data base which is assumed to be useful for studies on offspring with or without a family history of hypertension, has been established. The offspring studies include BP, 24-h ambulatory BP, electrocardiography, echocardiography, endocrine parameters, electrolytes and anthropometric variables.

Adult↗
PubMed1992

Hemodynamics of elevated blood pressure.

In young hypertensives (less than 30 years) there are signs of increased sympathetic drive with higher than normal heart rates and cardiac output. Over the years, established hypertension is associated with an elevated total peripheral resistance, an abnormally low cardiac output (particularly during exercise), and reduced coronary reserve.

Adolescent↗
PubMed1992

Hemodynamic profiles of antihypertensive agents.

Alpha-blockers tend to normalize central hemodynamics and only modestly reduce the systolic blood pressure-heart rate (SBP x HR) product. Similarly, dihydropyridine calcium antagonists normalize central hemodynamics, but at the expense of an increased heart rate (which tends to normalize chronic treatment). Non-dihydropyridine calcium antagonists tend to reduce resting heart rate. Angiotensin converting enzyme (ACE) inhibitors normalize central hemodynamics with no change in heart rate. Classic beta-blockers, particularly the non-selective agents, lower heart rate and cardiac output at rest and during exercise, with a reflex increase in total peripheral resistance (TPR), which lessens with chronic therapy. With dual-acting beta-blockers like carvedilol, the fall in blood pressure is accompanied by a fall in TPR and only a modest drop in cardiac output; the increase in AVO2 difference is less marked with carvedilol compared to a classic beta-blocker, suggesting that the body's reserve mechanisms may be less reduced.

Antihypertensive Agents↗
PubMed1992

The influence of vasodilating beta-blockers on cardiac function and vascular resistance in essential hypertension.

In nearly all forms of established hypertension, the cardinal hemodynamic disturbance is an increased total peripheral resistance, while cardiac output is abnormally low, particularly during exercise. When left untreated, total peripheral resistance increases, cardiac output falls, and blood pressure increases over time. The coronary reserve is reduced, and renal as well as cerebral resistance increases and blood flow falls. Antihypertensive agents effect central hemodynamics differently. Ordinary beta-blockers do usually not reduce total peripheral resistance much below pretreatment level, and cardiac output is chronically depressed, particularly during exercise. However, the beta-blockers greatly reduce the workload on the heart by decreasing the heart rate-pressure product. Modern beta-blockers with vasodilating activity--like carvedilol--are based on a combination of beta-blockade and vasodilatation. Such beta-blockers also induce a marked decrease in the pressure-heart rate product, and some reduction in total peripheral resistance. They cause less depression of exercise cardiac output than ordinary beta-blockers. Blood flow to the kidneys and the brain is maintained. From a theoretical point of view, this type of antihypertensive treatment should maintain good blood pressure control, reduce cardiac workload and be associated with less side-effects than ordinary beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1992

Carvedilol in hypertension: effects on hemodynamics and 24-hour blood pressure.

Nineteen men (mean age, 44 years) with moderately severe essential hypertension were studied invasively at rest and during exercise. After initial predrug recordings, patients received 25 mg carvedilol orally, and central hemodynamics at rest and during exercise were recorded 1 and 2 h after tablet intake to evaluate the immediate effects of carvedilol. Blood pressure decreased by 11% within 1 h, and the hemodynamic results indicated a combination beta-blocking and vasodilating effect. After 6-9 months of treatment (dose, 25-100 mg), supine hemodynamics were recorded, first 12-24 h after the last dose and then 1 and 2 h after an additional 25-mg dose. During chronic treatment (2 h after the last dose with the patient at rest and in the supine position), mean arterial pressure was reduced by 17% (p less than 0.001) and total peripheral resistance index was reduced by 6% (NS), whereas heart rate and cardiac index were reduced by 12%. Exercise hemodynamics demonstrated a decrease in blood pressure of 17% (p less than 0.001). Exercise stroke index increased by 5% (NS), in part compensating for the reduction in heart rate of 17%. Total peripheral resistance index was reduced by 5% (NS). Twenty-four-hour blood pressure monitoring (Accutracker II) demonstrated significant blood pressure reductions in awake as well as in asleep patients. Blood pressures decreased from 163/102 to 141/84 mm Hg in from 135/78 to 122/68 mm Hg in awake and asleep patients; respectively. Carvedilol is an effective antihypertensive agent, and the hemodynamic mode of action reflects alpha 1- and beta 1-blocking activities.

Administration, Oral↗
PubMed1991

Long-term haemodynamic effects of sustained-release trimazosin at rest and during exercise in essential hypertension.

The long-term haemodynamic effect of sustained-release trimazosin (mean daily dose 418 mg) at rest and during exercise has been examined in 14 male patients (age 30-61 y) with previously untreated mild or moderate essential hypertension. Cardiac output (dye dilution), heart rate and intra-arterial blood pressure were measured supine and sitting at rest, and during bicycle exercise. After 11 months of trimazosin treatment the mean casual blood pressure was reduced from 165/106 mmHg to 147/92 mmHg. The intra-arterial systolic and diastolic pressure was reduced by 3-7% at rest and during 50, 100 and 150 W exercise. Total peripheral resistance was reduced by 8-14% and cardiac output was slightly higher (2-8%) in all situations. Stroke volume and heart rate remained unchanged, as did body fluid volumes (isotope dilution) and body weight. Side effects were minor and transient. Thus, the haemodynamic responses to trimazosin are similar to but weaker than those of other alpha 1-adrenoceptor blockers. The efficacy of the sustained-release formulation of trimazosin was low and daily doses above 600 mg are likely to be needed by many patients.

Adult↗