Biomedical subjects

H Wedel

Publications and source records attributed to H Wedel.

At least 109 records · Page 6Linked to original sources

PubMed1985

Predictors of cardiovascular morbidity in treated hypertension: results from the primary preventive trial in Göteborg, Sweden.

Prognostic factors for cardiovascular disease (CVD) were studied in treated, middle-aged male hypertensives, derived from a random population sample and followed for more than 10 years. In multivariate analysis diastolic blood pressure, smoking, serum cholesterol, proteinuria, angina pectoris and previous stroke were found to be independent predictors of CVD morbidity (non-fatal myocardial infarction (MI), non-fatal stroke, or CVD death). Multivariate analyses for coronary heart disease (CHD), stroke and CVD mortality were also performed and the results are given. Life-table analyses showed a three times higher CVD incidence among smokers than amongst non-smokers and a doubled incidence for subjects with a serum cholesterol in the highest quartile, i.e. above 7.3 mmol/l, compared with those with levels below, and a three times higher incidence for subjects with proteinuria than those without. Non-smokers with a serum cholesterol below 7.3 mmol/l and free of any hypertensive organ manifestation at entry did not differ significantly in CVD morbidity from a normotensive comparison group that was derived from the same population sample. These findings in a well-defined population sample show that in spite of treatment for hypertension the CVD risk is still substantial if organ damage or other risk factors are present. These findings underline the importance of multiple risk intervention.

Angina Pectoris↗

PubMed1985

Tolerability to treatment with metoprolol in acute myocardial infarction in relation to age.

A double-blind trial with the beta 1-selective blocker metoprolol in suspected acute myocardial infarction and during 3 months' follow-up included 1395 patients, aged 40-74 years, 698 on metoprolol and 697 on placebo. In order to further evaluate the tolerability to beta-blockade in the elderly, the total series was divided into 2 groups according to median age (61 years) and into quartiles, the lowest quartile (40-57 years) being compared with the highest (67-74 years). The decrease in heart rate and systolic blood pressure after intravenous metoprolol in the acute phase was similar in the elderly and the younger patients. Hypotension was observed more often in the metoprolol-treated than in the placebo-treated younger patients, while no difference was observed in the elderly. Bradycardia was observed more often in the metoprolol group in both age groups, while there was no difference regarding the incidence of congestive heart failure in either the younger or in the elderly patients. The effect on mortality, serious ventricular arrhythmias and chest pain seemed to be similar in different age groups. From the present series we conclude that hemodynamic reactions and tolerability to beta-blockade can be expected to be similar in elderly and younger patients.

Adult↗

PubMed1984

Göteborg Metoprolol Trial: design, patient characteristics and conduct.

The Göteborg Metoprolol Trial was a double-blind, placebo-controlled, stratified trial aimed at evaluating the effect of the beta 1-selective blocker, metoprolol, in suspected acute myocardial infarction and during 2 years of follow-up. The primary end-point was 3-month mortality (blind treatment period). Secondary end-points were 2-year mortality, indirect signs of infarct size, chest pain, arrhythmias and tolerability. The entry criteria were fulfilled in 2,802 patients, 1,395 of whom were included in the trial. Treatment started as soon as possible after arrival in hospital with intravenous administration followed by oral treatment for 3 months. All patients were randomized 48 hours or less after estimated onset of infarction and 69% were randomized at 12 hours or less. The blind treatment had to be withdrawn in 19% of all randomized patients before the end of the 3-month follow-up.

Aged↗

PubMed1984

Göteborg Metoprolol Trial: clinical observations.

Heart rate, systolic blood pressure and rate-pressure product were analyzed during the first 18 hours and 4 days after intravenous metoprolol or placebo. On injection of metoprolol there was an immediate decrease in mean heart rate from 72.9 +/- 0.6 to 62.7 +/- 0.4 beats/min, but no change was found in the placebo group. The difference in heart rate remained during the first 4 days. Systolic blood pressure was reduced from 144.1 +/- 0.9 to 134.6 +/- 0.9 mm Hg after intravenous metoprolol and was lower than that in the placebo group during 4 days of follow-up. Indirect signs of congestive heart failure tended to be less severe in patients given metoprolol within 12 hours of the onset of symptoms than in those given placebo. The duration of hospitalization also tended to be shorter in patients given early metoprolol treatment than in those given placebo early.

Blood Pressure↗

PubMed1984

Göteborg Metoprolol Trial: tolerance.

During a 3-month follow-up, 131 patients (19.1%) withdrew from blind treatment in both metoprolol- and placebo-treated groups. More metoprolol-treated than placebo-treated patients withdrew because of cardiovascular adverse experience mainly during the very early phase. In all, 45 (6.5%) metoprolol-treated vs 14 (2.0%) placebo-treated patients were not given either a full intravenous dose or a full oral dose 15 minutes later. Bradycardia and hypotension were more common in the metoprolol group, whereas severe atrioventricular block did occur in a similar number of patients in both groups and severe congestive heart failure was more common in the placebo group. Results indicate that tolerance is generally good after intravenous and oral treatment with metoprolol in patients with suspected acute myocardial infarction.

Administration, Oral↗

PubMed1984

Prognostic importance of cholesterol levels after myocardial infarction.

The aim of this study was to analyze the relationship between serum cholesterol level and all causes mortality in men who sustained a first myocardial infarction. The cholesterol distribution 3 months after the infarction was established. Ten annual cohorts (n = 1,204) were followed for a maximum period of 11 years. Secondary risk factors were comparable among the groups of the serum cholesterol distribution quintiles according to a multiple logistic prognostic function based on left heart failure, atrial fibrillation, breathlessness on infarction, maximum S-ASAT, relative heart size, and a history of hypertension. When all ages were analyzed together, the total mortality was higher in the upper cholesterol quintiles (P = 0.02). This association was confirmed when analyzed with Coxian adjustments for age, change in smoking habits after infarction, and the previously mentioned prognostic function. When broken down by age (less than or equal to 49, 50-59, greater than or equal to 60) and period of follow-up (3-24 and 25-84 months), the association between mortality and cholesterol quintiles was confined to patients under 50 years during the late follow-up period (P = 0.01), whereas there was no association for the other age groups.

Adult↗

PubMed1984

Myocardial infarction among women in Göteborg, Sweden: a community study of mortality and incidence, 1968-1977.

Studies were made of all female cases below 65 years of age with acute myocardial infarction in Göteborg. Incidence and mortality rates were calculated. During the 10-year period 1968-1977, 1048 women were registered. More than half of the 491 fatal cases occurred outside hospital. In general, the incidence of myocardial infarction was unchanged during the study period except for women 50-54 years of age. In this group the incidence increased. There were no time trends as to case fatality and the proportion of the total mortality due to infarction.

Adult↗

PubMed1984

Sex differences in preinfarction characteristics and longterm survival among patients with myocardial infarction.

The prevalence of primary risk factors, previous medical history, and physical activity were assessed among 262 women and 1259 men who suffered a first nonfatal myocardial infarction between 1968 and 1977 in Göteborg, Sweden. The probability of suffering a myocardial infarction based on the conventional factors cholesterol level, systolic blood pressure and smoking habits was estimated in both sexes by means of a multiple risk function. Comparisons between sexes were made with age alone and age and estimated primary risk as confounders. Survival rate and reinfarction rate were calculated for a 5-year period of follow-up. Women with infarctions had higher serum cholesterol levels (p less than 0.001) and higher blood pressure values (p less than 0.001) but were less often smokers than men (p less than 0.001). The female patients also reported chest pain and dyspnea on exertion, and low physical activity both at work and during leisure time significantly more often than men; these differences remained after controlling for estimated primary risk. An overrepresentation of hypertension and diabetes prior to myocardial infarction was found among women below 45 years of age compared with men. A high frequency of women in this age group was also on sick leave or disability pension at onset of myocardial infarction, suggesting that mainly women with several risk factors including socioeconomic factors suffer an infarction at this age. No similar and consistent differences were found between women and men of older ages. The cumulative 5-year survival rate was 80% in women and 81% in men. Below age 45 the survival rate was lower among women than men (p less than 0.01). No sex difference was found in the recurrence rate of nonfatal reinfarctions. This indicates that once women have suffered a myocardial infarction they are exposed to at least as high a risk as men.

Adult↗

PubMed1984

Declining trend in mortality after myocardial infarction.

All patients under 60 years of age who were discharged from hospital after a first myocardial infarction between 1968 and 1977 in Göteborg were followed for a minimum of 24 months. The patients were unselected, and treatment was standardised. The patients were divided into five two yearly cohorts, and the prognostic comparability and mortality of these cohorts were assessed. There was a reduction in the two year mortality rate after discharge during the 10 year period. Small baseline differences between the cohorts were controlled by multivariate methods, and a subsequent analysis showed that there was a declining trend in mortality between 1968 and 1977. A higher tendency among smokers to give up smoking and a lower prevalence of angina pectoris could explain only part of the reduction in mortality. A small number of patients underwent a coronary bypass operation; the slight increase in the number of operations during the period cannot, however, account for the reduced mortality. Most of the patients in the later cohorts were treated with beta blockers, and this is the most likely explanation for the majority of the decline in mortality.

Adult↗

PubMed1984

Effect of metoprolol on chest pain in acute myocardial infarction.

A total of 1395 patients aged 40 to 74 years were included in a double blind trial with the beta 1 selective blocker metoprolol in suspected acute myocardial infarction. Metoprolol was given intravenously (15 mg) as soon as possible after admission to hospital followed by 200 mg daily for three months. A placebo was given in the same manner. The severity of chest pain in the acute phase was calculated by recording the number of injections of analgesics given and the time from the start of blind treatment to the time when the last analgesic was given (duration of pain). The patients receiving metoprolol were given a lower mean number of injections of analgesics during the first four days and after randomisation than those receiving a placebo. The estimated duration of pain was shorter in the metoprolol group than in the placebo group. These effects were related to the initial heart rate, the initial systolic blood pressure, and the final site of the infarct as determined electrocardiographically. Thus metoprolol given in the acute phase of suspected or definite myocardial infarction appears to reduce the severity of chest pain.

Adult↗

PubMed1984

Development of congestive heart failure after treatment with metoprolol in acute myocardial infarction.

In a double blind study of metoprolol in the treatment of suspected acute myocardial infarction 698 patients (study group) received metoprolol and 697 a placebo (control group). Metoprolol was given in an intravenous dose of 15 mg as soon as possible after admission to hospital followed by 50 g by mouth four times a day for two days and thereafter 100 mg twice a day for three months. A placebo was similarly given. Congestive heart failure occurred in a similar percentage of patients in both the study (27%) and the control groups (30%). Its severity was estimated by calculating the total dose of frusemide given during the first four days in hospital. Less frusemide was given to patients treated with metoprolol compared with those given a placebo in the total series. An appreciably lower total dose of frusemide was given to patients included in the trial less than or equal to 12 hours after the onset of pain and treated with metoprolol compared with a placebo, while no difference was seen among patients treated later. The initial heart rate, systolic blood pressure, and infarct site affected the results.

Adult↗

PubMed1983

Effect of metoprolol on indirect signs of the size and severity of acute myocardial infarction.

In a double-blind randomized trial, 1,395 patients with suspected acute myocardial infarction (MI) were investigated to evaluate the possibility of limiting indirect signs of the size and severity of acute MI with the beta 1-selective adrenoceptor antagonist metoprolol. Metoprolol (15 mg) was given intravenously and followed by oral administration for 3 months (200 mg daily). Placebo was given in the same way. The size of the MI was estimated by heat-stable lactate dehydrogenase (LD[EC 1.1.1.27]) analyses and precordial electrocardiographic mapping. Lower maximal enzyme activities compared with placebo were seen in the metoprolol group (11.1 +/- 0.5 mukat X liter-1) when the patient was treated within 12 hours of the onset of pain (13.3 +/- 0.6 mukat X liter-1; n = 936; p = 0.009). When treatment was started later than 12 hours, no difference was found between the 2 groups. Enzyme analyses were performed in all but 20 patients (n = 1,375). Precordial mapping with 24 chest electrodes was performed in patients with anterior wall MI. The final total R-wave amplitude was higher and the final total Q-wave amplitude lower in the metoprolol group than in the placebo group. Patients treated with metoprolol less than or equal to 12 hours also showed a decreased need for furosemide, a shortened hospital stay, and a significantly reduced 1-year mortality compared with the placebo group, whereas no difference was observed among patients treated later on. After 3 months, however, there was a similar reduction in mortality among patients in whom therapy was started less than or equal to 12 hours and greater than 12 hours after the onset of pain. The results support the hypothesis that intravenous metoprolol followed by oral treatment early in the course of suspected myocardial infarction can limit infarct size and improve long-term prognosis.

Aged↗

PubMed1983

A double-blind trial of metoprolol in acute myocardial infarction. Effects on ventricular tachyarrhythmias.

During a double-blind trial in which patients with suspected myocardial infarction received metoprolol or placebo, we analyzed the occurrence of ventricular tachyarrhythmias. Metoprolol (15 mg intravenously) was given as soon as possible after admission, and thereafter 200 mg was given daily for three months. Antiarrhythmic drugs were given only for ventricular fibrillation and sustained ventricular tachycardia (greater than 60 beats per second). Definite acute myocardial infarction developed in 809 of the 1395 participants, and probable infarction in 162. Metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia. However, there were 17 cases of ventricular fibrillation in the placebo group (697 patients) and only 6 in the metoprolol group (698 patients, P less than 0.05). During the hospital stay significantly fewer patients receiving metoprolol (16) than placebo (38) (P less than 0.01) required lidocaine. In a separate analysis of 145 patients, metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia during the first 24 hours of treatment. Despite a lack of effect on less serious ventricular tachyarrhythmias, metoprolol had a prophylactic effect against ventricular fibrillation in acute myocardial infarction.

Double-Blind Method↗

PubMed1983

Incidence and importance of metabolic side-effects during antihypertensive therapy.

Three long-term, randomised trials examining antihypertensive treatment with either diuretics or beta-blockers are in progress. On the basis of these, the following conclusions may be drawn regarding metabolic side-effects. Diuretics decrease whereas beta-blockers increase serum potassium. Neither drug has any obvious influence on total body potassium. Serum urate increases on both drugs but more so in those taking diuretics. Serum triglycerides increase while total serum cholesterol is unchanged in both treatments. It is still a matter of controversy whether there is a decrease in glucose tolerance and an increase in the incidence of diabetes in patients on diuretics. The possible negative influence of metabolic side-effects on morbidity and mortality may limit the beneficial effects of blood pressure reduction, especially in patients with low pressures before treatment. Thus, it seems crucial to minimise theses side-effects. Since they are dose-related for both diuretics and beta-blockers, the use of low doses and, if needed, combination treatment is preferable.

Adrenergic beta-Antagonists↗

PubMed1983

Cause of death in relation to social and alcoholic problems among Swedish men aged 35-44 years.

There have been conflicting reports concerning the relationship between increased alcohol intake and mortality from ischaemic heart disease. In this investigation, social register data also containing life-long registration data for alcoholic intemperance were related to cause of death for 302 men aged 35-44 in 1968-74. A random population sample of 940 male survivors of the same age was used for comparison. "Social problems only" were less common for the deceased, irrespective of cause of death, than for the controls. Registration for alcoholic problems was significantly more common for ischaemic heart disease, accidents, suicide and "other deaths" but not for cancer. The variables "detained by the police for drunkenness" and "in prison for crime" showed similar associations. Possible explanations are discussed, especially the association between alcoholic intemperance and death from ischaemic heart disease. The most probable mechanism is effects on the myocardial cell enzyme functions with following arrhythmias in subjects susceptible to malignant arrhythmias due to coronary artery disease and myocardial ischaemia.

Accidents↗

PubMed1983

Cessation of smoking after myocardial infarction. Effects on mortality after 10 years.

Ten annual cohorts of men suffering from their first myocardial infarction have been followed up to a maximum period of 10.5 years. One thousand and twenty-three male patients of 1306 were smokers. Three months after the infarction 55% had stopped smoking and 45% continued smoking. These two groups were then compared and followed with regard to non-fatal reinfarctions and deaths. Preinfarction characteristics were shown to be similar for the two groups. The prognostic comparability of the two groups was tested using two multiple logistic models. Those who stopped smoking had a slightly higher predicted two year mortality after the infarction. In different age groups it is shown with life table technique that those who stopped smoking had a considerably higher survival rate and lower cumulative frequency of reinfarction. The present study shows a reversion of the expected prognosis after myocardial infarction caused by changing the smoking habit.

Adult↗

PubMed1983

Prognostic value of angiographic indices of coronary artery disease from the Coronary Artery Surgery Study (CASS).

The Coronary Artery Surgery Study, CASS, enrolled 24,959 patients between August 1975 and June 1979 who were studied angiographically for suspected coronary artery disease. This paper compares the prognostic value for survival without early elective surgery of eight different indices of the extent of coronary artery disease: the number of diseased vessels, two indices using the number of proximal arterial segments diseased, two empirically generated indices from the CASS data, and the published indices of Friesinger, Gensini, and the National Heart and Chest Hospital, London. All had considerable prognostic information. Typically 80% of the prognostic information in one index was also contained in another. Our analysis shows that good prediction from angiographic data results from a combination of left ventricular function and arteriographic extent of disease. Prognosis may reasonably be obtained from three simple indices: the number of vessels diseased, the number of proximal arterial segments diseased, and a left ventricular wall motion score. These three indices account for an estimated 84% of the prognostic information available. 6-yr survival varies between 93 and 16% depending upon the values of these three indices.

Angiography↗

PubMed1983

The Göteborg metoprolol trial. Effects on mortality and morbidity in acute myocardial infarction.

In the Göteborg Metoprolol Trial, 1395 patients with suspected acute myocardial infarction were, on admission, randomly allocated to double-blind treatment, 697 to placebo and 698 to metoprolol (15 mg i.v. + 200 mg/day) for 90 days. During this period, there were 62 deaths in the placebo group (8.9%) and 40 in the metoprolol group (5.7%), a mortality reduction of 36% (p less than 0.03). This effect persisted regardless of age, previous infarction or previous chronic beta blockade. All deaths were classified as cardiovascular. After 3 months, all patients were recommended open treatment with metoprolol, and the difference in mortality between the two groups was maintained after 1 year. Early institution of metoprolol (within 12 hours) influenced infarct development during the first 3 days (infarct diagnosis and indirect measures of infarct size). Metoprolol also reduced the incidence on fatal and nonfatal infarction during the next 4-90 days by 35%. Furthermore, fewer episodes of ventricular fibrillation were recorded in the metoprolol than in the placebo group (six vs 17 patients). The tolerance was judged to be very good. The same percentage of patients (19%) was withdrawn from the blind treatment in the two groups. Fewer patients in the metoprolol group used lidocaine, furosemide and analgesics. We conclude that metoprolol therapy instituted on admission in patients with suspected acute myocardial infarction reduced 3-month mortality and exerted beneficial clinical effects.

Adult↗