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Biomedical subjects

F Waagstein

Publications and source records attributed to F Waagstein.

At least 91 records · Page 5Linked to original sources
PubMed1989

Early use of metoprolol and serum potassium in suspected acute myocardial infarction.

In 1350 patients with suspected acute myocardial infarction, serum potassium was analysed in the emergency ward. The effect of metoprolol was compared with placebo in a double-blind randomized trial. Metoprolol increased serum potassium from 4.11 +/- 0.02 mmol/l to 4.27 +/- 0.02 mmol/l (P less than 0.001) during the 1st day after hospital admission, whereas serum potassium levels remained fairly constant in patients given placebo during the same time (4.11 +/- 0.02 to 4.14 +/- 0.02 mmol/l; P greater than 0.2). Similar results were obtained when analysing patients with a confirmed myocardial infarction separately. The effects appeared homogeneously distributed in subgroups related to sex, clinical history, infarct site, infarct size and delay time from onset of symptoms to start of treatment. We conclude that early treatment with the beta-1-selective blocker metoprolol in patients with suspected acute myocardial infarction increases serum potassium.

Clinical Trials as Topic↗
PubMed1989

Treatment of pain in acute myocardial infarction.

The treatment of pain in acute myocardial infarction varies with local practice. Narcotic analgesics are still the usual treatment in many hospitals. Knowledge of optimal doses, duration of pain relief, and time between drug administration and pain relief is inadequate. Many studies indicate that the relief of pain is often incomplete after treatment with narcotic analgesics. There is often a need for alternative treatments. Large randomised studies consistently show that beta blockade, initially given intravenously and then orally, relieves pain and reduces the need for analgesics. Studies also indicate that early administration of streptokinase and glyceryl trinitrate relieves pain. There is evidence that drugs that limit ischaemic damage also relieve pain.

Adrenergic beta-Antagonists↗
PubMed1989

Influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing.

The influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing was studied in 11 patients with severe coronary artery disease. The patients were catheterised and treated with transcutaneous electrical nerve stimulation on two occasions, double blind and in random order, with a single intravenous dose of saline or with a single intravenous dose of 50 mg naloxone. Treatment with transcutaneous electrical nerve stimulation increased tolerance to pacing and significantly improved lactate metabolism with placebo and with naloxone. The positive effects of transcutaneous electrical nerve stimulation were thus reproducible and not reversed by single intravenous doses of naloxone. The results indicate that the effects of transcutaneous electrical nerve stimulation on the heart are not mediated by beta endorphin but they do not exclude activation of more short-acting opioids such as delta or kappa receptor agonists (met-enkephalin or dynorphin or both) because naloxone has a low affinity for these receptors. Non-opioid mechanisms may also be important.

Aged↗
PubMed1989

Long-term beta-blockade in dilated cardiomyopathy. Effects of short- and long-term metoprolol treatment followed by withdrawal and readministration of metoprolol.

To evaluate the short- and long-term effects of beta-adrenergic blockade (metoprolol) as well as the reaction to withdrawal and readministration of metoprolol in severe heart failure, 33 patients (25 men and eight women; mean age, 47.6 +/- 14.0 years) with dilated cardiomyopathy were studied by right and left heart catheterization, right ventricular biopsy, two-dimensional and Doppler echocardiography, and external pulse recordings. Twenty-six of 33 patients survived more than 6 months, and 24 of the 26 patients improved their functional class (from mean 3.3 to 1.8, p less than 0.0001). These 24 patients were subjected to withdrawal of metoprolol until the number of symptoms increased and deterioration occurred as observed noninvasively (group 1, n = 16), whereas the eight patients did not deteriorate during a 12-month period (group 2). During long-term treatment with metoprolol, there was an increase in ejection fraction from 0.24 to 0.42 (p less than 0.0001), whereas there was a decrease in the left ventricular (LV) end-diastolic dimension (from 7.3 to 6.4 cm, p less than 0.0001), in the grade of mitral regurgitation (from 1.7 to 0.4, p less than 0.0001), and in the grade of tricuspid regurgitation (from 0.6 to 0.05, p less than 0.007). There was a decrease in pulmonary wedge pressure (from 23.8 to 10.7 mm Hg, p less than 0.0001), LV end-diastolic pressure (from 24.1 to 13.4 mm Hg, p less than 0.002), and systolic vascular resistance (from 1,782 to 1,499 dynes/sec/cm, p less than 0.04). There was an increase in systolic blood pressure (from 116 to 132 mm Hg, p less than 0.003), cardiac index (from 2.17 to 2.58 l/min/m2, p less than 0.005), and LV stroke work index (from 31 to 65 g.m/m2, p less than 0.0001). During withdrawal of metoprolol, the heart rate and left atrial dimension increased (p less than 0.0001), whereas ejection fraction decreased (p less than 0.0001). The 12 (of 16) patients in group 1 who survived the withdrawal period had metoprolol readministered, and subsequently, ejection fraction increased (from 0.23 to 0.33, p less than 0.002). Patients had a low number of ventricular beta-adrenergic receptors compared with healthy control subjects (30.3 +/- 2.9 vs. 97.4 +/- 8.7 fmol/mg protein, p less than 0.001), but long-term treatment with metoprolol caused a moderate up-regulation (from 30.3 +/- 2.9 to 49.0 +/- 7.1 fmol/mg protein, p less than 0.05), which may facilitate a more normal response to sympathetic stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1988

Effects on mortality during five years after early intervention with metoprolol in suspected acute myocardial infarction.

This study reports the mortality over a 5-year-period determined a double-blind trial, which evaluated the effect of early intervention with metoprolol in suspected acute myocardial infarction. In all, there were 1,395 randomized patients, 698 and 697 of whom were allocated to metoprolol 200 mg daily and placebo treatments, respectively, for the first 3 months. Thereafter, the two groups were treated in a similar fashion implying beta-blockade to a majority. Within the first 3 months, mortality in the metoprolol group was 5.7% versus 8.9% of the placebo group (p = 0.02). This difference persisted after 2 years (metoprolol 13.2%; placebo 17.2%; p = 0.04). Over a 5-year-period, 24.2% of the patients who originally were allocated to metoprolol had died as compared to 25.7% of those originally allocated to placebo (p greater than 0.2). Among patients in whom treatment started early (less than or equal to 8 hours after onset of pain = the median delay time), enzyme activities in the metoprolol group was lower (p = 0.03) than in the placebo group. Mortality during the first 2 years among these patients treated early was lower in the metoprolol (11.8%) than in the placebo group (17.3%; p = 0.04). Corresponding figures after 5 years were 22.0% and 25.3%, respectively (p greater than 0.2). Among patients in whom treatment started later than 8 hours onset of pain, there was neither any difference in enzyme activity nor in mortality after 2 and 5 years. It can be concluded that early treatment with metoprolol in suspected acute myocardial infarction reduced mortality during the first 3 months compared with placebo. The difference persisted after 2 years. However, 5 years after randomization, no significant difference in mortality was observed between the two treatment groups.

Adult↗
PubMed1987

Catecholamine metabolism during pacing-induced angina pectoris and the effect of transcutaneous electrical nerve stimulation.

The arterial levels of norepinephrine and epinephrine were estimated in 14 patients with severe coronary artery disease in order to assess the catecholamine metabolism during pacing-induced angina pectoris and to evaluate the effects of transcutaneous electrical nerve stimulation (TENS). Arterial levels of epinephrine and norepinephrine increased significantly during pacing to angina pectoris (p less than 0.05 and p less than 0.001, respectively), indicating that maximal atrial pacing induced an increase in sympathetic tone. At the corresponding pacing rate during TENS, myocardial lactate production was improved (p less than 0.01) and the ST segment depression was less pronounced (p less than 0.05). The maximal pacing rate during TENS was 141 +/- 24 compared to 123 +/- 19 (p less than 0.01) and the heart rate-blood pressure product was also significantly higher (p less than 0.01), suggesting an elevation of the anginal threshold by TENS. Systemic vascular resistance and systolic blood pressure were significantly reduced (both p less than 0.01). These beneficial results may be caused by a decrease in left ventricular afterload as reflected by a fall in systolic blood pressure and may be explained by reduced sympathetic activity. TENS may decrease the sympathetic activity either directly or indirectly as a consequence of pain inhibition. This hypothesis is supported by the fact that arterial levels of epinephrine and norepinephrine dropped during TENS in TENS responders.

Angina Pectoris↗
PubMed1986

The influence of early intervention in acute myocardial infarction on long-term mortality and morbidity as assessed in the Göteborg metoprolol trial.

The mortality and morbidity were assessed during a 2-year follow-up in an acute intervention trial in suspected acute myocardial infarction with metoprolol (a selective beta 1-blocker). On admission to the trial, the 1395 participating patients were randomly allocated to metoprolol or placebo for 3 months. Thereafter, if there was no contraindication, patients with infarction and/or angina pectoris were continued on metoprolol for 2 years. A lower mortality was observed after 3 months in patients randomised to metoprolol. The difference remained after 2 years. The difference in 2-year mortality rate was restricted to patients randomised early after onset of pain. Late infarction was observed more often in the placebo group during the first 3 months. When the two groups thereafter were treated similarly, the difference successively declined and did not remain after 2 years. A similar incidence of angina pectoris was observed in the two groups at each check up. During the early recovery period, more patients in the metoprolol group returned to work. No such difference was observed later on.

Adult↗
PubMed1986

Variability, prediction and prognostic significance of chest pain in acute myocardial infarction.

The variability of chest pain is described in 389 patients with acute myocardial infarction. Whereas 17% were free from severe pain after arrival in hospital, 11% required more than 10 analgesic injections. In 27% of the series analgesics were given more than 24 h after arrival in hospital. Predictors for the severity of chest pain were the rate-pressure product and degree of chest pain soon after arrival in hospital as well as electrocardiographic signs of myocardial infarction at entry. Patients with more severe chest pain had a higher 2-year mortality rate and a higher incidence of ventricular fibrillation and congestive heart failure during hospitalization.

Analgesia↗
PubMed1985

Acute haemodynamic effects of felodipine in congestive heart failure.

The haemodynamic effects of felodipine 0.1 mg/kg p.o., a new arteriolar dilator, were studied in 7 patients with severe congestive heart failure of NYHA Class IV (Group A) and in 3 patients in Class II-III (Group B). In Group A, measurements were made before and 1 and 4 h after felodipine administration. There was a substantial fall in systemic arterial pressure, which was not associated with a compensatory tachycardia. In fact, there was a fall in heart rate from 92 to 82 beats/min 1 h after drug administration. The pulmonary capillary wedge pressure was reduced from 22 to 14 mm Hg and the cardiac index and stroke volume index rose significantly. Consequently, there was a marked reduction in systemic vascular resistance. In Group B measurements were performed at rest and during exercise before and 1 h after felodipine. The pulmonary wedge capillary pressure during exercise was lower than in the control situation. Coronary sinus flow was increased and there was a pronounced fall in coronary vascular resistance. The results would suggest that felodipine, by virtue of its ventricular unloading potency, might be a valuable drug in the treatment of congestive heart failure.

Adult↗
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↗
PubMed1985

The effects of transcutaneous electrical nerve stimulation in patients with severe angina pectoris.

The pain-relieving effects of transcutaneous electrical nerve stimulation (TENS) were investigated in patients with severe angina pectoris first with respect to systemic and coronary hemodynamics and myocardial metabolism during pacing-induced angina and second in a controlled long-term study. Two series of patients with severe angina pectoris (NYHA class III to IV) were studied (13 patients in the pacing study and 23 in the long-term study). In the pacing-induced angina study there was increased tolerance to pacing (142 +/- 23 compared with 124 +/- 20 beats/min tolerated, p less than .001), improved lactate metabolism (2 +/- 36% compared with -18 +/- 43%, p less than .01), and less pronounced ST segment depression (2.3 +/- 1.1 compared with 2.9 +/- 2.6 mm, p less than 0.05) with TENS. In the long study the effects of TENS were measured by means of repeated bicycle ergometer test, frequency of anginal attacks, and consumption of short-acting nitroglycerin. TENS was used regularly for 1 hr three times per day. The TENS treatment group had increased work capacity (637 +/- 308 vs 555 +/- 277 W . min, p greater than .001), decreased ST segment depression (2.3 +/- 1.1 vs 3.6 +/- 1.6 mm, p less than .001), reduced frequency of anginal attacks (p less than .05), and reduced consumption of short-acting nitroglycerin per week (p less than .05) compared with the control group. The observed effects were mainly due to decreased afterload resulting from systemic vascular dilatation.

Adult↗
PubMed1985

Pharmacologic treatment of dilated cardiomyopathy with special reference to the role of beta-blockers.

The pharmacologic treatment of dilated cardiomyopathy encompasses measures such as temporary administration of amino acids and calories for those who may be undernourished and avoidance of drugs such as alcohol, nicotine, amphetamines and high doses of tricyclic antidepressants. Anticoagulants should be used in patients with persistent failure or marked dilatation of the cardiac chambers since about 20% suffer from major embolic complications. In patients with ventricular tachycardia, R-on-T, or multifocal ventricular ectopic beats, class I antiarrhythmic drugs, or if unsuccessful, amiodarone should be administered since the risk of sudden death is substantial. In addition to digitalis and diuretics, the use of vasodilators is generally accepted to be of clinical value for reduction of symptoms in heart failure. Reports concerned with long-term clinical and hemodynamic effects with drugs such as prazosin, captopril and the combination of hydralazine and isosorbide dinitrate are conflicting and, so far, there is no evidence that any vasodilator prolongs survival. The beta-agonists, such as prenalterol, are limited in their usefulness by tachycardia induction, a tendency to provoke serious arrhythmias, tremor and anxiety as well as hemodynamic tolerance development. While the noncatecholamine inotropics such as milrinone may provide symptomatic relief in severe congestive heart failure, they also increase heart rate, induce ventricular arrhythmias and are associated with high one-year mortality rates. The beneficial effect of long-term beta-blockade, which we first reported in 1975 to include a decrease in functional class, increase in exercise tolerance, improvement in physical findings, increase in ejection fraction and enhanced survival, has been met with scepticism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1984

Göteborg Metoprolol Trial: electrocardiographically estimated infarct size.

In 236 patients with anterior myocardial infarction (MI), infarct size was estimated by analyzing the R- and Q-wave amplitude in 24 precordial leads 4 days after randomization. In 254 patients with inferior MI, the final R- and Q-wave amplitude was evaluated in leads II, III and aVF. Electrocardiographic signs of a smaller MI were observed in anterior MI in the metoprolol group compared with the placebo group when treatment was started 12 hours or less after the onset of pain, but no difference was found when treatment was started later. There was no sign of an effect of metoprolol in inferior MI. An immediate reduction in ST-segment elevation was observed after metoprolol treatment regardless of infarct localization or delay between the onset of pain and treatment.

Clinical Trials as Topic↗
PubMed1984

Göteborg Metoprolol Trial: effects on arrhythmias.

During the initial hospitalization, ventricular fibrillation (VF) developed in 6 metoprolol-treated patients (0.9%) vs 17 placebo-treated patients (2.4%) after inclusion in the study (p = 0.035). There were 6 episodes of VF in the metoprolol group compared with 41 episodes in the placebo group (p less than 0.001). During the same period, 14 metoprolol-treated patients had treated ventricular tachycardia vs 26 placebo-treated patients (p = 0.076). Similar favorable results were found when the incidence of severe ventricular arrhythmias during the first rehospitalization within the 3-month double-blind treatment period was analyzed.

Adult↗