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Biomedical subjects

K Swedberg

Publications and source records attributed to K Swedberg.

At least 199 records · Page 11Linked to original sources
PubMed1984

Relationship between infarct size and incidence of severe ventricular arrhythmias in a double-blind trial with metoprolol in acute myocardial infarction.

In 585 patients having an acute myocardial infarction for the first time the relationship was investigated between estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia during hospitalization. The size of the infarct was estimated from analyses of heat stable lactate dehydrogenase (LD) (EC 1.1.1.27.) in serum collected every 12 hr for 48-108 hr. All patients participated in a double-blind comparison of the beta 1-selective blocker metoprolol with placebo in suspected acute myocardial infarction. A correlation was observed between the enzymatically estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia in patients on placebo (P less than 0.001), while this could not be demonstrated in patients on the beta-blocker (P greater than 0.2). In placebo treated patients there was a correlation between the maximum heat stable LD activity and early ventricular fibrillation (P = 0.034), late ventricular fibrillation (P less than 0.001), primary ventricular fibrillation (P = 0.002) as well as secondary ventricular fibrillation (P = 0.034). It is concluded that there seems to be a relatively strong correlation between the final size of the infarction and the occurrence of severe ventricular arrhythmias. Treatment with beta-blockade appeared to disturb this correlation.

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↗
PubMed1984

Alterations in angina threshold with nifedipine during pacing induced angina.

Changes in coronary haemodynamics and angina threshold were determined during atrial pacing in 11 patients with fixed obstructive coronary artery disease with effort angina before and after the administration of 20 mg of oral nifedipine. Coronary vascular resistance decreased at resting and at "subangina" heart rates but not at "angina" rates. Primary coronary vasodilatation with nifedipine was also suggested by higher coronary sinus oxygen content whether at rest or at subangina or angina heart rates. After nifedipine angina occurred at a lower double product and lower myocardial oxygen consumption. These findings suggest that nifedipine is a coronary vasodilator, but angina can occur at a lower angina threshold in some patients with obstructive coronary artery disease.

Aged↗
PubMed1984

Enzymatically and electrocardiographically estimated infarct size in relation to pain in acute myocardial infarction.

In 563 patients with acute myocardial infarction and no previous myocardial infarction, the estimated infarct size was related to the estimated duration of pain and the amount of analgesics given. The size of infarction estimated from analyses of heat-stable lactate dehydrogenase (EC 1.1.1.27) at 12-hour intervals for 48-108 h and from Q- and R-wave changes in the ECG correlated positively, although weakly with duration of the pain and the amount of analgesics given. These data support the hypothesis that larger infarcts, as a group, evolve over a longer time period than smaller infarcts and that the duration of pain in many patients might be an indicator of the infarct size. In the individual patient, however, one cannot predict the size of the infarction from the severity of pain.

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

The time course in acute myocardial infarction evaluated with precordial mapping and standard ECG.

Fifty-six patients with acute transmural anterior wall myocardial infarction (MI) were investigated with a 24-electrode grid and 34 patients with an acute transmural inferior wall MI were investigated with standard ECG leads II, III, and aVF in order to study the length of time after the onset of pain during which the development of Q waves and reduction of R waves progress. These ECG changes continued for 18-26 h after onset of pain but the majority appeared during the first 12 h.

Adult↗
PubMed1983

Enalapril: a new angiotensin-converting enzyme inhibitor in chronic heart failure: acute and chronic hemodynamic evaluations.

Hemodynamic effects of the new oral angiotensin-converting enzyme inhibitor, enalapril, were evaluated acutely in 15 patients with chronic heart failure and in 7 patients after 4 weeks of maintenance therapy. Initial hemodynamic effects were characterized by a significant increase in cardiac index (from 2.1 +/- 0.7 to 2.6 +/- 0.7 liters/min per m2) and a decrease in pulmonary capillary wedge pressure (from 30 +/- 6 to 24 +/- 7 mm Hg), right atrial pressure (from 14 +/- 5 to 11 +/- 4 mm Hg), mean arterial pressure (from 96 +/- 16 to 80 +/- 17 mm Hg) and systemic vascular resistance (from 1,820 +/- 480 to 1,200 +/- 410 dynes . s . cm-5) without any significant change in heart rate, pulmonary artery pressure and pulmonary vascular resistance. During maintenance therapy, the dose of diuretic drugs had to be increased because of systemic venous hypertension. Repeat hemodynamic study showed that after chronic therapy, cardiac index (2.1 +/- 0.7 vs. 3.0 +/- 0.08 liters/min per m2) and stroke volume index (24 +/- 10 vs. 36 +/- 7 ml/m2) remained elevated and pulmonary capillary wedge pressure was lower than control (30 +/- 6 vs. 16 +/- 6 mm Hg), indicating sustained improvement in left ventricular performance. Plasma renin activity increased and plasma norepinephrine levels decreased after enalapril therapy and these humoral changes persisted during maintenance therapy. All patients receiving chronic therapy had symptomatic improvement. Significant hypotension, which occurred in five patients at the initiation of therapy, appears to be the major side effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Possible adrenergic effects on heart protein metabolism.

It is known that the heart will adapt to actual demand by increasing or decreasing its size through different mechanisms. In this presentation, the possible role of catecholamines in regulating heart protein synthesis and developing cardiac hypertrophy and cardiomyopathy is discussed. Injecting animals with catecholamines has been found to induce cardiac hypertrophy. In vitro perfusion of rat heart in the presence of catecholamines has been found to induce a time-dependent and dose-dependent stimulation of amino acid transport and incorporation into proteins. Acute haemodynamic effects of catecholamines increase cardiac performance while long-term treatment seems to cause depression of cardiac function, especially during ischaemic conditions. Chronic beta-blockade in patients with primary congestive cardiomyopathy improved both cardiac function and clinical condition in more than half the patients. Furthermore, a beneficial effect on survival was also found, when compared with a matched control group. It is hypothesised that catecholamines may play a role in developing cardiac hypertrophy as well as congestive cardiomyopathy.

Adrenergic beta-Antagonists↗
PubMed1983

Correlation between enzymatic estimation of infarct size and early mortality rate.

In 585 patients with a first acute myocardial infarction the maximum activity of heat stable lactate dehydrogenase (EC 1.1.1.27) was correlated with mortality at three months. The patients participated in a double blind trial with metoprolol in acute myocardial infarction. In all patients not taking a beta blocker a highly significant correlation was found, but this was not evident in those who were. When patients with anterior or inferior infarctions treated with a placebo were analysed separately the correlation remained, as it did when the patients who were alive on the fourth day after the onset of pain were analysed separately. No correlation was observed between enzyme activity and three month mortality in these subgroups if only patients treated with metoprolol were included. In a subsample of only 171 patients it was found that the maximum activity of creatine kinase (EC 2.7.3.2) and creatine kinase subunit B did not correlate with three month mortality regardless of treatment. Thus it is concluded that when a sufficiently large number of patients are investigated there is a highly significant correlation between the enzymatic estimation of infarct size and early mortality in acute myocardial infarction. This relation did not persist when patients treated with beta blockade were analysed.

Adult↗
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↗
PubMed1981

Effect on mortality of metoprolol in acute myocardial infarction. A double-blind randomised trial.

The effect of metoprolol on mortality was compared with that of placebo in a double blind randomised trial in patients with definite or suspected acute myocardial infarction. Treatment with metoprolol or placebo started as soon as possible after the patient's arrival in hospital and was continued for 90 days. Metoprolol was given as a 15 mg intravenous dose followed by oral administration of 100 mg twice daily. 1395 patients (697 on placebo and 698 on metoprolol) were included in the trial. Definite acute myocardial infarction developed in 809 and probable infarction in 162. Patients were allocated to various risk groups and within each group patients were randomly assigned to treatment with metoprolol or placebo. There were 62 deaths in the placebo group (8.9%) and 40 deaths in the metoprolol group (5.7%), a reduction of 36% (p less than 0.03). Mortality rates are given according to the treatment group to which the patients were initially randomly allocated.

Adult↗
PubMed1981

Clinical and biochemical heterogeneity of globoid cell leukodystrophy.

The residual galactosylceramide beta-galactosidase activity in cultured skin fibroblasts from a child with late-onset globoid cell leukodystrophy (GLD) was distinctly different from that found in the typical infantile form of the disease. The residual enzyme activity and maximum velocity of the enzyme reaction were higher in this patient, while the Michaelis constant was similar in controls and in the two forms of GLD. The pH optimum of enzyme activity from the patient was similar to that of controls and a more acidic pH optimum was found in the infantile form. Cultured skin fibroblasts from the patient accumulated less [6(3)H]-galactosylceramide than did cells from the infantile form. These various biochemical measurements correlated well with the age of onset of the disease and suggest that different allelic mutations of the galactosylceramide beta-galactosidase locus are responsible for the different clinical forms of GLD.

Cells, Cultured↗