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Biomedical subjects

G Olsson

Publications and source records attributed to G Olsson.

At least 109 records · Page 6Linked to original sources
PubMed1988

Trends in coronary care. A retrospective study of patients with myocardial infarction treated in coronary care units.

Data on the 2,008 patients in the Swedish Co-operative Study from 1969 were compared with 773 consecutive cases with definite myocardial infarction (MI) admitted to the coronary care unit (CCU) of Danderyd Hospital in Stockholm 1984-85. We found a significant decrease in hospital mortality from 26.6% to 12.9% despite the admission of older patients to our CCU. Mean age for men was 63.8 vs. 65.6 years and for women, 69.8 vs. 72.3. The incidence of previous hypertension and diabetes was higher and the incidence of heart failure and angina lower in 1984-85. No differences were noted as regards the incidence of ventricular fibrillation, atrial fibrillation and AV-block III in the acute phase despite a much more frequent use of antiarrhythmics in 1969 (33% vs. 4%). A decreased use of cardiac glucosides was also noted (34% vs. 16%). Asystole, however, was noted in 10% of the patients in 1969 compared with 3% in our patients. beta-Adrenergic blockers were not used in 1969 but commonly given in 1984-85 (67%), also in those with heart failure (54%). Delay between onset of symptoms and admission was longer in 1969, 47% being admitted within 6 hours compared with 75% in 1984-85. In conclusion, our study shows a marked change in the use of various cardiac drugs in the treatment of MI. Differences between the populations as regards mortality and different clinical findings are more difficult to evaluate and may also be explained by change in the selection of patients treated in the CCU.

Age Factors↗
PubMed1987

Lipomas have characteristic structural chromosomal rearrangements of 12q13-q14.

Cytogenetic analysis was performed in 10 consecutive lipomas; 6 had typical benign histology whereas four had foci of atypia. Three tumors had supernumerary ring chromosomes, 6 had different balanced rearrangements, and one had a normal karyotype. Chromosome 12 was involved in 5 of the balanced rearrangements and, although less certainly, in all the ring chromosomes, with breakpoints localized to 12q13 or q14. The other rearranged chromosomes were numbers 2, 3, 7, 8, 11, 17 and 22. These results demonstrate the non-random involvement of chromosomal region 12q13-q14 in benign lipogenic tumors. The combined data from this and previous studies on benign and malignant lipogenic tumors indicate that different levels of cytogenetic specificity exist within this group of neoplasms. We suggest that myxoid liposarcoma development requires the recombination of 2 specific chromosomal bands (12q13 and 16pII), whereas for some types of benign lipogenic tumors structural changes in 12q13-q14 may be sufficient for neoplastic growth.

Aged↗
PubMed1987

Economic consequences of postinfarction prophylaxis with beta blockers: cost effectiveness of metoprolol.

Treatment with certain beta adrenoceptor blocking agents after myocardial infarction reduces mortality and the incidence of reinfarction. Data from a randomised placebo controlled study of the beta 1 selective blocker metoprolol given as secondary prophylaxis were therefore analysed for the possible cost effectiveness of extending this treatment to the general population of patients with myocardial infarction. Metoprolol 100 mg twice daily and matching placebo were given to 154 and 147 patients, respectively, for three years. During this period drug costs for the beta blocker, digitalis, and diuretics were analysed as well as costs of readmission for cardiac problems and indirect costs arising from sick leave or early retirement. Active treatment with metoprolol significantly reduced costs of readmission as well as indirect costs. The net effect per patient over the three years was a reduction of roughly kr 19,000 (1930 pounds). These results suggest that beta blocker treatment given as secondary prophylaxis after myocardial infarction is highly cost effective.

Aged↗
PubMed1987

Serum lipids and lipoproteins in ischaemic heart disease following withdrawal of long-term metoprolol treatment.

In 39 patients who had been treated with metoprolol 100-200 mg daily or placebo for three years after acute myocardial infarction, serum lipids and lipoproteins were studied while the patients were on treatment as well as after its withdrawal. Withdrawal was performed over 1 week. Treatment had to be reinstituted in 6 patients (1 ex placebo and 5 ex metoprolol) because of aggravated symptoms. During the entire study period total cholesterol was significantly higher in the metoprolol withdrawal group and LDL cholesterol tended to be higher. HDL cholesterol in both groups increased significantly during the initial 28-day period following withdrawal of treatment. In both groups VLDL triglycerides tended to decrease during the first 28 days without treatment. Other lipoprotein fractions in both groups were unchanged. Overall, in patients who tolerated the ending of 3 years of treatment with metoprolol after myocardial infarction, there was no significant effect on lipoprotein fractions as compared to a placebo group.

Adult↗
PubMed1987

Metoprolol in acute myocardial infarction reduces ventricular arrhythmias both in the early stage and after the acute event.

Fifty three of the 5778 patients included in the MIAMI (Metoprolol in Acute Myocardial Infarction) trial were investigated with long-term ECG recordings in order to evaluate the effect of acute beta-blockade on premature ventricular complexes in and after acute myocardial infarction. Twenty five patients were given placebo and 28 metoprolol in a double-blind randomized fashion for 15 days. After this period the patients were put on open beta-blockade without breaking individual study codes. The mean number of premature ventricular complexes during the inclusion day (day 0) was the same in the two groups. The median numbers were also similar in the two groups: 190 and 154 in the placebo and metoprolol groups, respectively. Metoprolol significantly reduced the median number of premature ventricular complexes in the randomized period. The median numbers on days 1, 2 and 15 were 146, 101, 84 in the placebo group and 73, 59 and 10 in the metoprolol group, respectively (P less than 0.05). Also during the further follow-up, when investigated 1, 3 and 6 months after the infarction, the median number of premature ventricular complexes was lower in the metoprolol group (74, 257, 142 in the placebo group and 7, 5 and 11 in the metoprolol group, P less than 0.05). This indicates that metoprolol treatment in the acute phase of myocardial infarction reduces ventricular arrhythmias both in the early stage and also after the acute event.

Arrhythmias, Cardiac↗
PubMed1987

Postinfarction metoprolol treatment: effects on prognosis in relation to serum cholesterol concentrations.

In a double-blind randomized study of 154 postmyocardial infarction patients assigned to metoprolol (100 mg twice daily) and 147 patients assigned placebo, the outcome during a 3-year follow-up according to serum cholesterol concentrations was evaluated. There was no indication that metoprolol influenced the total serum cholesterol concentration. The median cholesterol value at 3 months was 6.7 mmol/l. In patients with cholesterol less than or equal to 6.7 mmol/l, nonfatal reinfarctions were reduced in the metoprolol group (7 vs. 24%; p less than 0.01). In patients with cholesterol greater than 6.7 mmol/l, mortality was lower in those treated with metoprolol (8 vs. 20%; p less than 0.05). The beneficial effect of conventional postinfarction beta-blockade with metoprolol is independent of serum cholesterol concentration.

Cholesterol↗
PubMed1987

Abrupt withdrawal of isosorbide 5-mononitrate (Imdur) after long term treatment in stable angina pectoris. A preliminary report.

32 patients with stable angina pectoris who had been receiving a controlled-release formulation Durules of isosorbide 5-mononitrate (Imdur) 60 to 120 mg daily with concomitant beta-blocker therapy for at least 1 year were entered into a study to evaluate possible rebound phenomena from the abrupt withdrawal of isosorbide 5-mononitrate and to determine whether nitrate tolerance had developed. Isosorbide 5-mononitrate was abruptly withdrawn and substituted with placebo for 2 weeks, after which the active drug was reintroduced. No deterioration of exercise performance could be detected during withdrawal of therapy, but an increase was seen after reinstitution. No tolerance was found for systolic blood pressure and ST segment changes or for the number of anginal attacks and short-acting glyceryl trinitrate tablets consumed. Three patients had to be hospitalised because of a sudden deterioration of symptoms on withdrawal of isosorbide 5-mononitrate. It was concluded that isosorbide 5-mononitrate in Durules has a beneficial effect and that tolerance does not appear to be clinically relevant.

Adrenergic beta-Antagonists↗
PubMed1987

Pharmacokinetics of felodipine and effect on digoxin plasma levels in patients with heart failure.

Some calcium antagonist drugs used in hypertension and cardiac diseases have been shown to increase plasma digoxin levels mainly as a result of reduced renal clearance. Felodipine is a new dihydropyridine calcium antagonist drug with cardiovascular effects, whose pharmacokinetics and effects on plasma digoxin levels have been studied in patients with left ventricular failure. 12 patients (11 men) on long term digoxin therapy were given 2.5 or 5 mg felodipine bid for 7 days followed by 1 week on 10mg bid. Plasma levels of digoxin and felodipine were measured before dosage and 30, 60 and 90 minutes and 2, 3, 4, 6, 8, 10 and 24 hours after the first dose and after 1 week of therapy (steady state). The area under plasma concentration versus time curve was calculated after the first dose and in steady state both for digoxin and felodipine. The absorption characteristics Cmax and Tmax were calculated both for felodipine and digoxin on the different felodipine doses. There was a linear relationship between dose and plasma level of felodipine. Plasma half-life in the 4- to 10-hour period of felodipine was 5.5 hours after a 10mg single dose, and 12 hours after 10mg bid. Felodipine 2.5mg, 5mg and 10mg all transiently increased peak plasma digoxin concentrations (by about 40%) at 1 hour after intake. Urinary excretion of digoxin during the day was unchanged, but impaired renal clearance may account for the transient increase in digoxin plasma level after felodipine.

Aged↗
PubMed1987

Beta-blockade after myocardial infarction: practical implications of major clinical trials.

A survey of the literature concerning 20 years' experience of beta-blockade after myocardial infarction indicates that several positive effects are achieved and that these are neither marginal nor transient. Mortality is reduced during the first year from about 10 to 7%. This has been shown for the individual beta-blockers metoprolol, propranolol, and timolol, and also when the data on all beta-blocker trials have been pooled. The effect is further enhanced if therapy continues. Patients at high risk of mortality can be separated fairly accurately from those at low risk. Thus, prophylactic treatment with the sole purpose of reducing mortality can be individualized. Effects on reinfarction are also already present after 1 year and are enhanced during further follow-up. It has not yet been possible, however, to identify those patients in whom this end-point will not be influenced. Furthermore, during extended follow-up, the proportion of asymptomatic patients who are free of side effects increases during treatment with beta-blockade, whereas it decreases during placebo therapy, due mostly to increased numbers of patients suffering from complications such as reinfarction, angina pectoris, cerebrovascular incidents, arrhythmias, or disturbances in the peripheral circulation. Twenty percent of patients experienced improved fitness when beta-blockade treatment was withdrawn, which balances the beneficial effects. No other drugs have been shown to have comparable beneficial effects. We conclude that the practical implications of the clinical trials indicate that beta-blockade should be continued for at least 3 years after myocardial infarction in patients without severe side effects.

Adrenergic beta-Antagonists↗
PubMed1987

Beta-blockade in ischemic heart disease and hypertension.

The effect of beta-blocking agents on post-myocardial infarction patients with a history of hypertension or elevated blood pressure (BP) at baseline in two prospective placebo-controlled postinfarction studies using beta-adrenoceptor blocking agents (the Stockholm Metoprolol Trial and the Norwegian Timolol Study) is discussed. The results of both of these trials indicate that active beta-blockade reduces the incidence of nonfatal reinfarction, although the BP levels were similar in the two treatment groups. The differences in the efficacy of treatment in previous studies of hypertension are discussed. So far, none of the studies has shown a significant difference in mortality when different antihypertensive therapies have been compared in the same study. Some aspects of designing future trials comparing different treatment regimens in hypertension are discussed.

Adrenergic beta-Antagonists↗
PubMed1986

Quality of life after myocardial infarction: effect of long term metoprolol on mortality and morbidity.

A double blind randomised study of 154 patients with myocardial infarction assigned to metoprolol (100 mg twice daily) and 147 assigned to placebo compared the effects of treatment in relation to health state over three years. Health state was evaluated by a new method based on the average number of days spent in each of seven mutually exclusive categories of health. The scale took into account death, history of serious complications, functional state, and side effects of treatment. Of the maximum attainable 1095 days alive during the three years patients given metoprolol attained 992 days and those given placebo 964 days. During the period alive the metoprolol treated group spent an average of 278 days in an optimal functional state as compared with 176 days for the placebo treated group. This included 221 and 156 days respectively in a completely asymptomatic state (that is, without either cardiac symptoms or side effects of treatment). The time spent with a serious non-fatal complication was shortened by 56 days in the metoprolol group. The overall differences between the groups were statistically significant (p = 0.03). Aside from bringing an improved quality of life after myocardial infarction, metoprolol may add up to one month to life expectancy for three years of treatment.

Clinical Trials as Topic↗
PubMed1986

Left ventricular function following withdrawal of chronic metoprolol treatment in patients with ischaemic heart disease. A double blind study.

The effect on left ventricular function of a gradual withdrawal of chronic metoprolol treatment in postinfarction patients was studied. All patients were in a randomized double-blind postinfarction study with metoprolol (M 100-200 mg daily; N = 14) or placebo (P; N = 18). After three years treatment the study medication was gradually withdrawn during one week. M-mode echocardiography, guided by concomitant cross-sectional recordings, were performed before, one and 12 weeks after the withdrawal. Treatment (i.e. M or P) had to be reinstituted in eight patients (5 M; 3P) because of the development of disabling symptoms during the follow-up. Heart rate was lower in patients treated with M (57 +/- 4) than with P (69 +/- 10) (p less than 0.01). One week after withdrawal of M, heart rate had increased to 77 +/- 13 (p less than 0.001), while patients on P showed no significant change. In order to minimize the influence of heart rate on the evaluation of time intervals in the cardiac cycle, heart rate dependent correction factors were used. One week after M withdrawal there was a prolongation of the pre-ejection period (PEP) from 120 +/- 15 ms to 133 +/- 16 ms (p less than 0.01), mainly due to a prolongation of the interval for early isovolumetric contraction (Q Mc) from 87 +/- 10 ms to 101 +/- 11 ms (N = 11; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Evaluation of antiarrhythmic effect of metoprolol treatment after acute myocardial infarction: relationship between treatment responses and survival during a 3-year follow-up.

Three hundred and one patients were randomized to 3 years double-blind postinfarction treatment with metoprolol(N = 154) 100 mg b.i.d. or matching placebo (N = 147). Repeated 6 h electrocardiograms were performed pretreatment and after 3 days, 1 month, 6, 12, 24 and 36 months treatment. There were no significant differences in pretreatment ventricular arrhythmia in the two groups. In the placebo group there was an increase both in complexity of the arrhythmia (P less than 0.001) and frequency of premature ventricular complexes (PVCs) (P less than 0.001) by time. These increases were blunted by metoprolol treatment. Treatment effect on mortality was similar in patients both with and without complex PVCs before treatment. In a retrospective analysis, the outcome of patients with an initial PVC frequency of greater than 1 PVC h-1 was evaluated. In metoprolol treated patients in whom the arrhythmia frequency was reduced by greater than 75% after three days of treatment, mortality was lower as compared to those metoprolol treated patients who did not show this treatment response (3% vs 28%, P = 0.013). Mortality in placebo treated patients with frequent PVCs was 24%. In conclusion, chronic metoprolol treatment after acute myocardial infarction blunts the naturally occurring increase of PVC frequency and PVC complexity by time. Patients with frequent PVCs in the early postinfarction phase who respond to metoprolol with greater than 75% reduction of the arrhythmias may have an excellent prognosis. However, this latter hypothesis has to be further tested in a prospective study.

Aged↗
PubMed1986

Effect of metoprolol in postinfarction patients with increased heart size.

Mortality was analysed in relation to clinical and radiological signs of left ventricular failure in a double-blind randomized comparison of 154 post-myocardial infarction patients assigned to metoprolol (100 mg b.i.d.) and 147 patients assigned to placebo treatment. The maximal respiratory rate in the coronary care unit and the relative heart size measured by chest X-ray examination prior to discharge from hospital were used for evaluation of myocardial function. In the placebo group mortality was higher in those with elevated maximal respiratory rate (11% vs. 27%, P less than 0.05) and in those with larger hearts (8% vs. 33%, P less than 0.001). No increase in mortality in patients with findings of left ventricular dysfunction was found in the metoprolol treated group. This was not due to an excess mortality in patients with preserved left ventricular function, but rather due to a reduction in mortality among patients with impaired left ventricular function. In patients with relative heart sizes greater than 460 ml m-2 (= median), mortality was higher in the placebo treated patients as compared to metoprolol treated patients (33% vs 16%, P less than 0.05). During the three year follow-up, repeat chest X-ray examination showed similar heart sizes in the two treatment groups. Furthermore, treatment with digitalis and diuretics were similar in the two treatment groups although more patients in the metoprolol group were withdrawn due to uncontrolled left ventricular heart failure (7 vs 1, P less than 0.05). We conclude that elevated maximal respiratory rate in the coronary care unit and heart enlargement on a pre-discharge chest X-ray, indicate a worsened prognosis. This excess mortality is reduced by metoprolol treatment during a three year follow-up.

Cardiomegaly↗
PubMed1986

Cardiovascular reactivity to mental stress during gradual withdrawal of chronic postinfarction treatment with metoprolol.

In 34 patients on double-blind postinfarction treatment with metoprolol 100-200 mg daily (N = 20) or matching placebo, the study treatment was gradually withdrawn during one week. The patients were subjected to mental stress (a modified version of Stroop's colour word conflict test) before and 1 and 12 weeks after the completion of double-blind withdrawal. This stress increased heart rate (P less than 0.001), blood pressures (P less than 0.001) and adrenaline (P = 0.003), but not noradrenaline in venous plasma. In the placebo group similar responses were evoked on all three occasions. In the metoprolol group, heart rate responses were reduced while on treatment. Following withdrawal there was no rebound increase in the heart rate response. Rather, some blockade persisted one week after withdrawal. Twelve weeks after withdrawal heart rate and blood pressure responses to mental stress were normalized. During treatment the metoprolol group had fewer ventricular arrhythmias than the placebo group. Following withdrawal, ventricular arrhythmias during stress increased in 4 patients in the metoprolol group. Plasma adrenaline levels were reduced one week after withdrawal of metoprolol treatment. Plasma noradrenaline levels did not change within either group during the follow-up period. Thus, no rebound increase in cardiovascular reactivity to mental stress was found, in contrast to our previous findings with physical stressors in similar patients participating in this study. These differences in responsiveness after metoprolol withdrawal may be related to different clearance rates for metoprolol in different tissues. Our results indicate that central, presumably supramedullary, cardiovascular control mechanisms involving beta-adrenoceptors recover at a slow rate following withdrawal.

Adult↗