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Sökning: WFRF:(Waagstein F.)

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1.
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2.
  • Damman, K., et al. (författare)
  • Loop diuretics, renal function and clinical outcome in patients with heart failure and reduced ejection fraction
  • 2016
  • Ingår i: European Journal of Heart Failure. - : Wiley. - 1388-9842. ; 18:3, s. 328-336
  • Tidskriftsartikel (refereegranskat)abstract
    • AimWe aimed to study the relationships of loop diuretic dose with renal function and clinical outcomes in patients with chronic heart failure (HF). Methods and resultsLoop diuretic dose at baseline was recorded in patients included in the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA). The relationship to change in estimated glomerular filtration rate (eGFR) over time and to the first occurrence of the composite outcome of cardiovascular (CV) death or hospitalization owing to HF was examined in propensity score matched cohorts. Of the 5011 patients, 2550, 745, and 449 were receiving >80mg (high), 41-80mg (medium) and 40mg (low) of loop diuretics in furosemide equivalent daily dosages, respectively, which were used to assemble 229, 385, and 1045 pairs of propensity-matched high, medium, and low dose cohorts. Compared with matched no loop diuretic groups, eGFR declined 0.30.2, 0.3 +/- 0.3 and 1.2 +/- 0.5mL/min/1.73m(2)/year in the low-, medium-, and high-dose groups, respectively. Compared with matched no loop diuretic groups, hazard ratios (HR) (95% confidence intervals) for outcome associated with low-, medium- and high-dose groups were 1.71 (1.41-2.06), 1.99 (1.50-2.64), and 2.94 (1.95-4.41), respectively. Higher loop diuretic dose was particularly associated with increased risk for hospitalization owing to HF: HR 4.80 (2.75-8.37), P<0.001. ConclusionsThe use of loop diuretics was associated with a slightly greater rate of decline in eGFR, which did not vary significantly by diuretic dose.Loop diuretic dose was associated with higher risks of (CV) mortality and predominantly hospitalization owing to HF, which appeared to be higher among those receiving higher daily doses.
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3.
  • Herlitz, Johan, et al. (författare)
  • Correlation between enzymatic estimation of infarct size and early mortality rate.
  • 1983
  • Ingår i: British Heart Journal. - : BMJ Group. - 0007-0769. ; 50:6, s. 520-524
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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4.
  • Andersson, Bert, 1952, et al. (författare)
  • Changes in early and late diastolic filling patterns induced by long-term adrenergic beta-blockade in patients with idiopathic dilated cardiomyopathy.
  • 1996
  • Ingår i: Circulation. - 0009-7322. ; 94:4, s. 673-82
  • Tidskriftsartikel (refereegranskat)abstract
    • beta-Blockers have been used in patients with idiopathic dilated cardiomyopathy to improve cardiac performance and theoretically would be beneficial to diastolic function. However, there are few reports on changes in diastolic function during chronic pharmacological treatment of congestive heart failure.The present study was a substudy in the international Metoprolol in Dilated Cardiomyopathy Trial. Transmitral Doppler echocardiography was used to evaluate diastolic function in 77 patients randomly assigned to placebo (n = 37) or metoprolol (n = 40). The patients were treated for 12 months. Changes in Doppler flow variables in the metoprolol group implied a less restrictive filling pattern, expressed as an increase in E-wave deceleration time (placebo, 185 +/- 126 to 181 +/- 64 ms; metoprolol, 152 +/- 63 to 216 +/- 78 ms; P = .01, placebo versus metoprolol). Maximal increase in deceleration time had occurred by 3 months, whereas systolic recovery was achieved gradually and maximal effect was seen by 12 months of treatment. Although deceleration time was correlated to heart rate at baseline, changes in deceleration time were not significantly correlated to changes in heart rate during treatment.During the first 3 months of treatment, maximal effects on diastolic variables were reached, whereas the most prominent effect on systolic function was seen late in the study. It is suggested that effects on diastolic filling account for subsequent later myocardial systolic recovery. The E-wave deceleration time, which in recent studies has been shown to be a powerful predictor of survival, was significantly improved in the metoprolol-treated patients.
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5.
  • Cleland, John G F, et al. (författare)
  • Plasma concentration of amino-terminal pro-brain natriuretic peptide in chronic heart failure: prediction of cardiovascular events and interaction with the effects of rosuvastatin: a report from CORONA (Controlled Rosuvastatin Multinational Trial in Heart Failure).
  • 2009
  • Ingår i: Journal of the American College of Cardiology. - : Elsevier BV. - 1558-3597 .- 0735-1097. ; 54:20, s. 1850-9
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: We investigated whether plasma amino-terminal pro-brain natriuretic peptide (NT-proBNP), a marker of cardiac dysfunction and prognosis measured in CORONA (Controlled Rosuvastatin Multinational Trial in Heart Failure), could be used to identify the severity of heart failure at which statins become ineffective. BACKGROUND: Statins reduce cardiovascular morbidity and mortality in many patients with ischemic heart disease but not, overall, those with heart failure. There must be a transition point at which treatment with a statin becomes futile. METHODS: In CORONA, patients with heart failure, reduced left ventricular ejection fraction, and ischemic heart disease were randomly assigned to 10 mg/day rosuvastatin or placebo. The primary composite outcome was cardiovascular death, nonfatal myocardial infarction, or stroke. RESULTS: Of 5,011 patients enrolled, NT-proBNP was measured in 3,664 (73%). The midtertile included values between 103 pmol/l (868 pg/ml) and 277 pmol/l (2,348 pg/ml). Log NT-proBNP was the strongest predictor (per log unit) of every outcome assessed but was strongest for death from worsening heart failure (hazard ratio [HR]: 1.99; 95% confidence interval [CI]: 1.71 to 2.30), was weaker for sudden death (HR: 1.69; 95% CI: 1.52 to 1.88), and was weakest for atherothrombotic events (HR: 1.24; 95% CI: 1.10 to 1.40). Patients in the lowest tertile of NT-proBNP had the best prognosis and, if assigned to rosuvastatin rather than placebo, had a greater reduction in the primary end point (HR: 0.65; 95% CI: 0.47 to 0.88) than patients in the other tertiles (heterogeneity test, p = 0.0192). This reflected fewer atherothrombotic events and sudden deaths with rosuvastatin. CONCLUSIONS: Patients with heart failure due to ischemic heart disease who have NT-proBNP values <103 pmol/l (868 pg/ml) may benefit from rosuvastatin.
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6.
  • Eriksson, Jan W, et al. (författare)
  • Glucose turnover and adipose tissue lipolysis are insulin-resistant in healthy relatives of type 2 diabetes patients : is cellular insulin resistance a secondary phenomenon?
  • 1999
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 48:8, s. 1572-8
  • Tidskriftsartikel (refereegranskat)abstract
    • To elucidate potential mechanisms for insulin resistance occurring early in the development of type 2 diabetes, we studied 10 young healthy individuals, each with two first-degree relatives with type 2 diabetes, and 10 control subjects without known type 2 diabetic relatives. They were pairwise matched for age (35 +/- 1 vs. 35 +/- 1 years), BMI (23.6 +/- 0.6 vs. 23.1 +/- 0.4 kg/m2), and sex (four men, six women). Glucose turnover was assessed during a euglycemic clamp at two insulin levels (low approximately 20 mU/l; high approximately 90 mU/l), and abdominal subcutaneous adipose tissue (SAT) lipolysis and blood flow were concomitantly studied with microdialysis and 133Xe clearance. HbA1c was higher in patients with type 2 diabetic relatives than in control subjects (4.8 +/- 0.1 vs. 4.5 +/- 0.1%, P < 0.02), but fasting glucose, insulin, and C-peptide levels were similar. During the clamp, the insulin sensitivity index for glucose disposal was lower (P < 0.03) in relatives than in control subjects (low 12.0 +/- 1.6 vs. 18.1 +/- 1.4; high 9.4 +/- 0.8 vs. 12.9 +/- 0.6 [100 x mg x l x kg(-1) x mU(-1) x min(-1)]). This difference was partially attributed to slightly higher clamp insulin levels in the relatives (P < 0.03), suggesting an impaired rate for insulin clearance. SAT lipolysis measured as in situ glycerol release did not differ under basal conditions (2.0 +/- 0.2 vs. 2.1 +/- 0.2 micromol x kg(-1) x min(-1)), but the suppression during the insulin infusion was less marked in relatives than in control subjects (glycerol release: low 0.92 +/- 0.09 vs. 0.68 +/- 0.16; high 0.71 +/- 0.10 vs. 0.34 +/- 0.10 micromol x kg(-1) x min(-1); P < 0.03). Plasma nonesterified fatty acids also tended to be higher in relatives than in control subjects during the insulin infusion (NS). In contrast, in vitro experiments with isolated subcutaneous adipocytes displayed similar effects of insulin in relatives and control subjects with respect to both glucose uptake and antilipolysis. In conclusion, insulin action in vivo on both lipolysis and glucose uptake is impaired early in the development of type 2 diabetes. Since this impairment was not found in isolated adipocytes, it may be suggested that neural or hormonal perturbations precede cellular insulin resistance in type 2 diabetes.
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8.
  • Herlitz, Johan, et al. (författare)
  • Clinical observations after treatment with metoprolol in suspected acute myocardial infarction in relation to age
  • 1985
  • Ingår i: Acta Medica Scandinavica. - : Wiley-Blackwell Publishing Ltd.. - 0001-6101. ; 217:3, s. 293-298
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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9.
  • Herlitz, Johan, et al. (författare)
  • Development of congestive heart failure after treatment with metoprolol in acute myocardial infarction
  • 1984
  • Ingår i: British Heart Journal. - : BMJ Group. - 0007-0769. ; 51:5, s. 539-544
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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10.
  • Herlitz, Johan, et al. (författare)
  • Effect of metoprolol on chest pain in acute myocardial
  • 1984
  • Ingår i: British Heart Journal. - : BMJ Group. - 0007-0769. ; 51:4, s. 438-444
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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11.
  • Herlitz, Johan, et al. (författare)
  • Effect of metoprolol on indirect signs of the size and severity of acute myocardial infarction
  • 1983
  • Ingår i: American Journal of Cardiology. - : Elsevier Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 51:8, s. 1282-1288
  • Tidskriftsartikel (refereegranskat)abstract
    • 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 beta1-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 μkat · liter−1)when the patient was treated within 12 hours of the onset of pain (13.3 ± 0.6 μkat · 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 ≤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 12 hours and >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 longterm prognosis.
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12.
  • Herlitz, Johan, et al. (författare)
  • Effect of metoprolol on the prognosis among patients with suspected acute myocardial infarction and indirect signs of congestive heart failure. (A subgroup analysis of the Göteborg Metoprolol Trial)
  • 1997
  • Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 80:9B, s. 40J-44J
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study is to describe the impact of early treatment with metoprolol on prognosis during 1 year of follow-up in patients with suspected acute myocardial infarction (AMI) and indirect signs of congestive heart failure (CHF). Patients aged 40-74 years who presented within 48 hours of onset of symptoms raising suspicion of AMI were assessed for inclusion. All patients participated in the Göteborg Metoprolol Trial and had indirect indices of CHF according to various clinical criteria. As soon as possible after hospital admission, patients received either placebo or metoprolol (15 mg) divided into 3 intravenous injections, then oral treatment, 200 mg daily for 3 months. Thereafter, most patients in both treatment groups received metoprolol in an open manner. Among the 1,395 randomized patients, 262 (19%) had signs of mild-to-moderate CHF before randomization. Of these, 131 were randomized to metoprolol and 131 to placebo. During the first 3 months, mortality was 10% among patients randomized to metoprolol versus 19% among patients randomized to placebo (p = 0.036). The corresponding figures for the first year were 14% and 27%, respectively (p = 0.0099). Patients randomized to placebo who showed signs of CHF had a 1-year mortality rate of 28% compared with 10% among patients without such signs (p <0.001). The results suggest that early treatment with metoprolol markedly reduces mortality in patients having suspected AMI and signs of CHF.
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13.
  • Herlitz, Johan, et al. (författare)
  • Effects of work and acute beta-receptor blockade on myocardial noradrenaline release in congestive cardiomyopathy
  • 1979
  • Ingår i: Clinical Cardiology. - : John Wiley & Sons, Inc. - 0160-9289 .- 1932-8737. ; 2:6, s. 424-430
  • Tidskriftsartikel (refereegranskat)abstract
    • Systemic hemodynamic changes and noradrenaline concentrations in coronary sinus blood were studied at rest and during work before and after acute beta-receptor blockade. Patients with congestive cardiomyopathy were compared to patients with primary valvular diseases and to healthy subjects. Noradrenaline concentrations were higher in coronary sinus blood than in arterial blood and increased after beta blockade and during work. Noradrenaline concentrations were more increased in patients with more pronounced myocardial failure and did not seem to separate patients with congestive cardiomyopathy from those with valvular disease. Patients with congestive cardiomyopathy showed a good hemodynamic tolerance toward acute beta blockade.
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14.
  • Herlitz, Johan, et al. (författare)
  • Effects on mortality during five years follow-up after early intervention with metoprolol in suspected acute myocardial infarction
  • 1988
  • Ingår i: Acta Medica Scadinavica. - : Wiley-Blackwell. - 0001-6101. ; 223:3, s. 227-231
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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15.
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16.
  • Herlitz, Johan, et al. (författare)
  • Enzymatically and electrocardiographically estimated infarct size in relation to pain in acute myocardial infarction
  • 1984
  • Ingår i: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 71:5, s. 239-246
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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17.
  • Herlitz, Johan, et al. (författare)
  • Goteborg Metoprolol Trial : clinical observations
  • 1984
  • Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 53:13, s. 37-45
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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18.
  • Herlitz, Johan, et al. (författare)
  • Göteborg Metoprolol Trial : mortality and causes of death
  • 1984
  • Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 53:13, s. 9-14
  • Tidskriftsartikel (refereegranskat)abstract
    • During the 3-month blind treatment period there were 40 deaths in the metoprolol group compared with 62 deaths in the placebo group (p = 0.024). During the first year (after 3 months the 2 groups were treated similarly) there were 64 deaths in the metoprolol group vs 93 in the placebo group (p = 0.017) and during 2 years 92 patients died in the metoprolol group vs 120 in the placebo group (p = 0.043). The relative incidence of different causes of death did not differ significantly between the 2 treatment groups, indicating that metoprolol reduced all causes of death to the same extent as its effect on overall mortality.
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19.
  • Herlitz, Johan, et al. (författare)
  • Göteborg Metoprolol Trial : effects on arrhythmias
  • 1984
  • Ingår i: American Journal of Cardiology. - : Elsevier. - 0002-9149 .- 1879-1913. ; 53:13, s. 27-31
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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20.
  • Herlitz, Johan, et al. (författare)
  • Göteborg Metoprolol Trial : design, patient characteristics and conduct
  • 1984
  • Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 53:13, s. 3D-8D
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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21.
  • Herlitz, Johan, et al. (författare)
  • Göteborg Metoprolol Trial : electrocardiographically estimated infarct size
  • 1984
  • Ingår i: American Journal of Cardiology. - : Elsevier. - 0002-9149 .- 1879-1913. ; 53:13, s. 22-26
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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22.
  • Herlitz, Johan, et al. (författare)
  • Hemodynamic and clinical findings after combined therapy with metoprolol and nifedipine in acute myocardial infarction
  • 1984
  • Ingår i: Clinical Cardiology. - : John Wiley & Sons, Inc.. - 0160-9289 .- 1932-8737. ; 7:8, s. 425-432
  • Tidskriftsartikel (refereegranskat)abstract
    • In a double-blind trial, 30 patients with suspected acute myocardial infarction with onset of symptoms within the previous 24 h were randomized to treatment with 10 mg nifedipine/placebo orally 4 times a day during hospitalization. All patients were given 15 mg metoprolol intravenously 20 min after the initial administration of nifedipine/placebo, and thereafter, 50 mg 4 times a day. The combined therapy resulted only in moderate changes in systolic blood pressure and heart rate compared with metoprolol alone. Three of the 15 patients in the nifedipine group versus 2 of the 15 in the placebo group were withdrawn because of hypotension and/or bradycardia. None was withdrawn because of congestive heart failure or A-V block. It is concluded that the combination of nifedipine and metoprolol seems to be a relatively well-tolerated combination in acute myocardial infarction.
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23.
  • Herlitz, Johan, et al. (författare)
  • Relationship between enzymatically estimated infarct size and short- and long-term survival after acute myocardial infarction
  • 1984
  • Ingår i: Journal of Internal Medicine. - : Wiley-Blackwell Publishing Ltd.. - 0954-6820 .- 1365-2796. ; 216:3, s. 261-267
  • Tidskriftsartikel (refereegranskat)abstract
    • In 585 patients with acute myocardial infarction (AMI) and no previous MI the maximal activity of serum heat-stable lactate dehydrogenase (LD) (EC 1.1.1.27) activity was related to 1-year and 2-year mortality rates. All patients participated in a double-blind trial with metoprolol during the first three months after an AMI. Thereafter both groups were treated in a similar way. A strong relationship was found between LD maximum activity and the in-hospital prognosis (p<0.001), the 1-year survival rate (p<0.001) and the 2-year survival rate (p<0.001). When the patients who were alive after primary hospitalization were analyzed as a separate group, the relationship between LD maximum activity and 1-year and 2-year survival rates remained (p<0.001). In a subsample of 171 patients the maximal activity of creatine kinase (CK) (EC 2.7.3.2) and CK subunit B did not correlate either with in-hospital, 1-year or 2-year survival rates. We conclude that, when a sufficiently large number of patients are investigated, there is a strong relationship between serum enzyme maximum activity and short- and long-term survival.
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24.
  • Herlitz, Johan, et al. (författare)
  • Relationship between infarct size and incidence of severe ventricular arrhythmias in a double-blind trial with metoprolol in acute myocardial infarction
  • 1984
  • Ingår i: International Journal of Cardiology. - : Elsevier Ireland Ltd. - 0167-5273 .- 1874-1754. ; 6:1, s. 47-60
  • Tidskriftsartikel (refereegranskat)abstract
    • 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 β1-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 < 0.001), while this could not be demonstrated in patients on the beta-blocker (P > 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 < 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.
  •  
25.
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26.
  • Herlitz, Johan, et al. (författare)
  • The influence of early intervention in acute myocardial infarction on long-term mortality and morbidity as assessed in the Göteborg metoprolol trial
  • 1986
  • Ingår i: International Journal of Cardiology. - : Elsevier Ireland Ltd. - 0167-5273 .- 1874-1754. ; 10:3, s. 291-301
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
27.
  • Herlitz, Johan, et al. (författare)
  • The time course in acute myocardial infarction evaluated with precordial mapping and standard ECG
  • 1983
  • Ingår i: Clinical Cardiology. - : John Wiley & Sons, Inc.. - 0160-9289 .- 1932-8737. ; 6:10, s. 479-486
  • Tidskriftsartikel (refereegranskat)abstract
    • 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 a VF 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.
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28.
  • Herlitz, Johan, et al. (författare)
  • Treatment of pain in acute myocardial infarction
  • 1989
  • Ingår i: British Heart Journal. - : B M J Group. - 0007-0769. ; 61:1, s. 9-13
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
29.
  • Herlitz, Johan, et al. (författare)
  • Variability, prediction and prognostic significance of chest pain in acute myocardial infarction
  • 1986
  • Ingår i: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 73:1, s. 13-21
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
30.
  • Hjalmarson, A, et al. (författare)
  • The Göteborg metoprolol trial. Effects on mortality and morbidity in acute myocardial infarction
  • 1983
  • Ingår i: Circulation. - : SRDS. - 1539-3011. ; 67:suppl 1, s. 68-69
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
31.
  • Hjalmarson, Å, et al. (författare)
  • Effect on mortality of metoprolol in acute myocardial infarction
  • 1981
  • Ingår i: The Lancet. - : The Lancet Publishing Group. - 0140-6736 .- 1474-547X. ; 318:8251, s. 823-827
  • Tidskriftsartikel (refereegranskat)abstract
    • 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<0·03). Mortality rates are given according to the treatment group to which the patients were initially randomly allocated.
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32.
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33.
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34.
  • Hjamarson, A, et al. (författare)
  • Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure. The Metoprolol CR/XL randomized intervention trial in congestive heart failure
  • 2000
  • Ingår i: Journal of the American Medical Association. - : JAMA. - 0221-7678. ; 283:10, s. 1295-1302
  • Tidskriftsartikel (refereegranskat)abstract
    • Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored. OBJECTIVE: To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure. DESIGN: Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year. SETTING: Three hundred thirteen sites in 14 countries. PARTICIPANTS: Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy. INTERVENTIONS: Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001). MAIN OUTCOME MEASURES: Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients. RESULTS: The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P<.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P<.001), number of hospitalizations due to worsening heart failure (317 vs 451; P<.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P<.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively). CONCLUSIONS: In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.
  •  
35.
  • Inglis, S. C., et al. (författare)
  • Intermittent claudication as a predictor of outcome in patients with ischaemic systolic heart failure: analysis of the Controlled Rosuvastatin Multinational Trial in Heart Failure trial (CORONA)
  • 2010
  • Ingår i: European Journal of Heart Failure. - : Wiley. - 1388-9842. ; 12:7, s. 698-705
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: To examine the relationship between baseline intermittent claudication and outcomes in patients enrolled in the Controlled Rosuvastatin Multinational Trial in Heart Failure trial (CORONA). Intermittent claudication is an independent predictor of worse outcome in coronary heart disease, but its prognostic importance in heart failure (HF) is unknown. Patients aged >or=60 years with NYHA class II-IV, low ejection fraction HF of ischaemic aetiology were enrolled in CORONA. Rosuvastatin did not reduce the primary outcome or all-cause mortality. METHODS AND RESULTS: To determine whether intermittent claudication was an independent predictor of clinical outcomes, a three-step multivariable model was built: (i) demographic/clinical variables, (ii) biochemical measures added, (iii) high-sensitivity C-reactive protein and N-terminal pro B-type natriuretic-peptide added. Of the 5011 patients, 637 (12.7%) had intermittent claudication at baseline. Patients with intermittent claudication were more likely to be male (83 vs. 75%), be a current smoker (19 vs. 9%), and have diabetes mellitus (36 vs. 29%) relative to those without intermittent claudication. Over a median 33-month follow-up, 2168 patients died or were hospitalized for HF. Patients with intermittent claudication had an increased risk of death (any cause) (adjusted hazard ratio 1.36, 95% CI 1.19-1.56, P < 0.0001), death from worsening HF (1.35, 1.03-1.77, P = 0.028), sudden death (1.24, 1.00-1.54, P = 0.05), and risk of non-fatal or fatal myocardial infarction (time to first event 1.67, 1.24-2.27, P < 0.001). In the full multivariable model, intermittent claudication remained an independent predictor of most outcomes evaluated. CONCLUSION: Intermittent claudication is a relatively common symptom in ischaemic HF and an independent predictor of worse outcome. Clinical Trial Registration Information: NCT00206310-http://clinicaltrials.gov/ct2/show/NCT00206310?term=corona&ran k=2.
  •  
36.
  • Kjekshus, John, et al. (författare)
  • Rosuvastatin in older patients with systolic heart failure.
  • 2007
  • Ingår i: The New England journal of medicine. - 1533-4406. ; 357:22, s. 2248-61
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Patients with systolic heart failure have generally been excluded from statin trials. Acute coronary events are uncommon in this population, and statins have theoretical risks in these patients. METHODS: A total of 5011 patients at least 60 years of age with New York Heart Association class II, III, or IV ischemic, systolic heart failure were randomly assigned to receive 10 mg of rosuvastatin or placebo per day. The primary composite outcome was death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. Secondary outcomes included death from any cause, any coronary event, death from cardiovascular causes, and the number of hospitalizations. RESULTS: As compared with the placebo group, patients in the rosuvastatin group had decreased levels of low-density lipoprotein cholesterol (difference between groups, 45.0%; P<0.001) and of high-sensitivity C-reactive protein (difference between groups, 37.1%; P<0.001). During a median follow-up of 32.8 months, the primary outcome occurred in 692 patients in the rosuvastatin group and 732 in the placebo group (hazard ratio, 0.92; 95% confidence interval [CI], 0.83 to 1.02; P=0.12), and 728 patients and 759 patients, respectively, died (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.31). There were no significant differences between the two groups in the coronary outcome or death from cardiovascular causes. In a prespecified secondary analysis, there were fewer hospitalizations for cardiovascular causes in the rosuvastatin group (2193) than in the placebo group (2564) (P<0.001). No excessive episodes of muscle-related or other adverse events occurred in the rosuvastatin group. CONCLUSIONS: Rosuvastatin did not reduce the primary outcome or the number of deaths from any cause in older patients with systolic heart failure, although the drug did reduce the number of cardiovascular hospitalizations. The drug did not cause safety problems. (ClinicalTrials.gov number, NCT00206310.)
  •  
37.
  • Lam, P. H., et al. (författare)
  • Digoxin use and lower risk of 30-day all-cause readmission in older patients with heart failure and reduced ejection fraction receiving β-blockers
  • 2018
  • Ingår i: Clinical Cardiology. - : Wiley. - 0160-9289. ; 41:3, s. 406-412
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Digoxin use has been associated with a lower risk of 30-day all-cause admission and readmission in patients with heart failure and reduced ejection fraction (HFrEF). Hypothesis: Digoxin use will be associated with improved outcomes in patients with HFrEF receiving β-blockers. Methods: Of the 3076 hospitalized Medicare beneficiaries with HFrEF (EF <45%), 1046 received a discharge prescription for β-blockers, of which 634 were not on digoxin. Of the 634, 204 received a new discharge prescription for digoxin. Propensity scores for digoxin use, estimated for each of the 634 patients, were used to assemble a matched cohort of 167 pairs of patients receiving and not receiving digoxin, balanced on 30 baseline characteristics. Matched patients (n = 334) had a mean age of 74 years and were 46% female and 30% African American. Results: 30-day all-cause readmission occurred in 15% and 27% of those receiving and not receiving digoxin, respectively (hazard ratio [HR]: 0.51, 95% confidence interval [CI]: 0.31-0.83, P = 0.007). This beneficial association persisted during 4 years of follow-up (HR: 0.72, 95% CI: 0.57-0.92, P = 0.008). Digoxin use was also associated with a lower risk of the combined endpoint of all-cause readmission or all-cause mortality at 30 days (HR: 0.54, 95% CI: 0.34-0.86, P = 0.009) and at 4 years (HR: 0.76, 95% CI: 0.61-0.96, P = 0.020). Conclusions: In hospitalized patients with HFrEF receiving β-blockers, digoxin use was associated with a lower risk of 30-day all-cause readmission but not mortality, which persisted during longer follow-up. © 2018 Wiley Periodicals, Inc.
  •  
38.
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39.
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40.
  •  
41.
  •  
42.
  • Richterova, A, et al. (författare)
  • Goteborg Metoprolol Trial : effects on chest pain
  • 1984
  • Ingår i: American Journal of Cardiology. - : Excerpta Medica, Inc.. - 0002-9149 .- 1879-1913. ; 53:13, s. 32-36
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of metoprolol on chest pain was compared with that of placebo in all randomized patients. The pain score before and 15 minutes after the injection of trial medication was registered and a reduction in chest pain was observed in the metoprolol group. Increasing chest pain after blind injection was observed in only 16 and 9 patients from the placebo and metoprolol groups, respectively. Comparison with the placebo as well as detailed analysis of clinical data revealed that in these patients the increasing pain could not be explained by coronary spasm evoked by beta-blockade. Similarly, metoprolol did not exhibit any unfavorable effect on the 14 patients who were withdrawn (together with the 28 patients given placebo) from blind treatment due to angina pectoris. Either metoprolol does not induce coronary vasospasm or spasm does not play a role in these patients with definite and suspected acute myocardial infarction as well as unstable angina pectoris. Metoprolol reduced the need for analgesics during the first 4 days and shortened the duration of pain. The effects were similar in patients with early and late treatment, but may depend on initial heart rate, blood pressure and site of infarction.
  •  
43.
  • Rydén, L, et al. (författare)
  • A Double-Blind Trial of Metoprolol in Acute Myocardial Infarction : Effects on Ventricular Tachyarrhythmias
  • 1983
  • Ingår i: New England Journal of Medicine. - : Massachusetts Medical Society. - 0028-4793 .- 1533-4406. ; 308:11, s. 614-618
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
44.
  •  
45.
  •  
46.
  •  
47.
  • Waagstein, Finn, 1938, et al. (författare)
  • Increased exercise ejection fraction and reversed remodeling after long-term treatment with metoprolol in congestive heart failure: a randomized, stratified, double-blind, placebo-controlled trial in mild to moderate heart failure due to ischemic or idiopathic dilated cardiomyopathy.
  • 2003
  • Ingår i: European journal of heart failure. - 1388-9842. ; 5:5, s. 679-91
  • Tidskriftsartikel (refereegranskat)abstract
    • the effects of long-term administration of beta-blockers on left ventricular (LV) function during exercise in patients with ischemic heart disease (IHD) and idiopathic dilated cardiomyopathy (DCM) are controversial.patients with stable congestive heart failure (CHF) (New York heart association [NYHA] class II and III) and ejection fraction (EF) < or =0.40 were randomized to metoprolol, 50 mg t.i.d. or placebo for 6 months. Patients were divided into two groups: ischemic heart disease (IHD) and idiopathic dilated cardiomyopathy (DCM). The mean EF was 0.29 in both groups and 92% were taking angiotensin-converting enzyme (ACE) inhibitors. In the IHD group, 84% had suffered a myocardial infarction (MI) and 64% had undergone revascularization at least 6 months before the study. LV volumes were measured by equilibrium radionuclide angiography. Mitral regurgitation was assessed by Doppler echocardiography. All values are changes for metoprolol subtracted by changes for placebo.metoprolol improved LV function markedly both at rest and during sub-maximal exercise in both groups. The mean increase in EF was 0.069 at rest (P<0.001) and 0.078 during submaximal exercise (P<0.001). LV end-diastolic volume decreased by 22 ml at rest (P=0.006) and by 15 ml during exercise (P=0.006). LV end-systolic volume decreased by 23 ml both at rest (P=0.001) and during exercise (P=0.004). Exercise time increased by 39 s (P=0.08). In the metoprolol group, mitral regurgitation decreased (P=0.0026) and only one patient developed atrial fibrillation vs. eight in the placebo group (P=0.01).metoprolol improves EF both at rest and during submaximal exercise and prevents LV dilatation in mild to moderate CHF due to IHD or DCM.
  •  
48.
  • Waagstein, F, et al. (författare)
  • Metoder för effektregistrering vid hjärtinfarkt
  • 1983
  • Ingår i: Proceedings of Nordiskt Symposium "Klinisk Läkemedelsprövning", Göteborg 1982. - : A Lindrgren och söner AB. ; , s. 97-110
  • Konferensbidrag (refereegranskat)
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