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The hemodynamic effects of dobutamine (5 to 20 microg/kg/min intravenously) and enoximone (0.5 to 2 mg/kg intravenously) were assessed by pulmonary artery catheterization in 29 patients with chronic HF before and after 9 to 12 months of treatment with metoprolol or carvedilol at standard target maintenance oral doses. Hemodynamic studies were performed after >/=12 h of wash-out from all cardiovascular medications, except the beta-blockers that were administered 3 h before the second study.
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beta-Blockers, particularly propranolol, have been shown to be an effective treatment for neuroleptic-induced akathisia (NIA). To examine the relative contribution of beta-1 and beta-2 receptor blockade to the therapeutic effect of propranolol, we studied a beta-1 selective agent (low dose metoprolol) and a beta-2 specific blocker (ICI 118,551). Both agents ameliorated NIA. To further evaluate instruments for quantifying NIA we compared (a) two sets of clinical ratings during the metoprolol study and (b) clinical and electromechanical ratings of NIA during the ICI 118,551 study. The changes in clinical ratings of NIA after metoprolol were similar for most patients; however, the changes in electromechanical and clinical ratings after ICI 118,551 were similar in less than half of the patients studied.
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To estimate associations between use of β-blockers, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin receptor blockers (ARBs) and breast cancer recurrence in a large Danish cohort.
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The responder rate (that is reduction of headache days per month more than 50 %) was 7/10 at three months after the injection. On average the number of headache days per month was reduced from 19.2 days to a minimum of 10.1 days. After three to six months the number of headache days increased again in all responders. Slight local side effects such as redness or temporary pain were observed in all patients, but severe side effects such as infections, fever, ptosis or allergic reactions did not occur.
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The Stockholm Metoprolol Trial is a prospective double-blind placebo-controlled postmyocardial infarction study of 301 patients treated with metoprolol, 100 mg b.i.d., or matching placebo for three years. From this study we have retrospectively evaluated the outcome in patients with a history of treatment for hypertension prior to the index infarction. There were 41 such patients in the placebo group and 35 in the metoprolol group. Blood pressures during follow-up were nearly identical in the two groups. During the three years 11 patients died in the placebo group and 7 in the metoprolol group. Corresponding figures for nonfatal events such as reinfarction, coronary artery bypass surgery, cerebrovascular events and lower limb amputation were 12 vs. 1 (p less than 0.005), 3 vs. 0, 4 vs. 0 and 1 vs. 0, respectively. The numbers of patients with fatal and nonfatal events were 24 vs. 8 (p less than 0.01). In a retrospective subgroup analysis the results must always be interpreted with caution. The present results may, however, imply that postinfarction treatment with metoprolol reduces nonfatal atherosclerotic complications, especially nonfatal reinfarctions, in patients with a history of hypertension.
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The polarity of a drug is one of the most important parameters for the elaboration of switching systems. If the polarity of the drug is low or medium, "reversed-phase" chromatography is well adapted. The plasma or urine sample is diluted with water, centrifuged and injected first into a column of medium polarity (C2, CN or diol bonded phases). The compounds of interest are stopped on the top of the column and rinsed with water, then eluted and chromatographed on a C8 or C18 analytical column. A third column of still lower polarity can be added to improve the specificity of the system. In each successive step, the polarities of the mobile phases and columns should be decreased to reconcentrate the sample and reduce the band broadening that occurred in the previous step. Compounds of high polarity show almost no retention on reversed-phase columns, and normal-phase chromatography should be used. Aqueous solutions cannot be injected into polar bonded-phase columns as they lead to excessive band broadening. This problem can be solved by diluting plasma or urine with a large volume of a water-miscible organic solvent and injecting the clear supernatant. The compounds to be assayed are first reconcentrated on a polar column (NH2 or N(CH3)2 bonded phase) and then eluted. The selected "heart cut" of the eluate is chromatographed on another, more polar column. The influence of the polarity of drugs on the choice of switching systems is exemplified by assay methods for drugs of low, medium and high polarity.
The aim of this work was to evaluate binding capacity of quinidine, disopyramide and metoprolol to melanin in vitro. The antiarrhythmics studied cause adverse reactions to the eye. Synthetic DOPA-melanin was used in the studies and a UV spectrophotometric method was employed to determine the drugs. The studies of the kinetics of the formation of quinidine-melanin, disopyramide-melanin and metoprolol-melanin complexes indicate that for all the complexes investigated the maximum time to reach reaction equilibrium is 24 h. Binding parameters, i.e., the numbers of independent binding sites and the association constants were determined on the basis of the Scatchard plots. An analysis of the binding curves obtained supports our conclusion that both strong (n1) and weak (n2) binding sites are involved in the formation of the complexes investigated. The total numbers of binding sites in synthetic DOPA-melanin complexes with quinidine, disopyramide and metoprolol were 0.525, 0.493 and 0.387 micromol/mg, respectively. The quinidine-melanin complex is characterized by greater stability (K1 = 3.00 x 10(5) M(-1), K2 = 1.75 x 10(3) M(-1)) in comparison with biopolymer complexes with disopyramide (K1 = 1.12 x 10(4) M(-1), K2 = 6.04 x 10(2) M(-1)) and metoprolol (K1 = 1.42 x 10(4) M(-1), K2 = 7.89 x 10(2) M(-1)). The ability of these drugs to form complexes with melanin in vitro may be one of the reasons for their ocular toxicity in vivo, as a result of their accumulation in melanin in the eye.
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CO(thermo) ranged from 2.1 to 8.2 L/min. CO(PET) determined from both LV and RV was linearly related to CO(thermo) with slopes close to 1 (LV, r = 0.98; RV, r = 0.96; both P < 0.001). Interobserver reproducibility was r = 0.98, P < 0.001. The PCWP range was 6-14 mm Hg and the lung-uptake %ID was 2.7-8.5 %ID. When normalized to baseline, lung-uptake %ID was correlated with PCWP (r = 0.56, P = 0.01) and linearly correlated with LV input resistance (PCWP divided by CO(thermo); r = 0.91, P < 0.001). When both lung-uptake %ID and stroke volume were normalized to baseline, a piecewise linear relation was found (r = 0.95, P < 0.001).
A 58 year old man experienced an attack of squeezing chest pain. A contrast enhanced computed tomographic scan showed acute dissection of the descending aorta. Treatment with metoprolol and nicardipine kept his blood pressure below 130/90 mm Hg while he was supine at rest and after walking. Serial contrast enhanced computed tomographic scans showed opacification of the false lumen (which was not opacified initially) on the 42nd day; moderate regression of the false lumen on the 67th day, and resolution of the false lumen on the 266th day. This is the first in vivo demonstration of spontaneous resolution of aortic dissection detected by serial contrast enhanced computed tomographic scans.
D,l-sotalol significantly reduces the incidence of recurrences of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.
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The addition of flecainide in combination with sotalol/metoprolol may be an effective antiarrhythmic strategy for the control of ventricular arrhythmias in patients with ARVC refractory to single-agent therapy and/or catheter ablation.
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The average RHR at baseline and discharge were (71 ± 13) bpm and (63 ± 9) bpm. The proportion of patients reaching the RHR goals when discharged was 35.9% in stage 1 vs 48.3% (P < 0.001) in stage 2. The rate of β-blocker usage was 80.1% vs 81.0% (P = 0.162) in stage 1, 90.3% vs 91.3% (P < 0.001) in stage 2. The average dose of metoprolol succinate sustained-release tablet was (38 ± 18) vs (39 ± 42) mg/d (P < 0.001) in stage 1, (40 ± 23) vs (46 ± 23) mg/d (P < 0.001) in stage 2. The severe adverse events at both stages had no significant differences.
At 12 months, patients on carvedilol, compared with those continuing on metoprolol, showed a decrease in LV dimensions (end-diastolic volume -8+/-7 vs. +7+/-6 ml/m2, p = 0.053; end-systolic volume -7+/-5 vs. +6+/-4 ml/m2, p = 0.047), an improvement in LV ejection fraction (+7+/-3% vs. -1+/-2%, p = 0.045), a reduction in ventricular ectopic beats (-12+/-9 vs. +62+/-50 n/h, p = 0.05) and couplets (-0.5+/-0.4 vs. +1.5+/-0.6 n/h, p = 0.048), no significant benefit on symptoms and quality of life and a negative effect on peak oxygen consumption (-0.6+/-0.6 vs. +1.3+/-0.5 ml/kg/min, p = 0.03).
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In patients with CHF, physicians should aim to treat the LV dysfunction, not just the CHF symptoms. LV dysfunction is a chronic disease that is usually progressive, even when it seem compensated. The risk of sudden death or progressive CHF is very real. Adding a beta blocker to the treatment regimen while the disease is still compensated or after resolution of an acute exacerbation can stabilize or reverse the LV dysfunction and improve survival. Beta blockade is now a vital part of the standard of care for most patients with LV dysfunction.
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beta-blockers have been shown to benefit patients after myocardial infarction by decreasing mortality, sudden cardiac death, and reinfarction. Although beta-blockers are recommended for all patients with acute coronary syndromes (ACS) without contraindications, a target heart rate (HR) is recommended only for patients with unstable angina/non ST-elevation myocardial infarction. A contemporary series documenting trends in beta-blocker usage and achieved HR and blood pressures (BP) is not available. The study objectives were to monitor trends in HR and BP in relation to beta-blocker use in a contemporary series of patients with ACS.
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Patients are eligible if they have a positive tilt test and 3 syncopal spells preceding the tilt test. They are excluded if they have seizures or other causes of syncope; important heart disease; a contraindication to or need for beta blockers; a permanent pacemaker; a major noncardiovascular disease; or previous use of beta blockers at a dose greater than the equivalent of metoprolol 25mg twice daily for the purpose of suppressing vasovagal syncope.
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Verapamil sustained-release (SR)/trandolapril is a combination of a phenylalkylamine calcium antagonist and an angiotensin converting enzyme inhibitor for the management of essential hypertension. Verapamil SR/trandolapril does not adversely influence glucose, insulin or lipid parameters in patients with mild to moderate essential hypertension and type 2 (non-insulin-dependent) diabetes mellitus with or without elevated cholesterol and/or triglyceride levels. Verapamil SR/trandolapril reduces proteinuria to a greater extent than the individual components in patients with diabetic or non-diabetic proteinuria. The antihypertensive efficacy of once daily verapamil SR/trandolapril (180/1 or 180/2 mg) for 8 weeks or 6 months is similar to that of atenolol/chlorthalidone (100/25 mg) and lisinopril/hydrochlorothiazide (20/12.5 mg), and was at least as good as that of metoprolol/hydrochlorothiazide (100/12.5 mg) in a small trial. The reduction in sitting or supine diastolic and systolic blood pressure is greater after verapamil SR/trandolapril (180/2 to 240/4 mg) than after monotherapy with verapamil SR (180 and 240 mg/day) or trandolapril (2 to 8 mg/day). Fewer cardiac events occurred after verapamil SR/trandolapril (240/1 to 360/2 mg/day) than after trandolapril (1 to 2 mg/day) in postmyocardial infarction patients with congestive heart failure. The incidence of adverse events after verapamil SR/trandolapril is similar to that of comparator drugs and the individual components of the combination.
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A total of 49,673 patients receiving metoprolol were identified within a cohort of 3,649,285 insurance members. While the crude analysis revealed a higher risk for index events in patients receiving the generic drug (Bremen: RR 1.45; Northern Germany: RR 1.14), no elevated risk remained after confounder adjustment (Bremen: OR 1.06; Northern Germany: OR 1.04). Among co-morbid conditions considered as confounders, a previous CV event and an elevated thromboembolic risk exerted the strongest effect on index events.
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In a study of 48 patients with coronary artery disease and evidence of ischemia during exercise and daily life, metoprolol reduced the threshold of myocardial ischemia in a dose-dependent manner. This effect of beta blockers is probably due to increased coronary tone.
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In this first-in-man study, ten NYHA class III/IV patients were implanted with an ultrasonic pressure-monitoring device, followed a month later by loading with MXL 25 mg/day and uptitrated every two weeks to 200 mg/day. PAP was measured at each follow up. Diurnal variation was evaluated at baseline (no MXL), 100, and 200 mg/day MXL. Treadmill Test (TMT) was performed before and at each uptitration. Echocardiography was performed at one year.
Since 1990, 1322 patients with syncope of unknown origin have undergone tilt-table testing. Of those, 330 patients (24 X 9%) presented an abnormal response (syncope or pre-syncope). Furthermore, 58 of those patients (17 X 5%) suffered a period of asystole (> or = 3000 ms) during the test. Asystole (median (interquartile range)) lasted 10 (4, 19 X 2) s (range 3-90). Two different protocols (angles) of tilting (Westminster (60 degrees) n=1124; isoproterenol (80 degrees) n=198)) influenced the time to the syncopal episode (13 (6 X 5, 20 X 5) vs 2 (1, 6 X 5) min, P=0,0005) but not the duration of the asystole. During this period, therapy for asystole featured three different stages: first patients were treated with pacemakers; later drug therapy (metoprolol and/or etilefrine) was recommended; lastly (from 1995), no specific treatment was given. In a cohort age- and gender-matched study, those patients without were compared to those with asystole in a 2:1 basis. During 40 X 7 months of follow-up (17 X 7, 66 X 8), 12 patients (20 X 6%) with asystole had syncopal recurrences. Furthermore, 34 patients (28 X 8%) without asystole presented syncopal episodes during a follow-up of 51 X 6 months (29 X 3, 73 X 1) (P=ns). The Kaplan-Meier analysis in patients with and without asystole showed a mean time free of recurrence of 92 X 6 +/- 6 months vs 82 X 6 +/- 4 X 7 months (P=ns). The previous number of syncopes had a significant relationship with recurrences (P=0 X 002), but not therapy. There were no cardiac related deaths.
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Twenty-four heart failure patients were randomised to metoprolol or placebo for 6 months, followed by 6 months of open treatment with metoprolol. Rest and dobutamine stress echocardiography (DSE) was performed before and after each treatment period.
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The β1-adrenergic receptor gene (Entrez Gene:ADRB1), as the target of beta-blockers for hypertension, can directly influence the antihypertensive effect of metoprolol in the Chinese population. This therapeutic effect is often hindered by a lack of evidence-based medical information. To address this challenge, we report a novel assay based on graphene oxide and a CeO2 nanocomposite functionalized by 3-aminopropyltriethoxysilane supported Pt nanoparticles (GO/CeO2/PtNPs) as a signal probe. Due to the large specific surface area and good adsorption properties of the GO/CeO2 nanocomposite, large amounts of PtNPs were immobilized, which amplified the electrochemical signal and improved the sensitivity of the biosensor. To further improvement the sensitivity of the biosensor, Streptavidin (SA) was introduced because it can provide more active sites for the immobilization of the biotinylated capture probe (bio-CP). The electrochemical signal was primarily derived from the catalysis of H2O2 by GO/CeO2/PtNPs. Chronoamperometry was applied to record electrochemical signals, which linearly increased with target DNA. Under optimal conditions, the prepared biosensor had a wide linear range from 1fM to 10nM and a low detection limit of 0.33fM in the detecting of ADRB1 gene. Moreover, the proposed method had good stability and recovery, suggesting its potential for use in clinical research.
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We found that adrenaline increases COX-1 levels in the gastric tissue of both intact and adrenalectomized rats by stimulating alpha-2 receptors. Adrenaline decreases COX-2 levels by stimulating beta-2 adrenergic receptors. Prednisolone inhibits both COX-1 and COX-2 in the gastric tissue of intact rats. In adrenalectomized rats, prednisolone increases gastric COX-1 by stimulating alpha-2 receptors, and decreases COX-2 levels by stimulating beta-2 receptors.
Criteria for inclusion of patients were: migraine without aura or with short aura for at least 2 years, and 2-10 attacks per month. In all, 63 patients (11 men and 52 women) were each randomized for participation one of the three kinds of treatment. All patients declared their willingness to participate in all three different therapies. After neurological and psychological diagnosis the baseline phase of 2 months was started, followed by the intensive therapy phase lasting 3 months. The end of the intensive therapy is followed by a first 2-month follow-up period. A second follow-up of 2 months was started 6 months after the end of intensive therapy. Psychological diagnosis involved the following elements: a migraine questionnaire, a list of patient's complaints, a depression scale and a psychological exploration. All patients kept a diary during all phases of the study with daily descriptions of their headaches, the therapy and their mood. The psychological programme lasted for 12 sessions of 2 hours each. A psychologist worked with small groups of up to 5 patients This programme was composed of progressive relaxation techniques (Jacobson) and techniques aimed at overcoming pain and stress. The data on diagnosis, the baseline phase, the intensive therapy phase and the two follow-up phases were analysed by conventional statistics (comparison of mean values,t-test, variance analysis, non-parametric tests) and by time series analysis. The parameters analysed were: frequency of attacks, mean headache intensity, duration of headache and migraine, consumption of analgesic drugs and mood. Analysis of the questionnaires and the different diagnostic data revealed no significant differences between the three different groups of therapy.
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The aim of the present work was to evaluate drug release and quality of EVA/drug matrices at different PEO 7M concentrations (5 and 15%), manufactured using two different hot-melt extruders: a lab-scale mini extruder and a pilot-scale extruder. The process parameters used on both extruders (temperature and screw speed) and drug release from the matrices were compared. On the lab-scale extruder all formulations were extruded at 90 °C, whereas on the pilot-scale extruder the temperature of the die was adjusted to 100 °C in order to achieve a constant pressure at the extrusion die, hence constant material flow through the die to yield smooth extrudates. Screw speed was also adjusted from 60 rpm (lab-scale extruder) to 90 rpm (pilot-scale extruder) in order to obtain a balance between feeding rate and screw speed. Drug release from the obtained matrices on both extruders was also assessed. Despite the differences in diameter (diameter of 2 and 3mm for the lab-scale extruder and pilot-scale extruder, respectively), temperature and screw speed, drug release per surface area was similar. DSC analysis of a formulation [EVA40/MPT (50/50, w/w) with 5% PEO] indicated small changes in its solid state after extrusion on both extruders: drug crystallinity was reduced by max. 20%, PEO recrystallized after cooling and EVA remained semi-crystalline. Extrusion experiments on the pilot-scale extruder of EVA/MPT, 50/50 (w/w) formulations were also monitored in-line using Raman and NIR spectroscopy in order to evaluate the material behavior at a molecular level in the extrusion barrel as function of the process settings (extrusion temperature: 90, 110 and 140 °C; screw speed: 90 and 110 rpm). At 90 and 110 °C the crystallinity of the drug was reduced, but the majority of MPT remained in its crystalline state as specific peaks in the Raman spectra of the drug became broader. These differences were accentuated when extrusion was performed at 140 °C as the drug completely melted. Peak shifts to lower frequencies [(CO) groups of the drug and (CH(3)COO) groups of EVA] were registered at all extrusion temperatures, with maximum effect at 140 °C indicating molecular interactions. Increasing the screw speed did not result in peak shifts of Raman spectra. NIR confirmed these observations and showed an additional peak in the spectra characteristic of (OH) bounds.
Mean molar phenotypic ratios obtained after administering metoprolol (mean change of -11%) or tolbutamide (mean change of -0.3%) alone, were not significantly different from those obtained when other drugs were co-administered (P > 0.05). The mean within-subject coefficients of variation were 33%, 18%, 22%, 13%, 16%, 13% and 5% for CYP3A4, CYP2D6, CYP2C9, CYP2E1, CYP1A2, N-acetyltransferase 2 and xanthine oxidase metabolic ratios, respectively. No significant interactions (P > 0.5) were observed during the simultaneous administration of various combinations of the five probe drugs.
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Male Sprague-Dawley rats were randomly divided into three groups: the sham-operated group, the MI group without metoprolol, which was fed the vehicle, and the MI+metoprolol group receiving intragastric metoprolol. Each group was further divided randomly into three subgroups, depending on the dosage of epinephrine administered during subsequent CPR applied after the induction of asphyxial cardiac arrest.
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Hypertension induces left-ventricular hypertrophy (LVH) by mechanisms involving oxidative stress and unbalanced cardiac matrix metalloproteinase (MMP) activity. We hypothesized that β1-adrenergic receptor blockers with antioxidant properties (nebivolol) could reverse hypertension-induced LVH more effectively than conventional β1-blockers (metoprolol) when used at doses that exert similar antihypertensive effects. Two-kidney one-clip (2K1C) hypertension was induced in male Wistar rats. Six weeks after surgery, hypertensive and sham rats were treated with nebivolol (10 mg kg(-1)day(-1)) or metoprolol (20 mg kg(-1)day(-1)) for 4 weeks. Systolic blood pressure was monitored weekly by tail-cuff plethysmography. LV structural changes and fibrosis were studied in hematoxylin/eosin- and picrosirius-stained sections, respectively. Cardiac MMP levels and activity were determined by in situ zymography, gel zymography, and immunofluorescence. Dihydroethidium and lucigenin-derived chemiluminescence assays were used to assess cardiac reactive oxygen species (ROS) production. Nitrotyrosine levels were determined in LV samples by immunohistochemistry and green fluorescence and were evaluated using the ImageJ software. Cardiac protein kinase B/Akt (AKT) phosphorylation state was assessed by Western blot. Both β-blockers exerted similar antihypertensive effects and attenuated hypertension-induced cardiac remodeling. Both drugs reduced myocyte hypertrophy and collagen deposition in 2K1C rats. These effects were associated with lower cardiac ROS and nitrotyrosine levels and attenuation of hypertension-induced increases in cardiac MMP-2 levels and in situ gelatinolytic activity after treatment with both β-blockers. Whereas hypertension increased AKT phosphorylation, no effects were found with β-blockers. In conclusion, we found evidence that two β1-blockers with different properties attenuate hypertension-induced LV hypertrophy and cardiac collagen deposition in association with significant cardiac antioxidant effects and MMP-2 downregulation, thus suggesting a critical role for β1-adrenergic receptors in mediating those effects. Nebivolol is not superior to metoprolol, at least with respect to their capacity to reverse hypertension-induced LVH.