The detection of autoantibodies against the cardiac beta(1)-adrenergic receptors is related to severer cardiac dysfunction and autoantibodies title decrease was found with improved cardiac function after standard therapy (ACEI, digitalis, betablocker) in patients with CHF.
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A sensitive and selective method for simultaneous determination of carvedilol and dopamine was described. The emission wavelengths of carvedilol and dopamine were at 354 nm and 314 nm with the excitation at 290 nm, respectively. The determination of carvedilol and dopamine by normal fluorometry was difficult because the emission spectra of carvedilol and dopamine were overlapped seriously. The first derivative peaks of carvedilol and dopamine were at 336 nm and 302 nm, respectively. The linear regression equations of the calibration graphs of carvedilol and dopamine were C = 0.000557H-0.00569 and C = 0.00438H-0.0812, with the correlation coefficients were 0.9953 and 0.9988, respectively. The liner range for the determination of carvedilol was 0.002 microg ml(-1) to 0.02 microg ml(-1), and 0.05 microg ml(-1) to 0.6 microg ml(-1) for dopamine. The detection limits were 1 ng ml(-1) for carvedilol and 0.04 microg ml(-1) for dopamine, respectively. The relative standard derivative (RSD) of 4.38% and 4.35% was observed for carvedilol and dopamine, respectively. The recovery of carvedilol was from 95.00% to 106.7% in human serum and from 97.50% to 105.0% in urine sample. The recovery of dopamine was from 100.0% to 102.5% in human serum and from 97.50% to 105.0% in urine sample. This method is simple and can be used for determination of carvedilol and dopamine in human serum and urine sample with satisfactory results.
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The COMET trial was a prospective, double-blind, randomised trial comparing carvedilol, a comprehensive adrenergic receptor antagonist, with metoprolol, a beta-1-selective agent in patients with heart failure and left ventricular systolic dysfunction. The trial showed a reduction in mortality with carvedilol that was consistent across subgroups. The purpose of this report is to describe in greater detail the heterogeneity of this population at baseline with particular reference to the impact of symptomatic severity, age and gender on patient characteristics.
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Despite several limitations, this analysis confirms the efficacy of prophylactic BB against post-CABG AF in this era. We recommend continuing perioperative BB in the open heart surgery patients in the absence of contraindications.
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Randomized, double-blinded controlled studies are included, with 1,647 patients treated with bisoprolol, 3,034 treated with carvedilol, 2,432 treated with metoprolol, and 6,807 treated with placebo. Direct costs of BB treatment and of every hospitalization episode are assessed. Cost-effectiveness is assessed as cost in euros by prevented death, and cost-benefit as the difference between hospitalization costs and BB costs. The study is conducted from the perspective of a third-party payer.
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The BLOCADE Feasibility Study will inform the design of a larger clinical endpoint study to determine whether beta-blocking agents provide benefit to patients receiving dialysis, and define whether such a study is feasible.
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Catecholamines stimulate cardiac contractility through beta(1)-adrenergic receptors (beta(1)-ARs), which in humans are polymorphic at amino acid residue 389 (Arg/Gly). We used cardiac-targeted transgenesis in a mouse model to delineate mechanisms accounting for the association of Arg389 with human heart failure phenotypes. Hearts from young Arg389 mice had enhanced receptor function and contractility compared with Gly389 hearts. Older Arg389 mice displayed a phenotypic switch, with decreased beta-agonist signaling to adenylyl cyclase and decreased cardiac contractility compared with Gly 389 hearts. Arg389 hearts had abnormal expression of fetal and hypertrophy genes and calcium-cycling proteins, decreased adenylyl cyclase and G alpha(s) expression, and fibrosis with heart failure This phenotype was recapitulated in homozygous, end-stage, failing human hearts. In addition, hemodynamic responses to beta-receptor blockade were greater in Arg389 mice, and homozygosity for Arg389 was associated with improvement in ventricular function during carvedilol treatment in heart failure patients. Thus the human Arg389 variant predisposes to heart failure by instigating hyperactive signaling programs leading to depressed receptor coupling and ventricular dysfunction, and influences the therapeutic response to beta-receptor blockade.
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Carvedilol is a vasodilating beta-blocker and antioxidant approved for treatment of mild to moderate hypertension. angina, and congestive heart failure. Metoprolol is a beta1-selective adrenoceptor antagonist. When carvedilol and metoprolol were recently compared in clinical trials for heart failure, each showed beneficial beta-blocker effects such as improved symptoms, quality of life, exercise tolerance, and ejection fraction, with no between-group differences. When thiobarbituric acid reactive substance (TBARS) levels were measured in serum as an indirect marker of free radical activity, there were also no between-group differences. However, we had noted superior cardioprotection by carvedilol in comparison to metoprolol in ischemia and reperfusion models. We therefore examined antioxidant activity directly in cells and tissues. Here we show that in cultured rat cerebellar neurons, and in brain and heart membranes, carvedilol has far greater antioxidant activity than metoprolol, which is essentially inactive as an antioxidant in these model systems. The antioxidant activity of carvedilol could be explained by a greater degree of lipophilicity, as measured by its ClogP value of 3.841 as contrasted to a ClogP value of 1.346 for metoprolol. Alternatively, the molecular structure of carvedilol favors redox recycling, which the structure of metoprolol does not. Therefore, carvedilol could have additional pharmacologic effects that are favorable for long-term therapy.
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A 64-year-old woman with dilated hypertrophic cardiomyopathy was treated by beta-blocker, because of recurrent episodes of congestive heart failure. Carvedilol administration was started with a dose of 2.5 mg/day, and gradually increased to the dose of 20 mg/day 3 months later. Her functional class recovered from New York Heart Association stage IV to stage II. Thallium-201 scintigraphy demonstrated advanced myocardial damage: defect/low perfusion in the anteroseptal, infero-posterior and apical regions. Iodine-123 beta-methyl-p-iodophenyl-pentadecanoic acid scintigraphy confirmed these findings. However, the scintigraphic abnormalities had reversed to near normal perfusion and metabolism similar to those of stunned myocardium after an ischemic episode. This case demonstrates the recovery of myocardial impairment during beta-blocker therapy in a patient with dilated hypertrophic cardiomyopathy.
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A 27-year-old man diagnosed as having dilated cardiomyopathy (DCM) without myocardial accumulation of 123I-beta-methyl-iodophenylpentadecanoic acid, and he was found to have type I CD36 deficiency. This abnormality of cardiac free fatty acid metabolism was also confirmed by other methods: 18F-fluoro-2-deoxyglucose positron emission tomography, measurements of myocardial respiratory quotient and cardiac fatty acid uptake. Although the type I CD36 deficiency was reconfirmed after 3 months, the abnormal free fatty acid metabolism improved after carvedilol therapy and was accompanied by improved cardiac function. Apart from a cause-and-effect relationship, carvedilol can improve cardiac function and increase free fatty acid metabolism in patients with both DCM and CD36 deficiency.
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Preparation of floating microsphere by the emulsion solvent diffusion method, studying the effect of various process parameters and optimize the formulation using full factorial design.
Dose discontinuation (n=64) or reduction group (n=83) had significantly higher ventricular arrhythmia rates compared with dose continuation group (n=262) (65.6 vs. 33.7 vs. 15.3%, p < 0.001 for both comparisons). Dose discontinuation group also had a significantly higher ventricular arrhythmia event rate compared with dose reduction group (p<0.001). There were no significant differences in ventricular arrhythmia event rates among dose discontinuation or reduction subgroups.
Patients with DCM who were treated with carvedilol were enrolled in the study. All patients had undergone carvedilol therapy in addition to standard therapy for at least 6 months. Clinical, echocardiographic, and electrocardiographic parameters, and 24-h Holter records of patients were retrospectively evaluated before and after carvedilol treatment.
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After 3 months, only LV end-diastolic diameter was lower in the carvedilol group compared to the placebo group. Nevertheless, after 12 months, patients on carvedilol treatment showed a LV geometric and functional improvement compared to placebo. We found significant differences in: diastolic (P < 0.01) and systolic diameters (P < 0.001); on LV mass (P < 0.002); on LV systolic volume (P < 0.03); and on LV ejection fraction (P<0.01). Pulmonary pressure was also reduced in beta-blocker subjects (P < 0.001).
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Congestive heart failure (CHF) is characterized by an initial compensatory, but subsequently deleterious, activation of both the renin-angiotensin (RAS) and the sympathetic nervous system (SNS). Incomplete suppression of the SNS may contribute to the residual mortality during optimal ACE inhibitor therapy in CHF. Carvedilol, a mixed alpha and beta-blocker with antioxidant properties, and other pure beta-adrenoceptor blockers reduce morbidity and mortality in Caucasians with CHF. However, beta-blocker monotherapy is of poor efficacy in Blacks with essential hypertension or in the treatment of glaucoma. The efficacy of beta-blockers in the treatment of African Americans with congestive heart failure is a controversial issue with conflicting findings. The aims of the present study were to examine and compare the cardiovascular, autonomic, and clinical effects of additional alpha-1, or beta-1 blockade in ACE-inhibitor treated Black patients with moderate to severe CHF.
β-Blockers exert a prognostic benefit in the treatment of chronic heart failure. Their pharmacological properties vary. The only substantial comparative trial to date-the Carvedilol or Metoprolol European Trial-has compared carvedilol with short-acting metoprolol tartrate at different dose equivalents. We therefore addressed the relative efficacy of equal doses of carvedilol and metoprolol succinate on survival in multicenter hospital outpatients with chronic heart failure.
Four (18%) of 22 rats in group V died between days 28 and 84 after immunization. None of the rats in group C or N died. Heart weight, heart rate, LVEDP, and area of myocardial fibrosis in group C (1.14 +/- 0.04 g, 345 +/- 16 beats per minute, 7.6 +/- 1.5 mm Hg, and 12% +/- 1%) were significantly lower than those in group V (1.34 +/- 0.04 g, 389 +/- 10 beats per minute, 12.3 +/- 1.3 mm Hg, and 31% +/- 2%). Although the differential absorption ratio was lower at all time points in group V than in group N, uptake after treatment increased in group C, compared with group V, at 10 min (12.5 +/- 1.0 vs. 7.6 +/- 0.8, not significant), 30 min (10.1 +/- 1.1 vs. 6.3 +/- 0.9, not significant), and 240 min (6.5 +/- 0.5 vs. 2.5 +/- 0.2, P < 0.05). The late washout ratio from myocardial radioactivity between 30 and 240 min in group C was lower than that in group V (36% vs. 60%).
Metoprolol tartrate 50 mg bid and carvedilol 25 mg bid had similar effects on 24-h heart rate. This result suggests that the degree of beta1-blockade produced by these two drugs in these doses is comparable and the superior survival effect of carvedilol compared to metoprolol seen in COMET is likely to be due to actions of carvedilol other than beta1-blockade.
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Effects of chronic treatment of stroke-prone spontaneously hypertensive rats (SHRSP) with carvedilol, an agent which has both alpha and beta-adrenoceptor blocking actions, on spontaneous muscle tone and on structural and functional abnormalities of endothelium were studied. The treatment of SHRSP with the drug of the dose of 30 to 200 mg/kg/day lowered the blood pressure significantly. Spontaneous muscle tone in endothelium-removed preparation disappeared by the treatment. Noradrenaline-induced contraction was depressed by the treatment in endothelium intact preparation but not in endothelium removed preparation. The treatment prevented the structural and functional abnormalities of endothelium. Similar results were obtained by the treatment with propranolol. These results indicate that carvedilol prevented abnormal contraction of SHRSP aorta through protective effects on smooth muscle and endothelium. These effects may play roles in blood pressure lowering effect of carvedilol.
Blood samples were collected at before and 6 months after administration of carvedilol in 44 CHF patients. The hemodynamic parameters, echocardiography, plasma concentrations of brain natriuretic peptide (BNP), norepinephrine and adiponectin were measured. Six months after treatment, there were significantly decreased plasma concentrations of adiponectin (15.8 +/-1.4 to 11.0 +/-1.1 microg/ml, P<0.0001), BNP and norepinephrine and increased left ventricular ejection fraction (LVEF). On stepwise multivariable analyses, a higher plasma adiponectin concentration before treatment (rs=-0.561, P<0.0001) was a significant independent predictor of a greater decrease in adiponectin concentration and the decrease in plasma adiponectin concentration was significantly correlated with the improvement of LVEF (r=-0.561, P<0.0001).
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To assess the association of T190C polymorphism of β3 adrenergic receptor gene (β3-AR) with chronic heart failure (CHF), and to evaluate the effect of this polymorphism on clinical response to β-AR blockade among patients with CHF.
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The estimated cost of carvedilol therapy and related ambulatory care for the 1156 patients assigned to active treatment was pound530,771 ( pound44.89 per patient/month of follow-up). However, patients assigned to carvedilol were hospitalised less often and accumulated fewer and less expensive days of admission. Consequently, the total estimated cost of hospital care was pound3.49 million in the carvedilol group compared with pound4.24 million for the 1133 patients in the placebo arm. The cost of post-discharge care was also less in the carvedilol than in the placebo group ( pound479,200 vs. pound548,300). Overall, the cost per patient treated in the carvedilol group was pound3948 compared to pound4279 in the placebo group. This equated to a cost of pound385.98 vs. pound434.18, respectively, per patient/month of follow-up: an 11.1% reduction in health care costs in favour of carvedilol.
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A liquid chromatographic-mass spectrometric assay with atmospheric pressure chemical ionization (LC-APCI-MS) is presented for screening for, library-assisted identification (both in scan mode) and quantification (selected-ion mode) of the beta-blockers acebutolol, diacetolol, alprenolol, atenolol, betaxolol, bisoprolol, bupranolol, carazolol, carteolol, carvedilol, celiprolol, esmolol, labetalol, metoprolol, nadolol, nebivolol, oxprenolol, penbutolol, propranolol, sotalol, talinolol and timolol in blood plasma after mixed-mode (HCX) solid-phase extraction (SPE) and separation by reverse-phase liquid chromatography with gradient elution. The validation data were within the required limits. The assay was successfully applied to authentic plasma samples allowing confirmation of diagnosis of overdose situations as well as monitoring of patients' compliance.
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In multivariate analysis, ICD therapy was associated with a significant 39% increase in the risk of HF as compared with conventional medical therapy. ACE-I and beta-blockers exhibited a graded efficacy for the reduction in the risk of HF events in ICD-treated patients: the greatest risk reduction of HF was seen in patients taking combination therapy (HR = 0.36, P < 0.001), followed by patients using beta-blockers only (HR = 0.51, P = 0.017) and ACE-I only (HR = 0.64, P = 0.071). Beta-blocker subtypes (metoprolol [HR = 0.49, P = 0.001] and carvedilol [HR = 0.58, P = 0.004]) exhibited similar efficacy. Consistent results were demonstrated when the combined endpoint of HF or death was assessed.
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Most studies assessing the effects of beta-blockers were carried out with traditional, beta(1)-selective beta-blockers, such as metoprolol and atenolol. Pathophysiologic and pharmacologic studies have documented that not all beta-blockers are created equal. In particular, the pharmacologic and clinical profiles of the newer, vasodilating beta-blockers, such as carvedilol, have been shown to differ from those of the traditional beta-blockers. These differences, although relevant in the younger patient with hypertension, are particularly important in elderly patients in whom traditional beta-blockers may not be as effective or as well tolerated as the newer vasodilating agents.
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In 2008, during a nationwide educational project on HF management, 15 courses for GPs were conducted. Before the training, physicians filled out a standardized questionnaire about the diagnosis and treatment of HF. The answers were assessed in a three age-group of respondents: 24-39 years (n = 142), 40-55 years (n = 316), 56 years and above (n = 156). Of 614 physicians, 97% indicated echocardiography as obligatory diagnostic procedure in HF diagnosis. The oldest GPs more frequently pointed to the role of chest X-ray (63%, p < 0.001) and electrocardiography (32%, p < 0.001) in exclusion of systolic HF. There was a significant reverse relationship between physicians' age and their declarations in prescription of angiotensin II receptor blockers (p = 0.007; contingency coefficient, Cc= 0.13) and b-blockers (p = 0.01; Cc = 0.12) in patients with advanced HF (NYHA III-IV), and positive relation between application of spironolactone (p = 0.007; Cc = 0.13) and digitalis (p < 0.001; Cc = 0.16) in patients of NYHA class I-II. The new generation b-blockers (bisoprolol, carvedilol, nebivolol) were more frequently prescribed by the youngest physicians (respectively: 98%, 96%, 58%) compared to the oldest group (respectively: 88%, 87%, 50%; p < 0.05).
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The body of work described in this research paper outlines the use of PEO/PCL blends in the production of monolithic matrices for oral drug delivery. Several batches of matrix material were prepared with carvedilol used as the active pharmaceutical ingredient. The matrices were prepared using various extrusion parameters to investigate the effect of screw speed and barrel temperature on the properties of the drug delivery devices. The resultant extrudate was characterised using steady state parallel plate rheometry, differential scanning calorimetry (DSC) and dissolution testing. Higher screw speeds were observed to result in slightly lower matrix melt viscosity when compared with matrices compounded using lower screw speeds. Dissolution testing showed that the incorporation of the hydrophobic PCL polymer into a PEO matrix results in a retarded drug release profile.
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CsA (20 mg/kg s.c) administration for 21 days produced elevated levels of TBARS and deteriorated renal function as assessed by increased plasma creatinine, BUN and decreased creatinine and urea clearance as compared to vehicle-treated rats. The kidneys of CsA-treated rats showed severe striped interstitial fibrosis, arteriolopathy, glomerular basement thickening, tubular vacuolization and hyaline casts. Propranolol neither decreased TBARS nor improved the renal dysfunction and morphological changes induced by CsA. Both doses of carvedilol markedly reduced elevated levels of TBARS, whereas the higher dose of carvedilol significantly attenuated renal dysfunction and morphological changes in CsA-treated rats.
Oxidative stress is a major pathway mediating ethanol hepatotoxicity and liver injury. We previously found that carvedilol, which can block the sympathetic nervous system via β1-, β2- and α1-adrenoreceptors, modifies ethanol-induced production of lipogenesis- and fibrogenesis-related mediators from hepatic stellate cells (HSC). In the present study, we assessed the effects of carvedilol on ethanol-induced liver injury, hepatic insulin resistance, and the interaction between oxidative stress and sympathetic hyperactivity in rats with alcoholic fatty liver disease (AFLD).