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Seventeen patients in class IIIb/IV CHF (group 1) on intermittent intravenous milrinone therapy and 15 patients in class II/IIIa compensated CHF (group 2) on standard triple heart failure therapy were titrated on carvedilol. Success and adverse events during titration were compared between the 2 groups. Fifteen (88%) patients in group 1 and 14 (93%) patients in group 2 were successfully titrated on carvedilol over 8.1 +/- 1.8 weeks and 6.7 +/- 2.8 weeks, respectively. The target dose of carvedilol (25 or 50 mg twice daily) was achieved in 13 (87%) patients (group 1) and 14 (93%) patients (group 2). Seven (47%) patients in group 1 and 4 (28%) patients in group 2 had adverse events during carvedilol titration. Eight (53%) patients in group 1 were weaned off milrinone over a period of 8.4 weeks after carvedilol titration, whereas the rest of the patients had reduction in the frequency of infusion. Ten (63%) patients in group 1 improved by one or more functional classes.
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Patients with hypertensive left-ventricular hypertrophy (LVH) have lower coronary flow reserve (CFR). Whether carvedilol can improve CFR of patients with hypertensive LVH is unknown. We aimed to investigate the effects of carvedilol on CFR in patients with hypertensive LVH.
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Using Ca/Pi, carvedilol protected mitochondria from MPT induction, particularly in its high conductance form. Its effect was demonstrated by analyzing the decrease in mitochondrial swelling amplitude. Simultaneously, we observed inhibition of protein thiol group oxidation (p < 0.001). By contrast, carvedilol did not show any protective effect with Ca/Catr.
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Various beta-blockers with distinct pharmacological profiles are approved in heart failure, yet they remain underused and underdosed. Although potentially of major public health importance, whether one agent is superior in terms of tolerability and optimal dosing has not been investigated. The aim of this study was therefore to compare the tolerability and clinical effects of two proven beta-blockers in elderly patients with heart failure.
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Hospitalization for HF or death occurred in 30% of the patients on metoprolol and in 23% on carvedilol. Treatment with carvedilol was associated with a significantly decreased risk of hospitalization for HF or death when compared with metoprolol (hazard ratio [HR]: 0.70, [95% confidence interval (CI): 0.57 to 0.87], p = 0.001). This reduction in risk was further attenuated in the subgroup of cardiac resynchronization therapy with implantable cardioverter-defibrillator (CRT-D) patients (HR: 0.61 [95% CI: 0.46 to 0.82], p = 0.001) and CRT-D patients with left bundle branch block (LBBB) (HR: 0.51 [95% CI: 0.35 to 0.76], p < 0.001). Ventricular arrhythmias occurred in 26% and in 22%, respectively, of the patients receiving metoprolol or carvedilol (HR: 0.80 [95% CI: 0.63 to 1.00], p = 0.050). General use of beta-blockers and adherence in this study was high, and a clear dose-dependent relationship was found in carvedilol, but not in metoprolol.
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Cardiodynamic changes due to beta-blocker carvedilol and low-intensity infrared laser radiation were compared in 115 patients with ischemic heart disease (IHD). The comparison has shown a similar positive effect on heart contractility and diastolic function. This gave arguments for feasibility of laser beam usage as a neurohormonal modulator in IHD patients to reduce cardiac remodulation and prevent cardiac failure.
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Blood samples were collected for 24 hours after single doses of carvedilol were administered IV (175 microg/kg) or PO (1.5 mg/kg) by use of a crossover nonrandomized design. Carvedilol concentrations were detected in plasma by use of high-performance liquid chromatography. Plasma drug concentration versus time curves were subjected to noncompartmental pharmacokinetic analysis.
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Most DM patients were prescribed non-DM-friendly β-blockers-a practice that was associated with a trend toward worse glycemic control postdischarge. Although in need of further confirmation in larger studies, our findings highlight an opportunity to improve current practices of β-blockers use in patients with DM.
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Carvedilol in long term therapy of CHF with AF exerts substantial influence on adhesive function of endothelium and improves hemodynamics.
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The time interval between airway obstruction and CA in the treatment group was significantly longer than in the control group (230 ± 27 vs 203 ± 24 seconds; P < 0.05). The rate of return of spontaneous circulation in the treatment group was significantly higher than in the control group (92% vs 50%; P < 0.05). Acidosis and increased glucose and tumor necrosis factor-α concentrations in the treatment group were significantly lower than in the control group.
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In this single-centre, prospective, randomized study, 60 patients with dilated cardiomyopathy with an LVEF less than 40% and already receiving digoxin, ACE inhibitors and diuretics for six months as the standard therapy were randomly assigned to receive either carvedilol (n=30) or placebo (n=30). Patients received an initial dosage of 3.125 mg carvedilol or placebo twice daily for two weeks, which was then increased at two-week intervals (if tolerated), first to 6.25 mg, then to 12.5 mg, and, finally, to a target dosage of 25 mg twice daily. Clinical examinations, radionuclide studies, and determinations of plasma levels of tumour necrosis factor-alpha (TNF-a), interleukin (IL)-2 and IL-6 were performed at baseline and repeated four months after random assignment. Primary end points were New York Heart Association functional class, LV function and plasma cytokines levels. Eight patients died (seven in the placebo group, P=0.05). Patients treated with carvedilol had a significant improvement in functional class compared with the baseline values (P=0.001), with a decrease in the levels of cytokines (IL-6 [P=0.001] and TNF-a [P=0.001]). LVEF increased from 22.14+/-7.85% to 27.85+/-11.80% (P=0.002), but diastolic function did not change in the carvedilol group.
Spherically agglomerated solid dispersions of carvedilol (CAR) were prepared with polyvinyl-pyrrolidone (PVP) using acetone, water and dichloromethane as solvent, non-solvent and bridging liquid, respectively. The prepared agglomerates were evaluated for its percentage yield, drug content, morphology, thermal behavior, micromeritic properties, aqueous solubility and in vitro drug release. Differential scanning calorimetric and powder X-ray diffraction studies confirm that formulation process altered the crystalline nature of carvedilol. The recrystallized agglomerates exhibited significant increase (p < 0.05) in micromeritic properties than untreated carvedilol. Solubility and in vitro drug release studies indicated that the spherical agglomerates showed significant increase (p < 0.05) in solubility and dissolution rate than pure carvedilol alone.
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TAC rats showed an increased diastolic interventricular septal thickness at week 5. At 10 weeks, Masson staining showed that left ventricular and renal glomerular fibrosis were significantly reduced in RDN compared with Sham group. In comparison to Sham group, hepatic perivascular fibrosis was attenuated in both RDN and Carvedilol group, so were the media thickness and the media/lumen of aorta. The plasma levels of B-type natriuretic peptide (BNP), Cystatin C (Cys-C), Alanine Transaminase, angiotensin II (Ang II), transforming growth factor beta 1 (TGF-β1), and malondialdehyde increased, and total superoxide dismutase (T-SOD) decreased in Sham but not in RDN group, compared with Control group. Both RDN and Carvedilol reduced the Cys-C and TGF-β1 levels, and restored T-SOD concentration, compared with Sham group. While only RDN lowered the plasma levels of BNP and Ang II. No significant effects of RDN on blood pressure (BP) and heart rate (HR) were oberved.
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The effect of withdrawal of digoxin on left ventricular function in patients with a history of idiopathic dilated cardiomyopathy (IDCM) following normalization of left ventricular ejection fraction (LVEF) with beta blockers remains unknown.
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The subdivision of alpha adrenoceptors into the alpha 1 and alpha 2 classes was the impetus for the design of the selective alpha 1-adrenoceptor antagonists, which remain useful antihypertensives. alpha 2-Adrenoceptor agonists also have application as antihypertensive drugs, based on their ability to reduce sympathetic outflow. Likewise, subdivision of the beta adrenoceptors has lead to the development of selective beta 1-adrenoceptor antagonists as antihypertensive and selective beta 2 agonists as bronchodilators. In the past decade, both the alpha 1 and alpha 2 adrenoceptors have been further subdivided, each into three subclasses. In addition, there is strong functional evidence to suggest the presence of additional adrenoceptor subtypes, such as the "alpha 1L" adrenoceptor and "beta 4" adrenoceptor. alpha 1A (or alpha 1L)-Adrenoceptor antagonists have been evaluated for benign prostatic hyperplasia (BPH), and selective alpha 1A agonists for stress incontinence. Gene knockout experiments in mice suggest an important role for the alpha 1B adrenoceptor in the control of vascular tone. Hence, selective alpha 1B antagonists may offer a new approach toward hypertension. Although targeting of specific adrenoceptors can be used to optimize the therapeutic profile of a drug, there are also cases where blockade of multiple adrenoceptors is desirable, as with the alpha/beta-adrenoceptor antagonist carvedilol in congestive heart failure. It is possible that combination of affinities for selected adrenoceptor subtypes within a single molecule may be desirable for certain applications.
Fibroblasts isolated from hearts of adult rats were grown in 10% serum-containing media which induced an increase in cell number by 94%. After 48 h, treatment with 10 microM NE caused an even greater increase in cell number by 222%, i.e. another 128% (comitogenic effect). In contrast, NE alone had no effect on the growth of serum-deprived cells. EGF and PDGF-AA did not replace serum as the basic mitogen. After addition of NE to proliferating cells under serum conditions, there was a rapid, time-dependent significant activation of the p42/p44(MAPK) and of CREB for up to 60 and 120 min, respectively. In both cases, the maximum of activation was reached after 5 min. Application of FO (0.1-20 microM) caused a strong activation of CREB, while no increase in the phosphorylation of the p42/p44(MAPK) was detected. Treatment with 20 microM FO led to an identical increase in cell number as application of NE. Specific blockade of PKA with RpcAMPS prevented the activation of CREB and also the comitogenic effect of FO as well as of NE. The alpha- and beta-adrenergic receptor blocker carvedilol (10 microM) normalized all NE-induced effects. Prazosin and yohimbine, inhibitors of alpha(1)- and alpha(2)-adrenoceptor activation, respectively, did not influence the NE-evoked increase in cell number. In contrast, the non-selective beta-adrenoceptor blocker propranolol (1 microM) completely suppressed the comitogenic effect of NE. A similar effect was obtained with the specific beta(2)-adrenoceptor blocker ICI 118,551 (5 microM), while the beta(1)-adrenoceptor blocker metoprolol did not influence the increase in cell number.
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Carvedilol limits myocardial necrosis resulting from coronary artery occlusion and reperfusion in a more pronounced manner than the pure beta adrenoceptor antagonist, propranolol. The cardioprotective effect of carvedilol, which reduced infarct size by 91%, may result from the combined effects of beta adrenoceptor blockade and vasodilatation, and possibly also from inhibition of intracellular calcium overload in cardiac cells resulting from antagonism of myocardial alpha 1 adrenoceptors and/or calcium channel blockade. The cardioprotection provided by carvedilol may ultimately be of benefit in hypertensive patients who are at risk for acute myocardial infarction.
The Cox proportional hazards model was used to calculate hazard ratios (HR) for convenience expressed as relative risks (risk reduction = 1-HR), and 95% confidence intervals (CI).
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Beta-adrenoceptor blockade did not affect a visual assessment of the autoradiographic image of 9MPA in hearts subjected to ischemia-reperfusion, but it accelerated the clearance of 9MPA in both the IR and non-IR. The administration of beta-blockade before ischemia could accelerate the recovery from ischemia-reperfusion injury by inhibiting myocardial FA accumulation before beta-oxidation.
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Constipation is one of most frequent non-motor symptoms of Parkinson's disease (PD) and it may precede the clinical diagnosis of PD by years, with negative effects on quality of life. In contrast to motor features, levodopa is ineffective and possibly detrimental on constipation. Treatment of constipation in PD is non-specific and frequently unsuccessful. Stemming from a clinical observation of unexpected relief of bothersome constipation, abdominal bloating and pain after treatment with the beta-blocker carvedilol in one patient, we have evaluated the association between the use of beta-blockers and the presence of constipation in a large, unselected PD cohort.
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A capillary electrophoresis method was used for assay of some degradation products of carvedilol. The optimized parameters were as; running buffer 80 mM acetate dissolved in methanol/ethanol mixture (65:35% v/v), applied voltage of 19 kV, temperature is 20 ºC and the wavelength range of 200-350 nm. The results indicate that the proposed capillary electrophoresis method could effectively separate carvedilol from its degradation products and can be employed as a stability indicating assay method. In addition, the presence of a new unknown degradation product was discovered by this method. In addition, capillary electrophoresis behaviour of carvedilol in photo/force degradation conditions gave valuable information concerning the dissimilarities of their ionization. Results indicated that the capillary electrophoresis proposed method can be used for the determination of carvedilol in human serum. Finally, accuracy of the proposed method was established by recovery experiments from spiked human serum samples.
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Tablet splitting could be safer and easier when drug- and patient-specific criteria have been met. Tablet size, shape, and hardness may also play a role in the decision to split a tablet or not. Tablets containing drugs with a wide therapeutic index and long half-life might be more suitable candidates for division. Dose variation exceeded a proxy USP specification for more than one-third of sampled half tablets of bromazepam, carvedilol, bisoprolol, and digoxin. Drug content variation in half tablets appeared to be attributed to weight variation due to fragment or powder loss during the splitting process.
Prospective propensity-adjusted cohort study over 5 years on 1085 adults diagnosed with HF-PSF for the first time, in an integrated university-based health organization in Spain. The independent relationship between CT-βB and mortality and morbidity was analyzed, stratifying patients for comorbidity, after a multivariable adjustment for potential confounders.
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Although we recently demonstrated that opening of a native aortic valve (AV) after left ventricular assist device (LVAD) implantation is a sufficient condition to prevent development of aortic insufficiency (AI), its preoperative predictors remain unknown. Data were obtained from 58 patients who had been treated with continuous flow LVAD for ≥ 6 months at our institute between 2006 and 2014. Opening of native AV was accomplished in 21 patients (36%) at postoperative 6 months. Uni/Multivariate logistic regression analyses demonstrated that a preoperative lower cumulative dose of β-blocker was the only independent predictor for postoperative opening of native AV (P = 0.020, OR 0.905) at the cutoff level of 4.5g (equivalent dose of carvedilol), calculated by an ROC analysis. Prevalence of native AV opening was increased gradually along with improvement of LV ejection fraction only in patients with preoperative insufficient β-blocker treatment during postoperative 6 months (P < 0.05 for both). Patients with opening of native AV had higher exercise capacity and a lower re-admission rate than those with closed native AV during 2-year LVAD support (5% versus 44%, P < 0.05). Opening of native AV during LVAD support is profoundly associated with LV reverse remodeling especially in patients with insufficient preoperative β-blocker exposure probably due to their better responsiveness to combination therapy with β-blocker and LVAD. Patients who accomplished native AV opening can enjoy better exercise performance and avoid re-admission due to cardiovascular events.
The primary outcome was a composite measure of heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo. Secondary efficacy variables included individual components of this composite, echocardiographic measures, and plasma b-type natriuretic peptide levels.
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Carvedilol exerts antiarrhythmogenic effects by ameliorating sympathetic nerve sprouting and electrical remodeling in MI rats. The effects of carvedilol on amelioration of electrical remodeling may be partly related to the inhibition of sympathetic remodeling.