At antihypertensive equipotent doses, the inhibition of alpha 1-receptors improves the endothelial fibrinolytic activity and the lipid profile. beta-Blockade has an anti-ischaemic action, but reduces the lipoprotein ratio (ApoA/ApoB) and does not improve endothelial fibrinolytic activity.
coreg 80 mg
This pilot study suggests that oxidative stress in CHF may be due to increased free radical production or inefficient free radical clearance by scavengers. beta-Blockers, but not ACE inhibitors, reduced lipid peroxidation in patients with CHF. No relation was demonstrated between a reduction in oxidative damage and endothelial damage/dysfunction.
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Exercise performance is better preserved with nebivolol than with carvedilol under acute exposure to HA hypoxia in healthy subjects.
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Eighty-five patients (42%) were responders; 26 patients (13%) were partial responders, and 90 patients (45%) were nonresponders. The percentage of responders progressively decreased as the time from the end of chemotherapy to the start of HF treatment increased; no complete recovery of LVEF was observed after 6 months. Responders showed a lower rate of cumulative cardiac events than partial and nonresponders (5%, 31%, and 29%, respectively; p < 0.001).
Portal hypertension is a common complication of chronic liver diseases associated with liver fibrosis and cirrhosis. At present, beta-blockers such as carvedilol remain the medical treatment of choice for protection against variceal bleeding and other complications. Since carvedilol has powerful antioxidant properties we assessed the potential antifibrotic effects of carvedilol and the underlying mechanisms that may add further benefits for its clinical usefulness using a chronic model of carbon tetrachloride (CCl4)-induced hepatotoxicity. Two weeks after CCl4 induction of chronic hepatotoxicity, rats were co-treated with carvedilol (10mg/kg, orally) daily for 6weeks. It was found that treatment of animals with carvedilol significantly counteracted the changes in liver function and histopathological lesions induced by CCl4. Also, carvedilol significantly counteracted lipid peroxidation, GSH depletion, and reduction in antioxidant enzyme activities; glutathione-S-transferase and catalase that was induced by CCl4. In addition, carvedilol ameliorated the inflammation induced by CCl4 as indicated by reducing the serum level of acute phase protein marker; alpha-2-macroglobulin and the liver expression of nuclear factor-kappa B (NF-κB). Finally, carvedilol significantly reduced liver fibrosis markers including hydroxyproline, collagen accumulation, and the expression of the hepatic stellate cell (HSC) activation marker; alpha smooth muscle actin. In conclusion, the present study provides evidences for the promising antifibrotic effects of carvedilol that can be explained by amelioration of oxidative stress through mainly, replenishment of GSH, restoration of antioxidant enzyme activities and reduction of lipid peroxides as well as amelioration of inflammation and fibrosis by decreasing collagen accumulation, acute phase protein level, NF-κB expression and finally HSC activation.
The objective of this study was to estimate the incidence rates of severe hypersensitivity reactions (angioedema and anaphylactic reactions) for various β-blockers and to examine the risk of severe hypersensitivity reactions in patients exposed to carvedilol extended-release compared with carvedilol and compared with other β-blockers.
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All subjects were given either carvedilol (25 mg/day) or placebo for 2 weeks in a random order with a 2-week wash-out period. At the end of each treatment period they underwent a 30-minute exercise test on a bicycle ergometer with a fixed load of 20 W.
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Neuroprotective mechanisms were studied using an in vitro ischemia model of cultured rat cerebellar granule cell neurons exposed to either glutamate or oxygen free radical-generating systems. Prevention of lipid peroxidation by carvedilol was studied by measuring the formation of thiobarbituric acid-reactive substance. Gerbil CA1 neuron survival was examined by direct neuronal count 7 days after 6 minutes of global ischemia with reperfusion.
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The problem of heart failure (HF) has become a topic of great interest. Until recently, the use of beta-blockers in patients with HF was considered as one of the contraindications which were taught to medical students as realities with a strict policy to avoid them in HF patients. Times have changed and the contraindicated drug is now an advised and preferred one to be used in HF patients with certain advised recommendations for its use in a safe and beneficial way. Even though the use of beta-blockers in HF patients is an important and necessary step towards an optimal treatment of these patients as most of the big studies have proved, still we need to emphasize these benefits in order to achieve more application of these agents in HF patients. Here we analyse the major studies which used beta-blockers in HF patients. It seems that beta-blockers have to be used in all patients with HF with reduced ejection fraction unless a real contraindication exists as they bring up a great benefit towards decreasing mortality and morbidity.
Until recently, beta-blocking drugs were considered to be contraindicated in patients with chronic heart failure. However, several well-conducted randomised clinical trials have now proven otherwise. Yet, it was still not clear whether nonselective alpha-, beta 1- and beta 2-receptor blockade with carvedilol would be superior to selective beta 1-receptor blockade with metoprolol. One of the studies ('Carvedilol or metoprolol European trial' (COMET)) demonstrated a statistically significant 17% reduction of all-cause mortality with carvedilol. Although striking, the results may have been influenced by differences in blood pressure and heart rate, as well as the short-acting formula of metoprolol that was used. Furthermore, the 'Carvedilol hibernation reversible ischaemia trial; marker of success' (CHRISTMAS) study demonstrated myocardial hibernation in the majority of ischaemic heart-failure patients, and showed beneficial effects on left-ventricle function with carvedilol in both hibernated and non-hibernated patients. Despite this and the rest of the overwhelming evidence, at present only a minority of eligible chronic heart-failure patients are treated with beta-blockers.
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Transporter proteins such as P-glycoprotein are major determinants of intracellular drug concentrations. Moreover, inhibition or induction of transporters is an important mechanism underlying drug interactions in humans. However, very little is known whether beta-adrenoceptor antagonists are substrates and/or inhibitors of P-glycoprotein. Therefore, we investigated the P-glycoprotein-mediated transport of propranolol, metoprolol, bisoprolol, carvedilol and sotalol in P-glycoprotein-expressing Caco-2 monolayers and inhibition of P-glycoprotein-mediated digoxin transport by the beta-adrenoceptor antagonists. A significant inhibition of polarized, basal to apical drug transport by the P-glycoprotein inhibitor PSC-833 was observed for bisoprolol (0.5 and 5 microm) and carvedilol (0.5 microm). Moreover, propranolol and carvedilol inhibited P-glycoprotein-mediated digoxin transport with IC(50) values of 24.8 and 0.16 microm, respectively, whereas metoprolol and sotalol had no effect. Bisoprolol significantly inhibited directional digoxin transport at 50 and 250 microm by 31% and 44%, respectively. Taken together, P-glycoprotein is likely to be one determinant of bisoprolol and carvedilol disposition in humans. In addition, the beta-adrenoceptor antagonists propranolol and carvedilol significantly inhibit P-glycoprotein function thereby possibly contributing to drug interactions in humans (e.g. digoxin-carvedilol and cyclosporine-carvedilol).
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To (a) investigate the effect of tablet characteristics on weight and content uniformity of half tablets, resulting from splitting 16 commonly used medications in the outpatient setting and (b) provide recommendations for safe tablet-splitting prescribing practices.
coreg missed dose
We randomized 1546 consecutive patients with a left ventricular ejection fraction <45% found on echocardiography at 1 of 3 laboratories to a reminder for use of beta-blockers or no reminder. Patients were excluded from analysis if they died within 30 days of randomization (n=89), did not receive medications through the Veterans Affairs system after 30 days (n=180), or underwent echocardiography at >1 laboratory (n=6). The primary outcome was a prescription for an oral beta-blocker between 1 and 9 months after randomization. The mean age of the 1271 included patients was 69 years; 60% had a history of heart failure, and 51% were receiving treatment with beta-blockers at the time of echocardiography. More patients randomized to the reminder had a subsequent beta-blocker prescription (74%, 458 of 621) compared with those randomized to no reminder (66%, 428 of 650; P=0.002). The effect of the reminder was not significantly different for subgroups based on patient location (inpatient versus outpatient) or prior use of beta-blockers.
coreg renal dosing
Carvedilol and nebivolol both prevent development of nephropathy related to CMs by decreasing oxidative stress. Neither is superior to the other.
Our purpose was to measure the effect of non-benefit drug use on observed associations between exposure and outcome, thereby documenting an empirical example of the potential magnitude of biases introduced when exposure status is misclassified from a restrictive drug coverage policy.
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It is unclear whether improvement in left ventricular (LV) ejection fraction (LVEF) following treatment with a combined α(1),β(1),β(2)-blockade can be attributed to improvement in LV contractility, to a reduction in afterload, and/or to improvements in LV remodeling and chamber size. We aimed to examine whether the observed improvement in LVEF following carvedilol treatment is due to changes in intrinsic myocardial contractility beyond changes in LV chamber size or loading conditions.
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Beta-blockers (BB) have proven to be effective in the treatment of congestive heart failure (CHF). This study is an economic analysis for the addition of BB to standard treatment of CHF.
Some 4.6 million Americans are estimated to suffer from heart failure, and approximately 400,000 new cases are diagnosed each year. Each year 260,000 patients die as a direct or indirect result of the disorder, with annual costs estimated between $21 billion to $40 billion.
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During a 2-week placebo run-in period, patients were required to have two treadmill exercise tests (modified Bruce Protocol) differing by not more than 15% with regard to total exercise time (TET). Of 313 patients enrolled, 248 were randomized and 212 completed the study according to the protocol.
coreg usual dose
Carvedilol ([1-[carbazolyl-(4)-oxy]-3-[2-methoxyphenoxyethyl) amino]-propanol-(2)]) has been shown to protect cardiac mitochondria from oxidative stress. In this work we examined the mechanisms responsible for an observed depressive effect in the mitochondrial transmembrane potential (delta psi). Two possible mechanisms were considered: a protonophoretic activity and the opening of mitochondrial ATP-sensitive potassium channels. We show that carvedilol increases mitochondrial inner membrane permeability to protons, but not to potassium, causing an increase in state IV respiration in the presence and absence of oligomycin. By contrast, a K(ATP)-channel inhibitor, 5-hydroxydecanoic acid, did not affect carvedilol-induced depolarizations. Hence, our results suggest that carvedilol depresses mitochondrial delta psi by a weak protonophoretic mechanism.
The study aimed at in vivo pharmacokinetic evaluation of carvedilol loaded nanocapsules (CLN) followed by in silico predictions and establishment of IVIVC.
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Beta blockers are known to have favorable effects on endothelial function partly because of their capacity to reduce oxidative stress. To determine whether beta blockers can also prevent dextrose-induced endoplasmic reticulum (ER) stress in addition to their antioxidative effects, human coronary artery endothelial cells and hepatocyte-derived HepG2 cells were treated with 27.5 mM dextrose for 24 hours in the presence of carvedilol (a lipophilic beta blockers with alpha blocking activity), propranolol (a lipophilic nonselective beta blockers), and atenolol (a water-soluble selective beta blockers), and ER stress, oxidative, stress and cell death were measured. ER stress was measured using the placental alkaline phosphatase assay and Western blot analysis of glucose regulated protein 78, c-Jun-N-terminal kinase (JNK), phospho-JNK, eukaryotic initiating factor 2α (eIF2α), and phospho-eIF2α and measurement of X-box binding protein 1 (XBP1) mRNA splicing using reverse transcriptase-polymerase chain reaction. Superoxide (SO) generation was measured using the superoxide-reactive probe 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-A]pyrazin-3-one hydrochloride (MCLA) chemiluminescence. Cell viability was measured by propidium iodide staining method. The ER stress, SO production, and cell death induced by 27.5 mM dextrose were inhibited by all 3 beta blockers tested. The antioxidative and ER stress reducing effects of beta blockers were also observed in HepG2 cells. The salutary effects of beta blockers on endothelial cells in reducing both ER stress and oxidative stress may contribute to the cardioprotective effects of these agents.
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Although beta-blockers have been classically contraindicated in heart failure patients, their administration at progressively increasing doses provides long-term benefit in such patients with altered left ventricular function, and prevents the direct and indirect deleterious cardiac effects of catecholamines. By improving left ventricular function and preventing severe arrhythmias, beta-blockade improves survival, reduces the occurrence of sudden death and hospital admissions for worsening heart failure. The degree of benefit is dose dependent, although few prospective data confirm this fact. Among tested compounds, bisoprolol, metoprolol and carvedilol have produced similar improvements in survival with a 34% reduction in mortality in large-scale clinical trials. Bucindolol, however, did not significantly improve survival in the BEST trial. Different hypotheses may explain such results. In terms of therapeutic strategy, beta-blocker treatment must be initiated in stabilised patients already receiving diuretics and an angiotensin-converting enzyme inhibitor. Ongoing studies are evaluating the potential benefit of starting treatment first with beta-blockers in order to better prevent sudden death, particularly as this most often occurs in the early stages of the disease.
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Infarct size (IS) reduction by ischemic preconditioning (IPC) has been assessed in the heart in which coronary stenosis (CS)-induced chronic ischemia was not present. The aim of this study is to assess whether and how IS reduction by IPC is modified in the heart in which CS has occurred, and how further therapeutics, if any, modify it.
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Despite the wide use of beta-blockers, HR is insufficiently controlled in the analyzed sample of stable CAD patients in Latvia. Target HR ≤60bpm is achieved only in 25% of the patients while more than one third have increased HR ≥70bpm.