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Coreg

Coreg is a high-quality medication which is taken in treatment of hypertension, heart failure, and in the treatment and prevention of heart attack. Coreg acts by affecting circulation and heart. It is a beta-blocker.

Other names for this medication:
Coreg CR, Cardivas, Caarca, Carloc, Carzec, Carvil, Carvistar, Carvipress, Carviflo, Carvibeta, Cardol

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Also known as:  Carvedilol.

Description

Coreg is a perfect remedy in struggle against hypertension, heart failure. Its target is to treat and prevent heart attack.

Coreg acts by affecting circulation and heart. It is a beta-blocker.

Coreg is also known as Carvedilol, Dilatrend, Eucardic, Carloc.

Generic name of Coreg is Carvedilol.

Brand names of Coreg are Coreg, Coreg CR.

Dosage

Coreg is available in tablets and extended-release capsules which are used orally with food.

Do not crush or chew it.

Take Coreg tablets twice a day, extended-release capsules are taken once a day in the morning.

If you want to achieve most effective results do not stop taking Coreg suddenly.

Overdose

If you overdose Coreg and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Coreg overdosage: bluish-colored fingernails, weakness, short breathing, fainting, uneven heartbeats, convulsions, lightheadedness.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Coreg are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Coreg if you are allergic to Coreg components.

Do not take Coreg if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Coreg if you have a history of asthma, emphysema, thyroid disorder, pheochromocytoma, myasthenia gravis, low blood pressure, liver, kidney or heart disease diabetes, hyperthyroidism, depression, Prinzmetal's angina, bronchitis.

Be careful using Coreg if you take monoamine oxidase inhibitors (tranylcypromine (such as Parnate), isocarboxazid (such as Marplan), selegiline (such as Zelapar, Eldepryl, Emsam), phenelzine (such as Nardil)); verapamil (such as Calan,Verelan, Covera-HS); paroxetine (such as Paxil); cimetidine (such as Tagamet); rifampin (such as Rifadin, Rimactane); clonidine (such as Catapres), cyclosporine (such as Sandimmune, Neoral); digoxin (such as Lanoxin, Lanoxicaps); quinidine; diltiazem (such as Tiazac, Cardizem); fluoxetine (such as Prozac); epinephrine (such as Epipen); oral diabetes medicines and insulin; propafenone (such as Rythmol); reserpine (such as Serpalan).

Do not use potassium supplements or salt substitutes.

Avoid quickly physical movements.

If you are going to have a surgery, be careful with Coreg.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Avoid driving machine.

Do not stop taking Coreg suddenly.

coreg 40 mg

When 20 mg/day carvedilol plus 25 mg/day spironolactone plus 5 mg/day enalapril maleate (enalapril, group A) or 8 mg/day candesartan cilexetil (candesartan, group B) plus 40 mg/day furosemide were used concomitantly, the mean serum potassium increased significantly in both groups of patients. Seven of 59 (11.9%) patients had hyperkalemia (>5.5 mEq/L) during 12 months of treatment whereas 8.5% of patients (five of 59) had hypokalemia (< or =3.5 mEq/L).

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Cardiovascular disease is the leading cause of death worldwide. Within the treatment armamentarium, beta-blockers have demonstrated efficacy across the spectrum of cardiovascular disease--from modification of a risk factor (ie, hypertension) to treatment after an acute event (ie, myocardial infarction). Recently, the use of beta-blockers as a first-line therapy in hypertension has been called into question. Moreover, beta-blockers as a class are saddled with a misperception of having poor tolerability. However, vasodilatory beta-blockers such as carvedilol have a different hemodynamic action that provides the benefits of beta-blockade with the addition of vasodilation resulting from alpha 1-adrenergic receptor blockade. Vasodilation reduces total peripheral resistance, which may produce an overall positive effect on tolerability. Recently, a new, controlled-release carvedilol formulation has been developed that provides the clinical efficacy of carvedilol but is indicated for once-daily dosing. This review presents an overview of the clinical and pharmacologic carvedilol controlled-release data.

coreg oral tablet

Carvedilol (2.0 and 4.0 mg/kg i.p.) and propranolol (10 mg/kg i.p.) were administered to separate group of animals 24 h before and concurrently with CsA (20 mg/kg s.c.) for 21 days. Renal function was assessed by estimating plasma creatinine, blood urea nitrogen (BUN), creatinine and urea clearance. Tissue lipid peroxidation was measured as thiobarbituric acid-reacting substances (TBARS). Renal morphological alterations were assessed by histopathological examination of hematoxylin-eosin, PAS and Masson's trichrome stained sections of the kidneys.

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To determine the acute effects of carvedilol (beta-blocker) on cardiovascular and renal function and its pharmacokinetics in dogs. Fifteen mature mongrel dogs (7-15 kg) of both sexes were used in these experiments. Eight dogs served as controls, and seven dogs served as iatrogenic mitral regurgitation (MR) experimental animals. Carvedilol (0.2, 0.4, and 0.8 mg/kg, P.O.) was administered, and the blood carvedilol concentration was analyzed by reverse-phase high-performance liquid chromatography. The response to isoproterenol or phenylephrine was also evaluated. Isoproterenol (0.025 microg/kg/min) was infused via the saphenous vein for 5 min, and phenylephrine (5 microg/kg) was injected with carvedilol (0.2, 0.4 mg/kg) or placebo for 4 days. The heart rate and arterial blood pressure were measured, and LV fractional shortening was measured by echocardiography. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by intravenous infusion of sodium thiosulfate and sodium para-aminohippurate. Carvedilol (0.2 mg/kg) decreased the heart rate, whereas renal function, arterial blood pressure, and left ventricular contractile function were not affected. Carvedilol (0.4 mg/kg) decreased heart rate, blood pressure, and renal function. The tachycardic response to isoproterenol was significantly diminished for 36 hr by 0.4 mg/kg carvedilol. Carvedilol 0.2 mg/kg inhibited this effect for 24 hr. Thus, it is necessary to titrate the dosage of carvedilol, it should be initiated at less than 0.2 mg/kg and titrated up to 0.4 mg/kg for heart failure dogs.

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We sought to evaluate the effects of beta-blocker therapy on regional and global myocardial mechanics in addition to ventricular synchrony in patients with heart failure and normal QRS by using tissue Doppler and strain echocardiography.

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N588K-KCNH2 and V307L-KCNQ1 mutations lead to a gain-of-function of IKr and IKs thus causing short-QT syndromes (SQT1, SQT2). Combined pharmacotherapies using K(+) -channel-blockers and β-blockers are effective in SQTS. Since β-blockers can block IKr and IKs , we aimed at determining carvedilol's and metoprolol's electrophysiological effects on N588K-KCNH2 and V307L-KCNQ1 channels.

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The apoptotic indices of the infracted/scar, border and non-infarcted areas at any time-point of Group MI were all significantly higher than those of Group S (all P < 0.05). Only the apoptotic indices of the infracted/scar and border areas of the C-4 week subgroup were significantly lower than those of the MI-4 week subgroup (both P < 0.05), and were close to those of the non-infarcted area. DNA gel electrophoresis showed that the positive rate of Group S at any time-point were both 0, the positive rate of MI-48 h subgroup and C-48 h subgroup were both significantly higher than that of Group S (both P < 0.05) without significant difference between these 2 groups, and the positive rates of the MI-4 week subgroup and C-4 week subgroup were both 0. Immunohistochemistry showed that the bax gene expression was slightly to significantly increased in the infarcted/scar, border, and non-infarcted areas of the MI-48 h and MI-4 week subgroups. The bcl-2 expression was significantly increased only in the infracted area of the MI-48 h subgroup. The bcl-2 expression was slightly increased in the infracted and border areas of the C-48 h subgroup and the bax expression was significantly decreased in the infracted/scar area of the C-4 week subgroup. Western blotting showed that (1) the bcl-2 expression of the S-4 week subgroup was significantly higher than that of the S-48 h subgroup (P < 0.05), (2) the bcl-2 expression and bax expression of the MI-48 h subgroup were significantly higher than that of the S-48 h subgroup (P < 0.05 - 0.01), the bcl-2/bax ratio of the MI-48 h subgroup was significantly lower that that of the S-48 h subgroup, however, there were no significant differences in the bcl-2 and bax expression and bcl-2/bax ratio between the MI-4 week subgroup and S-48 h subgroup (all P > 0.05), and (3) There were no significant difference in the bcl-2 and bax expression between Group A and Group S (all P > 0.05), however, the bcl-2/bax ratios at the 2 time-points of Group C were both significantly higher than those of Group MI.

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In vitro, human cultured endothelial cells were treated with native low-density lipoprotein (LDL), oxidized LDL or tumor necrosis factor (TNF)alpha in the absence and in the presence of carvedilol (40 micro M); 8-iso-prostaglandin (PG)F(2alpha), as parameter of oxidative stress, was determined in the supernatants. In a double-blind, randomized, cross-over study, 17 healthy men received 25 mg carvedilol b.i.d., 100 mg metoprolol b.i.d. or placebo for 6 days. After each treatment, systemic oxidative stress was assessed by measuring urinary excretion of 8-iso-PGF(2alpha) and 2,3-dinor-5,6-dihydro-8-iso-PGF(2alpha), and the plasma concentration of 3-nitrotyrosine by means of gas chromatography-tandem mass spectrometry. In addition, thiobarbituric acid-reactive substances (TBARS) in plasma were assessed using spectrophotometry.

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The precise mechanism by which beta-adrenoceptor blockers exert their beneficial actions in patients with heart failure remains unclear. Several possibilities have been proposed, including heart rate reduction, beta2-adrenoceptor-mediated modulation of catecholamine release, antagonism of the receptor-mediated toxic actions of norepinephrine on the myocardium, and favorable effects on myocardial energetics. In the present study we evaluated the effect of 3 months of carvedilol therapy on hemodynamics, total systemic and cardiac norepinephrine spillover (isotope dilution method), and myocardial metabolism (myocardial oxygen consumption and carbon dioxide release) in 10 patients with severe congestive heart failure. Although carvedilol treatment was associated with a significant improvement in left ventricular ejection fraction (17+/-1% to 28+/-3%; P<0.01) and left ventricular stroke work (87+/-13 to 119+/-21 g. m per beat; P<0.05), this effect was unrelated to changes in total systemic or cardiac norepinephrine spillover. The rise in left ventricular stroke work was accompanied by a modest rise in myocardial oxygen consumption per beat (0.33+/-0.04 to 0.42+/-0.04; P=0.05), although contractile efficiency was unchanged. The favorable effects of carvedilol on ventricular function in the failing heart are not explained by alterations in norepinephrine release or by changes in myocardial contractile efficiency.

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The aim of this study was to evaluate the efficacy of nebivolol, carvedilol or metoprolol succinate on the outcome of patients presenting with acute myocardial infarction (AMI) complicated by left ventricular dysfunction.

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Carvedilol significantly increased RRIs and lowered BP, CBFV, and 0.1 Hz RRI-, BP-, and CBFV-powers at baseline (P=0.041 for CBFV-powers), and during 0.1 Hz NS-induced sympathetic activation (P<0.05). At baseline and during 0.2 Hz NS-induced parasympathetic activation, atropine lowered RRIs and 0.2 Hz RRI-powers, but did not change BP, CBFV, and 0.2 Hz BP- and CBFV-powers.

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ClinicalTrials.gov Identifier: NCT02619526 , registered on 25 November 2015.

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AF occurred in 29 of 120 patients (24.0%). The incidence of postoperative AF was 15.0% (9 of 60) in the carvedilol group and 33% (20 of 60) in the metoprolol group (P = .022). The carvedilol group was treated with mean daily dose of 46 +/- 9 mg and metoprolol group with mean daily dose of 93 +/- 11 mg. There were no differences between the study groups regarding any known preoperative, perioperative, or postoperative characteristics (all values were P >.05). No significant adverse effect was observed in either group.

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ECMO and plasma exchange should be considered as a therapeutic option in selected patients under resuscitation without return to spontaneous circulation after severe intoxication.

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The baseline characteristics of both groups were well balanced. Both carvedilol and atenolol significantly reduced heart rate from baseline (76 ± 11 to 66 ± 9 beat/min, p < 0.001; 74 ± 9 to 64 ± 9 beat/min, p < 0.001, respectively) with no significant changes in systolic and diastolic blood pressure. Improvement of time to ST-segment depression during the treadmill exercise and the SAQ scores for angina stability and frequency after 6 months of treatment were similar between groups. There was no significant change from baseline in the level of fasting glucose, insulin, or glycated hemoglobin in either group. However, total cholesterol and low-density lipoprotein cholesterol levels significantly reduced to a greater extent with carvedilol than with atenolol (-23 vs. -10 and -38 vs. -24 %, respectively, p < 0.05 for both), although the rate of statin use was comparable. No changes were seen in high-density lipoprotein cholesterol and triglyceride levels after 6 months of treatment in both groups compared with baseline.

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coreg mg 2017-01-02

With carvedilol, 11/18(61.1%) and 11/17(64.7%) patients responded acutely and after 7 days, respectively, while 9/18(50%) and 10/16(62.5%) did so to propranolol. However, HVPG reduction (percent) by carvedilol was not superior to that by propranolol either acutely (27.67 +/- 31.49 compared to 22.98 +/- 27.40, P = 0.6) or after 7 days (28.2 +/- 29.05 compared to 23.25 +/- 20.15, P = 0.6). With carvedilol, the acute HVPG response (P < 0.001) and responder status (P = 0.018) were good predictors of the response after 7 days, but were Cordarone Iv Dosing weak predictors in the case of propranolol (0.1 > P > 0.05 and P = 0.059, respectively). On carvedilol, only one patient (with ascites) developed symptomatic systemic hypotension with oliguria.

coreg normal dose 2015-02-18

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coreg cr generic 2016-06-15

Fifty-seven patients with New York Heart Association functional class II or III with a radionuclide left ventricular ejection fraction (LVEF) of less than 40% received carvedilol or metoprolol in a randomized fashion. The VE/VCO2 slope, LVEF and plasma brain natriuretic peptide (BNP) concentration were Asacol Medicine determined before and after 16 weeks of treatment. LVEF improved (p<0.01), but the VE/VCO2 slope and BNP did not. A significant improvement in the VE/VCO2 slope was observed in patients with LVEF <29% or BNP >63 pg/ml (respective baseline median values) (p<0.05, p<0.05). In patients with BNP >63 pg/ml, the improvement effect on the VE/VCO2 slope with carvedilol was significantly greater than that with metoprolol (p<0.05) and a significant improvement in the VE/VCO2 slope was observed only in those who took carvedilol (p<0.01).

coreg heart medication 2017-07-23

Ultraviolet (UV) spectrophotometric and nonaqueous volumetric methods are described for the determination of carvedilol in pharmaceutical formulations. Linearity, precision, and accuracy were evaluated according to the validation guidelines of the International Conference on Harmonization and the United States Pharmacopeia for both methods. The UV spectrophotometric procedure was performed in ethanol at 244 nm. Good linearity was obtained between 2 and 7 microg/mL with a correlation coefficient of 0.9999. The intra- and interday precision values were <2% for all samples analyzed. The accuracy, determined from recovery studies, was between 97.5 and 102.2%. The other procedure was based on the volumetric quantitation of carvedilol in a nonaqueous medium with 0.01 M perchloric acid and 1% violet crystal as the indicator. The validation of the volumetric method Sporanox Review yielded good results that included linearity (r of > 0.999), precision (relative standard deviations of <2% for intra- and interday precision), and accuracy (96.4-102.4%). The methods were applied to tablets and compounded capsules. Statistical analysis by analysis of variance showed no significant difference between the results obtained by the proposed methods.

coreg 5 mg 2015-10-28

Cytokine and sFas levels are elevated in patients with PPC. Despite treatment with ACE inhibitors and beta-blockers, mortality remains high. However, in 34% of the Detrol Generic Dosing patients, left ventricular function almost completely normalized.

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coreg cost 2017-04-19

With the mean follow-up period of 5.17 years and 4.93 years in the carvedilol and noncarvedilol cohorts Effexor 25 Mg , respectively, the patients in the carvedilol cohort had a 26% reduction of cancer risk compared with those in the noncarvedilol cohort (hazard ratio [HR]=0.74; 95% confidence interval [CI]=0.63-0.87; p<.001). The sex-specific carvedilol to noncarvedilol relative risk was lower for both women (HR=0.73; 95% CI=0.56-0.94) and men (HR=0.75; 95% CI=0.61-0.92). Moreover, stratified by cancer site, treatment with carvedilol in the carvedilol cohort resulted in significantly lower incidence of stomach and lung cancers than in the noncarvedilol cohort.

coreg 40 mg 2016-10-23

We explored the prescription of β-blockers with ivabradine in patients with systolic heart failure, focusing on the most frequently Levitra 10mg Dosage coprescribed β-blocker, carvedilol.

coreg user reviews 2016-03-18

Carvedilol is a new beta-blocker antihypertensive agent with vasodilating properties secondary to alpha 1-blocking activity. Peripheral vascular resistance is reduced and cardiac output and renal function are not altered with carvedilol. The antihypertensive effects of this agent are equivalent to those of other beta-blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, and diuretics. Carvedilol has a neutral effect on lipids and glucose metabolism. The percentage of responders is increased when carvedilol is combined with a diuretic. This agent has several unique Detrol Generic properties. In addition to its antihypertensive effects, carvedilol in vitro and in vivo has been shown to have antiproliferative effects on smooth muscle cells and to inhibit the action of oxygen-free radicals. The antioxidant properties of this compound are significantly greater than those of vitamin E. In animal models, carvedilol may slow the process of atherogenesis, reduce infarct size, and improve postinfarction survival to a greater degree than other beta-blockers. Recent studies have demonstrated that carvedilol reduces morbidity and mortality in patients with congestive heart failure who are already receiving angiotensin converting enzyme inhibitors, diuretics, and digitalis. The antioxidant and antiproliferative activities of carvedilol may present an advantage over other available antihypertensive medications.

coreg medication 2017-11-20

The blood pressure (BP) lowering effect of low doses of antihypertensive agents is not usually explored because of the difficulty in detecting small changes in BP. Since ambulatory blood pressure monitoring in a cross-over trial design can reliably detect differences of 5 mmHg with less than 20 subjects, we have used this technique to assess the dose-response curve of a new beta-blocker, carvedilol. Twenty subjects were enrolled after diagnostic ambulatory BP monitoring had shown a day-time average diastolic BP of over 90 mmHg. Three doses of carvedilol (6.25, 12.5 and 25 mg daily) and placebo were then given double-blind in random order for periods of 4 weeks each. No period effects were detected. The antihypertensive effect was statistically significant at doses of 12.5 mg and 25 mg daily. There was, however, no evidence that 25 mg/day produced the peak effect. The lowest dose (6.25 mg/day) produced a small fall in both systolic and diastolic BP but Discount Cialis Online neither of these were significant. We conclude that doses of 12.5 and 25 mg carvedilol once a day are adequate for the treatment of hypertension.