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Carvedilol and nebivolol reduce HVPG in cirrhotic patients; however, the effect of carvedilol on the HVPG reduction might be superior to that of nebivolol, especially after 14 days of treatment.
To show the effectiveness of emergency extracorporeal membrane oxygenation (ECMO) and plasmaspheresis in severe polyintoxication.
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The influence of beta-blocker therapy (bisoprolol or carvedilol) (bB) on the prognosis of heart failure (HF) patients with diabetes mellitus (DM) is uncertain.
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In the United States, carvedilol and metoprolol (tartrate or succinate) are the most commonly employed beta-adrenoreceptor antagonists for the treatment of heart failure. However, use of these agents in patients with heart failure remains extremely low despite overwhelming evidence of their beneficial short- and long-term effects. Because the myocardial pathophysiology associated with heart failure involves not only beta-1 adrenoreceptors but also beta-2 and alpha-1 adrenoreceptors, this indicates a more complex disease process that may require pan-receptor antagonism to provide optimal clinical benefit. Relative to metoprolol (tartrate or succinate), carvedilol represents an extremely complex molecular entity that not only possesses the ability to antagonize all of the principle adrenoreceptors involved in heart failure but also reduces oxidative stress and provides an antiarrhythmic benefit independent of beta-adrenoreceptor antagonism. Taken together, an interesting pharmacologic premise for the superiority of carvedilol relative to metoprolol (tartrate) may exist, but the lack of clinical trials comparing an optimal dose of either extended-release metoprolol (ie, succinate) or immediate-release metoprolol (ie, tartrate) to carvedilol limits the clinical application of the pharmacologic differences between the agents.
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Male, adult Sprague-Dawley rats.
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This study aimed to compare whether reduced heart rate (HR) or higher beta-blocker (BB) dose affected outcomes to a greater extent in the HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training) trial population.
Cardiac function was examined by echocardiography and levels of autoantibodies against cardiac beta(1)-adrenergic receptor were detected in 65 patients with CHF by means of enzyme linked immune assay. Carvedilol was added on ACEI, diuretics and digitalis regimen for a target dose of 50 mg/d. All patients were followed up for 6 months.
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Among 2058 patients receiving chronic BB treatment, 1990 were analyzed: BBM 530 (27 %), BBW 1460 (73 %). Compared to BBM, BBW had a higher in-hospital mortality (5.5 vs 3.0 %; p < 0.05), 30-day mortality (8.7 vs 4.5 %; p < 0.01), and 30-day combined endpoint (29.8 vs 23.4 %; p < 0.05). Multivariate adjustment confirmed an independent direct association between BBW and in-hospital mortality (OR 1.89; 95 % CI 1.09-3.26) and 30-day mortality (OR 2.01; 95 % CI 1.28-3.15). Stratified analysis indicated no interaction by all the subgroups analyzed, except for HR (p = 0.01 for interaction), which showed a greater negative impact of BBW in patients with HR >80 bpm (OR 2.74; 95 % CI 1.13-6.63).
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Data from the US Carvedilol Heart Failure Trials Program indicate that carvedilol reduces mortality in patients with heart failure; our study suggests that it also may be cost-saving over a period of approximately six months.
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The ANZ trial, a carvedilol study in heart failure, is characterized by a considerable number of early withdrawals in the carvedilol group. Using the ANZ trial database, the percentage of withdrawals was calculated as well as the number of days on treatment. Fourteen out of 21 deaths (67%) in the carvedilol group occurred after discontinuation of carvedilol. At the time of death, 14 out of 29 (48%) patients in the placebo group had withdrawn from treatment. Mean time of patients on medication who withdrew and died later were 301 days for placebo, but only 204 days for carvedilol. We performed a conventional ITT analysis, and an ITT-based Cox-proportional hazards model (modified ITT) in which the actual time on trial medication was entered into the model as an explanatory variable. The risk ratio in conventional ITT analysis was 0.71 (95% confidence interval (CI) 0.41 to 1.24, p = 0.228) and 0.50 (95% CI 0.28-0.90, p < 0.001 ) in modified ITT analysis.
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Eighty-seven subjects with uncomplicated essential hypertensive (49% men; age = 52.2 ± 11.1 years) from Jilin province of China were enrolled in the study, and 5 of them discontinued the treatment due to adverse effects. Both systolic and diastolic blood pressures (DBPs) were measured before and after 7 days of treatment with carvedilol (10 mg/d). Genotypes of the β1-adrenergic receptor (ADRB1 Ser49Gly and Arg389Gly) and β2-adrenergic receptor (ADRB2 Gly16Arg and Glu27Gln) were determined by polymerase chain reaction with restriction fragment length polymorphism.
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Beta-blockers are not considered to be contraindicated in patients with peripheral artery disease, and carvedilol and bisoprolol are commonly used in patients with PAD in Japan. Because there have been only a few reported comparative studies of the effects of different beta-blockers, we compared the clinical outcomes in patients treated with these beta-blockers after undergoing femoropopliteal stenting.
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One hundred and six patients (aged 65 12 [mean +/- SD] years) with ACHF were enrolled and treated with OMT, in which carvedilol was titrated up to the maximal dose (phase 1). Subsequently, patients with left ventricular (LV) ejection fraction < or = 35%, NYHA class III-IV and QRS interval > or =120 msec were assigned to CRT. Both CRT and NO-CRT patients underwent a long-term follow-up of 7 years (1193.98 +/- 924 days), while efforts to up titrate the carvedilol dose were continued during the second phase (471 + 310 days). Phase 1 was completed by 84 patients (79%), and 15 (18%) underwent CRT. The mean carvedilol dose in the CRT group was 19.0 +/- 17.8 mg, against 32.7 +/- 19.1 mg in the remaining 69 patients (P = 0.018). At the end of phase 2, CRT patients presented a significantly greater variation of increasing in the carvedilol dose than NO-CRT patients (+20.0 +/- 19.8 mg vs. -0.3 +/- 20.5 mg; P = 0.015), a greater NYHA class reduction (-0.8 +/- 0.6 vs. -0.2 +/- 0.7; P = 0.011), and a greater increase in LV ejection fraction (10.8 +/- 9 vs. 3.1 +/- 6.1; P = 0.018).
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The authors recently reported that urinary 8-hydroxy-2'-deoxyguanosine (U8-OHdG) derived from cardiac tissue reflects clinical status and cardiac dysfunction severity in patients with chronic heart failure (CHF). The aim of the present study was to investigate whether U8-OHdG levels can accurately predict cardiac events in CHF patients and their response to β-blocker treatment.
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Carvedilol ameliorated MI-induced apoptosis in a dose-dependent manner. In parallel, carvedilol also decreased the ratio of Bax to Bcl-2, the expression of TLR4 and NF-κB induced by MI. The extent of apoptosis and Bax-Bcl-2 ratio was strongly correlated with the TLR4 levels.
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In this report we describe the case of a 56-year-old man with a medical history of onset of asthenia, palpitations and dyspnoea for mild efforts. After a negative ergometric test for myocardial ischaemia and 24-h Holter monitoring showing frequent ventricular premature beats, but an echocardiogram with significant dilation and dysfunction of the left ventricle, coronary angiography was performed and did not show haemodynamically significant stenosis. Regarding the anamnesis of snoring, daytime sleepiness and the relationship between sleep-related breathing disorder and cardiovascular disease, we performed a cardiorespiratory sleep study that indicated a diagnosis of sleep-related breathing disorder with prevalent obstructive apnoea. In addition to optimal medical therapy for cardiovascular disease, the patient began therapy with continuous positive airway pressure during the night. This showed a considerable decrease in ventricular premature beats (VPBs) during the night, a better control of ventricular ectopy during the day and a better compliance with medical therapy.
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Predischarge initiation of carvedilol in stabilized patients hospitalized for HF improved the use of beta-blockade at 60 days without increasing side effects or length of stay. Predischarge initiation may be one approach to improve beta-blocker use in this population.
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A population-based inception cohort study that included all individuals aged ≥65 years with a first HF diagnosis in Quebec was conducted. β-Blockers initiation among 91,131 patients who were not using β-blockers at the time of HF diagnosis and discontinuation among those who initiated a β-blocker after HF diagnosis were assessed. Stepwise Cox regression analyses were used to calculate hazard ratios (HR) and to identify factors associated with β-blocker initiation and discontinuation.
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Oxidative stress is closely related to the pathogenesis of neurodegenerative disorders such as Parkinson's disease. Carvedilol, a nonselective β-adrenergic receptor blocker with pleiotropic activity has been shown to exert neuroprotective effect due to its antioxidant property. However, the neuroprotective mechanism of carvedilol is still not fully uncovered. The phosphotidylinositol 3-kinase (PI3K)/Akt signaling pathway plays key role in cell survival and the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is the major cellular defense mechanism against oxidative stress. Here we investigated the effects of carvedilol on 6-hydroxydopamine (6-OHDA)-induced cell death as well as the Akt and Nrf2/ARE pathways in PC12 cells. We found that carvedilol significantly increased cell viability and decreased reactive oxygen species in PC12 cells exposed to 6-OHDA. Furthermore, carvedilol activated the Akt and Nrf2/ARE pathways in a concentration-dependent manner, and increased the protein levels of heme oxygenase-1(HO-1) and NAD(P)H quinone oxidoreductase-1(NQO-1), two downstream factors of the Nrf2/ARE pathway. In summary, our results indicate that carvedilol protects PC12 cells against 6-OHDA-induced neurotoxicity possibly through activating the Akt and Nrf2/ARE signaling pathways.
From results, carvedilol and bisoprolol were associated with better outcomes, with no difference between these two β-blockers in patients with HF in Taiwan.
The purpose of this study was to evaluate the acute and long-term effects on blood pressure and hemodynamics both at rest and during acute exposure to loud noise of drugs with beta-adrenoceptor blocking and vasodilating properties. Prizidilol and carvedilol both act as nonselective beta-blocking and precapillary vasodilating compounds. Prizidilol (200 mg X 2) was compared to propranolol (80 mg X 2) plus hydralazine (25 mg X 2) and showed similar antihypertensive effect in a long-term double-blind randomized trial. Carvedilol was evaluated acutely with invasive (dye-dilution) and noninvasive (plethysmography) technique and showed an acute antihypertensive effect without causing a rise in TPR and with a decrease in regional resistance in the fore-arm. Acutely, carvedilol (25 mg and 50 mg) decreased blood pressure and regional resistance (50 mg) in contrast to propranolol (80 mg) which did not lower blood pressure acutely and caused an increase in regional resistance. In a long-term double-blind, randomized comparison, both propranolol (80 mg X 2) and carvedilol (25 mg X 2 and 50 mg X 2) showed a useful antihypertensive effect. After 29 days, however, it was still possible to demonstrate an acute decrease in resistance with carvedilol (50 mg) after tablet intake, indicating the vasodilating activity of this compound. When patients with essential hypertension were exposed to an even broad band noise (100 dBA), there was a rise in blood pressure due to an increase in TPR. Alpha 1-adrenoceptor blockade (prazosin 2 mg) prevented the rise in TPR but blood pressure increased in spite of this due to a rise in CO. Moreover, nonselective beta-adrenoceptor blockade and alpha 1-adrenoceptor blockade in combination (labetalol 200 mg) were unable to prevent the rise in blood pressure induced by noise. Finally, precapillary vasodilatation and beta-adrenoceptor blockade (prizidilol 400 mg) given as long-term treatment were also inefficient in preventing the noise-induced (105 dBA) rise in blood pressure. The absolute level of blood pressure obtained, however, was significantly lower than during placebo administration.
These data show that alpha1 and beta3-adrenergic receptors may contribute to the mediation of MDMA-induced hyperthermia and that drugs targeting these receptors, such as carvedilol, warrant further investigation as novel therapies for the treatment of psychostimulant-induced hyperthermia and its sequelae.
The IMPACT-HF was a prospective, randomized open-label trial conducted in 363 patients hospitalized for HF. Patients were randomized to carvedilol initiation pre-hospital discharge or to postdischarge initiation (>2 weeks) of beta-blockade at the physicians' discretion. The primary end point of the study was the number of patients treated with beta-blockade at 60 days after randomization. Secondary end points included the number of patients discontinuing beta-blockade, median dose achieved, and a composite of death, rehospitalization, unscheduled visit for HF, or > or =50% increase in oral diuretic, new oral diuretic, or any intravenous therapy with diuretics, inotropes, or other vasoactive agents.