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1 tentially be suppressed by carvedilol or (R)-carvedilol.
2 ailure and systolic dysfunction treated with carvedilol.
3 ontribute to the cardioprotective effects of carvedilol.
4 ad heart failure at study entry; 34 received carvedilol.
5 ling by the ryanodine stabilizer JTV-519 and carvedilol.
6 of the patients on metoprolol and in 23% on carvedilol.
7 at does not seem to occur with metoprolol or carvedilol.
8 patients were assigned to receive placebo or carvedilol.
10 to twice-daily dosing with placebo, low-dose carvedilol (0.2 mg/kg per dose if weight <62.5 kg or 12.
11 dose if weight > or =62.5 kg), or high-dose carvedilol (0.4 mg/kg per dose if weight <62.5 kg or 25
13 ial in normal subjects (single dose of 25 mg carvedilol, 100 mg metoprolol tartrate, and placebo).
14 ibernators, respectively) but increased with carvedilol (2.5 [0.9] and 3.2 [0.8], respectively; p<0.0
15 ated cardiomyopathy (DCM) were randomized to carvedilol (25 mg twice daily, Coreg, Glaxo Smith Kline,
16 e, heart rates were significantly reduced by carvedilol (308 +/- 25 versus 351 +/- 31 beats per minut
17 l medications; atenolol: 92 mg versus 68 mg; carvedilol: 44 mg versus 20 mg; metoprolol: 80 mg versus
19 hanged (15%); among 103 patients assigned to carvedilol, 58 improved (56%), 25 worsened (24%), and 20
22 mbined risk of death or hospitalization with carvedilol (95 percent confidence interval, 13 to 33 per
23 5 percent decrease in the risk of death with carvedilol (95 percent confidence interval, 19 to 48 per
24 gned to establish the efficacy and safety of carvedilol, a "third-generation" beta -blocking agent wi
25 tion and improves its functional response to carvedilol, a beta blocker currently used in the treatme
26 holesterolemia and determined the effects of carvedilol, a beta-blocker with free radical-scavenging
32 hat the beta-arrestin-biased betaAR agonist, carvedilol, activates cellular pathways in the heart.
40 ction fraction < 45% (n = 49 patients; 24 on carvedilol and 25 on placebo), carvedilol showed attenua
42 ll-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard
44 admission occurred in 1116 (74%) of 1511 on carvedilol and in 1160 (76%) of 1518 on metoprolol (0.94
45 ic actions of the aforementioned drugs, with carvedilol and JTV-519 (but not flecainide or riluzole)
46 the efficacy of mixed adrenoceptor blockers carvedilol and labetalol, and the atypical antipsychotic
49 of this study was to evaluate the effects of carvedilol and metoprolol on the endpoint of inappropria
51 we examined the effects of standard doses of carvedilol and metoprolol succinate (metoprolol controll
52 ssed the relative efficacy of equal doses of carvedilol and metoprolol succinate on survival in multi
53 e to infused Ang II in patients treated with carvedilol and metoprolol, a selective beta-antagonist.
54 lol, carvedilol, and metoprolol; 2 of these, carvedilol and metoprolol, have Food and Drug Administra
56 Although there was no difference between the carvedilol and placebo groups in the number of patients
59 h greater responsiveness for metoprolol than carvedilol) and beta(1)-adrenergic receptor Arg389Gly po
60 available in the United States, bisoprolol, carvedilol, and metoprolol; 2 of these, carvedilol and m
67 were randomly assigned to receive placebo or carvedilol (at doses of 6.25 to 50 mg twice daily) for u
69 - + beta1,2,3-adrenergic receptor antagonist carvedilol before or after a thermogenic challenge of MD
73 were started on one of three beta-blockers (carvedilol, bucindolol or metoprolol) and the dose was a
74 F patients have better responses not only to carvedilol but to certain other beta blockers as well.
77 ent of the hypercholesterolemic rabbits with carvedilol, but not propranolol, significantly preserved
78 on fraction was not altered significantly by carvedilol, but stroke volume was higher at pre-hospital
79 Here we show that only alprenolol (Alp) and carvedilol (Car) induce beta(1)AR-mediated transactivati
80 cations included chlorthalidone, amlodipine, carvedilol, cholecalciferol, erythropoietin, and a phosp
81 .0%, 6.7%, and 1.1% with increasing doses of carvedilol compared with 15.5% in the placebo group, P <
82 ation was also reduced in patients receiving carvedilol compared with metoprolol (HR: 0.50 [95% CI: 0
85 Moreover, when administered 1 hr after MDMA, carvedilol completely reversed established hyperthermia
89 he alpha- and beta-adrenergic blocking agent carvedilol demonstrated a significant survival advantage
90 se in cardiac beta-receptor density, whereas carvedilol did not change cardiac beta-receptor expressi
91 of the third-generation beta-blocking agent carvedilol differs considerably from second-generation c
93 g 16 clinically relevant betaAR antagonists, carvedilol displays a unique profile of in vitro signali
94 subjects, whereas chronic administration of carvedilol does not attenuate the vasoconstrictor respon
96 The change in LVEF was also influenced by carvedilol dose, etiology of heart failure, baseline hea
97 racemic carvedilol and the non-beta-blocking carvedilol enantiomer, (R)-carvedilol, suppressed sponta
99 he BB dose at baseline was standardized with carvedilol equivalents and analyzed as a continuous vari
101 rrhythmias by beta-blockers (propranolol and carvedilol), flecainide, and the neuronal sodium-channel
102 ind, randomised trial to compare placebo and carvedilol for 6 months in individuals with stable, chro
103 placebo and 1156 patients to treatment with carvedilol for a mean period of 10.4 months, during whic
104 trials of tacrine for Alzheimer disease and carvedilol for congestive heart failure typify the use o
105 ratios of the relative risks associated with carvedilol for these two outcome variables in black as c
106 lure, which treated patients with placebo or carvedilol for up to 15 months (median, 6.5 months).
107 that: (i) The beta-AR antagonists nadolol or carvedilol, given as a single i.v. injection (acute trea
109 found that 304 (27.2%) patients died in the carvedilol group and 1066 (36.8%) in the metoprolol grou
111 , all-cause mortality alone was lower in the carvedilol group than in the placebo group (116 [12%] vs
112 mproved and fewer patients felt worse in the carvedilol group than in the placebo group after 6 month
114 orsened outcome for patients in the combined carvedilol group vs the placebo group was 0.79 (95% CI,
115 he placebo group and 22 to 975 (2.3%) in the carvedilol group, giving a carvedilol/placebo hazard rat
119 in the placebo group and 3.2 percent in the carvedilol group; the reduction in risk attributable to
121 -related and was present in both placebo and carvedilol groups, although the effect was statistically
122 F] units in the low-, medium-, and high-dose carvedilol groups, respectively, compared with 2 EF unit
125 t rate reductions, short-term treatment with carvedilol had superior hemodynamic and metabolic effect
127 he purpose of this study was to test whether carvedilol has an antioxidant effect in humans in vivo.
128 receptor (beta2AR)-expressing HEK-293 cells, carvedilol has inverse efficacy for stimulating G(s)-dep
129 The third-generation beta-blocking agent carvedilol has substantially different effects on left v
131 d patients entered into the Multicenter Oral Carvedilol Heart failure Assessment (MOCHA) trial, a 6-m
137 ely, of the patients receiving metoprolol or carvedilol (HR: 0.80 [95% CI: 0.63 to 1.00], p = 0.050).
139 beta-blocker treatment, including the use of carvedilol, improves myocardial betaAR signaling and red
141 To prospectively evaluate the effects of carvedilol in children and adolescents with symptomatic
142 hese data suggest that long-term benefits of carvedilol in heart failure are not mediated by alpha-ad
143 diated beta-arrestin1 signaling activated by carvedilol in miR biogenesis, which may be linked, in pa
145 ed, multicenter, dose-response evaluation of carvedilol in patients with chronic stable symptomatic h
147 in patients randomized to metoprolol versus carvedilol in the Carvedilol Or Metoprolol European Tria
148 ght to compare the effects of metoprolol and carvedilol in the MADIT-CRT (Multicenter Automatic Defib
149 All patients receiving either metoprolol or carvedilol in the MADIT-CRT study were identified and co
150 th beta-blockers were well tolerated; use of carvedilol in the presence of RAS blockade did not affec
151 ng may contribute to the special efficacy of carvedilol in the treatment of heart failure and may ser
153 fications to the three principal subunits of carvedilol, including the carbazole and catechol moietie
156 riluzole; a direct antiarrhythmic action of carvedilol (independent of its alpha/beta-adrenergic blo
157 strate for the first time that nebivolol and carvedilol induce relaxation of renal glomerular microva
158 A-mediated down-regulation of MARCH2 ablated carvedilol-induced ubiquitination, endocytosis, and degr
159 wn for any Galphas-coupled receptor, whereby carvedilol induces the transition of the beta1AR from a
161 -initiated study to evaluate if predischarge carvedilol initiation in stabilized patients hospitalize
163 patients (91.2%) randomized to predischarge carvedilol initiation were treated with a beta-blocker,
165 Taken together, these data indicate that carvedilol is able to stabilize a receptor conformation
166 ta1-selective, the third-generation compound carvedilol is beta-nonselective, with ancillary pharmaco
167 non-selective beta- and alpha-blockade with carvedilol is well tolerated in patients with COPD who d
168 heart failure outcomes in patients receiving carvedilol (low- and high-dose combined) vs placebo.
169 receive treatment with placebo, 6.25 mg BID carvedilol (low-dose group), 12.5 mg BID carvedilol (med
171 In response to beta blocker therapy with carvedilol, MARCH2 E3 ligase activity regulates cell sur
175 BID carvedilol (low-dose group), 12.5 mg BID carvedilol (medium-dose group), or 25 mg BID carvedilol
176 heart failure treated with beta-AR blockers (carvedilol, metoprolol, or atenolol), 9 from patients wi
177 d bioassay of ca. 100 compounds based on the carvedilol motif to identify features that correlate wit
178 double-blind) to either placebo (n = 145) or carvedilol (n = 133; target dose, 25 to 50 mg BID) for 6
179 In subjects randomized to treatment with carvedilol (n = 231), LVEF improved 9.5 +/- 0.9 EF units
180 inhibitors, were randomized double-blind to carvedilol (n = 232) or placebo (n = 134) and followed u
182 ndomized to receive a 6.25- to 25-mg dose of carvedilol (n = 498) or 50- to 200-mg dose of metoprolol
187 We investigated the long-term efficacy of carvedilol on morbidity and mortality in patients with l
189 to explore whether the protective effects of carvedilol on the ischemic myocardium include inhibition
193 ly substantial comparative trial to date-the Carvedilol or Metoprolol European Trial-has compared car
196 ure were randomly assigned to receive either carvedilol or metoprolol in addition to standard therapy
197 tween all-cause mortality and treatment with carvedilol or metoprolol succinate was observed after ei
198 chronic heart failure who were using either carvedilol or metoprolol succinate were identified in th
199 wo concurrent placebo-controlled trials with carvedilol or metoprolol that had common substudies focu
200 , nonselective beta-adrenergic blockade with carvedilol or propranolol does not prevent patients with
201 d 23 patients with CHF who were treated with carvedilol or propranolol in addition to ACE inhibitors,
202 tion of trained patients treated with either carvedilol or propranolol increased from 12.9 +/- 1.4 to
204 l benefit was greater for trials of the drug carvedilol (OR 0.54, 95% CI 0.36 to 0.81) than for nonca
209 curred in 21% of placebo patients and 11% of carvedilol patients, reflecting a 48% (P = .008) reducti
210 975 (2.3%) in the carvedilol group, giving a carvedilol/placebo hazard ratio (HR) of 0.41 (95% confid
211 rs were equally randomized to the SCS, MEDS (carvedilol plus ramipril 2.5 mg PO QD), SCS plus MEDS (c
212 a placebo-controlled multicenter trial, the Carvedilol Post-Infarct Survival Control in Left Ventric
214 Taken together, these results suggest that carvedilol prevents myocardial ischemia/reperfusion-indu
215 ate heart failure from systolic dysfunction, carvedilol produced dose-related improvements in LV func
217 iciency Bisoprolol Study (CIBIS II), and the Carvedilol Prospective Randomized Cumulative Survival St
218 vention Trial in Heart Failure), COPERNICUS (Carvedilol Prospective Randomized Cumulative Survival tr
220 ischemic cardiomyocytes, and treatment with carvedilol reduced both the intensity of staining as wel
223 ed by left-ventricular systolic dysfunction, carvedilol reduced the frequency of all-cause and cardio
227 ts with heart failure have demonstrated that carvedilol reduces morbidity and mortality and inhibits
236 non-beta-blocking carvedilol enantiomer, (R)-carvedilol, suppressed spontaneous Ca(2+) oscillations i
238 with chronic heart failure to treatment with carvedilol (target dose 25 mg twice daily) and 1518 to m
240 ignificantly higher in patients treated with carvedilol than in those treated with metoprolol (20 [ra
241 (123)I-MIBG cardiac washout was lower during carvedilol than metoprolol treatment (12.9% +/- 3.9% vs.
243 n to microalbuminuria was less frequent with carvedilol than with metoprolol (6.4% vs 10.3%; odds rat
244 sociated with higher mortality compared with carvedilol therapy (hazard ratio, 1.49; 95% confidence i
246 n for 2 hours 3 times a day), medicine (MED; carvedilol therapy at 12.5 mg PO BID), or control (CTRL;
247 ment Predischarge: Process for Assessment of Carvedilol Therapy in Heart Failure (IMPACT-HF) trial wa
251 esized that the nonselective beta-antagonist carvedilol, through its alpha1-adrenergic blocking prope
252 rest or on minimal exertion, the addition of carvedilol to conventional therapy ameliorates the sever
253 ht to evaluate the efficacy of enalapril and carvedilol to prevent chemotherapy-induced left ventricu
266 l and placebo (isometric handgrip -3.5 U for carvedilol versus -1.2 U for metoprolol and -2.2 U for p
267 o, P=0.15; cold pressor test 3.1+/-8.9 U for carvedilol versus 9.0+/-2.7 U for metoprolol and 8.2+/-5
269 nd long-term (6 months, oral) treatment with carvedilol versus placebo in 151 consecutive patients wi
270 hat drugs targeting these receptors, such as carvedilol, warrant further investigation as novel thera
272 group; the reduction in risk attributable to carvedilol was 65 percent (95 percent confidence interva
273 partial agonist activity at either receptor; carvedilol was a genotype-independent neutral antagonist
275 class I and II and with wide QRS complexes, carvedilol was associated with a 30% reduction in hospit
276 plantable cardioverter-defibrillator device, carvedilol was associated with a 36% lower rate of inapp
288 of hibernator status on response of LVEF to carvedilol was not significant (0.7 [-2.2 to 3.5]; p=0.6
289 A novel beneficial and synergistic effect of carvedilol was seen in patients with CRT-D and LBBB.
290 to Ang II infusion in patients treated with carvedilol was significantly lower than in patients trea
292 ese measures of outcome and clinical status, carvedilol was superior to placebo within each racial co
293 The maximum of NO release for nebivolol and carvedilol was very similar (188+/-14 and 226+/-17, resp
295 result, estimated inpatient care costs with carvedilol were 57% lower for cardiovascular admissions
299 ol or Metoprolol European Trial-has compared carvedilol with short-acting metoprolol tartrate at diff
300 ed that alpha-adrenergic-blocking effects of carvedilol would limit vasoconstriction in response to a
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