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1 pnea relief and a possible clinical role for tolvaptan.
2 sferase level were reversible after stopping tolvaptan.
3 on of the vasopressin V2 receptor antagonist tolvaptan.
4 justed life-year gained was even greater for tolvaptan.
5 e associated with the hemodynamic effects of tolvaptan.
7 significantly greater weight reduction with tolvaptan (-2.4 +/- 2.1 kg vs. -0.9 +/- 1.8 kg; p < 0.00
10 0 (-1.60 to 0.00) kg in the groups receiving tolvaptan 30, 60, and 90 mg/d, and placebo, respectively
11 Patients were randomized to receive either tolvaptan (30 mg/d) or matching placebo, within 48 hours
12 on of the vasopressin V2-receptor antagonist tolvaptan (30 mg/day) on reducing left ventricular end-d
13 were randomly assigned to placebo (n=63) or tolvaptan [30 mg (n=64), 45 mg (n=64), or 60 mg (n=63)]
14 ients were randomly assigned to receive oral tolvaptan, 30 mg once per day (n = 2072), or placebo (n
16 er minute or more, in a 2:1 ratio to receive tolvaptan, a V(2)-receptor antagonist, at the highest of
17 tricular ejection fraction < or =40% to oral tolvaptan, a vasopressin antagonist, or placebo and foll
22 with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor antagonist, w
30 The other three drugs namely lansoprazole, tolvaptan and roflumilast, were less potent in suppressi
31 Notably, the V2R-selective inverse agonists tolvaptan and satavaptan completely silenced the constit
32 helin [tezosentan], vasopressin [conivaptan, tolvaptan], and adenosine) and non-cAMP-mediated inotrop
34 re randomized to double-blind treatment with tolvaptan at a single oral dose (15, 30, or 60 mg) or pl
37 The oral vasopressin-2 receptor antagonist tolvaptan causes aquaresis in patients with volume overl
38 espite rapid and persistent weight loss with tolvaptan compared with placebo, in patients with AHF wh
41 hinese translation BACKGROUND: In the TEMPO (Tolvaptan Efficacy and Safety in Management of Autosomal
42 tagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST) between October 7, 2003, and Februar
43 tagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial investigated the effects of to
44 tagonist in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial with baseline hemoglobin data,
45 agonism in Heart Failure: Outcome Study with Tolvaptan (EVEREST) trial, which enrolled 4133 patients
46 tagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial, which randomized 4133 patient
48 tagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST), an event-driven, randomized, double
49 tagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST), an event-driven, randomized, double
51 111 patients with hyponatremia received oral tolvaptan for a mean follow-up of 701 days, providing 77
52 t improvement from baseline to day 30 in the tolvaptan group according to scores on the Mental Compon
53 p of 9.9 months, 537 patients (25.9%) in the tolvaptan group and 543 (26.3%) in the placebo group die
54 occurred in 38 of 681 patients (5.6%) in the tolvaptan group and in 8 of 685 (1.2%) in the placebo gr
55 re fewer ADPKD-related adverse events in the tolvaptan group but more events related to aquaresis (ex
57 talization for heart failure occurred in 871 tolvaptan group patients (42.0%) and 829 placebo group p
58 sodium concentrations increased more in the tolvaptan group than in the placebo group during the fir
59 , the increase in total kidney volume in the tolvaptan group was 2.8% per year (95% confidence interv
60 idence interval [CI], -2.81 to -1.87) in the tolvaptan group, as compared with -3.61 ml per minute pe
61 (5%) and 21 HF hospitalizations (18%) in the tolvaptan group, compared with 11 deaths (9%) and 34 HF
63 L/24 hours at day 1 for 30-, 45-, and 60-mg tolvaptan groups, and placebo, respectively; P<0.001).
64 2 kg was observed in the 30-, 45-, and 60-mg tolvaptan groups, respectively, and a body weight increa
65 tients hospitalized with heart failure, oral tolvaptan in addition to standard therapy including diur
66 rize evidence for decongestion benefits with tolvaptan in AHF and describe the design of the Targetin
68 esign of the Targeting Acute Congestion With Tolvaptan in Congestive Heart Failure Study (TACTICS) an
69 TACTICS-HF (Targeting Acute Congestion with Tolvaptan in Congestive Heart Failure) study was conduct
71 Study of the Short Term Clinical Effects of Tolvaptan in Patients Hospitalized for Worsening Heart F
74 (EVEREST) trial investigated the effects of tolvaptan in patients with worsening heart failure and e
75 y 7 or discharge improved significantly with tolvaptan in trial B (P = .02) but did not reach signifi
77 ered 2.5% of administered ECVs in the urine; tolvaptan increased recovery five-fold and reduced ECV d
81 In conclusion, prolonged administration of tolvaptan maintains an increased serum sodium with an ac
83 ast to diuretics, the vasopressin antagonist tolvaptan may increase net volume loss in heart failure
84 (SD) body weight reduction was greater with tolvaptan on day 1 (trial A, 1.71 [1.80] vs 0.99 [1.83]
86 s of vasopressin V2 receptor antagonism with tolvaptan on the changes in left ventricular (LV) volume
87 there was a significant favorable effect of tolvaptan on the composite of mortality or heart failure
88 In this study, we evaluated the effects of tolvaptan (OPC-41061), a novel, oral, nonpeptide vasopre
91 ction </=40% within 48 hours of admission to tolvaptan or placebo for a median follow-up of 9.9 month
92 tion, and were randomized to either 30 mg of tolvaptan or placebo given at 0, 24, and 48 h, with a fi
93 omized to receive 30, 60, or 90 mg/d of oral tolvaptan or placebo in addition to standard therapy, in
95 t ascites showed directional favorability of tolvaptan over placebo for the primary endpoint compared
99 , the oral vasopressin-2 receptor antagonist tolvaptan, provides benefits related to decongestion and
103 period that included sequential placebo and tolvaptan run-in phases, during which each patient's abi
105 stic Kidney Disease and Its Outcomes) trial, tolvaptan significantly reduced expansion of kidney volu
106 ute), the vasopressin V2-receptor antagonist tolvaptan slowed the growth in total kidney volume and t
108 patients, there was no significant effect of tolvaptan therapy on LV volumes observed during 1 year o
112 It was hypothesized that the addition of tolvaptan to a background diuretic improved dyspnea earl
113 HF, dyspnea, and congestion, the addition of tolvaptan to a standardized furosemide regimen did not i
116 nd net fluid loss compared with placebo, but tolvaptan-treated patients were more likely to experienc
117 hoc analysis, 60-day mortality was lower in tolvaptan-treated patients with renal dysfunction or sev
121 ry end point showed greater improvement with tolvaptan vs placebo (trial A, mean [SD], 1.06 [0.43] vs
122 h (25% moderately or markedly improved with tolvaptan vs. 28% placebo; p = 0.59) and at 24 h (50% to
126 , placebo-controlled trials, the efficacy of tolvaptan was evaluated in patients with euvolemic or hy
129 enefit from vasopressin receptor inhibition, tolvaptan was not associated with greater early improvem
131 he most common adverse effects attributed to tolvaptan were pollakiuria, thirst, fatigue, dry mouth,
133 n increase in urine volume was observed with tolvaptan when compared with placebo (3.9+/-0.6, 4.2+/-0
134 ed natural history data favored therapy with tolvaptan, with a reduction in the combined end point of
135 during which each patient's ability to take tolvaptan without dose-limiting side effects was assesse
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