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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.
6 rescue therapy was also similar at 24 h (21% tolvaptan, 18% placebo; p = 0.57).
7  significantly greater weight reduction with tolvaptan (-2.4 +/- 2.1 kg vs. -0.9 +/- 1.8 kg; p < 0.00
8 igned to oral placebo (223 patients) or oral tolvaptan (225) at a dose of 15 mg daily.
9 ble-blind trial, patients were randomized to tolvaptan 30 mg/day or placebo.
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
15                      More patients receiving tolvaptan (684 [76.7%] and 678 [72.1%] for trial A and t
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
18         In decompensated heart failure (HF), tolvaptan, a vasopressin V(2) receptor antagonist, has b
19                                              Tolvaptan, a vasopressin V2 receptor blocker, shows prom
20                                              Tolvaptan administered in addition to standard therapy m
21                                              Tolvaptan also reduced right atrial pressure (-4.4 +/- 6
22 with euvolemic or hypervolemic hyponatremia, tolvaptan, an oral vasopressin V2-receptor antagonist, w
23                                              Tolvaptan, an oral, nonpeptide, selective vasopressin V2
24                      We investigated whether tolvaptan, an orally active vasopressin V(2)-receptor an
25   A total of 120 patients were randomized to tolvaptan and 120 were randomized to placebo.
26 at 24 h (primary study endpoint) was 16% for tolvaptan and 20% for placebo (p = 0.32).
27                            Compounds such as tolvaptan and pasireotide, which indirectly reduce adeny
28 rsening heart failure at 60 days between the tolvaptan and placebo groups (P =.88 for trend).
29  investigating the effects of three doses of tolvaptan and placebo in patients with CHF.
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
33                                              Tolvaptan, as compared with placebo, slowed the increase
34 re randomized to double-blind treatment with tolvaptan at a single oral dose (15, 30, or 60 mg) or pl
35                                              Tolvaptan at all doses significantly reduced pulmonary c
36                                              Tolvaptan caused increased thirst and dry mouth, but fre
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
39                          At $5760 per month, tolvaptan cost $744 100 per quality-adjusted life-year g
40         Finally, a specific Avpr2 inhibitor, tolvaptan, does not affect bone formation or bone mass,
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
47 tagonism in Heart Failure Outcome Study With Tolvaptan (EVEREST) trial.
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
50 agonism in Heart Failure: Outcome Study with Tolvaptan [EVEREST]; NCT00071331).
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
56 ients with hyponatremia were observed in the tolvaptan group but not in the placebo group.
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
62 d placebo, respectively (P< or =.008 for all tolvaptan groups vs placebo).
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
67             (Targeting Acute Congestion With Tolvaptan in Congestive Heart Failure [TACTICS-HF]; NCT0
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
70 xtension of the Study of Ascending Levels of Tolvaptan in Hyponatremia (SALT-1 and SALT-2).
71  Study of the Short Term Clinical Effects of Tolvaptan in Patients Hospitalized for Worsening Heart F
72  for the symptomatic improvements noted with tolvaptan in patients with decompensated HF.
73                   The efficacy and safety of tolvaptan in patients with later-stage ADPKD are unknown
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
76                 Side effects associated with tolvaptan included increased thirst, dry mouth, and incr
77 ered 2.5% of administered ECVs in the urine; tolvaptan increased recovery five-fold and reduced ECV d
78                                              Tolvaptan increased urine output by 3 h in a dose-depend
79                                              Tolvaptan initiated for acute treatment of patients hosp
80                To investigate the effects of tolvaptan initiated in patients hospitalized with heart
81   In conclusion, prolonged administration of tolvaptan maintains an increased serum sodium with an ac
82                                              Tolvaptan may allow for less intensification of loop diu
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]
85     During the week after discontinuation of tolvaptan on day 30, hyponatremia recurred.
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
89                               Treatment with tolvaptan or pasireotide alone markedly reduced cyst pro
90  randomly assigned in a 1:1 ratio to receive tolvaptan or placebo for 12 months.
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
94              The composite end point favored tolvaptan over placebo (44 vs. 50 events per 100 follow-
95 t ascites showed directional favorability of tolvaptan over placebo for the primary endpoint compared
96 At day 3, dyspnea reduction was greater with tolvaptan (p = 0.01).
97                Assuming that the benefits of tolvaptan persist in the longer term, the drug may slow
98                                              Tolvaptan prolonged the median age at ESRD onset by 6.5
99 , the oral vasopressin-2 receptor antagonist tolvaptan, provides benefits related to decongestion and
100                                              Tolvaptan resulted in a slower decline than placebo in t
101                In patients with advanced HF, tolvaptan resulted in favorable but modest changes in fi
102                                              Tolvaptan resulted in greater weight loss and net fluid
103  period that included sequential placebo and tolvaptan run-in phases, during which each patient's abi
104                                              Tolvaptan significantly improved secondary end points of
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
107                                              Tolvaptan therapy increased the proportion of patients w
108 patients, there was no significant effect of tolvaptan therapy on LV volumes observed during 1 year o
109                            Patients received tolvaptan therapy until death, development of ESRD, or l
110 opment of ESRD, or liver complications or no tolvaptan therapy.
111                              After 1 year of tolvaptan, there was a small reduction in LV volume (dec
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
114 dy was conducted to address the acute use of tolvaptan to improve congestion in AHF.
115        (Heart Pressure Assessment Study With Tolvaptan to Treat Congestive Heart Failure; NCT00132886
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
118                                              Tolvaptan treatment increased AVP levels during follow-u
119 p of patients who had improved outcomes with tolvaptan treatment.
120 agonism in Heart Failure: Outcome Study with Tolvaptan) trial.
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
123  vs. 28% placebo; p = 0.59) and at 24 h (50% tolvaptan vs. 47% placebo; p = 0.80).
124 acebo groups, respectively; p < 0.05 for all tolvaptan vs. placebo).
125                                              Tolvaptan was associated with a slower decline in kidney
126 , placebo-controlled trials, the efficacy of tolvaptan was evaluated in patients with euvolemic or hy
127                                  The dose of tolvaptan was increased to 30 mg daily and then to 60 mg
128             The decrease in body weight with tolvaptan was not associated with changes in heart rate
129 enefit from vasopressin receptor inhibition, tolvaptan was not associated with greater early improvem
130                        In patients with CHF, tolvaptan was well tolerated; it reduced body weight and
131 he most common adverse effects attributed to tolvaptan were pollakiuria, thirst, fatigue, dry mouth,
132            To evaluate short-term effects of tolvaptan when added to standard therapy in patients hos
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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