ライフサイエンスコーパス: sotalol

1 talization between amiodarone, Class Ic, and sotalol.

2 tal admission is warranted for initiation of sotalol.

3 ointes (TdP) developed in the presence of dl-sotalol.

4 to the QT-prolonging antiarrhythmic drug d,l-sotalol.

5 developing TdP during-administration of d,l-sotalol.

6 lained by phototransformation, partially for sotalol.

7 interfering RNA reduced their sensitivity to sotalol.

8 rhythmic drugs: Ranolazine, Domperidone, and Sotalol.

9 l effects of vernakalant, ranolazine, and dl-sotalol.

10 vernakalant and ranolazine, but not with dl-sotalol.

11 Seven patients continued on sotalol.

12 by vernakalant and ranolazine, but not by dl-sotalol.

13 with either 20 nmol/L E-4031 or 10 mumol/L d-sotalol.

14 response to a pharmacological challenge with sotalol.

15 TDR induced by the selective I(Kr) blocker d-sotalol.

16 r amiodarone, propafenone, disopyramide, and sotalol.

17 machinery as underlying high sensitivity to sotalol.

18 , including methanesulfonanilides such as Dd-sotalol.

19 ter sequential administration of esmolol and sotalol.

20 caine 0.75 mg.kg(-1).h(-1) (n=7), low-dose d-sotalol (0.16 mg.kg(-1).h(-1)) (n=4), high-dose d-sotalo

21 ol (0.16 mg.kg(-1).h(-1)) (n=4), high-dose d-sotalol (0.5 mg.kg(-1).h(-1)) (n=6), or saline (n=7).

22 est detectable half-lives were estimated for sotalol (0.7 h) and sitagliptin (0.2 h) along the shorte

23 Both E-4031 (20 nmol/L) and d-sotalol (10 mumol/L) increased MAPD(90) and BVR at all s

24 The beta-adrenergic antagonist sotalol (10-4 M) reduced LL absorption rate from -1.47 +

25 Sotalol (10-4 M) reduced LL absorption rate from -3.39 +

26 ocardial infarction were randomly assigned d-sotalol (100 mg increased to 200 mg twice daily, if tole

27 mimic an increase in beta-adrenergic tone, d-sotalol (100 micromol/L) to block I(Kr) (LQT2 model), an

28 gnificantly (p = 0.008) lower in patients on sotalol (12.5%) as compared with placebo (38%).

29 /m(2)/day (range: 40 to 150 mg/m(2)/day) and sotalol 175 mg/m(2)/day (range: 100 to 250 mg/m(2)/day).

30 Sotalol (23.2%) and dofetilide (19.2%) were each more co

31 lation to receive amiodarone (267 patients), sotalol (261 patients), or placebo (137 patients) and mo

32 of beta-blockers (38%), amiodarone (14%), or sotalol (30%).

33 peripherally acting beta-adrenergic blocker sotalol (4 or 10 mg/kg ip) immediately or 2 hr after the

34 failure), were randomized to receive either sotalol (40 patients; mean dose = 190 +/- 43 mg/day) sta

35 6 patients randomized between amiodarone and sotalol, 60% versus 38% were successfully treated, respe

36 use by drug was as follows: dofetilide 93%, sotalol 66%, flecainide 68%, propafenone 48%, and droned

37 values for Domperidone (0.71 muM-0.29 muM), Sotalol (7.61 muM-0.27 muM), and Ranolazine (53.08 muM-5

38 niline, N,N-dimethyl-4-cyanoaniline (DMABN), sotalol (a beta-blocker) and sulfadiazine (a sulfonamide

39 Sotalol, a beta-adrenergic blocking agent with class III

40 We tested the efficacy and safety of sotalol, a beta-blocker with class III antiarrhythmic ef

41 e, a sodium (Na(+))-channel blocker, and d,l-sotalol, a potassium channel blocker, were studied in li

42 We investigated whether d-sotalol, a pure potassium-channel blocker with no clinic

43 We postulate that Dd-sotalol accesses its receptor in the open pore, and the

44 nsitivity (HS) or lowest sensitivity (LS) to sotalol administration in vivo (ie, on the basis of the

45 Sotalol also reduced the mean (+/-SD) frequency of shock

46 odels to quantify ECG alterations induced by sotalol, an IKr blocker associated with TdP, aiming to p

47 A total of 416 patients (199 in sotalol and 217 in amiodarone strata) were followed for

48 antiarrhythmic drugs that became available, sotalol and amiodarone, also have potent antiadrenergic

49 Although both dl-sotalol and azimilide rarely induced EADs in canine left

50 erature are supportive (as has occurred with sotalol and azimilide), and patients who are to receive

51 tes (TdP) with QT prolongation induced by dl-sotalol and azimilide.

52 In 183 patients randomized between sotalol and class I agents, 34% versus 23% were successf

53 t commonly prescribed AAD for AF followed by sotalol and dofetilide.

54 Sotalol and dronedarone are both used for maintenance of

55 drawal, occurred in 2 of 40 (5%) patients on sotalol and none in the placebo group (p = 0.2).

56 Torsadogenic hERG blockers, such as sotalol and quinidine, produced statistically and physio

57 33% and 40% of embryoid bodies treated with sotalol and quinidine, respectively, compared with negli

58 atheter ablation are compared with those for sotalol and to amiodarone separately.

59 the dynamics of hERG channels in response to sotalol and to identify regulators of the susceptibility

60 at 3 years were 47% for amiodarone, 50% for sotalol, and 44% for Class 1C versus 40%, 40%, and 36%,

61 Isoproterenol+chromanol 293B, d-sotalol, and ATX-II produced preferential prolongation o

62 paration of the beta-blockers, labetalol and sotalol, and the binaphthyl derivatives, 1,1'-bi-2-napht

63 ith concomitant antiarrhythmic drug therapy, sotalol appears to decrease the defibrillation threshold

64 o the cytoskeleton-associated fractions upon sotalol application.

65 Amiodarone and sotalol are equally efficacious in converting atrial fib

66 beta-adrenergic blockers, amiodarone, and sotalol are the most effective at preventing postoperati

67 med models using QTc to identify exposure to sotalol [area under the receiver operating characteristi

68 ythmic agents including either flecainide or sotalol as single agents before initiating combination t

69 Unlike dl-sotalol, azimilide (>3 micromol/L) increased epicardial

70 darone + beta-blockers, amiodarone alone, or sotalol +/- beta-blockers).

71 efinitive role for inactivation gating in Dd-sotalol block of HERG, using interventions complementary

72 ed steady-state inactivation also reduced Dd-sotalol block of HERG: 100 micromol/L Cd(2+) reduced ste

73 ivation by depolarizing to +60 mV reduced Dd-sotalol block to 49% (P:<0.05 versus +20 mV), suggesting

74 -disabling mutation (G628C-S631C) reduced Dd-sotalol block to only 11% (P:<0.05 versus wild type).

75 on inactivation gating and did not modify Dd-sotalol block.

76 channel-mediated parameters, and those of dl-sotalol by reverse rate-dependent prolongation of APD(90

77 miodarone, statins, steroids, magnesium, and sotalol can be effective in preventing postoperative atr

78 The combination of flecainide and sotalol can safely and effectively control refractory SV

79 d-Sotalol caused a preferential prolongation of the M cell

80 ranolazine caused rate-dependent, whereas dl-sotalol caused reverse rate-dependent, prolongation of E

81 ecreased after exposure of HS iPS-CMs to low sotalol concentrations.

82 None of the patients on sotalol developed Torsade de pointes or sustained ventri

83 Dronedarone, compared with sotalol, did not demonstrate a significant association w

84 Several antiarrhythmic drugs such as sotalol, disopyramide, and amiodarone, can be effective

85 congestive heart failure (P < .001), and d,l-sotalol dose > 320 mg/d (P < .001) as factors most predi

86 ed their first AAD prescription (amiodarone, sotalol, dronedarone, or Class Ic) within 14 days post-f

87 e amiodarone, disopyramide, propafenone, and sotalol (drugs listed in alphabetical order).

88 In the sotalol-eligible patients, ablation led to lower risk of

89 CNN models predicting sotalol exposure also accurately detected the presence a

90 An increase in TDR by dl-sotalol facilitated transmural propagation of EADs that

91 s has improved with greater experience using Sotalol for atrial flutter, and digoxin and amiodarone f

92 of the combination therapy of flecainide and sotalol for the treatment of refractory supraventricular

93 Patients in the sotalol group had a nonsignificantly shorter length of h

94 of the amiodarone group, 24.2 percent of the sotalol group, and 0.8 percent of the placebo group, and

95 days in the amiodarone group, 74 days in the sotalol group, and 6 days in the placebo group according

96 In the sotalol group, the reduction in the risk of death from a

97 deaths in the placebo group and four in the sotalol group.

98 In four sheep aged 6-12 weeks, sotalol had no effect on LL absorption rate, whereas the

99 In four sheep aged 6-12 weeks, sotalol had no effect on resting LL absorption rate, whe

100 aged 10-14 days, while rolipram given after sotalol had no effect.

101 ed 4-13 days, while theophylline given after sotalol had no effect.

102 that the class III antiarrhythmic effect of sotalol has a reverse use-dependent positive inotropic e

103 rolol HR = 1.5, 95% CI, 1.2 to 1.8; adjusted sotalol HR = 2.0, 95% CI, 0.99 to 4.0).

104 ne HR: 1.20, 95% CI: 1.03 to 1.40, p = 0.02, sotalol HR: 1.364, 95% CI: 1.16 to 1.611, p < 0.001, Cla

105 one versus Class Ic (HR 0.68; 0.57-0.80) and sotalol (HR 0.63; 0.53-0.75).

106 -2.24), amiodarone (HR 2.63; 1.77-3.89), and sotalol (HR 1.72; 1.17-2.54), but lower with amiodarone

107 o ablation and 18 of 104 (17.3%) assigned to sotalol (HR: 0.12; 95% CI: 0.03-0.5; P = 0.004).

108 ablation and in 62 of 104 (59%) assigned to sotalol (HR: 0.64; 95% CI: 0.43-0.94; P = 0.02).

109 ence interval [CI]: 1.03 to 1.36, p = 0.02), sotalol (HR: 1.32, 95% CI: 1.13 to 1.54, p < 0.001), and

110 cine corneal penetration of timolol maleate, sotalol hydrochloride, or brinzolamide incubated with or

111 trial fibrillation prescribed dronedarone or sotalol in 2012 or later.

112 ly and postoperatively administered oral d,l sotalol in preventing the occurrence of postoperative at

113 The administration of sotalol, in dosages ranging from 80 to 120 mg, was assoc

114 bsorption rate, whereas rolipram given after sotalol increased absorption rate from -1.27 +/- 0.1 to

115 but did not change ERP dispersion, whereas d-sotalol increased ERP dispersion by 140% (P<0.001) witho

116 ption rate, whereas theophylline given after sotalol increased LL absorption rate from -1.06 +/- 0.1

117 Conversely, regional low- and high-dose d-sotalol infusion did not alter DER values or conduction

118 orts: 1029 healthy subjects before and after sotalol intake (n = 14 135 ECGs); 487 cLQTS patients; an

119 -Tpeak interval as the best discriminator of sotalol intake.

120 reverse use-dependent prolongation of APD by sotalol is associated with a positive inotropic effect.

121 to 10 micromol/L) increased APD more than dl-sotalol, its EADs often failed to propagate transmurally

122 I(Kr) block with d-sotalol (LQT2) and augmentation of late I(Na) with ATX-I

123 sed 6212 patients (3106 dronedarone and 3106 sotalol; mean [+/-SD] age, 71+/-10 years; 2.5% female; m

124 ng 3135 adult patients who received oral d,l-sotalol (median follow-up, 164 days), TdP developed in 4

125 cell types, more in the ATX-II than in the d-sotalol model, but decreased TDR equally in the two mode

126 ere much steeper in the ATX-II than in the d-sotalol model.

127 c drugs (most commonly amiodarone [n=103] or sotalol [n=78]) and AF catheter ablation (n=49) or the M

128 ation of quinidine and disopyramide, but not sotalol, normalized APD and suppressed arrhythmia induct

129 sought to study the rate related effects of sotalol on myocardial contractility and to test the hypo

130 erformed within 14 days after randomization; sotalol or amiodarone was administered as antiarrhythmic

131 e was more effective at one year than either sotalol or class I agents for the strategy of maintenanc

132 a-blockers or no treatment, 41 (15%) were on sotalol or class I antiarrhythmic drugs, and 62 (22%) we

133 e first drug treatment to: 1) amiodarone, 2) sotalol, or 3) a class I drug.

134 er treatment with amiodarone, beta-blockers, sotalol, or ablation.

135 porcine corneal drug penetration of timolol, sotalol, or brinzolamide.

136 were randomized double-blind to amiodarone, sotalol, or placebo.

137 Amiodarone was superior to sotalol (P<0.001) and to placebo (P<0.001), and sotalol

138 hundred twenty-nine amiodarone patients, 606 sotalol patients, and 268 Class 1C patients were matched

139 double-blind treatment with 160 to 320 mg of sotalol per day (151 patients) or matching placebo (151

140 dl-Sotalol preferentially prolonged action potential durati

141 world cohort of outpatients on dofetilide or sotalol presenting to the hospital or emergency room for

142 In contrast, ranolazine and dl-sotalol produced consistent concentration- and reverse r

143 In the steady state pacing experiments, sotalol prolonged the APD in a reverse use-dependent man

144 Regional infusion of lidocaine and d-sotalol prolonged VF cycle length by 23% to 41% (P<0.05)

145 We found that treatment with sotalol promoted translocation of the hERG channel from

146 HERG to classic proarrhythmic HERG blockers (sotalol, quinidine, dofetilide) in both cardiac and nonc

147 ct relation between APD and LV (+)dP/dt with sotalol (r = 0.46, p < 0.001), but there was no signific

148 , block of HERG current by 300 micromol/L Dd-sotalol reached 80% after a 10-minute period of repetiti

149 lly relevant ventricular arrhythmia while on sotalol remained significant after multivariable adjustm

150 However, while sotalol requires initial monitoring for QT prolongation

151 = 0.80 (95% CI 0.03-25.14)], and infusion of sotalol [RR = 0.91 (95% CI 0.08-10.65)] were associated

152 zed ARVC subjects, neither beta-blockers nor sotalol seemed to be protective.

153 Sotalol should be considered for the prevention of posto

154 Sotalol significantly increased VT recurrence and ICD sh

155 In the sotalol stratum, a primary endpoint occurred in 44 of 95

156 In the sotalol stratum, sustained VT below detection occurred i

157 s, LV (+)dP/dt was significantly higher with sotalol than it was with esmolol.

158 ngth >600 ms) were significantly higher with sotalol than they were with esmolol.

159 ys with amiodarone therapy and 428 days with sotalol therapy (P=0.53).

160 rrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify f

161 s admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determi

162 monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for ini

163 Among 1549 patients assigned d-sotalol, there were 78 deaths (5.0%) compared with 48 de

164 s on INa-L, from marked increases (E-4031, d-sotalol, thioridazine, and erythromycin) to little or no

165 ntifying infants who required flecainide and sotalol to control refractory SVT.

166 fects of 293B+/-isoproterenol and those of d-sotalol to increase APD(90) and TDR and to induce TdP in

167 rogated the translocation of hERG channel in sotalol-treated HS iPS-CMs.

168 was 55+/-11 and 58+/-10 for dronedarone and sotalol users, correspondingly.

169 mortality was not significantly different in sotalol versus placebo (0% vs. 2%, p = 1.0).

170 were considered eligible to be allocated to sotalol vs ablation if they met all the following criter

171 Sotalol was approved for treatment of atrial fibrillatio

172 Sotalol was associated with a greater risk of any clinic

173 As compared with placebo, treatment with sotalol was associated with a lower risk of death from a

174 1549 patients evaluated, administration of d-sotalol was associated with increased mortality, which w

175 Sotalol was associated with increased risk of VT recurre

176 Compared with amiodarone, sotalol was associated with significantly increased ICD

177 simulated RRD of APD caused by E-4031 and d-sotalol was attenuated when late I(Na) was inhibited.

178 n (VF) in 6 of 7 animals, whereas regional d-sotalol was not proarrhythmic.

179 Sotalol was recently shown to be effective in reducing t

180 Oral sotalol was safe and efficacious in reducing the risk of

181 alol (P<0.001) and to placebo (P<0.001), and sotalol was superior to placebo (P<0.001).

182 d-Sotalol was used to mimic LQT2, whereas ATX-II mimicked

183 Dronedarone, compared with sotalol, was associated with a lower risk of ventricular

184 cted beta blockers-atenolol, metoprolol, and sotalol-was examined during nitrification using batch ex

185 association with recurrence, metoprolol and sotalol were associated with increased recurrence rates

186 In vitro, the responses to sotalol were highly variable but strongly correlated to

187 Metoprolol and sotalol were not biodegraded by the nitrification enrich

188 - 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for com

189 herapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related.