ライフサイエンスコーパス: sotalol

1 response to a pharmacological challenge with 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 l effects of vernakalant, ranolazine, and dl-sotalol.

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

8 Seven patients continued on sotalol.

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

10 machinery as underlying high sensitivity to sotalol.

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

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

13 r amiodarone, propafenone, disopyramide, and sotalol.

14 , including methanesulfonanilides such as Dd-sotalol.

15 ter sequential administration of esmolol and sotalol.

16 talization between amiodarone, Class Ic, and sotalol.

17 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

18 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).

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

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

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

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

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

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

25 /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).

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

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

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

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

30 6 patients randomized between amiodarone and sotalol, 60% versus 38% were successfully treated, respe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 33% and 40% of embryoid bodies treated with sotalol and quinidine, respectively, compared with negli

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

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

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

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

50 Amiodarone and sotalol are equally efficacious in converting atrial fib

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 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

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

84 -2.24), amiodarone (HR 2.63; 1.77-3.89), and sotalol (HR 1.72; 1.17-2.54), but lower with amiodarone

85 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 dl-Sotalol preferentially prolonged action potential durati

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

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

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

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

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

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

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

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

119 Sotalol should be considered for the prevention of posto

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

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

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

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

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

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

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

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

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

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

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

131 Sotalol was approved for treatment of atrial fibrillatio

132 Sotalol was associated with a greater risk of any clinic

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

134 1549 patients evaluated, administration of d-sotalol was associated with increased mortality, which w

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

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

137 Sotalol was recently shown to be effective in reducing t

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

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

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

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

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

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

144 Metoprolol and sotalol were not biodegraded by the nitrification enrich

145 - 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for com

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