ライフサイエンスコーパス: flecainide

1 ic Scn5a+/- hearts treated with (1.0 microM) flecainide.

2 cation of the sodium channel-blocking agent, flecainide.

3 syndrome elicit proarrhythmic sensitivity to flecainide.

4 are insufficient to explain the efficacy of flecainide.

5 tically to the sodium channel blocking agent flecainide.

6 Ia and Ic antiarrhythmic drugs quinidine and flecainide.

7 nd with the maximum plasma concentrations of flecainide.

8 hmic drugs quinidine and ranolazine, but not flecainide.

9 e and tetracaine and the antiarrhythmic drug flecainide.

10 ilure was rare in the quarter of patients on flecainide.

11 onths (3.8-5.3), ECG remained normal despite flecainide.

12 modes of action underlie RyR2 inhibition by flecainide.

13 ical activity with the Na(+) channel blocker flecainide.

14 ely than traditional Na+-channel blockade by flecainide.

15 ggested because of the hydrophilic nature of flecainide.

16 during exercise was significantly reduced by flecainide (0 [range, 0-2] vs 2.5 [range, 0-4] for place

17 Flecainide (0.1 micromol/L) produced bidirectional condu

18 Flecainide 1 mumol/l was more effective in suppressing a

19 Flecainide (1 micromol/L) tonic block was only 16.8+/-3.

20 Flecainide (1-300 mM) caused tonic and use-dependent blo

21 The effectiveness of flecainide (1.5 umol/L) and ibutilide (20 nmol/L), alone

22 so examined the safety of the combination of flecainide (1.5 umol/L) and ibutilide (50 nmol/L) using

23 The addition of flecainide (1.5 umol/L) partially reversed these effects

24 In contrast, flecainide (10 muM) and thapsigargin (10 muM) eliminated

25 The median doses used were: flecainide 100 mg/m(2)/day (range: 40 to 150 mg/m(2)/day

26 ng propafenone 300 to 900 mg/day (n = 46) or flecainide 100 to 300 mg/day (n = 25), presented for ibu

27 n a 1:1:1 ratio after PFO closure to receive flecainide (150 mg once daily in a sustained-release dos

28 y in a sustained-release dose) for 3 months, flecainide (150 mg once daily in a sustained-release dos

29 entricle epicardial surface before and after flecainide (2 mg/kg per 10 minutes).

30 aline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patien

31 of either chloroquine (4 micromol/L, n=7) or flecainide (2-4 micromol/L, n=5).

32 mic drug treatment (control); treatment with flecainide (200-300 mg per day) for 4 weeks (short-term

33 Ca(2+) transients, which were unaffected by flecainide (6 mumol/L).

34 was as follows: dofetilide 93%, sotalol 66%, flecainide 68%, propafenone 48%, and dronedarone 80%.

35 the combination of a Na(+) channel blocker (flecainide, 7 micromol/L) and acetylcholine (ACh, 2 to 3

36 re each more commonly prescribed than either flecainide (9.8%) or propafenone (4.8%).

37 Flecainide, a class I antiarrhythmic drug, inhibits Na(+

38 a truncated rat Na(v) 1.5 in the presence of flecainide, a class Ic agent, reveals distinct binding p

39 n, we show synergistic functional effects of flecainide, a proarrhythmic Na+ channel blocker, and oxi

40 The effects of flecainide, a sodium (Na(+))-channel blocker, and d,l-so

41 Furthermore, treatment with quinidine and flecainide abolished LBLPS-induced ventricular arrhythmi

42 Flecainide acetate directly suppresses sarcoplasmic reti

43 rillation (for <=48 hours) self administered flecainide acetate inhalation solution using a nebulizer

44 f delivering flecainide via oral inhalation (flecainide acetate inhalation solution) for acute conver

45 Our data support a model of flecainide action in which Na(+)-dependent modulation of

46 The mechanism of flecainide action remains controversial.

47 Here we examine whether flecainide administration can similarly reduce axonal de

48 Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevati

49 Flecainide administration significantly reduced the mean

50 masked using sodium channel blockers such as flecainide, ajmaline or procainamide, thus identifying p

51 e has been proposed as a treatment for LQT3, flecainide also evokes "Brugada-like" ST-segment elevati

52 We synthesized N-methylated flecainide analogues (QX-flecainide and N-methyl flecain

53 ciate slowly from the sodium channel such as flecainide and ajmaline unmask the Brugada syndrome elec

54 When used alone, flecainide and ibutilide cardioverted sustained AF in 40

55 In our experimental model, a combination of flecainide and ibutilide significantly improves cardiove

56 treatment strategies include beta-blockade, flecainide and ICD implementation--none of which is full

57 Flecainide and Ivabradine influenced BRV parameters sign

58 ally, comparable outcomes were found between flecainide and labetalol antiarrhythmic effects in vitro

59 Newer options such as flecainide and left cardiac sympathetic denervation are

60 sarcoplasmic reticulum Ca release, while QX-flecainide and N-methyl flecainide did not.

61 esized N-methylated flecainide analogues (QX-flecainide and N-methyl flecainide) and showed that N-me

62 us adverse events did not differ between the flecainide and placebo arms.

63 ias during exercise was compared between the flecainide and placebo arms.

64 ute arrhythmogenesis and its modification by flecainide and quinidine to alterations in DeltaAPD90 in

65 Electrophysiological effects of flecainide and quinidine were compared in Langendorff-pe

66 murine hearts in the presence and absence of flecainide and quinidine, and the extent to which Scn5a+

67 y with class I antiarrhythmic drugs, such as flecainide and quinidine, which may reduce ventricular a

68 Flecainide and RAD-243 retained their use-dependent bloc

69 scopic current relaxation during exposure to flecainide and RAD-243.

70 After radiofrequency ablation, flecainide and remap confirmed elimination of abnormal s

71 The combination of flecainide and sotalol can safely and effectively contro

72 acy and safety of the combination therapy of flecainide and sotalol for the treatment of refractory s

73 s performed identifying infants who required flecainide and sotalol to control refractory SVT.

74 ced from 307+/-35 to 269+/-27 ms (P<.001) by flecainide and subsequently to 217+/-4 ms (P<.001) with

75 d from 198+/-23 to 182+/-17 ms (P=.005) with flecainide and to 164+/-10 ms (P=.004) with isoprotereno

76 ainide analogues (QX-flecainide and N-methyl flecainide) and showed that N-methylation reduces flecai

77 lone, acetylcholine+ibutilide, acetylcholine+flecainide, and acetylcholine+ibutilide+flecainide, resp

78 ith WT, DeltaKPQ I(Na) was more sensitive to flecainide, and flecainide preferentially inhibited late

79 iverse drugs including lidocaine, phenytoin, flecainide, and quinidine, suggesting that these drugs i

80 ts alpha/beta-adrenergic blocking activity), flecainide, and riluzole; and suppression of abnormal Ca

81 d the open-channel blockers disopyramide and flecainide, and the lidocaine derivative RAD-243.

82 beta-blockers (propranolol and carvedilol), flecainide, and the neuronal sodium-channel blocker rilu

83 n respond more favourably to amiodarone than flecainide, and the opposite is found in atria with low

84 responded more favourably to amiodarone than flecainide, and the opposite was found in atria with low

85 Preliminary results with flecainide appear encouraging.

86 Flecainide applied to either the cytoplasmic or luminal

87 ntly, the synergy between catecholamines and flecainide at depolarized Vm and the shortened APD95 cou

88 for predicting proarrhythmic sensitivity to flecainide based on the identification of specific SCN5A

89 e tested lower dose combination therapy with flecainide, beta-blockade and CaMKII inhibition, our mod

90 utions of the open and inactivated states to flecainide binding and inhibition remain controversial.

91 n on repetitive depolarization suggests that flecainide binding is facilitated by channel opening and

92 se data provide insights into mechanisms for flecainide block and provide a rationale at the cellular

93 Flecainide block of Na(+) current (I(Na)) was investigat

94 4-fold delay in recovery from use-dependent flecainide block.

95 o direct evidence to support the notion that flecainide blocks RyR2 Ca(2+) flux in the physiologicall

96 s as the single dose oral loading regimen of flecainide but was superior to those of quinidine and am

97 ma and devoid of sodium channel contribution-flecainide, but not its analogues, suppressed RyR2-media

98 Recently, flecainide, but not lidocaine, has been found to correct

99 investigated the state-dependent binding of flecainide by examining its inhibition of rapidly inacti

100 the substrate identified in the presence of flecainide can eliminate the BrS phenotype and warrants

101 a(+) channel alpha-subunit C-terminus in the flecainide/channel interaction.

102 Flecainide completely prevented CPVT in two human subjec

103 ntials (Vm) ([K+]o=5.4 micromol), 1 micromol flecainide decreased Vmax from 698+/-55 to 610+/-72 V/s

104 We hypothesized that flecainide delivered by oral inhalation would quickly re

105 In intact antral tissue preparations, flecainide depolarized the membrane potential between sl

106 urrent-clamp conditions, exposure to 4-AP or flecainide depolarized the membrane potential by 7-10 mV

107 Flecainide did not affect Ca(2+) transient amplitude, de

108 Moreover, flecainide did not alter RyR2 channel gating and had neg

109 d actions of the drug at the cellular level, flecainide did not inhibit RyR2-dependent sarcoplasmic r

110 , even at supraphysiological concentrations, flecainide did not inhibit the physiologically relevant,

111 Flecainide did not prevent AA after PFO closure.

112 Ca release, while QX-flecainide and N-methyl flecainide did not.

113 ol, metoprolol, celiprolol, propranolol, and flecainide) displayed EFr.

114 placebo, evidence was strong for ibutilide, flecainide, dofetilide, propafenone, amiodarone, and qui

115 To determine whether flecainide dosed to therapeutic levels and added to beta

116 vant, DG channels are blocked selectively by flecainide (EC(50), WT=11.0 and DG=1.7 micromol/L), but

117 In contrast, flecainide effectively prevented triggered activity indu

118 In vivo, flecainide effectively suppressed catecholamine-induced

119 channel effects are insufficient to explain flecainide efficacy in CPVT.

120 channel effects are insufficient to explain flecainide efficacy in CPVT.

121 kinase II inhibition, or by using Mg(2+) or flecainide eliminated delayed afterdepolarizations and d

122 ndependent trials), and rats received either flecainide (Flec) (30 mg/kg/day) or vehicle (Veh) from t

123 day) for 4 weeks (short-term treatment); or flecainide for 6 months (long-term treatment).

124 6.3%), and 5 of 63 (7.9%) patients receiving flecainide for 6 months, for 3 months, or standard of ca

125 .8%) and 16 of 63 (25.4%) patients receiving flecainide for at least 3 months or standard of care, re

126 The mechanism of therapeutic efficacy of flecainide for catecholaminergic polymorphic ventricular

127 ents crossed over to treatment B (placebo or flecainide) for 3 months, followed by exercise testing.

128 ricular outflow tract, which increased after flecainide from 17.6 cm(2) (12.1-24.2) to 28.5 cm(2) (21

129 s with abnormal electrograms increased after flecainide from 19.0 (17.5-23.6) to 27.3 cm(2) (24.0-31.

130 Flecainide further reduced theta', accentuating this RV

131 With K+ depolarization to Vm=-70 mV, flecainide further reduced Vmax from 306+/-101 to 245+/-

132 Flecainide had lesser effects on core size and reentry f

133 rhythmias in Casq2-/- mice, whereas N-methyl flecainide had no significant effect on arrhythmia burde

134 Secondly, our study suggests that flecainide has antiarrhythmic effects on AF due to impai

135 The class IC antiarrhythmia drug flecainide has been shown to depress ventricular ectopy

136 Recently, flecainide has gained considerable interest in CPVT trea

137 Two sodium channel blockers, phenytoin and flecainide, have been reported to protect axons in exper

138 ensitive to low micromolar concentrations of flecainide (IC(50) = 11 microM).

139 ls replicated the increased effectiveness of flecainide in blocking human Nav1.5 channels in HEK293 c

140 nts with genetic arrhythmia syndromes (e.g., flecainide in catecholaminergic polymorphic ventricular

141 been proposed that the clinical efficacy of flecainide in CPVT is because of the combined actions of

142 The principal action of flecainide in CPVT is not via a direct interaction with

143 ncipal mechanism of antiarrhythmic action of flecainide in CPVT.

144 ssible explanation behind the AAD effects of flecainide in patients with Pitx2 deficiency.

145 and the response to the antiarrhythmic agent flecainide in Purkinje cells and ventricular myocytes fr

146 Chloroquine is more effective than flecainide in terminating SAF in isolated sheep hearts b

147 indings demonstrate proarrhythmic effects of flecainide in WT and Scn5a+/- murine hearts that recapit

148 Flecainide increased EGD ratios in WT (at 10 microM) and

149 Flecainide increased the effective refractory period in

150 g of membrane depolarization will potentiate flecainide-induced conduction slowing.

151 the addition of isoproterenol magnified the flecainide-induced reduction of Vmax an additional 24% t

152 depolarized Vm, isoproterenol amplified the flecainide-induced reduction of Vmax and theta2, suggest

153 the frequency of stimulation potentiated the flecainide inhibition (IC(50) = 7.4 microM), which progr

154 Although the flecainide inhibition of Nav1.5 is typically enhanced by

155 age sensitivity and strong dependence of the flecainide inhibition on repetitive depolarization sugge

156 states, which failed to promote significant flecainide inhibition.

157 Although flecainide inhibits single RyR2 channels in vitro, repor

158 Flecainide is a Class I antiarrhythmic drug and a potent

159 who develops a Brugada electrocardiogram on flecainide is diagnosed with "asymptomatic BrS" and coul

160 We assessed whether flecainide is effective to prevent AA during the first 3

161 sure, and whether 6 months of treatment with flecainide is more effective than 3 months to prevent AA

162 reports have claimed that RyR2 inhibition by flecainide is not relevant for its mechanism of antiarrh

163 Oral and intravenous flecainide is recommended for cardioversion of atrial fi

164 u = 7.4 +/- 0.1 s) channels, suggesting that flecainide is trapped and not tightly bound within the p

165 The effect of Flecainide, Ivabradine and Metoprolol was tested.

166 revious drug therapy, duration of treatment, flecainide levels and corrected QT intervals were record

167 shown that the class IC agents encainide and flecainide may increase the energy requirements for paci

168 cted superior therapeutic efficacy than with flecainide monotherapy.

169 it sodium channels and isolate the effect of flecainide on RyR2, flecainide significantly reduced the

170 tudy is to identify inhibitory mechanisms of flecainide on RyR2.

171 Patients received oral flecainide or placebo twice daily, with the dosage guide

172 atients were then randomized to treatment A (flecainide or placebo) for 3 months, followed by exercis

173 ing incremental pacing, before and following flecainide or quinidine challenge.

174 Flecainide or quinidine decreased the pacing rates at wh

175 ck and upstroke slowing after treatment with flecainide or quinine.

176 drugs, with carvedilol and JTV-519 (but not flecainide or riluzole) acting primarily through sarcopl

177 t two antiarrhythmic agents including either flecainide or sotalol as single agents before initiating

178 OR=0.673, 95% CI [0.596 to 0.758], p<0.001), flecainide (OR=0.301, 95% CI [0.118 to 0.641], p<0.001),

179 Electrocardiograms and flecainide plasma concentrations were obtained, cardiac

180 omized clinical trial of patients with CPVT, flecainide plus beta-blocker significantly reduced ventr

181 At diastolic cytoplasmic [Ca(2+)] (100 nM), flecainide possesses an additional inhibitory mechanism

182 I(Na) was more sensitive to flecainide, and flecainide preferentially inhibited late I(Na) (mean cur

183 Flecainide prevented catecholamine-induced sustained ven

184 Flecainide prevented initiation of VT in 13 out of 16 ar

185 We discovered that flecainide prevents arrhythmias in a mouse model of CPVT

186 Flecainide prevents catecholaminergic polymorphic ventri

187 To elucidate the potential mechanism for the flecainide proarrhythmia observed in CAST, the voltage d

188 channel blockers (SCB) with either ajmaline, flecainide, procainamide, or pilsicainide to unmask the

189 Flecainide produced a time-dependent decay in the curren

190 he tibial nerve of EAN animals revealed that flecainide provided significant protection against axona

191 we analyse the effects of the drug compounds flecainide, quinidine, nifedipine, verapamil, blebbistat

192 The data indicate that flecainide rapidly gains access to its binding site when

193 Flecainide remains an effective inhibitor of RyR2-mediat

194 line+flecainide, and acetylcholine+ibutilide+flecainide, respectively.

195 During pacing (n=11), flecainide reversibly reduced conduction velocity ( appr

196 holding potentials eliminated differences in flecainide's effects between wild-type and Pitx2c(+/-) a

197 odium channel block alone is responsible for flecainide's efficacy in CPVT.

198 N-methylation did not alter flecainide's inhibitory activity on human cardiac sodium

199 inide) and showed that N-methylation reduces flecainide's inhibitory potency on RyR2 channels incorpo

200 activation and intermediate inactivation) to flecainide sensitivity in patients carrying LQT3 and Bru

201 nhibitor ivabradine and the Na(v)1.5 blocker flecainide significantly decreased beating rates in muta

202 nd isolate the effect of flecainide on RyR2, flecainide significantly reduced the frequency of sponta

203 At hyperpolarized voltages, flecainide slowed the recovery of both the rapidly inact

204 The antiarrhythmic drug flecainide specifically targets the central cavity of th

205 e safe and to yield plasma concentrations of flecainide sufficient to restore sinus rhythm in patient

206 f epicardial and endocardial Ito channels to flecainide, suggesting that the current is produced by t

207 c modulation of impulse propagation in eight flecainide-superfused canine Purkinje fibers was examine

208 The addition of 1 micromol isoproterenol to flecainide-superfused fibers at physiological Vm increas

209 Flecainide testing was performed at each follow-up visit

210 ude that DeltaKPQ interacts differently with flecainide than with WT, leading to increased block and

211 Flecainide then increased arrhythmic tendency and EGD ra

212 Our simulations suggest that flecainide therapeutic efficacy in CPVT is unlikely to d

213 It is possible for flecainide to directly affect the cardiac ryanodine rece

214 AFLOAT (Assessment of Flecainide to Lower the Patent Foramen Ovale Closure Ris

215 The binding of flecainide to open channels was further investigated in

216 C(50), WT=894 and DG=205 micromol/L) but not flecainide tonic block in a concentration range that is

217 0% of the normal number of axons survived in flecainide-treated rats compared with 62.8% in vehicle-t

218 e (10 microM) prevented VT in six out of six flecainide-treated WT and 13 out of the 16 arrhythmogeni

219 VT occurred in 11 out of 16 (10 microM) flecainide-treated WT and nine out of the 13 initially n

220 ol-induced arrhythmias that are prevented by flecainide treatment.

221 onse on expressed channels; (2) suggest that flecainide use-dependent block of DG channels underlies

222 Flecainide, verapamil and atenolol significantly reduced

223 e tested: digoxin, dobutamine, isoprenaline, flecainide, verapamil and atenolol.

224 alation study, the feasibility of delivering flecainide via oral inhalation (flecainide acetate inhal

225 Administration of flecainide via oral inhalation was shown to be safe and

226 Flecainide was also potent in suppressing microglial act

227 The effect of flecainide was not abolished by inhibiting enteric neuro

228 Flecainide was not effective in preventing arrhythmias i

229 ollow-up data from 242 patients showing that flecainide was superior to no treatment (Kaplan-Meier su

230 Flecainide was used in 24% and left cardiac sympathetic

231 ith those observed with oral and intravenous flecainide were uncommon and included postconversion pau

232 on of spontaneous Ca(2+) release events with flecainide, whereas in RyR2(R4496C/+) mice, the Purkinje

233 were substantially reduced by amiodarone or flecainide, which are drugs that have sodium channel-blo

234 For quinidine and flecainide, which bind preferentially to the open Na+ ch

235 the classical sodium channel blocking agent, flecainide, which has no recognized monoamine oxidase B

236 Flecainide, which preferentially inhibits mutation-alter

237 Applying flecainide while briefly depolarizing from a relatively

238 4-aminopyridine (4-AP) and was inhibited by flecainide, with an IC(50) of 35 microM.

239 he activation or the inactivation gate traps flecainide within the pore resulting in the slow recover