ライフサイエンスコーパス: antiarrhythmic

1 with antiarrhythmics, with 43% requiring >1 antiarrhythmic.

2 thmic, whereas parasympathetic activation is antiarrhythmic.

3 ft ventricular pressure (0.06 mg/kg) was not antiarrhythmic.

4 conduction in epicardial border zones and be antiarrhythmic.

5 lation and demonstrate that wild-type ANP is antiarrhythmic.

6 beta-blocker use, and propensity to receive antiarrhythmics.

7 3.0 [1.6-5.5]) or used no confounding drugs (antiarrhythmics, 2.4 [1.4-4.3]; QT-prolonging drugs, 3.1

8 or persistent AF not receiving conventional antiarrhythmic (AA) therapy.

9 al sodium-channel blocker riluzole; a direct antiarrhythmic action of carvedilol (independent of its

10 nistic insights were gained on the different antiarrhythmic actions of the aforementioned drugs, with

11 Our data suggest that the antiarrhythmic activity of the drug is caused by reducti

12 thmias and that c-Src inhibitors might exert antiarrhythmic activity.

13 ed to investigate the cellular uptake of the antiarrhythmic agent amiodarone, a phospholipidosis-indu

14 Dronedarone is an antiarrhythmic agent approved in 2009 for the treatment

15 Celivarone is a new antiarrhythmic agent developed for the treatment of vent

16 heteroaromatic derivatives of the class III antiarrhythmic agent dofetilide was synthesized and asse

17 a(2+) release events and the response to the antiarrhythmic agent flecainide in Purkinje cells and ve

18 AZD1305 is an investigational antiarrhythmic agent for management of atrial fibrillati

19 ocytes expressing Kv1.5-GFP with the class I antiarrhythmic agent quinidine resulted in a dose- and t

20 hythmic drug therapy; and (3) intolerance to antiarrhythmic agent requiring drug cessation.

21 Dronedarone is a new antiarrhythmic agent that was recently approved for the

22 of 40 derivatives of clofilium, a class III antiarrhythmic agent.

23 and these findings support its utility as an antiarrhythmic agent.

24 ients) or therapy with class IC or class III antiarrhythmic agents (148 patients).

25 ence of atrial arrhythmias without using any antiarrhythmic agents after the catheter ablation.

26 Because conventional antiarrhythmic agents aiming at ion channels have proven

27 was reported in 1 of 1 RCT (100%) of class 1 antiarrhythmic agents and 5 of 5 RCTs (100%) of warfarin

28 isproportionate reporting similar to that of antiarrhythmic agents known to promote torsade de pointe

29 Rhythm control options are either antiarrhythmic agents or ablation, with each having its

30 hus, there is a recognized need for improved antiarrhythmic agents with actions that are selective fo

31 a that it may be possible to develop class I antiarrhythmic agents with optimized pharmacodynamic pro

32 drugs with narrow therapeutic indexes (e.g., antiarrhythmic agents, anticoagulant agents) have demons

33 story of diabetes mellitus, and prior use of antiarrhythmic agents.

34 ate hERG currents and thus may act as potent antiarrhythmic agents.

35 ee of atrial fibrillation without the use of antiarrhythmic agents; 84% were arrhythmia free when tho

36 This study examined the antiarrhythmic and anti-inflammatory effects of LLTS in

37 ion of Ca(2+) sensitivity in myofilaments is antiarrhythmic and might be beneficial to individuals wi

38 ction of Ca2+ sensitivity in myofilaments is antiarrhythmic and might be beneficial to individuals wi

39 trial fibrillation and explore the potential antiarrhythmic and/or arrhythmogenic effect of modulatio

40 Most patients were treated with antiarrhythmics and one third required electrophysiology

41 channel inhibitors used as local anesthetic, antiarrhythmic, and anticonvulsant drugs.

42 study investigates the electrophysiological, antiarrhythmic, and proarrhythmic effects of a clinicall

43 els are inhibited by many local anesthetics, antiarrhythmics, and antiepileptic drugs.

44 ble of precipitating arrhythmias and include antiarrhythmics, antianginals, antiemetics, gastrointest

45 ch autonomic activation is arrhythmogenic or antiarrhythmic are complex and different for specific ar

46 freedom from AF and 84% freedom from AF off antiarrhythmics at 2 years.

47 I(KAS) upregulation may be antiarrhythmic by preserving the repolarization reserve

48 ns were rediscovered causing increasing INR (antiarrhythmics class III [amiodarone], other opioids [t

49 We hypothesized that empirical antiarrhythmic drug (AAD) therapy for 6 weeks after AF a

50 whether an early reablation was superior to antiarrhythmic drug (AAD) therapy in patients with previ

51 n 6 months of enrollment and failure of >/=1 antiarrhythmic drug (Class I to IV).

52 ther, these data reveal a novel mechanism of antiarrhythmic drug action and highlight the possibility

53 PITX2-dependent mechanisms of antiarrhythmic drug action were studied in human embryon

54 7 patients who did not respond to at least 1 antiarrhythmic drug and who experienced at least 3 AF ep

55 rane potential may provide novel targets for antiarrhythmic drug development and companion therapeuti

56 atrial ablation, whereas all had at least 1 antiarrhythmic drug failure.

57 Amiodarone is the most effective antiarrhythmic drug for maintaining sinus rhythm for pat

58 of 329+/-124 days, the single procedure off antiarrhythmic drug freedom from recurrent atrial fibril

59 Sixty-one patients in the antiarrhythmic drug group and 66 in the radiofrequency a

60 the ablation group and 2.2% per year in the antiarrhythmic drug group, with an unadjusted hazard rat

61 tomatic paroxysmal AF, for whom at least one antiarrhythmic drug has failed, with risks within accept

62 Choice of an antiarrhythmic drug is based on safety first vs efficacy

63 emonstrated in an efficient synthesis of the antiarrhythmic drug N-acetylprocainamide.

64 f cryoblation patients compared with 7.3% of antiarrhythmic drug patients (absolute difference, 62.6%

65 The antiarrhythmic drug quinidine is a partial antagonist of

66 m a median of 8 per month to 1; P<0.001) and antiarrhythmic drug requirement although 55% of patients

67 This opens a novel avenue for antiarrhythmic drug research.

68 rents is a potentially valuable AF-selective antiarrhythmic drug strategy.

69 line antiarrhythmic medications or escalated antiarrhythmic drug therapy (escalated-therapy group).

70 and in 451 of 696 (65%) patients who were on antiarrhythmic drug therapy (relative risk, 0.40; 95% co

71 ong-term outcomes of VT control and need for antiarrhythmic drug therapy after endocardial (ENDO) and

72 blanking period allowed for optimization of antiarrhythmic drug therapy and reablation if necessary.

73 gulation therapy, and assess the efficacy of antiarrhythmic drug therapy and/or ablation procedures.

74 paring radiofrequency catheter ablation with antiarrhythmic drug therapy as first-line treatment in p

75 In comparing radiofrequency ablation with antiarrhythmic drug therapy as first-line treatment in p

76 ) were without arrhythmia recurrence and off antiarrhythmic drug therapy at the end of the 12-month f

77 of catheter ablation (CA) when compared with antiarrhythmic drug therapy both as first- and second-li

78 Few data exist to guide antiarrhythmic drug therapy for sustained ventricular ta

79 the CA group when compared with those in the antiarrhythmic drug therapy group (relative risk, 2.04;

80 CA seems to be superior to antiarrhythmic drug therapy in drug naive, resistant, an

81 Antiarrhythmic drug therapy is generally recommended as

82 The efficacy of antiarrhythmic drug therapy is incomplete, with response

83 , the Charlson index, hypertension, smoking, antiarrhythmic drug therapy, and the summed stress score

84 interventions include volume replenishment, antiarrhythmic drug therapy, defibrillators, and adjustm

85 AF are less likely to receive rhythm control antiarrhythmic drug therapy, electric cardioversion, or

86 ICD who had ventricular tachycardia despite antiarrhythmic drug therapy, there was a significantly l

87 isk of stroke or heart failure compared with antiarrhythmic drug therapy.

88 heart failure hospitalizations compared with antiarrhythmic drug therapy.

89 than among those receiving an escalation in antiarrhythmic drug therapy.

90 rter-defibrillator (ICD) is frequent despite antiarrhythmic drug therapy.

91 sion, cardioversion, or initiation/change of antiarrhythmic drug therapy; and (3) intolerance to anti

92 t would support using iPSC-CM to personalize antiarrhythmic drug therapy?

93 in permuted blocks of six per centre to: no antiarrhythmic drug treatment (control); treatment with

94 INTERPRETATION: Short-term antiarrhythmic drug treatment after cardioversion is les

95 herefore, we investigated whether short-term antiarrhythmic drug treatment after cardioversion is non

96 patients with paroxysmal AF without previous antiarrhythmic drug treatment, radiofrequency ablation c

97 r pulmonary vein isolation in the absence of antiarrhythmic drug treatment.

98 ion after myocardial infarction according to antiarrhythmic drug treatment.

99 ly failed therapy with >/= 1 membrane active antiarrhythmic drug underwent 2:1 randomization to eithe

100 -defibrillator, and VT storm despite greater antiarrhythmic drug use (P<0.01).

101 xysmal atrial fibrillation and no history of antiarrhythmic drug use to an initial treatment strategy

102 Antiarrhythmic drug use was associated with electrogram

103 to anticoagulation, heart rate control, safe antiarrhythmic drug use, and patient education and follo

104 on, New York Heart Association class III/IV, antiarrhythmic drug use, cerebrovascular disease, and ch

105 ersistent AF, longer history of AF, previous antiarrhythmic drug use, previous use of diuretics, incr

106 with symptomatic persistent AF, despite >/=1 antiarrhythmic drug(s), who were scheduled for pulmonary

107 te-dependent Na(+)-channel blocking (class I antiarrhythmic drug) action, along with mathematical mod

108 were 20.1% and 55.9%, respectively (80% off antiarrhythmic drug).

109 ther direct acting antivirals (DAAs) and the antiarrhythmic drug, amiodarone (AMIO).

110 Almost 90% of patients received >/=1 antiarrhythmic drug, but >60% had European Heart Rhythm

111 Flecainide, a class I antiarrhythmic drug, inhibits Na(+) and RyR2 channels an

112 ysmal AF who had not responded to at least 1 antiarrhythmic drug, the use of catheter ablation compar

113 We used lidocaine, a local anesthetic and antiarrhythmic drug, to probe the role of conserved Asn

114 Antiarrhythmic drug-free multiple procedure success was

115 Fifty-four of 108 antiarrhythmic drug-free relatives (50%) had a CPVT phen

116 ted by screening a CPVT patient registry for antiarrhythmic drug-naive individuals that reached >85%

117 One hundred twenty-four patients with antiarrhythmic drug-refractory atrial fibrillation with

118 lation (SA) have become accepted therapy for antiarrhythmic drug-refractory atrial fibrillation.

119 ent) and experienced failure of at least one antiarrhythmic drug.

120 ers or no treatment, 21 were on class 1 or 3 antiarrhythmic drugs (11 for atrial arrhythmias), and 2

121 with electrophysiologically guided class 1A antiarrhythmic drugs (AAD) is limited.

122 Antiarrhythmic drugs (AADs) are used to reduce the frequ

123 study tested the hypothesis that response to antiarrhythmic drugs (AADs) is modulated by 3 common loc

124 The impact of individual antiarrhythmic drugs (AADs) on mortality and hospital st

125 f follow-up, 72% achieved AF elimination off antiarrhythmic drugs (AADs), 15% achieved AF control wit

126 more likely to achieve long-term freedom off antiarrhythmic drugs (hazard ratio, 2.2; 95% confidence

127 interval, 1.5-3.2; P<0.0001), freedom on/off antiarrhythmic drugs (hazard ratio, 2.5; 95% confidence

128 Patients were treated with antiarrhythmic drugs (most commonly amiodarone [n=103] o

129 01), with 16% and 42.4%, respectively, using antiarrhythmic drugs (p = 0.004).

130 60%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.40).

131 34%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.84).

132 Arrhythmia-free survival off antiarrhythmic drugs 12 months after EAM was 77%.

133 m left atrial arrhythmia >30 seconds without antiarrhythmic drugs after 12 months, was 36.5% for CA a

134 wo patients (9.5%) remained controlled under antiarrhythmic drugs after unsuccessful endocardial/epic

135 tions, post-translational modifications, and antiarrhythmic drugs alter NaV1.5 at the molecular level

136 y-seven patients with VT refractory to 4+/-2 antiarrhythmic drugs and 2+/-1 previous endocardial/epic

137 ry-vein isolation, 88% of patients receiving antiarrhythmic drugs and 71% of those not receiving such

138 It is a prime target for class 1 antiarrhythmic drugs and a number of antidepressants.

139 roxysmal or persistent AF refractory to >/=2 antiarrhythmic drugs and drug-resistant hypertension (sy

140 Using previously ineffective antiarrhythmic drugs and reablation procedures, arrhythm

141 ith VT that is otherwise uncontrollable with antiarrhythmic drugs and standard percutaneous catheter

142 Ventricular tachycardia (VT) refractory to antiarrhythmic drugs and standard percutaneous catheter

143 ociated with AF-selective actions of class-I antiarrhythmic drugs and support the idea that it may be

144 Antiarrhythmic drugs are commonly used for prevention of

145 Antiarrhythmic drugs are effective for reduction of recu

146 Antiarrhythmic drugs are important in protecting against

147 eat or prevent repetitive ICD therapies when antiarrhythmic drugs are ineffective or not desired.

148 Various marketed antiarrhythmic drugs are limited by ventricular adverse

149 It is unknown whether antiarrhythmic drugs are safe and effective when nonshoc

150 Antiarrhythmic drugs are used commonly in out-of-hospita

151 Antiarrhythmic drugs are widely used to treat patients w

152 oint was freedom from atrial arrhythmias off antiarrhythmic drugs at 1 year after a single-ablation p

153 35+/-5 months, single-procedural success off antiarrhythmic drugs at 12 months (CFAE: 30/65 [46%] ver

154 urrent symptomatic atrial arrhythmia off all antiarrhythmic drugs at 12 months.

155 Ablation in conjunction with antiarrhythmic drugs can help palliate VT in this high-r

156 Conventional treatment with antiarrhythmic drugs carries a high risk for proarrhythm

157 vable in the majority of patients with fewer antiarrhythmic drugs compared with preablation (2.1+/-0.

158 Generally, antiarrhythmic drugs do not provide sufficient protectio

159 ll patients were free of arrhythmias without antiarrhythmic drugs during the 8.4+/-5.6-month follow-u

160 The development of effective and safe antiarrhythmic drugs for atrial fibrillation (AF) rhythm

161 l Question: Is catheter ablation better than antiarrhythmic drugs for the prevention of nonparoxysmal

162 is an accepted therapy in patients for whom antiarrhythmic drugs have failed; however, its role as a

163 dy sought to examine the efficacy of empiric antiarrhythmic drugs in a rigorously characterized cohor

164 ndria-targeted antioxidants may be effective antiarrhythmic drugs in cases of renin-angiotensin syste

165 atheter ablation was found to be superior to antiarrhythmic drugs in preventing recurrences of nonpar

166 Use of antiarrhythmic drugs is limited by the high incidence of

167 Class III antiarrhythmic drugs like dofetilide sensitize the heart

168 as, especially in combination with class III antiarrhythmic drugs like dofetilide.

169 r 2-4 weeks of sinus rhythm, suggesting that antiarrhythmic drugs might not be needed beyond that per

170 Antiarrhythmic drugs offer a noninvasive option to help

171 han a group of patients with AF managed with antiarrhythmic drugs only (5.5% per year), with an unadj

172 s. 36.7%; p = 0.01) and AF-free survival off antiarrhythmic drugs or repeat ablation following PVI (6

173 Antiarrhythmic drugs prolong the atrial action potential

174 tment, radiofrequency ablation compared with antiarrhythmic drugs resulted in a lower rate of recurre

175 Conventional antiarrhythmic drugs target the ion permeability of chan

176 doses of their assigned drug, and ancillary antiarrhythmic drugs than recipients of a placebo (P<0.0

177 rate dependence is a problematic property of antiarrhythmic drugs that prolong the cardiac action pot

178 Recently, investigators have developed antiarrhythmic drugs that target the connections between

179 nths, freedom from arrhythmia recurrence off-antiarrhythmic drugs was achieved in most patients with

180 ngiotensin-converting enzyme inhibitors, and antiarrhythmic drugs was prohibited.

181 n, the sinus rhythm maintenance rate without antiarrhythmic drugs was significantly higher (P=0.027)

182 Most antiarrhythmic drugs were developed at a time when the m

183 Antiarrhythmic drugs were discontinued at 3 to 6 months.

184 After a 3-month blanking period, all antiarrhythmic drugs were discontinued.

185 Patients on antiarrhythmic drugs were included as long as they were

186 s treated with catheter ablation (n=3194) or antiarrhythmic drugs without ablation (n=6028) between 2

187 fore ablation, patients failed a median of 2 antiarrhythmic drugs), including amiodarone, in 166 (59%

188 up, 70% remained in sinus rhythm (85% out-of-antiarrhythmic drugs).

189 r arrhythmia controlled (69.1% not receiving antiarrhythmic drugs).

190 fraction of 29% were refractory to multiple antiarrhythmic drugs, and 1 to 4 previous catheter ablat

191 eatment, 41 (15%) were on sotalol or class I antiarrhythmic drugs, and 62 (22%) were on amiodarone.

192 aintained sinus rhythm after reinitiation of antiarrhythmic drugs, and an additional 15 (10.0%) patie

193 rrence of any atrial tachyarrhythmia, use of antiarrhythmic drugs, and need for repeat ablations were

194 Without antiarrhythmic drugs, freedom from AF at 12 months after

195 urviving SCD and discuss landmark studies of antiarrhythmic drugs, ICD, and cardiac resynchronization

196 tion, 54 of 62 patients failed a mean of 2.4 antiarrhythmic drugs, including amiodarone in 29 (47%) p

197 Antiarrhythmic drugs, including beta-blockers, were disc

198 Among antiarrhythmic drugs, only amiodarone reduces VAs, altho

199 atrial flutter or atrial tachycardia, use of antiarrhythmic drugs, or repeat ablation) following a 90

200 New antiarrhythmic drugs, such as dronedarone and vernakalan

201 Unlike antiarrhythmic drugs, the safety and beneficial effects

202 epresents a paradigm shift from conventional antiarrhythmic drugs, which block downstream events to a

203 m control in these trials was achieved using antiarrhythmic drugs, with evidence of increased mortali

204 death led to significant investigation with antiarrhythmic drugs.

205 egy for the design of potentially beneficial antiarrhythmic drugs.

206 was achieved in 21/26 (81%) at 6 months off antiarrhythmic drugs.

207 sponsible for cardiogenic shock resistant to antiarrhythmic drugs.

208 remained free from AF/atrial tachycardia off antiarrhythmic drugs.

209 atrial fibrillation, which was refractory to antiarrhythmic drugs.

210 m any AF/AT (>30 s) after discontinuation of antiarrhythmic drugs.

211 r cardiogenic shock in patients resistant to antiarrhythmic drugs.

212 arin, statins, beta-blockers, diuretics, and antiarrhythmic drugs.

213 beta-adrenergic blockers, and class I or III antiarrhythmic drugs.

214 %) patients, including 24 patients receiving antiarrhythmic drugs.

215 l use-dependence, the hallmark of successful antiarrhythmic drugs.

216 arrying such genetic variations with Class I antiarrhythmic drugs.

217 d ventricular tachycardia despite the use of antiarrhythmic drugs.

218 At 1 year, 82% of patients were not taking antiarrhythmic drugs.

219 5 months (4-12), including 17/32 patients on antiarrhythmic drugs.

220 2c on LA electrophysiology and the effect of antiarrhythmic drugs.

221 tolerance, and safety concerns limit current antiarrhythmic drugs.

222 %) patients remained in sinus rhythm without antiarrhythmic drugs.

223 hout amiodarone therapy and limited need for antiarrhythmic drugs.

224 AF is commonly treated with antiarrhythmic drugs; the most effective block many ion

225 s, and that dietary omega3-FAs have an added antiarrhythmic effect based on action potential (AP) sho

226 onstrated that stochastic pacing sustains an antiarrhythmic effect by moderating the slope of the act

227 tion, stochastic pacing exerted a protective antiarrhythmic effect by reducing the spatial APD hetero

228 gly high levels of pacing stochasticity, the antiarrhythmic effect is hampered by increasing APD vari

229 .01), which suggests a primary extracellular antiarrhythmic effect mediated by Na(+) channel blockade

230 n heterologous cell systems and assessed the antiarrhythmic effect of Nav1.8 block on isolated mouse

231 there is no model that directly assesses the antiarrhythmic effect of pacing stochasticity per se.

232 ow levels are cardioprotective through their antiarrhythmic effect.

233 malarial quinoline chloroquine exerts potent antiarrhythmic effects by interacting with the cytoplasm

234 king the prediction of arrhythmogenic and/or antiarrhythmic effects difficult.

235 nhibition of these with AP14145 demonstrates antiarrhythmic effects in a vernakalant-resistant porcin

236 , sodium channel inhibitor exhibiting potent antiarrhythmic effects in various in vitro and in vivo m

237 were found between flecainide and labetalol antiarrhythmic effects in vitro and the clinical results

238 KVI-020 (4g) successfully demonstrated antiarrhythmic efficacy in a canine arrhythmia model, an

239 mulated AF and greatly reduces the predicted antiarrhythmic efficacy of IKur block.

240 treated with mexiletine, was to evaluate the antiarrhythmic efficacy of mexiletine by comparing the n

241 criticality of the delivery platform to SkM1 antiarrhythmic efficacy.

242 ore, offer an advantage for hemodynamics and antiarrhythmic efficiency, particularly in diseased hear

243 Forty-four patients (72.1%) in the antiarrhythmic group and in 36 patients (54.5%) in the a

244 ent in heart and represents a new target for antiarrhythmic intervention.

245 Antiarrhythmic management of atrial fibrillation (AF) re

246 The antiarrhythmic mechanism has been attributed to preferen

247 Antiarrhythmic medication consisted mostly of beta-block

248 ation is a safe and effective alternative to antiarrhythmic medication for the treatment of patients

249 Patients receiving antiarrhythmic medication were at higher risk of SCD (ha

250 igh favoring pulmonary vein isolation versus antiarrhythmic medications (OR, 5.87 [CI, 3.18 to 10.85]

251 At 5 years, 73% were in sinus rhythm off antiarrhythmic medications after single intervention, 1

252 r, or atrial tachycardia while not receiving antiarrhythmic medications at least 3 months after the p

253 Pulmonary vein isolation is better than antiarrhythmic medications at reducing recurrences of AF

254 Of the 120 patients taking antiarrhythmic medications before CSD, 39 (32%) no longe

255 blation group) with continuation of baseline antiarrhythmic medications or escalated antiarrhythmic d

256 ian, 867 days), arrhythmia-free survival off antiarrhythmic medications was more likely in group 1 th

257 Antiarrhythmic medications were used for initial therapy

258 Antiarrhythmic medications were utilized in a majority o

259 ent strategies such as exercise restriction, antiarrhythmic medications, and implantable cardioverter

260 to antithrombotic therapy, rate control, and antiarrhythmic medications.

261 30%) in group 2 remained arrhythmia-free off antiarrhythmic medications.

262 Antiarrhythmic medicines were examined in all subjects w

263 (n = 50, 4.4%), both (n = 110, 9.8%), or no antiarrhythmic (n = 302, 26.8%).

264 performed (cMSCs or cMSC/SkM1) were neither antiarrhythmic nor proarrhythmic.

265 confounders, ie, concomitant disease, use of antiarrhythmic or QT-prolonging drugs, and acute myocard

266 Comorbidity, use of antiarrhythmic or QT-prolonging drugs, or acute myocardi

267 ay contribute to establishment of an optimal antiarrhythmic pacing protocol in a future study.

268 Rotigaptide (3) is an antiarrhythmic peptide that improves cardiac conduction

269 uch as GS-458967 may constitute an effective antiarrhythmic pharmacological strategy.

270 results open a novel path toward discovering antiarrhythmic pharmacophores that target specific resid

271 ve of the present study was to determine the antiarrhythmic potential of RDN in a postinfarct animal

272 re of the dramatic complications of invasive antiarrhythmic procedures and their atypical and late pr

273 studies suggested that statin therapy exerts antiarrhythmic properties among patients with coronary a

274 Magnesium has antiarrhythmic properties in cellular and experimental m

275 y the ones to benefit most from the presumed antiarrhythmic properties of ranolazine.

276 s a Na(V)1.5 antagonist with antianginal and antiarrhythmic properties.

277 of the 2 most commonly used medications for antiarrhythmic prophylaxis of SVT in infants: digoxin an

278 l problems, yet forward rate dependent (FRD) antiarrhythmics remain elusive.

279 tine blocks Nav1.5 by binding to the class 1 antiarrhythmic site.

280 .x as a promising atrium-specific target for antiarrhythmic strategies.

281 indings raise caution in targeting Ito as an antiarrhythmic strategy.

282 elevant to the potential value of IKur as an antiarrhythmic target for the treatment of AF.

283 may serve as a useful platform to test novel antiarrhythmic therapeutics.

284 sociated with pregnancy, and the appropriate antiarrhythmic therapies available, almost all cases can

285 s, of whom 17 had altogether 114 appropriate antiarrhythmic therapies by the device and none suffered

286 Though antiarrhythmic therapies have limited efficacy, ameliora

287 ar mechanisms and potential effectiveness of antiarrhythmic therapies.

288 roxysmal AF undergoing ablation to empirical antiarrhythmic therapy (AAD group) or no antiarrhythmic

289 cal antiarrhythmic therapy (AAD group) or no antiarrhythmic therapy (no-AAD group) for the first 6 we

290 The lack of efficacy of antiarrhythmic therapy and the life-saving role of the i

291 Pharmacological treatment and antiarrhythmic therapy for ChHD is mostly based on resul

292 brillation is demonstrated to be superior to antiarrhythmic therapy for the control of symptomatic an

293 Europe and North America to received either antiarrhythmic therapy or ablation.

294 aling appears an attractive novel target for antiarrhythmic therapy.

295 tion, and may offer potential for innovative antiarrhythmic therapy.

296 mine patient compliance and effectiveness of antiarrhythmic treatment by the wearable cardioverter-de

297 patients using rhythm (class Ia, Ic, and III antiarrhythmics), versus rate control (beta-blockers, ca

298 dom from AF was 93%, and freedom from AF off antiarrhythmics was 82%, at a mean follow-up time of 3.6

299 In addition, novel antiarrhythmics with more atrial specific effects may re

300 A total of 95% of patients were treated with antiarrhythmics, with 43% requiring >1 antiarrhythmic.