ライフサイエンスコーパス: antiarrhythmic

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

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

3 thmic, whereas parasympathetic activation is antiarrhythmic.

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

5 3.0 [1.6-5.5]) or used no confounding drugs (antiarrhythmics, 2.4 [1.4-4.3]; QT-prolonging drugs, 3.1

6 nths follow-up, 68% remained AF-free off all antiarrhythmics; 74% remained AF-free and 66% remained A

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

8 cainide is not relevant for its mechanism of antiarrhythmic action and concluded that sodium channel

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

10 ikely constitutes the principal mechanism of antiarrhythmic action of flecainide in CPVT.

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

12 nt of epilepsy and has been reported to have antiarrhythmic actions on the heart.

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

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

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

18 Because conventional antiarrhythmic agents aiming at ion channels have proven

19 mechanistic insights into the effects of the antiarrhythmic agents in the setting of AF-induced SND.

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

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

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

23 Numerous antiarrhythmic agents, antimicrobial drugs, psychotropic

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

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

26 Therefore, we examined the antiarrhythmic and anti-inflammatory effects of noninvas

27 the understanding of molecular mechanisms of antiarrhythmic and local anesthetic drug interactions wi

28 ics simulations to study the interactions of antiarrhythmic and local anesthetic drugs with hNa(V)1.5

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

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

31 current sustained VT and had failed multiple antiarrhythmics and radiofrequency ablations.

32 and they are key targets for antiepileptic, antiarrhythmic, and analgesic drugs.

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

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

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

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

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

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

39 odarone (AMD), a widely prescribed class III antiarrhythmic, could inhibit hERG currents with relativ

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

41 ing from stroke prophylaxis to monitoring of antiarrhythmic drug (AAD) therapy.

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

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

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

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

46 The antiarrhythmic drug flecainide specifically targets the

47 inhibitors dantrolene and tetracaine and the antiarrhythmic drug flecainide.

48 e raises the possibility of repurposing this antiarrhythmic drug for the treatment of patients with p

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

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

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

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

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

54 he effects of GS-967 and eleclazine with the antiarrhythmic drug lidocaine, the prototype I (NaL) inh

55 We report chemical refinement of the antiarrhythmic drug mexiletine via high-throughput scree

56 al fibrillation and treatment failure with 1 antiarrhythmic drug or beta-blocker, with 4-year follow-

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

58 te success, duration of hospitalization, and antiarrhythmic drug prescription between the study cohor

59 The antiarrhythmic drug quinidine is a partial antagonist of

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

61 This opens a novel avenue for antiarrhythmic drug research.

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

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

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

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

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

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

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

69 , AND PARTICIPANTS: The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation tria

70 The CABANA (Catheter Ablation Versus Antiarrhythmic Drug Therapy for Atrial Fibrillation) tri

71 tion with a cryothermy balloon or to receive antiarrhythmic drug therapy for initial rhythm control.

72 on, catheter ablation is more effective than antiarrhythmic drug therapy for maintaining sinus rhythm

73 t atrium by catheter ablation is superior to antiarrhythmic drug therapy for maintaining sinus rhythm

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

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

76 Antiarrhythmic drug therapy is generally recommended as

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

78 with catheter cryoballoon ablation than with antiarrhythmic drug therapy, as assessed by continuous c

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

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

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

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

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

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

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

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

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

88 drug use (52% versus 40%, P=0.005), baseline antiarrhythmic drug use (34.8% versus 26.8%, P=0.045), a

89 at baseline (18% versus 8%; P=0.0004), prior antiarrhythmic drug use (52% versus 40%, P=0.005), basel

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

91 n with modest short-term risks, reduction in antiarrhythmic drug use, and improvement in quality of l

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

93 as associated with a significant decrease in antiarrhythmic drug use, cardioversion rate, and hospita

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

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

96 Antiarrhythmic drug utilization decreased by 69% at 12 t

97 es in procedure-related rehospitalization or antiarrhythmic drug utilization were observed between co

98 y emergency medical services personnel to an antiarrhythmic drug versus placebo in the ALPS trial (Re

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

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

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

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

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

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

105 Antiarrhythmic drug-free multiple procedure success was

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

107 er catheter ablation or the initiation of an antiarrhythmic drug.

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

109 ; p = 1.00), or in combination with Class Ic antiarrhythmic drugs (1.46 per 100 py, p = 1.00).

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

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

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

113 rhythmogenesis and variable effectiveness of antiarrhythmic drugs (AADs) in patients in the presence

114 mly assigned (1:1) to receive treatment with antiarrhythmic drugs (class I or III agents) or pulmonar

115 ablation and in 26.2% of those who received antiarrhythmic drugs (hazard ratio, 0.39; 95% CI, 0.22 t

116 of 149 patients (67.8%) assigned to receive antiarrhythmic drugs (hazard ratio, 0.48; 95% confidence

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

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

119 ase responds to quinidine therapy when other antiarrhythmic drugs (including intravenous amiodarone)

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

121 ion ablation (n = 79) or previously untested antiarrhythmic drugs (n = 76).

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

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

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

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

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

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

128 randomized controlled trials that evaluated antiarrhythmic drugs and CA in patients with ICD was con

129 study to evaluate the efficacy and safety of antiarrhythmic drugs and catheter ablation (CA) in the t

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

131 ) with CA (P=0.036) on/off previously failed antiarrhythmic drugs and in 53.5% (53/99) versus 32.0% (

132 Using previously ineffective antiarrhythmic drugs and reablation procedures, arrhythm

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

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

135 Antiarrhythmic drugs are effective for reduction of recu

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

137 Various marketed antiarrhythmic drugs are limited by ventricular adverse

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

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

140 Although antiarrhythmic drugs are useful, AF ablation has become

141 Antiarrhythmic drugs are widely used to treat patients w

142 35+/-5 months, single-procedural success off antiarrhythmic drugs at 12 months (CFAE: 30/65 [46%] ver

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

144 high freedom from AF/atrial tachycardia off antiarrhythmic drugs at long-term follow-up.

145 Guidelines recommend a trial of one or more antiarrhythmic drugs before catheter ablation is conside

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

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

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

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

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

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

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

153 Antiarrhythmic drugs have not proven to significantly im

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

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

156 Class III antiarrhythmic drugs like dofetilide sensitize the heart

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

158 Antiarrhythmic drugs offer a noninvasive option to help

159 present study were to examine the effect of antiarrhythmic drugs on human ESC (hESC) und human induc

160 genic shock and concomitant VT refractory to antiarrhythmic drugs on mechanical support.

161 The effect of antiarrhythmic drugs on spontaneously beating cardiomyoc

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

163 Early rhythm control included treatment with antiarrhythmic drugs or atrial fibrillation ablation aft

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

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

166 Other antiarrhythmic drugs should be considered if those initi

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

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

169 of previously failed/intolerant class I/III antiarrhythmic drugs through 12 months.

170 , single procedure freedom from AF on or off antiarrhythmic drugs was 72.5% (95% CI, 63.9%-80.3%).

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

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

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

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

175 All antiarrhythmic drugs were discontinued at least 5 half-l

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

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

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

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

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

181 hycardia/atrial flutter-free on or off AADs (antiarrhythmic drugs).

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

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

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

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

186 30 seconds after a single procedure, without antiarrhythmic drugs, at both 6 and 12 months.

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

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

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

190 Antiarrhythmic drugs, including beta-blockers, were disc

191 Among antiarrhythmic drugs, only amiodarone reduces VAs, altho

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

193 Outcomes included use of antiarrhythmic drugs, rate of cardioversions and cardiov

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

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

196 sponsible for cardiogenic shock resistant to antiarrhythmic drugs.

197 atrial fibrillation, which was refractory to antiarrhythmic drugs.

198 r cardiogenic shock in patients resistant to antiarrhythmic drugs.

199 d ventricular tachycardia despite the use of antiarrhythmic drugs.

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

201 5 months (4-12), including 17/32 patients on antiarrhythmic drugs.

202 2c on LA electrophysiology and the effect of antiarrhythmic drugs.

203 tolerance, and safety concerns limit current antiarrhythmic drugs.

204 %) patients remained in sinus rhythm without antiarrhythmic drugs.

205 hout amiodarone therapy and limited need for antiarrhythmic drugs.

206 death led to significant investigation with antiarrhythmic drugs.

207 egy for the design of potentially beneficial antiarrhythmic drugs.

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

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

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

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

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

213 0.13% (interquartile range, 0 to 1.60) with antiarrhythmic drugs.

214 ion were free from AF/atrial tachycardia off antiarrhythmic drugs.

215 lation and in 6 patients (4.0%) who received antiarrhythmic drugs.

216 sus 32.0% (16/50; P=0.0128) respectively off antiarrhythmic drugs.

217 tion or altering conductive properties using antiarrhythmic drugs.

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

219 Although class III antiarrhythmics, e.g., dofetilide, rescue congenital and

220 injury during SBRT for VT, which may have an antiarrhythmic effect before the onset of fibrosis.

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

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

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

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

225 The antiarrhythmic effect of UDCA may be partially mediated

226 c sympathetic activity that may result in an antiarrhythmic effect on atrial fibrillation.

227 No antiarrhythmic effect was observed in the acute UDCA adm

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

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

230 e novel sodium channel inhibitors exhibiting antiarrhythmic effects in various in vitro and in vivo m

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

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

233 Antiarrhythmic effects of anti-TASK-1-siRNA were associa

234 The potential antiarrhythmic effects of prolonged UDCA administration

235 ndly, our study suggests that flecainide has antiarrhythmic effects on AF due to impaired Pitx2 by pr

236 substantial UDB contributes to the observed antiarrhythmic efficacy of GS-967 and eleclazine.

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

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

239 tudy used a porcine AF model to evaluate the antiarrhythmic efficacy of TASK-1 inhibition by adeno-as

240 Antiarrhythmic efficacy was tested utilizing a Casq2 (ca

241 ich we propose contributes to their observed 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 acid (UDCA) has previously been shown to be antiarrhythmic in fetal hearts.

245 Antiarrhythmic management of atrial fibrillation (AF) re

246 The antiarrhythmic mechanism has been attributed to preferen

247 The antiarrhythmic mechanism has been attributed to preferen

248 We investigated antiarrhythmic mechanisms of ranolazine in sheep models

249 Antiarrhythmic medication consisted mostly of beta-block

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

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

252 Of 76 patients randomized to receive antiarrhythmic medication, 74 received it, including 8 w

253 mptomatic atrial fibrillation despite use of antiarrhythmic medication, the improvement in quality of

254 treated with catheter ablation compared with antiarrhythmic medication.

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

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

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

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

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

260 Use of dual antiarrhythmic medications decreased from 59% to 12% ( P

261 tients treated with AF catheter ablation and antiarrhythmic medications only.

262 matched 1:1 with 1087 patients treated with antiarrhythmic medications only.

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

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

265 Antiarrhythmic medications were used for initial therapy

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

267 30%) in group 2 remained arrhythmia-free off antiarrhythmic medications.

268 emplated the current best available class 1b antiarrhythmic, mexiletine, using the rat Langendorff pr

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

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

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

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

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

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

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

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

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 This promising antiarrhythmic strategy warrants further testing in expe

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

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

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

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

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

287 Though antiarrhythmic therapies have limited efficacy, ameliora

288 ar mechanisms and potential effectiveness of antiarrhythmic therapies.

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

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

291 s of such events, and define the efficacy of antiarrhythmic therapy in patients with ATS1.

292 l fibrillation (AF) catheter ablation versus antiarrhythmic therapy on outcomes have shown mixed resu

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

294 torms were always refractory to conventional antiarrhythmic therapy, including intravenous amiodarone

295 aling appears an attractive novel target for antiarrhythmic therapy.

296 e cardiac action potential and is target for antiarrhythmic therapy.

297 TASK-1 currents represents a new option for antiarrhythmic therapy.

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

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.