ライフサイエンスコーパス: antiarrhythmic drug

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

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

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

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

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

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

7 tolerance, and safety concerns limit current antiarrhythmic drugs.

8 %) patients remained in sinus rhythm without antiarrhythmic drugs.

9 hout amiodarone therapy and limited need for antiarrhythmic drugs.

10 death led to significant investigation with antiarrhythmic drugs.

11 egy for the design of potentially beneficial antiarrhythmic drugs.

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

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

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

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

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

17 %) patients, including 24 patients receiving antiarrhythmic drugs.

18 0.13% (interquartile range, 0 to 1.60) with antiarrhythmic drugs.

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

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

21 arrying such genetic variations with Class I antiarrhythmic drugs.

22 The patients did not receive antiarrhythmic drugs.

23 atrial flutter, and 3% had paroxysmal AF on antiarrhythmic drugs.

24 illators, the need is still pressing for new antiarrhythmic drugs.

25 ative strategies for discovering new cardiac antiarrhythmic drugs.

26 iscusses why there is a need for new cardiac antiarrhythmic drugs.

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

28 f 2,033 patients received 3,030 exposures to antiarrhythmic drugs.

29 in the search for more efficacious and safer antiarrhythmic drugs.

30 rapy, there is still a pressing need for new antiarrhythmic drugs.

31 d an ICD but not among patients who received antiarrhythmic drugs.

32 tion or altering conductive properties using antiarrhythmic drugs.

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

34 sponsible for cardiogenic shock resistant to antiarrhythmic drugs.

35 atrial fibrillation, which was refractory to antiarrhythmic drugs.

36 r cardiogenic shock in patients resistant to antiarrhythmic drugs.

37 d ventricular tachycardia despite the use of antiarrhythmic drugs.

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

39 5 months (4-12), including 17/32 patients on antiarrhythmic drugs.

40 2c on LA electrophysiology and the effect of antiarrhythmic drugs.

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

42 3 (49%) VF/pVT episodes were treated with an antiarrhythmic drug; 108 (40%) of these patients receive

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

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

45 57% of patients were in sinus rhythm without antiarrhythmic drugs, 32% had persistent AF, 6% had paro

46 33% of patients were in sinus rhythm without antiarrhythmic drugs, 38% had AF, 17% had both AF and at

47 dults (> 18 yrs old) with VF/pVT received an antiarrhythmic drug; 8,883 (60%) of these patients recei

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

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

50 cost-effectiveness of the ICD compared with antiarrhythmic drug (AAD) therapy, largely with amiodaro

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

52 erious ventricular arrhythmias compared with antiarrhythmic drug (AAD) use.

53 otal of 40 patients (mean age 57 years) with antiarrhythmic drug (AAD)-refractory AF (23 had also con

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

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

56 nts with post-Maze arrhythmias refractory to antiarrhythmic drugs (AADs) between January 2000 and Dec

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

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

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

60 Antiarrhythmic drugs (AADs) were associated with increas

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

62 2 converted to sinus rhythm after initiating antiarrhythmic drugs (AADs).

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

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

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

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

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

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

69 The antiarrhythmic drug amiodarone has fungicidal activity a

70 The antiarrhythmic drug amiodarone was recently demonstrated

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

72 Flecainide is a Class I antiarrhythmic drug and a potent inhibitor of the cardia

73 7 patients who did not respond to at least 1 antiarrhythmic drug and who experienced at least 3 AF ep

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

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

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

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

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

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

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

81 Using previously ineffective antiarrhythmic drugs and reablation procedures, arrhythm

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

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

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

85 masked by sodium channel blockers, including antiarrhythmic drugs and tricyclic antidepressants.

86 conduction in the left atrial septum due to antiarrhythmic drugs and/or atrial myopathy seems to pro

87 In 21 patients, VF storm was controlled with antiarrhythmic drugs and/or treatment of heart failure.

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

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

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

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

92 nts, the eclectic post-interventional use of antiarrhythmic drugs, and the lack of appropriate contro

93 Antiarrhythmic drugs are commonly used for prevention of

94 Antiarrhythmic drugs are effective for reduction of recu

95 Antiarrhythmic drugs are important in protecting against

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

97 Most antiarrhythmic drugs are ion channel blockers, and to da

98 Various marketed antiarrhythmic drugs are limited by ventricular adverse

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

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

101 Although antiarrhythmic drugs are useful, AF ablation has become

102 Antiarrhythmic drugs are widely used to treat patients w

103 rdia (VT), and torsade de pointes VT) in the antiarrhythmic drug arm of the AFFIRM study.

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

105 35+/-5 months, single-procedural success off antiarrhythmic drugs at 12 months (CFAE: 30/65 [46%] ver

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

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

108 Nine of the 11 patients were treated with antiarrhythmic drugs at the time of the study for concom

109 30 seconds after a single procedure, without antiarrhythmic drugs, at both 6 and 12 months.

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

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

112 omized to rhythm control, compared different antiarrhythmic drugs by randomly assigning the first dru

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

114 acy of drug treatment and the potential that antiarrhythmic drugs can provoke life-threatening arrhyt

115 rval syndrome; newer, more selective class 3 antiarrhythmic drugs; cardiac rhythm management devices;

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

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

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

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

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

121 have generated interest in new approaches to antiarrhythmic drug development.

122 Generally, antiarrhythmic drugs do not provide sufficient protectio

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

124 trolled trials would be helpful in assessing antiarrhythmic drug efficacy in children, because their

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

126 The antiarrhythmic drug flecainide specifically targets the

127 inhibitors dantrolene and tetracaine and the antiarrhythmic drug flecainide.

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

129 The most effective and safest antiarrhythmic drug for the treatment of AF is unknown.

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

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

132 rdioverter/defibrillator (ICD) compared with antiarrhythmic drugs for secondary prevention of sudden

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

134 This study evaluated the efficacy of antiarrhythmic drugs for the treatment of atrial fibrill

135 f proarrhythmic events in patients receiving antiarrhythmic drugs for treatment of atrial fibrillatio

136 Antiarrhythmic drug-free multiple procedure success was

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

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

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

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

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

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

143 s in understanding the proarrhythmic risk of antiarrhythmic drugs has led to development of safety gu

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

145 icacy and proarrhythmic potential of classic antiarrhythmic drugs have focused attention on nonpharma

146 Antiarrhythmic drugs have not proven to significantly im

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

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

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

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

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

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

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

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

155 f adverse arrhythmic events upon exposure to antiarrhythmic drugs in the AFFIRM study was reasonably

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

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

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

159 Antiarrhythmic drugs, including beta-blockers, were disc

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

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

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

163 on, rhythm control using currently available antiarrhythmic drugs is more expensive but not more effe

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

165 Class III antiarrhythmic drugs like dofetilide sensitize the heart

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

167 ic substrates and proarrhythmic responses to antiarrhythmic drugs may have influenced outcome.

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

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

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

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

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

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

174 Antiarrhythmic drugs offer a noninvasive option to help

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

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

177 The effect of antiarrhythmic drugs on spontaneously beating cardiomyoc

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

179 Among antiarrhythmic drugs, only amiodarone reduces VAs, altho

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

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

182 Adjunct therapy consisting of antiarrhythmic drugs or radiofrequency ablation is neces

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

184 ss IV heart failure, patients already taking antiarrhythmic drugs, or patients with valvular disease.

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

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

187 60%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.40).

188 34%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.84).

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

190 Azimilide dihydrochloride is a class III antiarrhythmic drug possessing Ikr and Iks channel-block

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

192 Antiarrhythmic drugs prolong the atrial action potential

193 The antiarrhythmic drug quinidine is a partial antagonist of

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

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

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

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

198 This opens a novel avenue for antiarrhythmic drug research.

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

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

201 Other antiarrhythmic drugs should be considered if those initi

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

203 New antiarrhythmic drugs, such as dronedarone and vernakalan

204 portant repolarizing current in heart, is an antiarrhythmic drug target and is markedly increased by

205 Conventional antiarrhythmic drugs target the ion permeability of chan

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

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

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

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

210 Unlike antiarrhythmic drugs, the safety and beneficial effects

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

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

213 were free of recurrent AF in the absence of antiarrhythmic drug therapy (p < 0.001).

214 solation were free from recurrent AF without antiarrhythmic drug therapy (p = 1.0).

215 were free of symptomatic PAF when not taking antiarrhythmic drug therapy (P=0.02).

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

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

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

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

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

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

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

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

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

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

226 Ablation is a reasonable alternative to antiarrhythmic drug therapy for controlling frequent ven

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

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

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

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

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

232 rdia are subject to frequent recurrences and antiarrhythmic drug therapy has been disappointing.

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

234 Antiarrhythmic drug therapy is generally recommended as

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

236 Therefore, temporary antiarrhythmic drug therapy may be more appropriate than

237 milarly, little is known about the effect of antiarrhythmic drug therapy on asymptomatic atrial fibri

238 Antiarrhythmic drug therapy was traditionally the mainst

239 escents with symptomatic, lone AF who failed antiarrhythmic drug therapy were evaluated.

240 were arrhythmia free (4 of whom were taking antiarrhythmic drug therapy), and one was having recurre

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

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

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

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

245 or anticoagulation, institution or change of antiarrhythmic drug therapy, or reprogramming of device

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

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

248 heart failure hospitalizations compared with antiarrhythmic drug therapy.

249 e free from AF and/or atrial flutter without antiarrhythmic drug therapy.

250 lucidate the underlying mechanisms and guide antiarrhythmic drug therapy.

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

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

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

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

255 rrent atrial fibrillation or flutter without antiarrhythmic-drug therapy at one year (P=0.05).

256 y 3 (4 percent) were in sinus rhythm without antiarrhythmic-drug therapy or ablation.

257 ein ablation independently of the effects of antiarrhythmic-drug therapy, cardioversion, or both.

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

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

260 llowing AF to persist, or rhythm-controlling antiarrhythmic drugs, to maintain sinus rhythm.

261 In antiarrhythmic drug-treated patients, dual-site RA reduc

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

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

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

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

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

267 ion after myocardial infarction according to antiarrhythmic drug treatment.

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

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

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

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

272 Among AFFIRM participants, antiarrhythmic drug use did not improve survival, stroke

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

274 Antiarrhythmic drug use was associated with electrogram

275 beta-Blocker use, antiarrhythmic drug use, and follow-up duration were sim

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

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

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

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

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

281 Mexiletine is a class 1b antiarrhythmic drug used for ventricular arrhythmias but

282 Baseline characteristics and antiarrhythmic drugs used were similar in both groups.

283 Antiarrhythmic drug utilization decreased by 69% at 12 t

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

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

286 Each time an antiarrhythmic drug was begun, it was counted as an expo

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

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

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

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

291 Azimilide, a novel class III antiarrhythmic drug, was investigated for its effects on

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

293 Antiarrhythmic drugs were discontinued at 3 to 6 months.

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

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

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

297 Strict criteria for the safe use of antiarrhythmic drugs were successful in minimizing proar

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

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

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