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

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

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

5 G channels by MK-499, a methanesulfonanilide antiarrhythmic drug.

6 atrial fibrillation, which was refractory to antiarrhythmic drugs.

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

8 r cardiogenic shock in patients resistant to antiarrhythmic drugs.

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

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

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

12 %) patients, including 24 patients receiving antiarrhythmic drugs.

13 d ventricular tachycardia despite the use of antiarrhythmic drugs.

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

15 arrying such genetic variations with Class I antiarrhythmic drugs.

16 The patients did not receive antiarrhythmic drugs.

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

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

19 ative strategies for discovering new cardiac antiarrhythmic drugs.

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

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

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

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

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

25 e in the cardiac substrate or treatment with antiarrhythmic drugs.

26 eatment of acute episodes of arrhythmia with antiarrhythmic drugs.

27 logic, immunosuppressive, anticoagulant, and antiarrhythmic drugs.

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

29 5 months (4-12), including 17/32 patients on antiarrhythmic drugs.

30 2c on LA electrophysiology and the effect of antiarrhythmic drugs.

31 tolerance, and safety concerns limit current antiarrhythmic drugs.

32 %) patients remained in sinus rhythm without antiarrhythmic drugs.

33 hout amiodarone therapy and limited need for antiarrhythmic drugs.

34 death led to significant investigation with antiarrhythmic drugs.

35 egy for the design of potentially beneficial antiarrhythmic drugs.

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

37 sponsible for cardiogenic shock resistant to antiarrhythmic drugs.

38 3 (49%) VF/pVT episodes were treated with an antiarrhythmic drug; 108 (40%) of these patients receive

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

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

41 57% of patients were in sinus rhythm without antiarrhythmic drugs, 32% had persistent AF, 6% had paro

42 33% of patients were in sinus rhythm without antiarrhythmic drugs, 38% had AF, 17% had both AF and at

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

44 ricular arrhythmias who were treated with an antiarrhythmic drug (AAD) or implantable cardioverter-de

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

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

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

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

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

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

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

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

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

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

55 Antiarrhythmic drugs (AADs) were associated with increas

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

57 2 converted to sinus rhythm after initiating antiarrhythmic drugs (AADs).

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

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

60 This represents a novel mechanism of antiarrhythmic drug action.

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

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

63 oportion of patients who required additional antiarrhythmic drugs after the administration of the stu

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

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

66 The antiarrhythmic drug amiodarone has fungicidal activity a

67 The antiarrhythmic drug amiodarone was recently demonstrated

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

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

70 7 patients who did not respond to at least 1 antiarrhythmic drug and who experienced at least 3 AF ep

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

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

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

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

75 Using previously ineffective antiarrhythmic drugs and reablation procedures, arrhythm

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

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

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

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

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

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

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

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

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

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

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

87 nel blocking properties with other class III antiarrhythmic drugs, and this may contribute to its ant

88 Antiarrhythmic drugs are commonly used for prevention of

89 Antiarrhythmic drugs are effective for reduction of recu

90 Recent data suggest that these new class III antiarrhythmic drugs are highly effective for treating p

91 Antiarrhythmic drugs are important in protecting against

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

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

94 Various marketed antiarrhythmic drugs are limited by ventricular adverse

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

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

97 uggest that when action potential-prolonging antiarrhythmic drugs are used for AF, excessive QT prolo

98 Antiarrhythmic drugs are widely used to treat patients w

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

100 tistically improved survival compared to the antiarrhythmic drug arm, most of whose patients were tak

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

102 35+/-5 months, single-procedural success off antiarrhythmic drugs at 12 months (CFAE: 30/65 [46%] ver

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

104 death, and 18 (72%) were receiving > or = 1 antiarrhythmic drugs at the time of death.

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

106 Participation of the selectivity ring in antiarrhythmic drug binding and access locates this stru

107 Local anesthetic antiarrhythmic drugs block voltage-gated Na(+) channels

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

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

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

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

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

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

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

115 n Hypothesis will support a new paradigm for antiarrhythmic drug classification, incorporating an ant

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

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

118 ast 10 years there has been a major shift in antiarrhythmic drug development from class I to class II

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

120 Generally, antiarrhythmic drugs do not provide sufficient protectio

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

122 We further show that the antiarrhythmic drug E-4031, which selectively blocks HER

123 ication, and is insensitive to the class III antiarrhythmic drug E-4031.

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

125 Newer antiarrhythmic drugs either block a specific ionic curre

126 The potential interaction with antiarrhythmic drugs, especially amiodarone, and drugs a

127 Antiarrhythmic drugs exert significant negative inotropi

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

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

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

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 ly, guidelines for allowance or avoidance of antiarrhythmic drug formulation substitution are suggest

137 Antiarrhythmic drug-free multiple procedure success was

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

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

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

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

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

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

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

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

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

147 Antiarrhythmic drugs have not been reliable in preventin

148 All antiarrhythmic drugs have the potential to provoke arrhy

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 Whether antiarrhythmic drugs improve the rate of successful resu

153 Na channel blockade by antiarrhythmic drugs improves the QT interval prolongati

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

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

156 plantable cardioverter-defibrillators versus antiarrhythmic drugs in patients with life-threatening v

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

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

159 the effectiveness of azimilide, a class III antiarrhythmic drug, in reducing the frequency of sympto

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

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

162 Antiarrhythmic drugs, including beta-blockers, were disc

163 :(Kr), a sensitive target for most class III antiarrhythmic drugs, including methanesulfonanilides su

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

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

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

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

168 Class III antiarrhythmic drugs like dofetilide sensitize the heart

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

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

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

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

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

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

175 Antiarrhythmic drugs offer a noninvasive option to help

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

177 Among antiarrhythmic drugs, only amiodarone reduces VAs, altho

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

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

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

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

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

183 60%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.40).

184 34%) in Group C were in sinus rhythm without antiarrhythmic drugs (p = 0.84).

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

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

187 Antiarrhythmic drugs prolong the atrial action potential

188 The antiarrhythmic drug quinidine is a partial antagonist of

189 ith implantable defibrillators, but not with antiarrhythmic drugs, reduces the risk of sudden death i

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

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

192 in blockade of the cardiac Na(+) channel by antiarrhythmic drugs remains uncertain.

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

194 This opens a novel avenue for antiarrhythmic drug research.

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

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

197 Sympathetic blockade-not class 1 antiarrhythmic drugs-should be the treatment of choice f

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

199 New antiarrhythmic drugs, such as dronedarone and vernakalan

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

201 Conventional antiarrhythmic drugs target the ion permeability of chan

202 siologically guided therapy and treated with antiarrhythmic drugs than among the patients assigned to

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

204 The first two class III antiarrhythmic drugs that became available, sotalol and

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

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

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

208 Unlike antiarrhythmic drugs, the safety and beneficial effects

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

210 m need for cardioversion, antithrombotic and antiarrhythmic drug therapies during dual-site atrial pa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Antiarrhythmic drug therapy had failed in 41 (79%) patie

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

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

229 Antiarrhythmic drug therapy is generally recommended as

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

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

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

233 months were randomized to regimens of either antiarrhythmic drug therapy or first-line RF ablation.

234 sooner and is unpredictable, suggesting that antiarrhythmic drug therapy should be considered after t

235 No new antiarrhythmic drug therapy was added.

236 Antiarrhythmic drug therapy was traditionally the mainst

237 incremental years of life due to ICD versus antiarrhythmic drug therapy were calculated.

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

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

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

241 Initial radiofrequency ablation, long-term antiarrhythmic drug therapy, and treatment of acute epis

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

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

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

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

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

247 heart failure hospitalizations compared with antiarrhythmic drug therapy.

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

249 lucidate the underlying mechanisms and guide antiarrhythmic drug therapy.

250 cardioverter-defibrillator implantation, and antiarrhythmic drug therapy.

251 ificant advances have been made in class III antiarrhythmic drug therapy.

252 or cost-effectiveness analyses of ICD versus antiarrhythmic drug therapy.

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

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

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

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

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

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

259 antable Defibrillators (AVID) trial compared antiarrhythmic-drug therapy with the implantation of def

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

261 ion: one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm, and the o

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

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

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

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

266 8), angina (n=2), hypokalemia (n=1), adverse antiarrhythmic drug treatment (n=1) and acute MI (n=1).

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

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

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

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

271 ion after myocardial infarction according to antiarrhythmic drug treatment.

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

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

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

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

276 Antiarrhythmic drug use was associated with electrogram

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

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

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

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

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

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

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

288 room, and day surgery stays and the costs of antiarrhythmic drugs were collected on 1008 patients.

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

290 Antiarrhythmic drugs were discontinued at 3 to 6 months.

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

292 nfarction or bypass surgery, and patients on antiarrhythmic drugs were excluded.

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

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

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

296 idine), and for patients who are to begin an antiarrhythmic drug while in a supraventricular tachyarr

297 Mexiletine is a class I antiarrhythmic drug with neuroprotective effects in mode

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

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

300 For antiarrhythmic drugs, women are at a higher risk for the