ライフサイエンスコーパス: atrial arrhythmia

1 ce or absence of induced bradyarrhythmias or atrial arrhythmias).

2 investigating the mechanisms responsible for atrial arrhythmia.

3 on (NVAF) in older adults with no history of atrial arrhythmia.

4 ng new target for understanding and managing atrial arrhythmia.

5 tion, nor did it facilitate sustenance of an atrial arrhythmia.

6 e pericardial knock, larger atrial size, and atrial arrhythmia.

7 cation of patients at risk for stroke during atrial arrhythmia.

8 ut was associated with a shorter duration of atrial arrhythmia.

9 to cause mitochondrial dysfunction or induce atrial arrhythmia.

10 Hypoxia-ischemia predisposes to atrial arrhythmia.

11 e older and more likely to have a history of atrial arrhythmia.

12 ovascular hospitalizations and recurrence of atrial arrhythmia.

13 ses with good rates of 12-month freedom from atrial arrhythmia.

14 is known about the potential role of JPH2 in atrial arrhythmias.

15 h sick sinus syndrome/dilated cardiomyopathy/atrial arrhythmias.

16 the treatment of cardiac disease, including atrial arrhythmias.

17 -up but did not reduce the recurrence of all atrial arrhythmias.

18 extrasystolic activity capable of initiating atrial arrhythmias.

19 that Pitx2 haploinsufficiency predisposes to atrial arrhythmias.

20 ated LRA-signaling pathways in prevention of atrial arrhythmias.

21 eased susceptibility to burst pacing-induced atrial arrhythmias.

22 s in the delay in cardiac repolarization and atrial arrhythmias.

23 r AF ablation would reduce the occurrence of atrial arrhythmias.

24 atrium and pulmonary veins may contribute to atrial arrhythmias.

25 velopment but an increased susceptibility to atrial arrhythmias.

26 ng that air pollution may be associated with atrial arrhythmias.

27 BB fibers may play a role in development of atrial arrhythmias.

28 hophysiology and mechanisms of postoperative atrial arrhythmias.

29 circuits are common mechanisms of recurrent atrial arrhythmias.

30 and its regulation by beta-AR stimulation on atrial arrhythmias.

31 cation of AVN conduction in the treatment of atrial arrhythmias.

32 associated with early or late postoperative atrial arrhythmias.

33 (WT) littermates that lack I Ks to prolonged atrial arrhythmias.

34 annel and prolongation of repolarization and atrial arrhythmias.

35 ponent in the development of Ca(2+)-mediated atrial arrhythmias.

36 luenced by the development of stress-induced atrial arrhythmias.

37 ycardia pacemaker therapy, and no persistent atrial arrhythmias.

38 priate sinus tachycardia, and 4 patients had atrial arrhythmias.

39 hannels has been proposed as a treatment for atrial arrhythmias.

40 sions for MV surgery provide a substrate for atrial arrhythmias.

41 esized that CRP is elevated in patients with atrial arrhythmias.

42 riod, it may contribute to the substrate for atrial arrhythmias.

43 mia-free periods in patients with paroxysmal atrial arrhythmias.

44 e most consistent predictor of postoperative atrial arrhythmias.

45 may contribute to the development of ectopic atrial arrhythmias.

46 red to be associated with the development of atrial arrhythmias.

47 urea nitrogen, congestive heart failure and atrial arrhythmias.

48 modalities, where diverges are observed for atrial arrhythmias.

49 of catheter ablation in preventing recurrent atrial arrhythmias.

50 s and atrial switch have a high incidence of atrial arrhythmias.

51 ) across the myocardium to guide ablation of atrial arrhythmias.

52 in PV isolation, and freedom from recurrent atrial arrhythmias.

53 characteristics may serve as predictors for atrial arrhythmias.

54 s that may modify atrial conduction or treat atrial arrhythmias.

55 s to dynamic instabilities that may underlie atrial arrhythmias.

56 chanisms by which mutant IKur contributes to atrial arrhythmias.

57 reathing (SDB) is frequently associated with atrial arrhythmias.

58 tribute to the initiation and maintenance of atrial arrhythmias.

59 relationship between sinus node disease and atrial arrhythmias.

60 susceptibility to re-entrant ventricular and atrial arrhythmias.

61 ented with sinus node dysfunction and 10 had atrial arrhythmias.

62 are their mapping resolution in scar-related atrial arrhythmias.

63 tients admitted for dofetilide reloading for atrial arrhythmias, 102 were reloaded at a previously to

64 ne the location of left atrial stasis during atrial arrhythmia; 2) define the degree of stasis associ

65 vs 9.7 days; P < 0.001); and lower rates of atrial arrhythmia (27% vs 19%; P = 0.013) and pulmonary

66 was associated with reductions in recurrent atrial arrhythmia (32.3% vs 53%; risk ratio [RR], 0.62;

67 intervention (10.7% vs 3.2%; P<.001) and new atrial arrhythmias (4.6% vs 1.5%; P =.004) occurred more

68 t ventricular ejection fraction (<50%; 45%), atrial arrhythmias (58%), and malignant ventricular arrh

69 he primary efficacy end point and to examine atrial arrhythmia (AA) burden and episode duration.

70 nt study sought to quantify the incidence of atrial arrhythmia (AA), ventricular arrhythmia (VA), and

71 There were no differences in post LVAD atrial arrhythmias (AA) (Adjusted OR = 0.45 [0.18-1.06],

72 ignificant difference in 1-year freedom from atrial arrhythmias (AA) between thermal (radiofrequency/

73 iomyopathy, atrioventricular block (AVB), or atrial arrhythmias (AAs) and ventricular arrhythmias (VA

74 n of the great arteries, atrial baffles, and atrial arrhythmia ablation was performed.

75 hanism of potentially lethal ventricular and atrial arrhythmias across the full spectrum of arrhythmi

76 outcome was freedom from clinical documented atrial arrhythmia (AF/atrial flutter/atrial tachycardia)

77 Rapid atrial arrhythmias affect the elderly who undergo cardia

78 is was a retrospective review of adults with atrial arrhythmia after Fontan operation who were evalua

79 nd embolic complication (TEC) in adults with atrial arrhythmia after Fontan operation.

80 Survival free of any atrial arrhythmia after one procedure was not significan

81 The freedom from atrial arrhythmia after pulmonary vein-based, linear-bas

82 2 months, the drug-free rate of freedom from atrial arrhythmias after 1 or 2 procedures was 60.2% (95

83 uperior to CA in achieving freedom from left atrial arrhythmias after 12 months of follow-up, althoug

84 Effectiveness outcomes included freedom from atrial arrhythmias after ablation and proportion of part

85 significantly associated with recurrence of atrial arrhythmias after catheter ablation for AF.

86 2 patients with congenital heart disease and atrial arrhythmias, age 32.0 +/- 18.0 years, 45.2% femal

87 Atrial fibrillation is the most common atrial arrhythmia and accounts for a significant burden

88 significant interaction between a history of atrial arrhythmia and percent pacing.

89 associated with reductions in recurrence of atrial arrhythmias and hospitalizations, with no differe

90 ter, in patients undergoing cardioversion of atrial arrhythmias and in patients with mitral valve dis

91 conduction disturbance and the occurrence of atrial arrhythmias and low left ventricular ejection fra

92 Increased expression of Rho GDIalpha led to atrial arrhythmias and mild ventricular hypertrophy in a

93 uces the incidence of clinically significant atrial arrhythmias and need for cardioversion/hospitaliz

94 ales who had ARVC compared with females, and atrial arrhythmias and P wave changes represented a comm

95 with ARVC also had an increased incidence of atrial arrhythmias and P wave changes.

96 Drug-induced BS is associated with atrial arrhythmias and SND.

97 cular symptoms, including a low incidence of atrial arrhythmias and syncope.

98 sion (FC) is associated with a lower risk of atrial arrhythmias and thromboembolism, but it is unknow

99 fter controlling for time-varying effects of atrial arrhythmias and thromboprophylaxis.

100 ons in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might pr

101 Whether beta-blockers reduce atrial arrhythmias and, when added to an angiotensin-con

102 ardia, atrioventricular conduction block, or atrial arrhythmias) and dilated cardiomyopathy.

103 on class 1 or 3 antiarrhythmic drugs (11 for atrial arrhythmias), and 2 were on amiodarone as a bridg

104 ablation reinterventions in 13 patients for atrial arrhythmia, and cardioversions in 15 patients.

105 1 with control patients by age, sex, type of atrial arrhythmia, and date of DCCV.

106 Eight patients (12.7%) experienced atrial arrhythmia, and seven of the eight continued ther

107 ation for non-AV nodal reentrant tachycardia atrial arrhythmias, and 4 patients underwent AV nodal re

108 ed by the implanted valve, the occurrence of atrial arrhythmias, and associated comorbidities.

109 ornia, CHD was associated with incident CHF, atrial arrhythmias, and fetal growth restriction and com

110 associated with myocardial ischemic damage, atrial arrhythmias, and intra-atrial conduction delay.

111 icated in the development and maintenance of atrial arrhythmias, and is characterized by expansion of

112 ter COVID-19 mainly from pulmonary embolism, atrial arrhythmias, and venous thromboses.

113 Cardiac conduction defects and atrial arrhythmia are common to both, but LMNA variants

114 Patients likely to have severe stasis during atrial arrhythmia are those with left ventricular dilati

115 The most common atrial arrhythmias are atrial flutters, which are mainly

116 Ventricular and atrial arrhythmias are common after acute myocardial inf

117 Atrial arrhythmias are common both before and after surg

118 Although stress-induced atrial arrhythmias are common during exercise testing, t

119 Atrial arrhythmias are common early after atrial fibrill

120 Atrial arrhythmias are common in patients with implantab

121 directed at prophylaxis and acute therapy of atrial arrhythmias are discussed as are recommendations

122 Despite the young age, bradyarrhythmias and atrial arrhythmias are frequent and represent the cause

123 Atrial arrhythmias are frequent, and atrial flutter may

124 -term ventricular dysfunction, although late atrial arrhythmias are more likely to be encountered.

125 Atrial arrhythmias are the most common complication enco

126 l use for the treatment of heart failure and atrial arrhythmia, are potent inhibitors of DNA double-s

127 for IART now includes algorithms to prevent atrial arrhythmias, as well as antitachycardia pacing, w

128 arrhythmias lasting more than 24 hours; (2) atrial arrhythmias associated with severe symptoms requi

129 y sought to assess the types and patterns of atrial arrhythmias, associated factors, and age-related

130 ) and 159 (43%) patients had a recurrence of atrial arrhythmia at 12 and 24 months, respectively.

131 adjunctive PWI did not improve freedom from atrial arrhythmia at 12 months compared with pulmonary v

132 e did not significantly improve freedom from atrial arrhythmia at 12 months compared with PVI alone.

133 Meta-regression showed freedom from atrial arrhythmia at 12 months has improved over time, w

134 lmonary vein isolation plus freedom from any atrial arrhythmia at 12 months.

135 specified efficacy criteria for freedom from atrial arrhythmias at 12 months compared with pulmonary

136 Freedom from atrial arrhythmias at 12 months postprocedure was simila

137 th ICD undergoing elective cardioversion for atrial arrhythmias at 13 centers were randomized in 1:1

138 In vivo ECGs demonstrated increased atrial arrhythmia burden in spike-injected mice vs. cont

139 our understanding of the pathophysiology of atrial arrhythmias, but also to the development of AF ma

140 I drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsade de pointes.

141 cutely predispose otherwise normal hearts to atrial arrhythmias by dynamically disrupting Na(V)1.5-ri

142 of Scn2b in mice results in ventricular and atrial arrhythmias, consistent with reported SCN2B mutat

143 Education, body mass index, atrial arrhythmias, depression, and anxiety were indepen

144 tected atrial high-rate episodes (AHREs) are atrial arrhythmias detected by implanted cardiac devices

145 devices capable of sensitive and continuous atrial arrhythmia detection.

146 bidities, including coronary artery disease, atrial arrhythmias, diabetes mellitus, and chronic kidne

147 Conversion was defined as termination of the atrial arrhythmia during or within 60 min after infusion

148 dy was to determine if atrial ectopy (AE) or atrial arrhythmias during exercise are predictive of an

149 , 123 patients (31.9%) experienced recurrent atrial arrhythmias during the 1-year follow-up.

150 fic subsets of IAB have been associated with atrial arrhythmias, elevated thromboembolic stroke risk,

151 n arms was observed for the freedom from any atrial arrhythmia endpoint after one ablation.

152 Electrocardiograms during atrial arrhythmia episodes were reviewed by an electroph

153 also increases the susceptibility to develop atrial arrhythmias facilitated by spontaneous Ca(2+) rel

154 Each species displayed an irregular atrial arrhythmia following oil exposure, indicating a h

155 usly identified as providing a substrate for atrial arrhythmias following an acute inflammatory insul

156 tcome was freedom from clinically documented atrial arrhythmia for 30 seconds or longer after a 3-mon

157 vascular hospitalizations and recurrences of atrial arrhythmia for patients with AF.

158 Although sinus node dysfunction (SND) and atrial arrhythmias frequently coexist and interact, the

159 Patients with CA scheduled for DCCV for atrial arrhythmias from January 2000 through December 20

160 ry end point was freedom from any documented atrial arrhythmia greater than 30 seconds, after a singl

161 At 12 months, freedom from recurrence of atrial arrhythmia >30 seconds after 1 ablation procedure

162 The primary end point, freedom from left atrial arrhythmia >30 seconds without antiarrhythmic dru

163 point was the composite of recurrence of any atrial arrhythmia >30 seconds, additional ablation proce

164 Patients with a history of sustained atrial arrhythmia had a stronger baroreflex than those w

165 its effect on the electrical remodeling and atrial arrhythmia have never been explored.

166 oximately one-third of patients experiencing atrial arrhythmias have AF secondary to pulmonary vein-l

167 The incidence and mechanisms of these late atrial arrhythmias have not been thoroughly described.

168 iabetes, coronary artery disease, history of atrial arrhythmias, history of ventricular arrhythmias,

169 n any particular venous drainage pattern and atrial arrhythmia; however, patients with a separate ost

170 r hazard of first inappropriate shock due to atrial arrhythmia (HR: 0.37; 95% CI: 0.19-0.71; P = 0.00

171 ndings provide insights into how HF promotes atrial arrhythmia in association with atrial alternans.

172 IART is the most common presenting atrial arrhythmia in patients with congenital heart dise

173 7.8%), and it was due to bradyarrhythmias or atrial arrhythmias in 3 cases (60%).

174 included dyspnea or heart failure in 67% and atrial arrhythmias in 62%.

175 observed to immediately precede the onset of atrial arrhythmias in 73% of episodes.

176 The pathophysiology of atrial arrhythmias in ARVC remains unclear.

177 1 mumol/l was more effective in suppressing atrial arrhythmias in atria with reduced Pitx2c mRNA lev

178 m generator that is involved in Ca-dependent atrial arrhythmias in CPVT.

179 We compared the incidence of atrial arrhythmias in double-lung transplant patients ve

180 argue that it may explain the propensity for atrial arrhythmias in HF.

181 c electrophysiology (EP) and inducibility of atrial arrhythmias in MHC-TGFcys33ser transgenic mice (T

182 ein demonstrates increased susceptibility to atrial arrhythmias in mice where Notch has been transien

183 Similar odds were found for atrial arrhythmias in noncomplex (OR, 8.2; 95% CI, 3.0-2

184 mortality rate but no significant impact on atrial arrhythmias in patients >50 years of age.

185 s of direct-current cardioversion (DCCV) for atrial arrhythmias in patients with CA are unknown.

186 ess effective when used for the treatment of atrial arrhythmias in pediatric patients compared with i

187 intervals and the appearance of progressive atrial arrhythmias in RTEF-1 mice.

188 lay an important role in the pathogenesis of atrial arrhythmias in scenarios where VIP release is inc

189 ac melanocyte-like cells and did not develop atrial arrhythmias in the absence of DCT.

190 Atrial arrhythmias in this population can lead to decomp

191 d stimulation, Pitx2(null+/-) adult mice had atrial arrhythmias, including AFL and atrial tachycardia

192 ortant role in triggering and/or maintaining atrial arrhythmias, including atrial fibrillation (AF).

193 he sinoatrial node (SAN) as a participant in atrial arrhythmias, including atrial flutter (AFL) and a

194 tions of n-3 PUFA effects on ventricular and atrial arrhythmias, including studies in patients with i

195 Permanent atrial arrhythmias increased with age from 3.1% to 22.6%

196 evices used as prophylaxis for postoperative atrial arrhythmias; intravenous amiodarone for destabili

197 Prior studies suggest that stroke during atrial arrhythmia is related to stasis in either the bod

198 branch block (kappa 0.78), and very good for atrial arrhythmias (kappa 0.83).

199 kappa 0.56 to 0.70); and good/very good for atrial arrhythmias (kappa 0.84 and 0.79) and bundle bran

200 d of 3 months, AF recurrence (defined as any atrial arrhythmia lasting >/=30 s) was detected using se

201 mia recurrence within 1 year, defined as any atrial arrhythmia lasting more than 30 seconds after the

202 nd point of the study was a composite of (1) atrial arrhythmias lasting more than 24 hours; (2) atria

203 Atrial arrhythmias may reflect underlying left atrial en

204 ence of advanced age at operation, symptoms, atrial arrhythmias, mitral regurgitation or moderately i

205 albumin levels increased, with tinnitus and atrial arrhythmias more common, in the salsalate group c

206 ies toward developing arrhythmias, with left atrial arrhythmias more commonly observed.

207 Atrial arrhythmias occur commonly after cardiac surgery

208 Atrial arrhythmias occur frequently, and their occurrenc

209 Atrial arrhythmias occur in 20-40% of patients with arrh

210 Atrial arrhythmias occur in a large group of patients wi

211 Transient atrial arrhythmia occurred in 5 patients after implantat

212 after index ablation, freedom from recurrent atrial arrhythmia occurred in 59 patients (35.5%) random

213 New-onset atrial arrhythmias occurred in 4.4, 1.2, and 1.0 cases p

214 AF recurrences were defined as any atrial arrhythmia occurring within the first week (early

215 endage thrombus formation, but stroke during atrial arrhythmia occurs frequently in the absence of ap

216 ible ventricular tachycardia were history of atrial arrhythmia (odds ratio, 8.56 [95% CI, 2.43-34.73]

217 confidence interval, 1.01-11.6, P<0.05) and atrial arrhythmias (odds ratio, 5.1; 95% confidence inte

218 ry end point was freedom from any documented atrial arrhythmia of more than 30 seconds without antiar

219 patients (86%) and 5 patients were free from atrial arrhythmia off AADs and on AADs, respectively.

220 veins and freedom from recurrent symptomatic atrial arrhythmia off all antiarrhythmic drugs at 12 mon

221 The primary study end point was freedom from atrial arrhythmias off antiarrhythmic drugs at 1 year af

222 Atrial arrhythmia often has mechanisms different from th

223 ued for 24 h, did not decrease postoperative atrial arrhythmias or delirium in patients recovering fr

224 d with a 2.82-fold higher risk of developing atrial arrhythmias (p < 0.001), with no difference betwe

225 dure (p < 0.001) and higher freedom from all atrial arrhythmias (p = 0.003).

226 Age, atrial arrhythmia, pacemaker, biventricular enlargement,

227 Male sex is likely to increase the risk of atrial arrhythmia, particularly in those with desmosomal

228 ial fibrillation increases in prevalence and atrial arrhythmias progressively become permanent as the

229 d mechanical ventilation, pneumonia, sepsis, atrial arrhythmias, pulmonary embolism, need for early r

230 dom from initial failure of the procedure or atrial arrhythmia recurrence after a 90-day blanking per

231 dpoints included freedom from any documented atrial arrhythmia recurrence after a single procedure, A

232 on of aggressive BP treatment did not reduce atrial arrhythmia recurrence after catheter ablation for

233 At 12 months, 164 patients experienced atrial arrhythmia recurrence as documented by the ICM (1

234 Colchicine did not prevent atrial arrhythmia recurrence at 2 weeks (31% versus 32%;

235 A did not significantly improve freedom from atrial arrhythmia recurrence at long-term follow-up.

236 perior to drug therapy for the prevention of atrial arrhythmia recurrence in patients with paroxysmal

237 , imaging revealed no PV stenosis, and early atrial arrhythmia recurrence occurred in only 10/39 (25.

238 s following catheter ablation did not reduce atrial arrhythmia recurrence or AF-associated clinical e

239 ntified (n = 163), women had a higher 1-year atrial arrhythmia recurrence rate (adjusted hazard ratio

240 rial surface and 18 months of follow-up, the atrial arrhythmia recurrence rate was 15% after 1.4 +/-

241 Freedom from atrial arrhythmia recurrence was 79.6% (39/49 patients)

242 Atrial arrhythmia recurrence was defined as AF, atrial f

243 The primary end point was atrial arrhythmia recurrence within 1 year, defined as a

244 ly, resulted in no significant difference in atrial arrhythmia recurrence.

245 lation remained as independent predictors of atrial arrhythmia recurrence.

246 ation of distal CS to LA connections reduced atrial arrhythmia recurrences compared with standard pul

247 ean follow-up of 170+/-22 days, there were 7 atrial arrhythmia recurrences in the standard group and

248 mean follow-up of 170 22 days, there were 7 atrial arrhythmia recurrences in the standard group and

249 better among participants without documented atrial arrhythmia recurrences.

250 rders, but its applicability for terminating atrial arrhythmias remains largely unexplored.

251 d consequent cardiac edema to the genesis of atrial arrhythmias remains unknown.

252 2/RyR2 ratios can promote SR Ca(2+) leak and atrial arrhythmias, representing a potential novel thera

253 lmonary connection are at risk for recurrent atrial arrhythmia requiring catheter ablation.

254 0.39-0.81; P=0.002) and fewer recurrences of atrial arrhythmias (RR, 0.42; 95% CI, 0.33-0.53; P<0.000

255 In 20 additional patients with scar-related atrial arrhythmias, similar sequential mapping with both

256 Exclusion criteria were history of atrial arrhythmia, stroke, valvular or congenital heart

257 Rapid atrial arrhythmias such as atrial fibrillation (AF) pred

258 duce the incidence of spontaneous or induced atrial arrhythmias, suggesting that neuromodulation may

259 s and severity of sinus node dysfunction and atrial arrhythmia susceptibility align with PITX2 dosage

260 F-induced vascular leak can acutely increase atrial arrhythmia susceptibility by disrupting ID nanodo

261 caused by Tbx5 haploinsufficiency, including atrial arrhythmia susceptibility, prolonged action poten

262 vein(s) tended to have a higher frequency of atrial arrhythmia than those with other patterns (P =.05

263 The CS may also generate focal atrial arrhythmias that may play a role in triggering an

264 seful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery.

265 In patients with scar-related atrial arrhythmias, the total area of bipolar voltage <0

266 Conversion of atrial arrhythmia to sinus rhythm was the primary effica

267 FA) is a novel technology for catheter-based atrial arrhythmia treatment.

268 PMCA1(cko) hearts became more susceptible to atrial arrhythmias under rapid programmed electrical sti

269 creased vulnerability to tachypacing-induced atrial arrhythmia, validating the direct mechanistic lin

270 Incident CHF, atrial arrhythmias, ventricular arrhythmias, and materna

271 Median time to recurrent atrial arrhythmia was 0.53 years (interquartile range 0.

272 Single-procedure 12-month freedom from atrial arrhythmia was 65.3% (95% CI, 57.7%-73.9%) overal

273 -year Kaplan-Meier estimate for freedom from atrial arrhythmia was 78.1% (95% CI, 76.0%-80.0%); clini

274 One-year freedom from atrial arrhythmia was 80.2% (95% CI, 69.7%-87.4%) for th

275 Early recurrence of atrial arrhythmia was an independent predictor of late r

276 pattern was determined, and association with atrial arrhythmia was assessed with the chi(2) and Fishe

277 Freedom from atrial arrhythmia was evaluated continuously through 12

278 d 82% (LPeAF) at 1 year and freedom from all atrial arrhythmias was 77% (PAF), 75% (PeAF), and 57% (L

279 ntrol study design, CRP in 131 patients with atrial arrhythmias was compared with CRP in 71 control p

280 Any recurrence of atrial arrhythmias was defined as the primary end point

281 Freedom from atrial arrhythmias was demonstrated in 12 of 20 (60%) an

282 Recurrence of atrial arrhythmias was the primary endpoint.

283 subcutaneous ICDs, while first shocks due to atrial arrhythmia were more common with transvenous ICDs

284 Subjects with a history of atrial arrhythmia were more likely to be paced < or =92%

285 Thromboembolic complications and new-onset atrial arrhythmia were reviewed and classified by a blin

286 -proven ATTRwt, poor functional capacity and atrial arrhythmias were common clinical features.

287 cardiomyopathy was identified in 6 patients, atrial arrhythmias were detected in 9 patients, and sudd

288 thy-linked JPH2 mutation not associated with atrial arrhythmias were not significantly different from

289 tients admitted for dofetilide reloading for atrial arrhythmias were retrospectively reviewed.

290 chronization therapy with defibrillator, and atrial arrhythmia) were identified.

291 ardia, sinus pauses, and a susceptibility to atrial arrhythmias, which contribute to a phenotype rese

292 red eighty-seven patients with no history of atrial arrhythmia who had a preoperative BNP level and h

293 The primary end point was freedom from atrial arrhythmia with absence of persistent complicatio

294 gnificant difference, including freedom from atrial arrhythmia with/without antiarrhythmic medication

295 e Cav1.3-null mutant mice showed evidence of atrial arrhythmias, with inducible atrial flutter and fi

296 us node dysfunction, conduction defects, and atrial arrhythmias, with infrequent VPB and ventricular

297 ned to PVI with PWI were free from recurrent atrial arrhythmia without antiarrhythmic medication afte

298 s with PVI plus PWI were free from recurrent atrial arrhythmia without the use of AAD therapy vs 61.5

299 n of the LAA improved long-term freedom from atrial arrhythmias without increasing complications.

300 of recurrence was defined as the absence of atrial arrhythmias without using any antiarrhythmic agen