ライフサイエンスコーパス: tachyarrhythmia

1 ed cardiac arrest or spontaneous ventricular tachyarrhythmia).

2 2) and are associated with fatal ventricular tachyarrhythmia.

3 was an ICD shock for adjudicated ventricular tachyarrhythmia.

4 tion to treat potentially lethal ventricular tachyarrhythmia.

5 ulnerability to life-threatening ventricular tachyarrhythmia.

6 iate ICD discharge for sustained ventricular tachyarrhythmia.

7 isodes of spontaneous, sustained ventricular tachyarrhythmia.

8 isodes of spontaneous, sustained ventricular tachyarrhythmia.

9 idered to be from sudden cardiac arrest from tachyarrhythmia.

10 ventricular systolic dysfunction, or atrial tachyarrhythmia.

11 s of atrial tachycardia and supraventricular tachyarrhythmia.

12 e cardiac monitoring device to detect atrial tachyarrhythmia.

13 lation and a higher risk of supraventricular tachyarrhythmia.

14 italization for heart failure or ventricular tachyarrhythmia.

15 jor predisposing factor for life-threatening tachyarrhythmias.

16 ICD shock defined as a shock for ventricular tachyarrhythmias.

17 with a decreased incidence of postoperative tachyarrhythmias.

18 optimal management in catecholamine-induced tachyarrhythmias.

19 04) and had a comparable incidence of atrial tachyarrhythmias.

20 cardiomyopathy at risk of fatal ventricular tachyarrhythmias.

21 IAT or by the development of in-trial atrial tachyarrhythmias.

22 tion but continuing proneness to ventricular tachyarrhythmias.

23 on or life-threatening catecholamine-induced tachyarrhythmias.

24 ue for managing children with JET and atrial tachyarrhythmias.

25 rred in 7 animals, simulating a rapid atrial tachyarrhythmias.

26 t-CRT-D LVEF and ICD therapy for ventricular tachyarrhythmias.

27 oanatomic scar substrate of life-threatening tachyarrhythmias.

28 n death previously attributed to ventricular tachyarrhythmias.

29 7% versus 4%, P=0.01)-a difference driven by tachyarrhythmias.

30 s were recurrence of AF and organized atrial tachyarrhythmias.

31 tween patients with and those without atrial tachyarrhythmias.

32 omyopathy, as well as atrial and ventricular tachyarrhythmias.

33 n and a reduction in the risk of ventricular tachyarrhythmias.

34 s an invariable trigger of paroxysmal atrial tachyarrhythmias.

35 with increased susceptibility to ventricular tachyarrhythmias.

36 iods for shock delivery to treat ventricular tachyarrhythmias.

37 ity to spontaneous and inducible ventricular tachyarrhythmias.

38 entry and may have important implications in tachyarrhythmias.

39 t disease are at higher risk for ventricular tachyarrhythmias.

40 QT prolongation, and spontaneous ventricular tachyarrhythmias.

41 , particularly in the setting of monomorphic tachyarrhythmias.

42 syncope and sudden death due to ventricular tachyarrhythmias.

43 ts presenting consecutively with ventricular tachyarrhythmias.

44 n the initiation and perpetuation of various tachyarrhythmias.

45 iarrhythmic device therapies for ventricular tachyarrhythmias.

46 ce were inducible into sustained ventricular tachyarrhythmias.

47 80% of O-CKO mice were inducible into lethal tachyarrhythmias.

48 d risk of sudden death caused by ventricular tachyarrhythmias.

49 ty and mortality rates from recurrent atrial tachyarrhythmias.

50 had a history of documented sustained atrial tachyarrhythmias.

51 alternans and thereby preventing ventricular tachyarrhythmias.

52 notype of ischemiainduced lethal ventricular tachyarrhythmias.

53 t of ventricular as well as supraventricular tachyarrhythmias.

54 f AF in patients presenting with ventricular tachyarrhythmias.

55 aphic risk factors in predicting ventricular tachyarrhythmias.

56 opriate ICD therapy or sustained ventricular tachyarrhythmias.

57 ectrical activation that promote ventricular tachyarrhythmias.

58 nary artery disease and unstable ventricular tachyarrhythmias.

59 ch may promote susceptibility to ventricular tachyarrhythmias.

60 may occur during catheter ablation of atrial tachyarrhythmias.

61 onally leading to unstable, self-terminating tachyarrhythmias.

62 ents, including life-threatening ventricular tachyarrhythmias.

63 increases in ventricular or supraventricular tachyarrhythmias.

64 d susceptibility to life-threatening cardiac tachyarrhythmias.

65 ality and appropriate shocks for ventricular tachyarrhythmias.

66 to epicardial fat pads for preventing atrial tachyarrhythmias.

67 oint (n=22 patients; 19 atrial/2 ventricular tachyarrhythmia, 1 death) included RV LGE presence and e

68 easons included the development of an atrial tachyarrhythmia (18%), loss of left ventricular capture

69 mia incidence between groups became similar: tachyarrhythmias (29% versus 31%; P=0.66), tachyarrhythm

70 edetomidine demonstrated significantly fewer tachyarrhythmias (29% versus 38%; P<0.001), tachyarrhyth

71 an in the placebo group had supraventricular tachyarrhythmia (3.1% vs. 0.4%; absolute difference, 2.7

72 tions of patients with sustained ventricular tachyarrhythmia (39.7% versus 48.2%; P=0.050) and approp

73 art rates were more likely to develop atrial tachyarrhythmias, a dual-chamber rate-modulated pacing m

74 rrence of symptomatic or asymptomatic atrial tachyarrhythmia (AF, atrial flutter, or atrial tachycard

75 risk of atrial fibrillation or other atrial tachyarrhythmias (AF/AT), or if postimplantation AF/AT m

76 12.9+/-9.4 months, and any documented atrial tachyarrhythmia after the 3-month blanking period was cl

77 rhythms and bradycardia-related ventricular tachyarrhythmias after AVB in mice.

78 ly meaningful difference in the incidence of tachyarrhythmias after congenital heart surgery, it may

79 herapy due to atrial fibrillation and atrial tachyarrhythmias, also evaluated as ATP or shock therapy

80 in the risk of life-threatening ventricular tachyarrhythmias among patients with NICM.

81 uce the risk of life-threatening ventricular tachyarrhythmias among patients with nonischemic cardiom

82 er, atrial tachycardia, and supraventricular tachyarrhythmias) among patients enrolled in MADIT-CRT (

83 During tachyarrhythmias, anatomically complex and simplified mo

84 itial treatment of AF, coexistence of atrial tachyarrhythmia and (2) progression of paroxysmal to (lo

85 dysplasia/cardiomyopathy is associated with tachyarrhythmia and an increased risk of sudden death.

86 dary outcomes included sustained ventricular tachyarrhythmia and appropriate ICD therapy.

87 se-limiting toxicities were supraventricular tachyarrhythmia and myelosuppression.

88 sodes, with correct detection of ventricular tachyarrhythmia and subsequent shock therapy.

89 outcomes measured were recurrence of atrial tachyarrhythmia and the incidence of adverse events.

90 98 patients, representing 32% of ventricular tachyarrhythmias and 76% of those that would be detected

91 ressor in selected patients with low risk of tachyarrhythmias and absolute or relative bradycardia.

92 ess rate of restoring sinus rhythm was high, tachyarrhythmias and bradyarrhythmias complicating DCCV

93 In-utero management of tachyarrhythmias and conduction system disease has impro

94 tion wavefronts during episodes of simulated tachyarrhythmias and fibrillatory arrhythmias, defined a

95 lecular and mechanistic insights into atrial tachyarrhythmias and identifies Kir3.x as a promising at

96 w the likely mechanism by which they lead to tachyarrhythmias and indicate a distinct role of I(KS) k

97 racking echocardiography predict ventricular tachyarrhythmias and provide incremental prognostic info

98 s included symptomatic recurrences of atrial tachyarrhythmias and quality of life measures assessed b

99 athetic stimulation precipitates ventricular tachyarrhythmias and sudden cardiac death except in Brug

100 Ventricular tachyarrhythmias and sudden cardiac death show a circadi

101 art failure have been plagued by ventricular tachyarrhythmias and sudden cardiac death.

102 redisposes to the development of ventricular tachyarrhythmias and sudden death.

103 sudden death and, in some cases, ventricular tachyarrhythmias and waxing and waning cardiomyopathy.

104 riefly discuss efforts to address aspects of tachyarrhythmia, and review advances in creating a biolo

105 ure, myocardial infarction, supraventricular tachyarrhythmia, and ventricular tachycardia or fibrilla

106 currence of atrial fibrillation, ventricular tachyarrhythmias, and stroke and length of stay after ca

107 Early recurrences (ERs) of atrial tachyarrhythmia are common after catheter ablation of at

108 Ventricular tachyarrhythmias are characteristic of giant cell myocar

109 ty of cardiovascular deaths, and ventricular tachyarrhythmias are mainly associated with severe metab

110 Tachyarrhythmias are more common in the Brugada syndrome

111 s therefore a relatively ideal agent against tachyarrhythmia at 37 degrees C, but should be more caut

112 n for EAM, and inducibility of any sustained tachyarrhythmia at the end of EAM procedure were identif

113 resulted in a lower rate of recurrent atrial tachyarrhythmias at 2 years.

114 strates a high rate of sustained ventricular tachyarrhythmias at 3 months in at-risk patients who are

115 myocardial biopsy and history of ventricular tachyarrhythmias at presentation (P<0.05 for all).

116 ac resynchronization therapy (CRT) on atrial tachyarrhythmia (AT) susceptibility in patients with lef

117 ndary endpoints included freedom from atrial tachyarrhythmias (AT) at 6 and 12 months, periprocedural

118 a subsequent reduction in the risk of atrial tachyarrhythmias (AT).

119 However, atrial tachyarrhythmias (ATA) are a common early complication a

120 he first documented recurrence of any atrial tachyarrhythmia (atrial fibrillation, atrial flutter, or

121 ical end point comprised new-onset sustained tachyarrhythmia (atrial/ventricular) or decompensated he

122 ng an association between subclinical atrial tachyarrhythmias (ATs) detected by cardiac implantable e

123 electrophysiologic studies for induction of tachyarrhythmias based on these trials.

124 ng upstream therapies to abort a ventricular tachyarrhythmia before its onset.

125 was observed in 12-month freedom from atrial tachyarrhythmias between an index ablative approach of s

126 polarizations (EADs) are a known trigger for tachyarrhythmias, but the conditions that cause surround

127 patients to an increased risk of ventricular tachyarrhythmias, but the incidence of cardiac or sudden

128 The rate of sustained ventricular tachyarrhythmias by 3 months was 3% among patients with

129 termination of life-threatening ventricular tachyarrhythmias by an ICD.

130 These tachyarrhythmias can also begin during cardiopulmonary r

131 Atrial and ventricular tachyarrhythmias can be perpetuated by up-regulation of

132 fectiveness and safety of terminating atrial tachyarrhythmias clinically.

133 a total of 14 patients (11%) had ventricular tachyarrhythmias, compared with 5 (3.8%) in the precedin

134 ays post-9/11, 16 patients (8%) demonstrated tachyarrhythmias, compared with only seven (3.5%) in the

135 d enhances the risk of malignant ventricular tachyarrhythmias complicating AVB.

136 ic mutation in a familial syndrome of atrial tachyarrhythmia, conduction system disease (CSD), and DC

137 ts from the Creighton University ventricular tachyarrhythmia database.

138 One-year freedom from symptomatic atrial tachyarrhythmia defined by continuous rhythm monitoring

139 One-year freedom from atrial tachyarrhythmia defined by continuous rhythm monitoring

140 outcome event, 11 had had subclinical atrial tachyarrhythmias detected by 3 months, and none had had

141 By 3 months, subclinical atrial tachyarrhythmias detected by implanted devices had occur

142 0/17 (59%) experienced sustained ventricular tachyarrhythmias during follow-up and 3 received intraca

143 mber of spontaneous nonsustained ventricular tachyarrhythmias during stage 2 and the occurrence of is

144 2 and the occurrence of ischemic ventricular tachyarrhythmias during stage 3 also were significantly

145 ith and those without device-detected atrial tachyarrhythmias during the first year.

146 ts for 3 months to detect subclinical atrial tachyarrhythmias (episodes of atrial rate >190 beats per

147 solation (PVI) as early recurrence of atrial tachyarrhythmia (ERAT) may be due to transient proarrhyt

148 was 83.0% for the first clinical ventricular tachyarrhythmia event; there were no differences in shoc

149 brillation (AF) in patients with ventricular tachyarrhythmias exist.

150 n result from coronary artery abnormalities, tachyarrhythmias, exposure to infection or toxins, or se

151 events were strongly associated with atrial tachyarrhythmia, extracardiac arteriopathy, and a high b

152 Premature stimulation induced ventricular tachyarrhythmia/fibrillation >60 seconds in 6 of 8 shams

153 incidence of inducible sustained ventricular tachyarrhythmia/fibrillation in canine infarcts.

154 reated by the WCD in response to ventricular tachyarrhythmia/fibrillation.

155 strong predictor of spontaneous ventricular tachyarrhythmia following ST-segment-elevation myocardia

156 n resulted in better 2-year organized atrial tachyarrhythmia-free survival (71% [62%-79%] versus 60%

157 Organized atrial tachyarrhythmia-free survival was similar after SRI and

158 ctional ectopic tachycardia [JET] and atrial tachyarrhythmias) frequently complicate recovery from op

159 Magnet response and tachyarrhythmia functions were disabled.

160 Tachyarrhythmia functions were disabled.

161 Patients with atrial tachyarrhythmia >/=30 s within the 3-month blanking peri

162 t and arrhythmic death caused by ventricular tachyarrhythmias >/=240 per minute was observed in 7 and

163 At 1 year, a recurrence of atrial tachyarrhythmia had occurred in 66 of 154 patients (42.9

164 Symptomatic atrial tachyarrhythmia had recurred in 11.0% of the patients wh

165 Ventricular tachyarrhythmias had a low positive and relatively high

166 had the Fontan procedure, those with atrial tachyarrhythmias had longer P-wave duration (159+/-28 ve

167 Patients with atrial tachyarrhythmias had longer paced (153+/-29 versus 145+/

168 Using more intervals to detect ventricular tachyarrhythmias has been associated with reducing unnec

169 Radiofrequency (RF) ablation treatment for tachyarrhythmias has been available only for the past 15

170 reases the incidence of postoperative atrial tachyarrhythmias have had mixed results and were not spe

171 ecutive patients presenting with ventricular tachyarrhythmias (i.e. ventricular tachycardia and fibri

172 ffect of both history of intermittent atrial tachyarrhythmias (IAT) and in-trial IAT on the risk of h

173 yocarditis presented as nonfatal ventricular tachyarrhythmia in 10 patients and as a fatal cardiac ar

174 There was recurrence of atrial tachyarrhythmia in 222 of 785 (28%) patients who underwe

175 aracterized by propensity toward ventricular tachyarrhythmia in the setting of well-preserved morphol

176 significant reduction in bradyarrhythmia and tachyarrhythmia in the whole group.

177 in 166 patients (19%), sustained ventricular tachyarrhythmias in 17 (2%), and permanent pacemakers we

178 d pre-specified protocol induced ventricular tachyarrhythmias in 40% of patients: arrhythmia inducibi

179 ere was a total of 120 sustained ventricular tachyarrhythmias in 41 patients, of whom 54% received ap

180 ppress sympathetic outflow and reduce atrial tachyarrhythmias in ambulatory dogs.

181 reduces the incidences of paroxysmal atrial tachyarrhythmias in ambulatory dogs.

182 suppressed catecholamine-induced ventricular tachyarrhythmias in Casq2-/- mice, whereas N-methyl flec

183 n (SCS) reduces the incidence of ventricular tachyarrhythmias in experimental models.

184 lead ECGs independently predicts ventricular tachyarrhythmias in ICD-eligible cardiomyopathy patients

185 lar rate during postoperative JET and atrial tachyarrhythmias in our young canine open heart surgery

186 as associated with the development of atrial tachyarrhythmias in pacemaker patients.

187 assist device (LVAD) therapy on ventricular tachyarrhythmias in patients with advanced congestive he

188 associated with greater risk of ventricular tachyarrhythmias in patients with cardiovascular disease

189 the treatment strategy of choice for atrial tachyarrhythmias in patients with congenital heart disea

190 y little apparent role in the maintenance of tachyarrhythmias in the rabbit ventricles and, contrary

191 In contrast, tachyarrhythmias in wild-type hearts (WT) were short-liv

192 LGE-SI is a better predictor of ventricular tachyarrhythmias (including nonsustained ventricular tac

193 ihood and increased frequency of ventricular tachyarrhythmias (including NSVT) on ambulatory Holter E

194 The incidence of ventricular tachyarrhythmia, including ventricular fibrillation, and

195 f atrial electrophysiology and induce atrial tachyarrhythmias, including atrial tachycardia and atria

196 The frequency of tachyarrhythmias increased significantly for the 30 days

197 orts of R-on-T extrasystoles and ventricular tachyarrhythmia induction as a result of biventricular p

198 ective shock delivery to convert ventricular tachyarrhythmia into sinus rhythm.

199 Fatal tachyarrhythmias invariably occurred in the presence of

200 In 8 of 9 patients with >1 event, atrial tachyarrhythmia, itself a known risk factor for mortalit

201 endpoint was any post-90-day blanking atrial tachyarrhythmias lasting 30 s or longer.

202 Patients with atrial tachyarrhythmias late after Fontan operation have longer

203 Ventricular tachyarrhythmias long enough to cause implantable cardio

204 ; 95% confidence interval, 0.60 to 0.95) and tachyarrhythmia mortality (adjusted hazard ratio, 0.40;

205 The cardiac and tachyarrhythmia mortality reductions were evident in sub

206 The reduction in tachyarrhythmia mortality with ICD therapy was similar i

207 elicited infrequent monomorphic ventricular tachyarrhythmias (MVT), and dominant frequencies (DFs) d

208 -defibrillator interventions for ventricular tachyarrhythmias (n=31), resuscitated out-of-hospital ca

209 monly with ICD interventions for ventricular tachyarrhythmias (n=33) or heart transplantation for adv

210 nfarction and 1 hypotensive supraventricular tachyarrhythmia), neither of which were fatal or life th

211 Ventricular tachyarrhythmia occurred in 35% of the patients in the l

212 The tachyarrhythmias occurred primarily within 8 days after

213 a, congestive heart failure, and ventricular tachyarrhythmias occurring during the index hospitalizat

214 The time to the first documented atrial tachyarrhythmia of more than 30 seconds (symptomatic or

215 Programming of ICD therapies for tachyarrhythmias of 200 beats per minute or higher or wi

216 We studied prevalence and frequency of tachyarrhythmias on 24-h ambulatory Holter electrocardio

217 f patients presenting with index ventricular tachyarrhythmias on admission (70% paroxysmal, 9% persis

218 Ventricular tachyarrhythmias on Holter electrocardiograms (ECG) have

219 reventing sudden death caused by ventricular tachyarrhythmia or fibrillation.

220 Significant clinical alerts (sustained tachyarrhythmias or an elevated fluid index value) were

221 indications, such as for known or suspected tachyarrhythmias or bradyarrhythmias.

222 w tract) per 24 h; and symptoms, ventricular tachyarrhythmias, or attenuated blood pressure response

223 nt was freedom from recurrence of any atrial tachyarrhythmia, outside a 90-day blanking period, at 12

224 tion is associated with an increased risk of tachyarrhythmia, palpitations, syncope, and sudden death

225 ortant reduction in all bradyarrhythmias and tachyarrhythmias pre-cardioneuroablation versus post-car

226 lity on the ECG and a diagnosis of an atrial tachyarrhythmia predict sudden death.

227 aneous and inducible polymorphic ventricular tachyarrhythmias (PVTs).

228 G features preceding polymorphic ventricular tachyarrhythmias (PVTs).

229 : tachyarrhythmias (29% versus 31%; P=0.66), tachyarrhythmias receiving intervention (14% versus 17%;

230 tachyarrhythmias (29% versus 38%; P<0.001), tachyarrhythmias receiving intervention (14% versus 23%;

231 Atrial tachyarrhythmias recurred in 28 PVI-only group patients

232 tion group patients, for 1-year freedom from tachyarrhythmia recurrence after a single ablation proce

233 l PVI in achieving freedom from total atrial tachyarrhythmia recurrence at long-term follow-up.

234 or persistent atrial fibrillation and atrial tachyarrhythmia recurrences despite previous successful

235 found a significantly higher risk of atrial tachyarrhythmia recurrences in patients with ECs compare

236 MIL ablation may reduce organized atrial tachyarrhythmia recurrences.

237 to 8.78) and a clinical diagnosis of atrial tachyarrhythmia (relative risk, 5.18; 95% CI, 2.28 to 11

238 igher risks for life-threatening ventricular tachyarrhythmias remain poorly understood.

239 Subclinical atrial tachyarrhythmias remained predictive of the primary outc

240 ut the rates of exercise intolerance, atrial tachyarrhythmias, right ventricular dysfunction, and pul

241 The occurrence of ventricular tachyarrhythmias seems to follow circadian, daily, and s

242 underlie a circadian pattern of ventricular tachyarrhythmia/sudden cardiac death.

243 ed as predictors of death due to ventricular tachyarrhythmias/sudden death in patients with nonischem

244 ery bypass graft provided substantial atrial tachyarrhythmia suppression both early as well as during

245 Children with incessant tachyarrhythmias (supraventricular arrhythmias [n=26], j

246 enefits, CRT may also ameliorate ventricular tachyarrhythmia susceptibility in HF patients.

247 zation therapy's (CRT) impact on ventricular tachyarrhythmia susceptibility in patients who, due to w

248 anner (relative to date) for all ventricular tachyarrhythmias (tachycardia or fibrillation) triggerin

249 Nonpost-operative JET is a rare tachyarrhythmia that is associated with a high rate of m

250 s can automatically detect and record atrial tachyarrhythmias that may be asymptomatic.

251 e substrate for the development of reentrant tachyarrhythmias that underlie rapid polymorphic VT/VF.

252 ients to assess the incidence of ventricular tachyarrhythmias, the occurrence of shocks, and possible

253 success rates and have made more complicated tachyarrhythmias treatable with ablation.

254 re for noncardiac surgery recommend that the tachyarrhythmia treatment algorithms of the ICD should b

255 The occurrence of ventricular tachyarrhythmias triggering ICD therapy in the 30 days b

256 and forty-four patients with CHD and atrial tachyarrhythmias undergoing radiofrequency catheter abla

257 CPAP nonusers." The recurrence of any atrial tachyarrhythmia, use of antiarrhythmic drugs, and need f

258 hip between RWT and the risk for ventricular tachyarrhythmia (VA) in patients enrolled in the MADIT-C

259 Programming of ventricular tachyarrhythmia (ventricular tachycardia [VT] or ventric

260 ionship between QRSd and risk of ventricular tachyarrhythmias (ventricular tachycardia/ventricular fi

261 conduction delay, and malignant ventricular tachyarrhythmias (ventricular tachycardia/ventricular fi

262 A total of 34 ventricular tachyarrhythmia/ventricular fibrillation episodes (20 in

263 e observed irrespective of index ventricular tachyarrhythmia (VT or VF), LV dysfunction or presence o

264 f complete heart block (CHB) and ventricular tachyarrhythmia (VT) after ASA to better understand when

265 Spontaneous ventricular tachyarrhythmia (VT)/ventricular fibrillation (VF) event

266 blation (CA) in the treatment of ventricular tachyarrhythmias (VT) in patients with an ICD.

267 eart disease (SHD) and recurrent ventricular tachyarrhythmias (VT).

268 he risk of life-threatening (LT) ventricular tachyarrhythmia (VTA) in patients with LMNA mutations is

269 nd the spontaneous initiation of ventricular tachyarrhythmias (VTA) in humans are unknown.

270 ization (ER) characteristics and ventricular tachyarrhythmias (VTAs) in patients with acute myocardia

271 of heart failure (HF) or death, ventricular tachyarrhythmias (VTAs), and death.

272 6%-50%, and >50%) on outcomes of ventricular tachyarrhythmias (VTAs), VTA >/=200 bpm, ICD shock, hear

273 (CRT) and the risk of subsequent ventricular tachyarrhythmias (VTAs).

274 n Ca(2+) waves, a major cause of ventricular tachyarrhythmias (VTs) and sudden death.

275 d activities, and stress-induced ventricular tachyarrhythmias (VTs) in a mouse model of cardiac ryano

276 with an enhanced propensity for ventricular tachyarrhythmias (VTs) under conditions of metabolic dem

277 One-year freedom from symptomatic atrial tachyarrhythmia was 77.2% in patients without ER compare

278 collapse rhythm was evaluated, a ventricular tachyarrhythmia was observed in 9.

279 embolism associated with subclinical atrial tachyarrhythmias was 13%.

280 patient with abolition of lethal ventricular tachyarrhythmias was 6:1, similar to randomized defibril

281 ences of atrial fibrillation or other atrial tachyarrhythmias was evaluated at the end of the follow-

282 First shock efficacy for ventricular tachyarrhythmias was high regardless of baseline DFT tes

283 Subclinical atrial tachyarrhythmias were associated with an increased risk

284 mice, spontaneous and inducible ventricular tachyarrhythmias were common, occurring in 60% and 86%,

285 terventions for life-threatening ventricular tachyarrhythmias were frequent and highly effective in r

286 ons terminating life-threatening ventricular tachyarrhythmias were frequent.

287 Adrenergically triggered tachyarrhythmias were more frequent in RyR2-V2475F(+/-)

288 tion, but appropriate shocks for ventricular tachyarrhythmias were noted only in a minority of patien

289 HCM cohort, ventricular and supraventricular tachyarrhythmias were particularly frequent and demonstr

290 ms (an indicator of potential of ventricular tachyarrhythmia) were reported.

291 siologic mechanism of atrial and ventricular tachyarrhythmias, whether they are sustained, nonsustain

292 s were incorrectly classified as ventricular tachyarrhythmia, which led to inappropriate shock delive

293 Ventricular tachyarrhythmias, which are difficult to induce in the h

294 Second, the patients with atrial tachyarrhythmias who had the Fontan procedure had larger

295 st 3 decades in the treatment of ventricular tachyarrhythmias with device-based therapy, sudden cardi

296 (ICD) therapy terminating potentially lethal tachyarrhythmias, with no difference in frequency of eve

297 one third of the patients had a ventricular tachyarrhythmia within the last hour of life.

298 n wild-type mice), and malignant ventricular tachyarrhythmias within minutes of ischemia.

299 y reduced sudden death caused by ventricular tachyarrhythmias without affecting heart failure deaths

300 Subclinical atrial tachyarrhythmias, without clinical atrial fibrillation,