ライフサイエンスコーパス: ventricular arrhythmia

1 failure, stroke, and sudden cardiac death or ventricular arrhythmia.

2 ify factors that may predispose to malignant ventricular arrhythmia.

3 nt with the absence of isoproterenol-induced ventricular arrhythmia.

4 RAGE suppression particularly on IR-induced ventricular arrhythmia.

5 GE delivery is protective against IR-induced ventricular arrhythmia.

6 d preserved cardiac function experienced any ventricular arrhythmia.

7 dissociating CaM from RyR2 can cause severe ventricular arrhythmia.

8 0.05), suggesting increased vulnerability to ventricular arrhythmia.

9 r heart failure, and sudden cardiac death or ventricular arrhythmia.

10 tion carriers without histories of sustained ventricular arrhythmia.

11 of human heart disease involving spontaneous ventricular arrhythmia.

12 mapping is used to localize the exit site of ventricular arrhythmia.

13 eve nondamaging and pain-free termination of ventricular arrhythmia.

14 y is a genetic disease with a proclivity for ventricular arrhythmias.

15 were enzymatic infarct size and incidence of ventricular arrhythmias.

16 aminergic surge, Scn8a(N1768D/+) mice showed ventricular arrhythmias.

17 corrected QT (QTc) prolongation and complex ventricular arrhythmias.

18 y with dilated cardiomyopathy and atrial and ventricular arrhythmias.

19 Patients with LVADs are at high risk for ventricular arrhythmias.

20 re were 11 278 appropriate ICD detections of ventricular arrhythmias.

21 rosis and cardiomyocyte apoptosis, and fewer ventricular arrhythmias.

22 tion slowing and increased susceptibility to ventricular arrhythmias.

23 tients exhibit left ventricular dilation and ventricular arrhythmias.

24 areas) may be used to estimate the risk for ventricular arrhythmias.

25 leads, and all had right bundle-branch block ventricular arrhythmias.

26 vel, increased susceptibility to polymorphic ventricular arrhythmias.

27 ged ventricular repolarization, and provoked ventricular arrhythmias.

28 and increased susceptibility to polymorphic ventricular arrhythmias.

29 function is induced or mediated by atrial or ventricular arrhythmias.

30 of supraventricular tachycardias (SVTs) and ventricular arrhythmias.

31 presenting alive (72%) experienced sustained ventricular arrhythmias.

32 r patients who are suffering from refractory ventricular arrhythmias.

33 tion toward improved prediction of malignant ventricular arrhythmias.

34 ) to study potential mechanisms of increased ventricular arrhythmias.

35 ailure, perforation, tamponade, or sustained ventricular arrhythmias.

36 kalaemia is a risk factor for development of ventricular arrhythmias.

37 Src activation, gap junction remodeling, and ventricular arrhythmias.

38 inked to a long list of inherited atrial and ventricular arrhythmias.

39 vel, increased susceptibility to polymorphic ventricular arrhythmias.

40 ions, TG animals were resistant to triggered ventricular arrhythmias.

41 eases characterized by catecholamine-induced ventricular arrhythmias.

42 wall stress, and apoptosis without inducing ventricular arrhythmias.

43 ibrillation, conductional abnormalities, and ventricular arrhythmias.

44 it gene are associated with life-threatening ventricular arrhythmias.

45 milial forms of exercise-induced polymorphic ventricular arrhythmias.

46 s accompanied with increased inducibility of ventricular arrhythmias.

47 afterdepolarization, triggered activity, and ventricular arrhythmias.

48 al duration and increasing susceptibility to ventricular arrhythmias.

49 ts with MVP who experienced life-threatening ventricular arrhythmias.

50 offer a noninvasive option to help suppress ventricular arrhythmias.

51 e, which is associated with life-threatening ventricular arrhythmias.

52 nduction velocity slowing, and the reentrant ventricular arrhythmias.

53 tients to mitigate the risks associated with ventricular arrhythmias.

54 tramural scar and to correlate the scar with ventricular arrhythmias.

55 turbance, atrial fibrillation, and malignant ventricular arrhythmias.

56 as not observed among patients who had prior ventricular arrhythmias.

57 ling and relevant mechanisms predisposing to ventricular arrhythmias.

58 of NSVT were not associated with ICD-treated ventricular arrhythmias.

59 le of myeloperoxidase for the development of ventricular arrhythmias.

60 est in patients at risk for life-threatening ventricular arrhythmias.

61 ICDs in patients without a history of prior ventricular arrhythmias.

62 using abnormal Ca(2+)-handling and malignant ventricular arrhythmias.

63 depolarisations (EADs), which trigger lethal ventricular arrhythmias.

64 tricular dysfunction is a known predictor of ventricular arrhythmias.

65 been proposed as an independent predictor of ventricular arrhythmias.

66 neous type 1 electrocardiogram and inducible ventricular arrhythmias.

67 (2+) (Ca) mishandling can initiate triggered ventricular arrhythmias.

68 RVD/C (40% versus 18%), experience sustained ventricular arrhythmias (11% versus 1%), and die from a

69 dle-branch block type or polymorphic complex ventricular arrhythmias (22 females; age range, 28-43 ye

70 5%), atrial arrhythmias (58%), and malignant ventricular arrhythmias (26%).

71 ients presented predominantly with sustained ventricular arrhythmias (268; 61%).

72 ients (16 heart failure hospitalizations, 10 ventricular arrhythmias, 5 cardiac deaths, and 5 thrombo

73 /tibia length; P<0.05), and strongly reduced ventricular arrhythmias (-70+/-22% premature ventricular

74 w QRS voltages on electrocardiography (33%); ventricular arrhythmias (82%); and frequent sudden cardi

75 METHODS AND Patients (n=68) undergoing ventricular arrhythmia ablation between March 2012 and J

76 s >40 mg were associated with lower risks of ventricular arrhythmia (adjusted hazard ratio=0.68, 95%

77 21-40 mg were associated with lower risks of ventricular arrhythmia (adjusted hazard ratio=0.80, 95%

78 R, 2.24; 95% CI, 2.05-2.43), sudden death or ventricular arrhythmia (aHR, 1.69; 95% CI, 1.44-1.98), a

79 ociated with future cardiovascular death and ventricular arrhythmia among patients referred to MRI fo

80 Incidence of ventricular arrhythmias among patients randomized to CRT

81 METHODS AND All ventricular arrhythmias among RAFT study participants we

82 opulation-based study comparing the risks of ventricular arrhythmia and cardiovascular death among pa

83 the small but significant increased risk of ventricular arrhythmia and cardiovascular death when pre

84 d with significant increases in the risks of ventricular arrhythmia and cardiovascular death.

85 ardiac sarcoidosis have an increased risk of ventricular arrhythmia and death.

86 emonstrates successful conversion of induced ventricular arrhythmia and reasonable rhythm discriminat

87 iated with an autosomal dominant syndrome of ventricular arrhythmia and sudden death that can present

88 individuals had a first episode of malignant ventricular arrhythmias and 33 (11%) had an end-stage he

89 ARVD/C) is a cardiomyopathy characterized by ventricular arrhythmias and an abnormal right ventricle.

90 an inherited cardiomyopathy characterized by ventricular arrhythmias and an increased risk of sudden

91 llenging because of concern about triggering ventricular arrhythmias and because a clinical benefit h

92 prolongation is a heritable risk factor for ventricular arrhythmias and can predispose to sudden dea

93 tion carriers are at high risk for malignant ventricular arrhythmias and end-stage heart failure, wit

94 sociated with an increased risk of malignant ventricular arrhythmias and end-stage heart failure.

95 Serious adverse effects (including ventricular arrhythmias and hypertension) are rare, and

96 35 athletes (80% men, age: 14-48 years) with ventricular arrhythmias and isolated LV subepicardial/mi

97 od1(-/-)-PMI mice showed significantly fewer ventricular arrhythmias and lower mortality after isopro

98 triction and complex CHD was associated with ventricular arrhythmias and maternal in-hospital mortali

99 sed relationships between citalopram use and ventricular arrhythmias and mortality.

100 ic resonance (group A) with 38 athletes with ventricular arrhythmias and no LGE (group B) and 40 heal

101 In vivo, Holter monitoring revealed ventricular arrhythmias and SAN dysfunctions in post-lef

102 /transporter dysfunction that predisposes to ventricular arrhythmias and SCD.

103 l study, extensive in 3 women with atrial or ventricular arrhythmias and short HV interval, and massi

104 massive in 6 men with atrial fibrillation or ventricular arrhythmias and short HV.

105 = 0.002); and 5) similar rates of malignant ventricular arrhythmias and sudden cardiac death (p = 0.

106 QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) a

107 Mitral valve prolapse (MVP) may present with ventricular arrhythmias and sudden cardiac death (SCD) e

108 The incidence and prevalence of sustained ventricular arrhythmias and sudden cardiac death are low

109 D), which is considered to be a precursor of ventricular arrhythmias and sudden cardiac death.

110 bit an abnormal ECG pattern and are prone to ventricular arrhythmias and sudden cardiac death.

111 nd subsequent increase in the propensity for ventricular arrhythmias and sudden cardiac death.

112 ) has been implicated in the pathogenesis of ventricular arrhythmias and sudden cardiac death.

113 larization abnormalities have been linked to ventricular arrhythmias and sudden cardiac death.

114 s and emotion have long been associated with ventricular arrhythmias and sudden death in animal model

115 e, which predisposes affected individuals to ventricular arrhythmias and sudden death.

116 mortality, recurrent myocardial Infarction, ventricular arrhythmia, and cerebrovascular accident dur

117 e of death, recurrent myocardial Infarction, ventricular arrhythmia, and cerebrovascular accident dur

118 known to cause torsade des pointes and other ventricular arrhythmias, and a recent observational stud

119 olic events, heart failure hospitalizations, ventricular arrhythmias, and cardiac death.

120 rcoidosis (CS) are conduction abnormalities, ventricular arrhythmias, and heart failure.

121 ture ventricular contractions, non-sustained ventricular arrhythmias, and increased heart rate variab

122 Incident CHF, atrial arrhythmias, ventricular arrhythmias, and maternal mortality were unc

123 comes of atrial fibrillation (AF), sustained ventricular arrhythmias, and sudden cardiac death are re

124 ar systolic dysfunction, AV block, atrial or ventricular arrhythmias, and sudden cardiac death.

125 Ventricular arrhythmias are among the most severe compli

126 Ventricular arrhythmias are associated with both increas

127 Preceding cardiac dysfunction or ventricular arrhythmias are associated with increased mo

128 Ventricular arrhythmias are the cardinal and typically e

129 Although ventricular arrhythmias are traditionally thought to con

130 cutaneous epicardial mapping and ablation of ventricular arrhythmias arising from the left ventricula

131 ive patients (49 +/- 14 years; 39% men) with ventricular arrhythmias arising from the left ventricula

132 Percutaneous epicardial ablation of ventricular arrhythmias arising from the left ventricula

133 instrumentation for mapping and ablation of ventricular arrhythmias arising from the left ventricula

134 Ventricular arrhythmias as a result of unintentional blo

135 activated neutrophils, can induce atrial and ventricular arrhythmias as well as repolarization abnorm

136 iac Purkinje cells are important triggers of ventricular arrhythmias associated with heritable and ac

137 criptional control of the Cspg4 locus led to ventricular arrhythmias, atrial fibrillation, atrioventr

138 arction, unstable angina, cardiogenic shock, ventricular arrhythmia, atrioventricular block, cardiac

139 llator (S-ICD) was developed to defibrillate ventricular arrhythmias, avoiding drawbacks of transveno

140 Patients are at risk of ventricular arrhythmias because of their underlying dise

141 for ventricular arrhythmias were spontaneous ventricular arrhythmias before enrollment and a younger

142 in follow-up included spontaneous sustained ventricular arrhythmias before ICD implantation and T-wa

143 ated with significant differences in overall ventricular arrhythmia burden in either group.

144 nergic agonist isoproterenol did not trigger ventricular arrhythmia but caused bradycardia-related pr

145 after infarction may prevent or reduce late ventricular arrhythmias but needs to be validated in cli

146 r current understanding of the mechanisms of ventricular arrhythmias by summarizing the state of know

147 We hypothesized that prevention of ventricular arrhythmias by the beta-blocker/sympatholyti

148 eration kindred with a history of atrial and ventricular arrhythmias, cardiac arrest, and sudden card

149 ts with a Heart Mate II device who underwent ventricular arrhythmia catheter ablation at 9 tertiary c

150 This study describes ventricular arrhythmia characteristics and ablation in p

151 ardiomyopathy (DCM) may be at lower risk for ventricular arrhythmias compared with those with ischemi

152 e, history of atrial arrhythmias, history of ventricular arrhythmias, current smoking, and cerebrovas

153 utcome was defined as all-cause mortality or ventricular arrhythmia, defined as aborted cardiac arres

154 CRT reduced the rate of onset of new ventricular arrhythmias detected by ICDs in patients wit

155 is effective for preventing life-threatening ventricular arrhythmias due to Brugada syndrome and idio

156 The primary end point of ventricular arrhythmias during exercise was compared bet

157 Ventricular arrhythmias during programmed electric stimu

158 onduction in addition to an earlier onset of ventricular arrhythmias during the early phase of acute

159 regarding the composite end point (malignant ventricular arrhythmias, end-stage heart failure, or dea

160 Hypokalemia is known to promote ventricular arrhythmias, especially in combination with

161 techolamine-induced stress, the frequency of ventricular arrhythmia events was markedly increased.

162 Ventricular arrhythmias evoked by catecholaminergic chal

163 h associations between NSVT- and ICD-treated ventricular arrhythmias examined.

164 ll myocarditis, the risk of life-threatening ventricular arrhythmias exceeds 50% at 5 years from admi

165 ars, 11 patients (16%) experienced sustained ventricular arrhythmias, exclusively in patients with bo

166 Ventricular arrhythmias have complex causes and mechanis

167 rioritized: chronic coronary artery disease, ventricular arrhythmias, heart failure, and cerebrovascu

168 hereditary cardiac condition associated with ventricular arrhythmias, heart failure, and sudden death

169 CI, 1.43-1.53), and sudden cardiac death or ventricular arrhythmia (HR, 1.65; 95% CI, 1.57-1.74).

170 ve stimulators are a promising treatment for ventricular arrhythmia in patients with heart failure.

171 d bradycardia, conduction abnormalities, and ventricular arrhythmia in response to Nav channel antago

172 for Ca2+ wave production and stress-induced ventricular arrhythmia in RyR2(ADA/+) mice.

173 ease outcome, and risk factors for malignant ventricular arrhythmias in a cohort of phospholamban R14

174 alve prolapse (MVP) and its association with ventricular arrhythmias in a cohort with "unexplained" o

175 RFA on outcome after ablation procedures for ventricular arrhythmias in a large single-center cohort.

176 group, CRT-D significantly reduced incidence ventricular arrhythmias in comparison to ICD (hazard rat

177 eath are less likely to experience sustained ventricular arrhythmias in comparison with men.

178 ellular mechanism responsible for triggering ventricular arrhythmias in CPVT-but has never been asses

179 ion, including genetic testing, the cause of ventricular arrhythmias in each of these infants remains

180 orth American ARVC Registry, the majority of ventricular arrhythmias in follow-up are monomorphic.

181 atients with ICDs, independent predictors of ventricular arrhythmias in follow-up included spontaneou

182 icardial illumination effectively terminated ventricular arrhythmias in hearts from transgenic mice a

183 nk between the iron deposition and malignant ventricular arrhythmias in humans with CMI is unknown.

184 The recurrence rate of ventricular arrhythmias in IVF patients is high.

185 e pathophysiology of atrial fibrillation and ventricular arrhythmias in MetS.

186 e concerning the occurrence and treatment of ventricular arrhythmias in patients supported with long-

187 h prevalence of QTc prolongation and complex ventricular arrhythmias in patients with anti-Ro antibod

188 redictors, characteristics, and treatment of ventricular arrhythmias in patients with ARVC.

189 was a powerful predictor of life-threatening ventricular arrhythmias in patients with BrS and no hist

190 or risk stratification of potentially lethal ventricular arrhythmias in patients with coronary artery

191 as a possible mechanism underlying triggered ventricular arrhythmias in patients with hypokalaemia.

192 RC strongly correlates with life-threatening ventricular arrhythmias in patients with idiopathic dila

193 We examined the influence of CRT on ventricular arrhythmias in patients with primary versus

194 total mortality, CD, and fatal and nonfatal ventricular arrhythmias in postacute myocardial infarcti

195 d arrhythmia syndrome characterized by fatal ventricular arrhythmias in structurally normal hearts du

196 entry, markedly reduced the burden of AF and ventricular arrhythmias in this model, suggesting a pote

197 of myocardial unloading are contributors to ventricular arrhythmias in this population.

198 fy and target the mechanisms contributing to ventricular arrhythmias in this population.

199 channel efficiently suppresses drug-induced ventricular arrhythmias in vitro by preventing potential

200 nging from uneventful palpitations to lethal ventricular arrhythmias, in the presence of pathologies,

201 eight patients had 502 sustained episodes of ventricular arrhythmias, including 489 that were monomor

202 th, resuscitated cardiac arrest, significant ventricular arrhythmia, indication for implantable defib

203 In 155 patients with ventricular arrhythmia-induced cardiac arrest, SN levels

204 to established risk indices in acute HF and ventricular arrhythmia-induced cardiac arrest.

205 Ventricular arrhythmia inducibility, spontaneous type I

206 Ventricular arrhythmias inducibility presented a hazard

207 Genesis of ventricular arrhythmias involves a complex interaction o

208 Ventricular arrhythmia is the leading cause of sudden ca

209 Radiofrequency ablation for ventricular arrhythmias is limited by inability to visua

210 ablation (RFA) from the epicardial space for ventricular arrhythmias is limited or impossible in some

211 Epicardial RFA for ventricular arrhythmias is often limited even when peric

212 ongation, a risk factor for life-threatening ventricular arrhythmias, is a potential side effect of m

213 However, the burden of idiopathic ventricular arrhythmias (IVA) in the general population

214 c cardiomyopathy, a disease characterized by ventricular arrhythmias leading to cardiac arrest and su

215 ology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD.

216 tion of myocardial fibrosis (a substrate for ventricular arrhythmia), microvolt T-wave alternans (a m

217 ardiac contractility but did neither provoke ventricular arrhythmias nor prolong cardiac repolarizati

218 sts were scored on an ordinal scale of worst ventricular arrhythmia observed (0 indicates no ectopy;

219 Ventricular arrhythmias occur more frequently in heart f

220 Ventricular arrhythmia occurred in 41 LGE-positive versu

221 A combined end point of death or ventricular arrhythmia occurred in 64 LGE-positive versu

222 The youngest age at which a malignant ventricular arrhythmia occurred was 20 years, whereas fo

223 deaths, lead failures, losses of capture, or ventricular arrhythmias occurred during MRI.

224 Clinically significant late atrial or ventricular arrhythmias occurred in 468 patients (44%).

225 Idiopathic ventricular arrhythmias of left bundle branch block infe

226 Ventricular arrhythmias often arise from the Purkinje-my

227 This large study found no elevated risks of ventricular arrhythmia or all-cause, cardiac, or noncard

228 1646 cases of ventricular arrhythmia or cardiac arrest and 379 cases o

229 tients with ARVC with histories of sustained ventricular arrhythmia or cardiac arrest were evaluated

230 ents (MACE), comprising significant nonfatal ventricular arrhythmia or death, was the primary outcome

231 risks of left ventricular non-compaction are ventricular arrhythmias or complete atrioventricular blo

232 GCM should be sought in patients who develop ventricular arrhythmias or high-grade heart block becaus

233 ciated with greater adjusted odds of serious ventricular arrhythmias (OR, 31.8; 95% CI, 4.3-236.3) an

234 the structural hallmark and correlates with ventricular arrhythmias origin.

235 magnetic resonance imaging and ECG malignant ventricular arrhythmia parameters for the prediction of

236 ants underlying exercise-induced polymorphic ventricular arrhythmia present in a large multigeneratio

237 ature ventricular contractions and sustained ventricular arrhythmia; proband status; extent of struct

238 PLN ablation diminishes ventricular arrhythmias promoted by CaMKII phosphorylati

239 hic, clinical, and geographic factors: prior ventricular arrhythmia (rate ratio [RR], 1.14; 95% CI, 1

240 ving role of catheter ablation in decreasing ventricular arrhythmia recurrence.

241 Ventricular arrhythmia recurrences occurred in 16 and in

242 Ventricular arrhythmia-related sudden cardiac arrest in

243 R), but the evaluation for and management of ventricular arrhythmia remain unclear.

244 RATIONALE: Ventricular arrhythmias remain the leading cause of deat

245 est tube drainage (>21 days), post-operative ventricular arrhythmias, renal insufficiency, and develo

246 The median ventricular arrhythmia score during exercise was signifi

247 There were no occurrences of sustained ventricular arrhythmia, sudden cardiac arrest, appropria

248 ch as atrial fibrillation (AF) predispose to ventricular arrhythmias, sudden cardiac death and stroke

249 e independently associated with a history of ventricular arrhythmias, sudden cardiac death, or implan

250 as independently associated with ICD-treated ventricular arrhythmias, supporting the importance of NS

251 nce between cardiac K(+) currents influences ventricular arrhythmia susceptibility.

252 associated with susceptibility to malignant ventricular arrhythmias, the gene-based risk stratificat

253 and without (control subjects; n=14) complex ventricular arrhythmias underwent a study protocol inclu

254 dysfunction) during ablation procedures for ventricular arrhythmias, using 64-electrode basket cathe

255 Catheter ablation for ventricular arrhythmia (VA) near the distal great cardia

256 sociated with CPVT may increase the risk for ventricular arrhythmia (VA).

257 LSG) hyperactivity promotes ischemia induced ventricular arrhythmia (VA).

258 Ablation of ventricular arrhythmias (VA) can be limited by intramura

259 The mechanisms of ventricular arrhythmias (VA) were probed by optical mapp

260 block (AVB), or atrial arrhythmias (AAs) and ventricular arrhythmias (VA).

261 rdiac death or syncope have higher risks for ventricular arrhythmias (VAs) and should undergo implant

262 Idiopathic left ventricular arrhythmias (VAs) and those caused by struct

263 In patients with A-HF, ventricular arrhythmias (VAs) are common.

264 Catheter radiofrequency ablation of ventricular arrhythmias (VAs) arising from the left vent

265 We report a series of patients with ventricular arrhythmias (VAs) arising from the PSP-LV an

266 enced episodes of ajmaline-induced sustained ventricular arrhythmias (VAs) compared with older patien

267 First, to evaluate whether ventricular arrhythmias (VAs) induced with programmed el

268 Risk stratification for ventricular arrhythmias (VAs) is important to refine sel

269 t to determine whether circadian patterns in ventricular arrhythmias (VAs) occur in a current primary

270 abnormality among patients with monomorphic ventricular arrhythmias (VAs) of left ventricular (LV) o

271 uency catheter ablation (RFCA) of idiopathic ventricular arrhythmias (VAs) originating from the basal

272 Idiopathic ventricular arrhythmias (VAs) originating from the left

273 diofrequency catheter ablation of idiopathic ventricular arrhythmias (VAs) originating from the left

274 Idiopathic ventricular arrhythmias (VAs) originating from the left

275 teristics and ablation outcome of idiopathic ventricular arrhythmias (VAs) originating from the parie

276 ntable cardioverter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutan

277 The prognosis for patients experiencing ventricular arrhythmias (VAs) while on continuous flow l

278 CD) is the most devastating manifestation of ventricular arrhythmias (VAs), and is the leading cause

279 The relationship of exercise with sustained ventricular arrhythmia (ventricular tachycardia/ventricu

280 tific) for the treatment of life-threatening ventricular arrhythmias (ventricular tachycardia/ventric

281 At least 1 intramural ventricular arrhythmia was eliminated in all but 2 patie

282 Ventricular arrhythmia was induced in 17 (81%) and was c

283 The adjusted ORs for ventricular arrhythmia were 4.32 (95% CI, 2.95-6.33) for

284 able cardioverter-defibrillator or sustained ventricular arrhythmias were excluded (n = 114).

285 h a metallic biliary Wallstent, epilepsy, or ventricular arrhythmias were excluded.

286 (83% plakophilin 2) without prior sustained ventricular arrhythmias were included.

287 y was performed in 321 (88.4%) patients, and ventricular arrhythmias were induced in 32 (10%) patient

288 Independent risk factors for malignant ventricular arrhythmias were left ventricular ejection f

289 n contrast to small-animal models, non-fatal ventricular arrhythmias were observed in hESC-CM-engraft

290 Risk factors for ventricular arrhythmias were spontaneous ventricular arr

291 rest with cardiopulmonary resuscitation, and ventricular arrhythmias were the most frequent complicat

292 presenting with exercise-induced polymorphic ventricular arrhythmia, which was followed for 10 years,

293 nts with DCM or ICM, no history of sustained ventricular arrhythmias, who underwent CRT implantation

294 in more than 30% of patients, and high-grade ventricular arrhythmias will be seen in about 10% of pat

295 f athletes with no or spotty LGE pattern had ventricular arrhythmias with a predominant left bundle b

296 All athletes with stria pattern showed ventricular arrhythmias with a predominant right bundle

297 ditive predictive value of HIC for malignant ventricular arrhythmias with an increased area under the

298 the nominal setting (18 of 24 intervals) for ventricular arrhythmias with cycle length </= 320 ms.

299 strong predictor of death and association of ventricular arrhythmias with sudden death led to signifi

300 l risk of sudden death, including death from ventricular arrhythmias, would predict the survival bene