ライフサイエンスコーパス: ventricular arrhythmia

1 rget for preventing heart failure-associated ventricular arrhythmia.

2 HCM myoarchitecture and its association with ventricular arrhythmia.

3 ventricular K(V) currents and predisposes to ventricular arrhythmia.

4 of human heart disease involving spontaneous ventricular arrhythmia.

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

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

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

8 ify factors that may predispose to malignant ventricular arrhythmia.

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

10 RAGE suppression particularly on IR-induced ventricular arrhythmia.

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

12 (CMs) in triggering heart failure-associated ventricular arrhythmia.

13 of D1R ameliorates heart failure-associated ventricular arrhythmia.

14 high prevalence of spontaneous and sustained ventricular arrhythmia.

15 d with cardiogenic shock and later developed ventricular arrhythmia.

16 c interval (range 505-725 ms) and documented ventricular arrhythmia.

17 hat may represent the anatomic substrate for ventricular arrhythmia.

18 iomyopathies are requiring therapy to reduce ventricular arrhythmias.

19 heart transplant, and 32 (20%) had malignant ventricular arrhythmias.

20 lausible molecular mechanism for some lethal ventricular arrhythmias.

21 cal course owing to a high rate of malignant ventricular arrhythmias.

22 turbance, atrial fibrillation, and malignant ventricular arrhythmias.

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

24 plained by QT prolongation leading to lethal ventricular arrhythmias.

25 y with dilated cardiomyopathy and atrial and ventricular arrhythmias.

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

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

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

29 ling and relevant mechanisms predisposing to ventricular arrhythmias.

30 y, which is associated with life-threatening ventricular arrhythmias.

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

32 le of myeloperoxidase for the development of ventricular arrhythmias.

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

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

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

36 tricular dysfunction is a known predictor of ventricular arrhythmias.

37 been proposed as an independent predictor of ventricular arrhythmias.

38 jection fraction (LVEF) face a high risk for ventricular arrhythmias.

39 neous type 1 electrocardiogram and inducible ventricular arrhythmias.

40 (2+) (Ca) mishandling can initiate triggered ventricular arrhythmias.

41 diac action potential that can trigger fatal ventricular arrhythmias.

42 tricular (His)-bundle associated with lethal ventricular arrhythmias.

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

44 were enzymatic infarct size and incidence of ventricular arrhythmias.

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

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

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

48 rosis and cardiomyocyte apoptosis, and fewer ventricular arrhythmias.

49 tion slowing and increased susceptibility to ventricular arrhythmias.

50 tients exhibit left ventricular dilation and ventricular arrhythmias.

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

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

53 vel, increased susceptibility to polymorphic ventricular arrhythmias.

54 ged ventricular repolarization, and provoked ventricular arrhythmias.

55 ystolic dysfunction, and a high incidence of ventricular arrhythmias.

56 nt morbidity and death from heart failure or ventricular arrhythmias.

57 ety and efficacy for catheter ablation of OT ventricular arrhythmias.

58 algorithms used to guide localization of OT ventricular arrhythmias.

59 1 patients were hospitalized for symptomatic ventricular arrhythmia (19.5% versus 25.3%; P=0.27).

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

61 5%), atrial arrhythmias (58%), and malignant ventricular arrhythmias (26%).

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

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

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

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

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

67 ow in silico, that for both human atrial and ventricular arrhythmias, activation of these channels le

68 ature >= 37.5 degrees C), and none developed ventricular arrhythmia after antimalarial treatment.

69 with DCM died suddenly or experienced severe ventricular arrhythmias although no adverse events were

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

71 Incidence of ventricular arrhythmias among patients randomized to CRT

72 is thought to increase the risk of malignant ventricular arrhythmias among patients with hypertrophic

73 METHODS AND All ventricular arrhythmias among RAFT study participants we

74 Patients who had ventricular arrhythmia and cardiogenic shock on presenta

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

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

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

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

79 imary end point was a composite of malignant ventricular arrhythmia and end-stage heart failure.

80 Low diastolic FA in HCM was associated with ventricular arrhythmia and is likely to represent disarr

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

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

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

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

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

86 35 athletes (80% men, age: 14-48 years) with ventricular arrhythmias and isolated LV subepicardial/mi

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

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

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

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

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

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

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

94 ing occur in failing hearts, contributing to ventricular arrhythmias and sudden cardiac death.

95 short QT syndromes associated with malignant ventricular arrhythmias and sudden cardiac death.

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

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

98 acquired long QT syndrome, which can lead to ventricular arrhythmias and sudden death.

99 ch may increase the risk of fentanyl-induced ventricular arrhythmias and sudden death.

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

101 ty Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Car

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

103 ac arrest, AMI, cardiogenic shock, sustained ventricular arrhythmia, and high-grade atrioventricular

104 condary end points were all-cause mortality, ventricular arrhythmias, and atrial fibrillation with me

105 pulation; the composite of ICD implantation, ventricular arrhythmias, and cardiac arrest: 0.96% (95%

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

107 failure admission, cardiac transplantation, ventricular arrhythmias, and cardiac device implantation

108 eases including Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy.

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

110 an acute cardiac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability in

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

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

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

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

115 n may be a biomarker for patients at risk of ventricular arrhythmias, and we have learned of the pote

116 Reentrant ventricular arrhythmias are a major cause of sudden deat

117 Ventricular arrhythmias are a major complication after m

118 Ventricular arrhythmias are a major early complication a

119 Ventricular arrhythmias are among the most severe compli

120 ces effectively improve survival, atrial and ventricular arrhythmias are common, predispose these pat

121 demiological studies have shown that SCD and ventricular arrhythmias are more likely to occur in the

122 erized by frequent arrhythmia, but malignant ventricular arrhythmias are most commonly associated wit

123 Ventricular arrhythmias are the cardinal and typically e

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

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

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

127 ated with QT prolongation, which may lead to ventricular arrhythmias as a possible explanation of thi

128 Ventricular arrhythmias as a result of unintentional blo

129 ly, and in heart failure and both atrial and ventricular arrhythmias, as well.

130 hospitalizations, and incidence of sustained ventricular arrhythmias at 24 months.

131 sient QT prolongation in some, and recurrent ventricular arrhythmias at a young age despite aggressiv

132 n potential (AP) variability in the onset of ventricular arrhythmias at high pacing rate, the knowled

133 ure ventricular complexes and pacing-induced ventricular arrhythmias at ZT14, and the hearts at ZT14

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

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

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

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

138 ablation is associated with markedly reduced ventricular arrhythmia burden with modest short-term ris

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

140 A decrease in FA of 0.05 increased odds of ventricular arrhythmia by 2.5 (95% confidence interval:

141 In this large cohort of patients with MVP, ventricular arrhythmia by Holter monitoring was frequent

142 itial edema in the heart can acutely promote ventricular arrhythmias by disrupting ventricular myocyt

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

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

145 This study describes ventricular arrhythmia characteristics and ablation in p

146 Idiopathic ventricular arrhythmias commonly originate from the righ

147 ied segment was reduced in HCM patients with ventricular arrhythmia compared to patients without (n =

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

149 SCEs included cardiac death or arrest, ventricular arrhythmias, congestive heart failure or arr

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

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

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

153 associated with an increased risk of de-novo ventricular arrhythmia during hospitalisation.

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

155 Ventricular arrhythmias during programmed electric stimu

156 Malignant ventricular arrhythmia end points most commonly occurred

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

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

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

160 age heart failure events, 24 [32%] malignant ventricular arrhythmia events).

161 Ventricular arrhythmias evoked by catecholaminergic chal

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

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

164 vere cardiac dysfunction, conduction defect, ventricular arrhythmias, fibrosis, apoptosis, and premat

165 ion <55% was strongly associated with severe ventricular arrhythmias for DSP cases (P<0.001, sensitiv

166 ents in cardiac function, high incidences of ventricular arrhythmias have been observed in animal mod

167 Ventricular arrhythmias have complex causes and mechanis

168 all-cause mortality (hazard ratio, 1.10) and ventricular arrhythmias (hazard ratio, 1.16).

169 sion in 61%, coronary artery disease in 25%, ventricular arrhythmia history in 1.4%, and no significa

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

171 Bailout ablation for refractory ventricular arrhythmia in cardiogenic shock allowed succ

172 the cardiac action potential and attenuated ventricular arrhythmia in catecholamine-challenged Casq2

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

174 cantly increase the risk of life-threatening ventricular arrhythmia in these patients.

175 %]; p = 0.007); complications in CA included ventricular arrhythmias in 2 and severe bradyarrhythmias

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

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

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

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

180 uction efficiencies as low as 40% suppressed ventricular arrhythmias in genetically modified mice wit

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

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

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

184 The risks of thromboembolism and ventricular arrhythmias in LVNC patients were similar to

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

186 The genesis of malignant ventricular arrhythmias in MVP probably recognizes the c

187 ia and reperfusion (I-R) are major causes of ventricular arrhythmias in patients with a history of co

188 osed to predict the 5-year risk of malignant ventricular arrhythmias in patients with ARVC.

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

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

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

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

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

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

195 ide guidance on the management of atrial and ventricular arrhythmias in this unique patient populatio

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

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

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

199 ation (RYR2(R176Q/+)) effectively suppressed ventricular arrhythmias induced by either beta-adrenergi

200 PVT; n=8) and in resuscitated patients after ventricular arrhythmia-induced cardiac arrest (n=155).

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

202 elevated in patients with CPVT and following ventricular arrhythmia-induced cardiac arrest.

203 Ventricular arrhythmias inducibility presented a hazard

204 Genesis of ventricular arrhythmias involves a complex interaction o

205 Ventricular arrhythmia is the leading cause of sudden ca

206 ring acute infections, the risk of malignant ventricular arrhythmias is increased, partly because of

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

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

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

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

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

212 ital mortality and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained vent

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

214 Ventricular arrhythmia occurred in 41 LGE-positive versu

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

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

217 Ventricular arrhythmias often arise from the Purkinje-my

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

219 wed for a composite end point of significant ventricular arrhythmia or sudden cardiac death.

220 None of the low-risk patients experienced ventricular arrhythmia or unexplained death, whereas 0.9

221 anned hospitalization for either symptomatic ventricular arrhythmia or worsening heart failure.

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

223 djusted OR = 0.45 [0.18-1.06], p = 0.31) and ventricular arrhythmias (OR = 0.65 [0.41-1.78], p = 0.41

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

225 g to death resulting from cardiogenic shock, ventricular arrhythmias, or multiorgan system failure.

226 the structural hallmark and correlates with ventricular arrhythmias origin.

227 ntaneous or ajmaline-induced type-1 pattern, ventricular arrhythmias originate from the right ventric

228 increased spontaneous atrial (p = 0.02) and ventricular arrhythmias (p = 0.03) in PVC-CM.

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

230 tion is the most widely used risk marker for ventricular arrhythmia potential and thus an important c

231 This study determined ventricular arrhythmia prevalence, severity, phenotypica

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

233 PLN ablation diminishes ventricular arrhythmias promoted by CaMKII phosphorylati

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

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

236 Ventricular arrhythmia recurrences occurred in 16 and in

237 In patients with recurrent ventricular arrhythmias refractory to medications and co

238 t greatest risk for SCD and life-threatening ventricular arrhythmias, regardless of the left ventricu

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

240 RATIONALE: Ventricular arrhythmias remain the leading cause of deat

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

242 5% with syncope and LVEF >35% with inducible ventricular arrhythmia, resulted in improved discriminat

243 dverse events, including clinically relevant ventricular arrhythmias, resuscitated cardiac arrest, ac

244 val: 3.1 to 3.8; p < 0.0001; IC(025): 1.46), ventricular arrhythmias (ROR: 4.7; 95% confidence interv

245 The median ventricular arrhythmia score during exercise was signifi

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

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

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

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

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

251 art's electrical system, typically caused by ventricular arrhythmias, that can lead to sudden cardiac

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

253 h fatalities that ranged from ~10% (SVAs and ventricular arrhythmias) to ~20% (CNS events, heart fail

254 cardiogenic shock and concomitant refractory ventricular arrhythmia undergoing bailout ablation due t

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

256 ndpoints like sudden cardiac arrest (SCA) or ventricular arrhythmia (VA).

257 4.9% vs 44.5%, p = 0.023), and more pre-LVAD ventricular arrhythmias (VA) (77% vs 60%, p = 0.048).

258 lar cardiomyopathy (ARVC) is associated with ventricular arrhythmias (VA) and sudden cardiac death (S

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

260 The association of the onset of ventricular arrhythmias (VA) with 0- to 21-day moving av

261 fective for eliminating most drug-refractory ventricular arrhythmias (VA).

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

263 e cardioverter-defibrillator utilization nor ventricular arrhythmia varied by sex.

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

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

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

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

268 Papillary muscles (PM) ventricular arrhythmias (VAs) exhibit QRS variability, a

269 Ventricular arrhythmias (VAs) have never been systematic

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

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 Idiopathic ventricular arrhythmias (VAs) originating from the left

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

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

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

279 ex substrate that may give rise to reentrant ventricular arrhythmias (VAs).

280 A composite outcome of severe ventricular arrhythmia was assessed.

281 Presence of ventricular arrhythmia was associated with male sex, bil

282 Ventricular arrhythmia was frequent (43% with at least v

283 Severe ventricular arrhythmia was independently associated with

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

285 Susceptibility to cardiac ventricular arrhythmias was significantly reduced in pro

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

287 mortality, acute kidney injury, stroke, and ventricular arrhythmia were found.

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

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

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

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

292 edium- and high-risk patients, including all ventricular arrhythmias, were identified within 15 days.

293 pital survival and an increased frequency of ventricular arrhythmias when used for treatment of COVID

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

295 homogenizing regions of scar contributing to ventricular arrhythmia with ablation or altering conduct

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

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

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

299 rmalities in the inferior leads, and complex ventricular arrhythmias with polymorphic/right bundle br

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