ライフサイエンスコーパス: arrhythmia

1 delays cardiac repolarization and can induce arrhythmia.

2 s in pHi impair cardiac function and trigger arrhythmia.

3 care to patients who have this debilitating arrhythmia.

4 d by pulmonary embolism, hypoxia, or primary arrhythmia.

5 either hypovolemia, hyperkalemia, or primary arrhythmia.

6 ed by hypovolemia, hyperkalemia, and primary arrhythmia.

7 te variability could protect against cardiac arrhythmia.

8 n abnormalities and premature death owing to arrhythmia.

9 like myocarditis, fibrosis, hypertrophy and arrhythmia.

10 embolism, compared with hypoxia and primary arrhythmia.

11 rt disease involving spontaneous ventricular arrhythmia.

12 Atrial fibrillation (AF) is a common arrhythmia.

13 l conduction that may be involved in cardiac arrhythmia.

14 fibrillation (AF), the most frequent cardiac arrhythmia.

15 ailored to address mechanisms underlying the arrhythmia.

16 gth (the distance between wavefronts) of the arrhythmia.

17 tial duration and an increased propensity to arrhythmia.

18 namic instabilities that may underlie atrial arrhythmias.

19 mals were resistant to triggered ventricular arrhythmias.

20 osure to CO causes early afterdepolarization arrhythmias.

21 s by which mutant IKur contributes to atrial arrhythmias.

22 n men and women that may affect the risk for arrhythmias.

23 er investigation in the treatment of cardiac arrhythmias.

24 teristics may serve as predictors for atrial arrhythmias.

25 ved among patients who had prior ventricular arrhythmias.

26 evant mechanisms predisposing to ventricular arrhythmias.

27 nction, and do not increase the incidence of arrhythmias.

28 t represent a new strategy to combat cardiac arrhythmias.

29 rial fibrillation, and malignant ventricular arrhythmias.

30 dex 1-4 min prior to the onset of the tachy-arrhythmias.

31 not associated with ICD-treated ventricular arrhythmias.

32 olecular mechanisms and treatment of cardiac arrhythmias.

33 eroxidase for the development of ventricular arrhythmias.

34 to perturbations and their susceptibility to arrhythmias.

35 ients without a history of prior ventricular arrhythmias.

36 nts at risk for life-threatening ventricular arrhythmias.

37 ed fatal severe hypoglycemia-induced cardiac arrhythmias.

38 ch could lead to heart failure and malignant arrhythmias.

39 a waves, protecting the heart from triggered arrhythmias.

40 al Ca(2+)-handling and malignant ventricular arrhythmias.

41 and exposed to isoproterenol showed reduced arrhythmias.

42 ons (EADs), which trigger lethal ventricular arrhythmias.

43 a(2+)) ions mediate various types of cardiac arrhythmias.

44 function is a known predictor of ventricular arrhythmias.

45 f these channels in mediating Ca(2+) -driven arrhythmias.

46 ebo group in rates of hypotension or cardiac arrhythmias.

47 may modify atrial conduction or treat atrial arrhythmias.

48 d K(+) currents, and increased propensity to arrhythmias.

49 for potential therapeutic approaches against arrhythmias.

50 ed cardiomyopathy and atrial and ventricular arrhythmias.

51 78 appropriate ICD detections of ventricular arrhythmias.

52 ntial and potentially trigger lethal cardiac arrhythmias.

53 rdepolarizations (DADs) that trigger cardiac arrhythmias.

54 he potential consequence of exercise-induced arrhythmias.

55 hat can ultimately lead to heart failure and arrhythmias.

56 d severe hypoglycemia induces lethal cardiac arrhythmias.

57 rrhythmogenic cardiomyopathies and inherited arrhythmias.

58 rcapnia, respectively), incidence of cardiac arrhythmias (196.0 +/- 239.9 vs. 576.7 +/- 472.9 events

59 h hypoxia: 23 mm (95% CI, 20-27) and primary arrhythmia: 25 mm (95% CI, 22-28)-the absolute differenc

60 Cardiac Excitation-Contraction Coupling and Arrhythmias (3-4 March 2016), a biennial event that brin

61 (14 vs 4, respectively; P = .02) and cardiac arrhythmias (57 vs 30; P = .004).

62 ac causes, whereas heart failure (22.5%) and arrhythmias (6.6%) were the most common cardiac causes o

63 by providers with greater specialization in arrhythmias (60.0%, 62.4%, and 67.0% for primary care ph

64 61% and 44%, respectively), supraventricular arrhythmias (69% and 52%, respectively), and dilated car

65 h; P<0.05), and strongly reduced ventricular arrhythmias (-70+/-22% premature ventricular contraction

66 betaARs increases the likelihood of cardiac arrhythmias, adverse ventricular remodelling, decline of

67 Noninducibility of any arrhythmia after a staged hybrid procedure seemed to be

68 only developed QT prolongation and malignant arrhythmias after exposure to QT-prolonging stressors, 1

69 out intervention), and if there was a lethal arrhythmia alarm (1.2 minutes [95% CI, -0.6 to 2.9] vs 1

70 Incidence of ventricular arrhythmias among patients randomized to CRT-D versus im

71 METHODS AND All ventricular arrhythmias among RAFT study participants were downloade

72 Both arrhythmia and cardiomyopathy genes are implicated.

73 hiPSC-CMs should be considered prior to pro-arrhythmia and cardiotoxicity screening in drug discover

74 erapeutic strategy protecting the heart from arrhythmia and contractile dysfunction.

75 ne artery blood flow associated with cardiac arrhythmia and high magnitude irregular fluctuations of

76 fibrillation (AF) is the most common cardiac arrhythmia and is associated with a 5-fold increase in t

77 rial fibrillation is the most common cardiac arrhythmia and leads to stroke.

78 of patients who are more likely to die of an arrhythmia and less likely to die of other causes is req

79 Risk of arrhythmia and tissue injury decreased with increasing a

80 ause of concern about triggering ventricular arrhythmias and because a clinical benefit has not been

81 n is a heritable risk factor for ventricular arrhythmias and can predispose to sudden death.

82 BPHL truncations may increase risk for human arrhythmias and cardiomyopathy.

83 Cardiac arrhythmias and conduction disturbances are accompanied

84 iverse ion channelopathies including cardiac arrhythmias and cystic fibrosis.

85 regular breathing, sympatho-vagal imbalance, arrhythmias and diastolic dysfunction.

86 thmogenic cardiomyopathy who exhibit cardiac arrhythmias and dysfunction, palmoplanter keratosis, and

87 Arrhythmias and heart failure are the most common late c

88 ion disturbance and the occurrence of atrial arrhythmias and low left ventricular ejection fraction,

89 mice showed significantly fewer ventricular arrhythmias and lower mortality after isoproterenol admi

90 complex CHD was associated with ventricular arrhythmias and maternal in-hospital mortality, although

91 mportant role in the pathogenesis of cardiac arrhythmias and may also contribute to the development o

92 ultures have proven useful for investigating arrhythmias and other conduction anomalies, and because

93 s on de novo variants associated with severe arrhythmias and structural heart diseases and investigat

94 ence and prevalence of sustained ventricular arrhythmias and sudden cardiac death are lower in women

95 ECG and increased susceptibility to cardiac arrhythmias and sudden death.

96 s vis-a-vis cardiac NaV s in triggering such arrhythmias and their potential as therapeutic targets i

97 it has already had on the fields of cardiac arrhythmias and whole-heart computational modeling, pres

98 tion within known AF susceptibility, cardiac arrhythmia, and cardiomyopathy gene regions.

99 on reinterventions in 13 patients for atrial arrhythmia, and cardioversions in 15 patients.

100 ly affect myocardial calcium handling, cause arrhythmia, and contribute to cardiac remodeling by indu

101 coronary syndrome, pericarditis, significant arrhythmia, and heart failure).

102 As BIN1 is implicated in cancers, arrhythmia, and late-onset Alzheimer disease, these find

103 sterase 2 in cardiac function, propensity to arrhythmia, and myocardial infarction.

104 no association between exercise intolerance, arrhythmia, and native T1 or LV extracellular volume.

105 ntial, and how their dysfunction can lead to arrhythmias, and discusses K(+) channel-based therapeuti

106 CHD was associated with incident CHF, atrial arrhythmias, and fetal growth restriction and complex CH

107 channels and transporters can cause acquired arrhythmias, and how these mechanisms might be targeted

108 ncident CHF, atrial arrhythmias, ventricular arrhythmias, and maternal mortality were uncommon during

109 by early afterdepolarizations and triggered arrhythmias, and reduced threshold for store overload-in

110 lial and genetic factors, ECG abnormalities, arrhythmias, and structural/functional ventricular alter

111 ial fibrillation (AF), sustained ventricular arrhythmias, and sudden cardiac death are recognized.

112 long-QT associated torsade de pointes (TdP) arrhythmias, and sympathetic discharge is a major factor

113 Atrial arrhythmias are the most common complication encountered

114 Previous studies in rats have indicated that arrhythmias arose as a result of augmentation of the lat

115 rction, angina, heart failure, hypertension, arrhythmias, arteriosclerosis, stroke, and venous thromb

116 eripheral arterial complication, and cardiac arrhythmia), as well.

117 validation of the Comprehensive In vitro Pro-Arrhythmia Assay (CiPA).

118 t to assess the types and patterns of atrial arrhythmias, associated factors, and age-related trends.

119 from patients who underwent ablation of this arrhythmia at the Tel Aviv and Sheba Medical Centers.

120 Freedom from atrial arrhythmias at 12 months postprocedure was similar compa

121 t, and atrial fibrillation are made, and the arrhythmia (atrial fibrillation) is indicative diagnosed

122 ontrol of the Cspg4 locus led to ventricular arrhythmias, atrial fibrillation, atrioventricular condu

123 D) was developed to defibrillate ventricular arrhythmias, avoiding drawbacks of transvenous leads.

124 isease and arrhythmias, with the most common arrhythmia being found in the atria of the heart.

125 e in the genesis of pump failure and related arrhythmias, both in control mice and in mice subjected

126 e in the genesis of pump failure and related arrhythmias, both in control mice and in mice subjected

127 gnificant differences in overall ventricular arrhythmia burden in either group.

128 fibrillation (AF) is the most common cardiac arrhythmia, but little is known about the molecular mech

129 ll ion channels leads to low heart rates and arrhythmia by an unknown route.

130 Last, we could reverse this 'worm arrhythmia' by the benzothiazepine S107, establishing th

131 and dialysate potassium concentrations with arrhythmias, cardiovascular events, and mortality.

132 spitalizations for AF and reports of serious arrhythmia caused by AF.

133 onary artery disease, heart failure, cardiac arrhythmia, cerebrovascular disease, congenital heart di

134 mia evaluation were collected from inherited arrhythmia clinics and the Rochester long-QT syndrome (L

135 y (DCM) may be at lower risk for ventricular arrhythmias compared with those with ischemic cardiomyop

136 nce of hypertension, hyperlipidemia, cardiac arrhythmias, coronary artery disease, congestive heart f

137 f atrial arrhythmias, history of ventricular arrhythmias, current smoking, and cerebrovascular accide

138 ed upon a total of 107049 beats from MIT-BIH arrhythmia database, our method has achieved average sen

139 Vinculin (VCL) was linked to sudden arrhythmia death in VCL knockout mice prior to the appea

140 nsurability of families affected with Sudden Arrhythmia Death Syndromes (SADS) for the determination

141 efined as all-cause mortality or ventricular arrhythmia, defined as aborted cardiac arrest or documen

142 reduced the rate of onset of new ventricular arrhythmias detected by ICDs in patients without a histo

143 Significant arrhythmias developed during six (18%) ablations.

144 Supraventricular arrhythmias developed over lifetime in 166 patients (19%

145 p junction protein, is often associated with arrhythmia, dilated cardiomyopathy (DCM), and heart fail

146 Our findings may have implications for arrhythmia disorders arising from mutations in the gatin

147 The proportion of arrhythmias due to IART increased with congenital heart

148 n-invasive identification of the presence of arrhythmia, due to irregularity in the ECG signal associ

149 These mechanisms could contribute to arrhythmias during clinical hypoglycemic episodes.

150 The primary end point of ventricular arrhythmias during exercise was compared between the fle

151 We previously observed an increase in arrhythmias during spontaneous prolonged hypoglycemia in

152 This simulation study investigated arrhythmia dynamics in multi-scale human ventricle model

153 Maternal outcomes included in-hospital arrhythmias, eclampsia or preeclampsia, congestive heart

154 e composite end point (malignant ventricular arrhythmias, end-stage heart failure, or death) compared

155 ge of complications raised at the horizon as arrhythmias, endocarditis, pulmonary hypertension, and h

156 pathogenic KCNE2 mutations identified during arrhythmia evaluation were collected from inherited arrh

157 one of the predefined subgroups of detected arrhythmia events.

158 ns between NSVT- and ICD-treated ventricular arrhythmias examined.

159 iarrhythmic drugs and reablation procedures, arrhythmia free-survival increased to 97% during follow-

160 et after 1.5 +/- 0.5 procedures per patient (arrhythmia free-survival: 85% vs. 59%; log-rank p < 0.00

161 .9% male, 69.2% with paroxysmal AF) who were arrhythmia-free at 12 months (excluding 3-month "blankin

162 Arrhythmia-free survival off antiarrhythmic drugs 12 mon

163 d to be the strongest correlate of long-term arrhythmia-free survival.

164 ation of these triggers resulted in improved arrhythmia-free survival.

165 ity of hypertension, coronary heart disease, arrhythmia, heart failure, and stroke.

166 , coronary artery disease, history of atrial arrhythmias, history of ventricular arrhythmias, current

167 ; these depolarized potentials cause cardiac arrhythmia; however, the underlying mechanism is unknown

168 ouse hearts, and that lack of PKP2 can cause arrhythmia in a structurally normal heart.

169 n HRV similar to mammalian respiratory sinus arrhythmia in an amphibian, the toad Rhinella schneideri

170 dysregulation and increases in incidence of arrhythmia in animal models of reduced ejection fraction

171 The model predicted increased risk for arrhythmia in females when acute sympathetic nervous sys

172 ock and sympathetic stimulation that induces arrhythmia in females with inherited and acquired long-Q

173 tricular conduction and an increased rate of arrhythmia in heterozygous and null mice.

174 ink between the V307L KCNQ1 mutation and pro-arrhythmia in human ventricles, and establishes partial

175 fibrillation (AF), the most common sustained arrhythmia in hypertrophic cardiomyopathy (HCM), is capa

176 IART is the most common presenting atrial arrhythmia in patients with congenital heart disease, wi

177 s of electrophysiological activity can cause arrhythmia in the heart.

178 with age to surpass IART as the most common arrhythmia in those >/=50 years of age (51.2% vs. 44.2%;

179 The 2014 Consensus Statement on Arrhythmias in ACHD patients and the 2015 European Socie

180 significantly reduced incidence ventricular arrhythmias in comparison to ICD (hazard ratio, 0.86; 95

181 s likely to experience sustained ventricular arrhythmias in comparison with men.

182 ng with miRYR2-U10 prevents life-threatening arrhythmias in CPVT mice, suggesting that the reduction

183 anism responsible for triggering ventricular arrhythmias in CPVT-but has never been assessed prospect

184 alone for the prevention of exercise-induced arrhythmias in CPVT.

185 Our data suggest that CO induces arrhythmias in guinea pig cardiac myocytes via the ONOO(

186 on are emerging as a critical determinant of arrhythmias in heart failure.

187 onstrates increased susceptibility to atrial arrhythmias in mice where Notch has been transiently act

188 correlates with life-threatening ventricular arrhythmias in patients with idiopathic dilated cardiomy

189 oteins can contribute to the pathogenesis of arrhythmias in patients with various types of heart dise

190 markedly increases the incidence of cardiac arrhythmias in rats with HFpEF.

191 ations and reduced the isoproterenol-induced arrhythmias in WT hearts.

192 ed AHI (7 +/- 2/h), RSNA (18 +/- 2% max) and arrhythmia incidence (46 +/- 13/h) as well as CBC respon

193 activity (SNA) are associated with increased arrhythmia incidence and contribute to mortality in chro

194 sensitivity, oscillatory breathing, RSNA and arrhythmia incidence during CHF.

195 Arrhythmias, including those in the atria, can arise as

196 Permanent atrial arrhythmias increased with age from 3.1% to 22.6% in pat

197 VT) is a condition of abnormal heart rhythm (arrhythmia), induced by physical activity or stress.

198 alter atrial ion channel gene expression and arrhythmia inducibility.

199 interval to drug-induced QT prolongation and arrhythmias is not known.

200 role of these currents in the development of arrhythmias is not well understood.

201 ing, underscoring that rewiring, rather than arrhythmia, is associated with physiological aging.

202 risk factor for life-threatening ventricular arrhythmias, is a potential side effect of many marketed

203 is grouped into 5 sections: (1) Overview of Arrhythmia, Ischemia, and QTc Monitoring; (2) Recommenda

204 nderstand how excitable tissues give rise to arrhythmias, it is crucially necessary to understand the

205 s it leads to a potentially life-threatening arrhythmia known as Torsade de Pointes (TdP).

206 Ectopic heartbeats can trigger reentrant arrhythmias, leading to ventricular fibrillation and sud

207 ients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and m

208 This method enables prediction of arrhythmia likelihood and its modulation by alterations

209 re death, generator or lead failure, induced arrhythmia, loss of capture, or electrical reset during

210 han previously believed suggesting that this arrhythmia may have a genetic component.

211 6-week postablation "blanking period" (when arrhythmias may occur owing to postablation inflammation

212 ardial fibrosis (a substrate for ventricular arrhythmia), microvolt T-wave alternans (a marker of ele

213 quantify contraction in in vitro and in vivo arrhythmia models and to measure pharmacological respons

214 merged that need to be addressed: overuse of arrhythmia monitoring among a variety of patient populat

215 periodic assessment of cardiac function and arrhythmia monitoring, is essential for all patients.

216 stable angina [n = 3], pericarditis [n = 2], arrhythmia [n = 12], and heart failure [n = 1]).

217 red on an ordinal scale of worst ventricular arrhythmia observed (0 indicates no ectopy; 1, isolated

218 failures, losses of capture, or ventricular arrhythmias occurred during MRI.

219 Cardiac arrhythmias occurred early and in the absence of cardiac

220 ific physiology, atrial pathology, impact on arrhythmia occurrence, imaging, mapping, and ablation.

221 comprising significant nonfatal ventricular arrhythmia or death, was the primary outcome.

222 greater adjusted odds of serious ventricular arrhythmias (OR, 31.8; 95% CI, 4.3-236.3) and maternal i

223 ffer in mortality, heart failure admissions, arrhythmias, or incident malignancy.

224 was larger for hypovolemia than for primary arrhythmia (p < 0.001).

225 ow-up of 11.3 +/- 9.4 years, the predominant arrhythmia pattern was paroxysmal in 62.3%, persistent i

226 and pulmonary hypertension, QT prolongation, arrhythmias, pericardial disease, and radiation-induced

227 ical impulse and are associated with various arrhythmia phenotypes.

228 n early screen for torsadogenic (causing TdP arrhythmias) potential in drug candidates.

229 rom fructose-rich diet (FRD) animals exhibit arrhythmias produced by exacerbated Ca(2+) /calmodulin-p

230 atrial fibrillation and as a determinant of arrhythmia progression.

231 rillation increases in prevalence and atrial arrhythmias progressively become permanent as the popula

232 During arrhythmia provocation induced by catecholamine injectio

233 n on extra-PV triggers had increased risk of arrhythmia recurrence (83.7% versus 64.0%; P=0.003).

234 ggressive BP treatment did not reduce atrial arrhythmia recurrence after catheter ablation for AF but

235 ibrillation (AF), and increased incidence of arrhythmia recurrence after pulmonary vein (PV) isolatio

236 strate-modification group (32%) were without arrhythmia recurrence and off antiarrhythmic drug therap

237 rface and 18 months of follow-up, the atrial arrhythmia recurrence rate was 15% after 1.4 +/- 0.5 pro

238 catheter ablation in decreasing ventricular arrhythmia recurrence.

239 o a level comparable to NYHA II and III with arrhythmia recurrence.

240 micro-RNAs and provide evidence that several arrhythmia-related target genes exhibit repression at po

241 ikelihood that candidate drugs will increase arrhythmias rely on small changes in APD and Q-T interva

242 RATIONALE: Ventricular arrhythmias remain the leading cause of death in patient

243 but its applicability for terminating atrial arrhythmias remains largely unexplored.

244 KEY POINTS: Arrhythmias result from disruptions to cardiac electrica

245 1-deficient mice recapitulated human cardiac arrhythmias resulting from loss of function of Nav1.5.

246 serve as a novel diagnostic tool to stratify arrhythmia risk and assess for progression of heart fail

247 in the screen were selected based on the pro-arrhythmia risk classification (Low risk, Intermediate r

248 predict prognosis, especially with regard to arrhythmia risk for certain subtypes.

249 t how various sex-based differences underlie arrhythmia risk in the setting of acute sympathetic nerv

250 her refine subtypes of DCM, especially where arrhythmia risk is increased, and ultimately contribute

251 ate of hiPSC-CMs determines the absolute pro-arrhythmia risk score calculated for these compounds.

252 The median ventricular arrhythmia score during exercise was significantly reduc

253 form for pre-clinical cardiotoxicity and pro-arrhythmia screening of drugs in development.

254 is end, here we developed a high content pro-arrhythmia screening platform consisting of either fetal

255 cific drug development and to study distinct arrhythmias, simple models are required to implement and

256 for investigation of QT interval changes and arrhythmia substrates.

257 n Kv7.1 and KCNE1 genes, which cause cardiac arrhythmias, such as the long-QT syndrome (LQT) and atri

258 were no occurrences of sustained ventricular arrhythmia, sudden cardiac arrest, appropriate defibrill

259 tly associated with a history of ventricular arrhythmias, sudden cardiac death, or implantable cardio

260 ntly associated with ICD-treated ventricular arrhythmias, supporting the importance of NSVT in hypert

261 cardiac K(+) currents influences ventricular arrhythmia susceptibility.

262 Cardiac Excitation-Contraction Coupling and Arrhythmias Symposium, a biannual event that aims to bri

263 cussed, including heart failure, infarction, arrhythmias, syncope, cardiomyopathy, angina, heart tran

264 n sequencing panel incorporated 38 inherited arrhythmia syndrome candidate genes and another 33 genes

265 ardia (CPVT) is a potentially lethal genetic arrhythmia syndrome characterized by polymorphic ventric

266 ardiac arrest may be because of an inherited arrhythmia syndrome.

267 es identifies a high proportion of inherited arrhythmia syndrome.

268 Inherited arrhythmia syndromes are responsible for a significant p

269 gory of potentially life-threatening genetic arrhythmia syndromes capable of producing severe long-QT

270 omatosis is an allelic disorder with cardiac arrhythmia syndromes caused by KCNQ1 mutations.

271 rrence of spatially discordant alternans, an arrhythmia that is widely believed to facilitate the dev

272 Atrial fibrillation (AF) is a common arrhythmia that poses a significant risk of stroke.

273 with susceptibility to malignant ventricular arrhythmias, the gene-based risk stratification for card

274 ents (death, heart failure, hospitalization, arrhythmia, thromboembolic events, and reintervention).

275 surgery (32%), catheter intervention (62%), arrhythmia treatment (32%), thrombosis (12%), and protei

276 ko) hearts became more susceptible to atrial arrhythmias under rapid programmed electrical stimulatio

277 respiratory acidosis in triggering the fatal arrhythmia underlying SUNDS.

278 tivity promotes ischemia induced ventricular arrhythmia (VA).

279 The mechanisms of ventricular arrhythmias (VA) were probed by optical mapping, whole-c

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

281 First, to evaluate whether ventricular arrhythmias (VAs) induced with programmed electrostimula

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

283 d ablation outcome of idiopathic ventricular arrhythmias (VAs) originating from the parietal band.

284 overter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutaneous coronar

285 ost devastating manifestation of ventricular arrhythmias (VAs), and is the leading cause of mortality

286 Incident CHF, atrial arrhythmias, ventricular arrhythmias, and maternal morta

287 The most common presenting arrhythmia was intra-atrial re-entrant tachycardia (IART

288 LPeAF) at 1 year and freedom from all atrial arrhythmias was 77% (PAF), 75% (PeAF), and 57% (LPeAF).

289 Qualifying arrhythmias were classified by a blinded adjudicating co

290 biliary Wallstent, epilepsy, or ventricular arrhythmias were excluded.

291 summary, severe hypoglycemia-induced cardiac arrhythmias were increased by insulin deficiency and dia

292 admitted for dofetilide reloading for atrial arrhythmias were retrospectively reviewed.

293 sinus pauses, and a susceptibility to atrial arrhythmias, which contribute to a phenotype resembling

294 s improved our understanding of this complex arrhythmia while unraveling more knowledge gaps and inad

295 survival from nonshockable-turned-shockable arrhythmias with amiodarone versus placebo were 2.3% (-0

296 have enabled noninvasive mapping of cardiac arrhythmias with electrocardiographic imaging and noninv

297 Thus, the EAD-induced arrhythmias with repolarisation reserve attenuation migh

298 increased risk of cardiovascular disease and arrhythmias, with the most common arrhythmia being found

299 dden death, including death from ventricular arrhythmias, would predict the survival benefit with an

300 channels is critical for preventing cardiac arrhythmia yet the mechanistic basis for the slow gating