ライフサイエンスコーパス: EAD

1 EAD occurred in 182 (27.6%) cases.

2 EAD production was strongest upon moving the activation

3 EAD was diagnosed in 41 (55.4%) of 74 patients with fact

4 EADs are mainly driven by voltage oscillations in the re

5 EADs are promoted by aberrant RyR-mediated Ca(2+) releas

6 EADs disappeared when the pacing cycle length was shorte

7 EADs occur in the setting of reduced repolarization rese

8 EADs were induced in isolated rabbit ventricular myocyte

9 EADs were then induced by a different method: increasing

10 14.44) and was predictive of PNF (P = 0.02), EAD (P = 0.05), and death <= POD90 (P = 0.06).

11 In the presence of phase-2 EADs, the cells may synchronously exhibit the same numbe

12 (2) EADs are reduced in absolute number of occurrence, which

13 azine (5-10 mumol/L) eliminated late phase 3 EAD- and DAD-induced triggered activity as well as isopr

14 In the presence of phase-3 EADs, regional synchronization leads to propagating EADs

15 t not its inactive analogue KN-92, abolished EADs and hypokalemia-induced ventricular tachycardia/fib

16 tate inactivation curve completely abolished EADs in myocytes while maintaining a normal Ca(i) transi

17 indow I(CaL,D-C) narrowing (10 mV) abolished EADs of all types (P < 0.05).

18 e development of early afterdepolarisations (EADs), which trigger lethal ventricular arrhythmias.

19 ase 3 early and delayed afterdepolarization (EAD and DAD)-induced triggered activity in SVC sleeves a

20 ie, by promoting early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is un

21 n slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1 but not in CA3 hippocampal

22 (2)O(2) initiated early afterdepolarization (EAD)-mediated triggered activity that led to sustained V

23 was initiated by early afterdepolarization (EAD)-mediated triggered activity.

24 Early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltag

25 likely caused by early afterdepolarizations (EADs) and polymorphic ventricular tachycardias (PVTs).

26 quent epicardial early afterdepolarizations (EADs) and spontaneous ventricular tachycardia (VT) in 4

27 shown to induce early afterdepolarizations (EADs) and triggered activity by impairing Na current (I(

28 can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodiu

29 Spontaneous early afterdepolarizations (EADs) and ventricular tachycardia/fibrillation occurred

30 s that result in early afterdepolarizations (EADs) are a known trigger for tachyarrhythmias, but the

31 Early afterdepolarizations (EADs) are linked to both triggered arrhythmias and reent

32 al alternans and early afterdepolarizations (EADs) are linked to cardiac arrhythmias.

33 w arrhythmogenic early afterdepolarizations (EADs) are triggered in failing heart cells.

34 Early afterdepolarizations (EADs) are triggers of cardiac arrhythmia driven by L-typ

35 Early afterdepolarizations (EADs) are voltage oscillations that occur during the rep

36 iac arrhythmias, early afterdepolarizations (EADs) during action potentials(APs) have been extensivel

37 ularly occurring early afterdepolarizations (EADs) in cardiac myocytes are traditionally hypothesized

38 blocker) induced early afterdepolarizations (EADs) in female base myocytes cultured for 1 day if incu

39 on and prominent early afterdepolarizations (EADs) in neonatal cardiomyocytes expressing the F1486del

40 illations called early afterdepolarizations (EADs) that can occur either during the plateau phase or

41 nd to facilitate early afterdepolarizations (EADs) when repolarization reserve is reduced.

42 illations called early afterdepolarizations (EADs), and premature death in paced adult rabbit ventric

43 Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointes.

44 Epicardial early afterdepolarizations (EADs), often accompanied by spontaneous ventricular tach

45 he occurrence of early afterdepolarizations (EADs), which are abnormal depolarizations during the rep

46 lations, such as early afterdepolarizations (EADs), which are associated with lethal arrhythmias.

47 ng proarrhythmic early afterdepolarizations (EADs).

48 hythmias such as early afterdepolarizations (EADs).

49 otential causing early afterdepolarizations (EADs).

50 nt that produces early afterdepolarizations (EADs).

51 Early-afterdepolarizations (EADs) are abnormal action potential oscillations and a k

52 Atrial early-afterdepolarizations (EADs) may contribute to atrial fibrillation (AF), perhap

53 tiguous susceptible myocytes required for an EAD and a barely suprathreshold DAD to trigger a propaga

54 ween an action potential with and without an EAD) is not sufficient to account for the large variatio

55 SH (4), NAD-beta-Ala-(Arg(11))CCMSH (5), and EAD-beta-Ala-(Arg(11))CCMSH (6) peptides were synthesize

56 herapeutic strategy for suppressing EADs and EAD-mediated arrhythmias.

57 Graft loss and EAD rate were 2% (n = 1) and 26% (n = 13).

58 Both MEAF and EAD were independent predictors of transplant survival w

59 lity) of AP duration in cardiac myocytes and EAD-mediated arrhythmias and suggests a novel possible m

60 Ten patients (3.4%) presented with PNF, and EAD occurred in 62 patients (20.9%); 9 patients died bef

61 propose a link between circadian rhythms and EAD formation and suggests that the efficacy of drugs ta

62 RNAs, 3- to 6-fold more viral Zta, Rta, and EAD proteins, 3- to 5-fold more viral DNA, and 7- to 9-f

63 locity, AP duration, conduction velocity and EAD incidence, as well as reflection incidence (29.2%, n

64 essing both pacing-induced re-entrant VF and EAD-mediated multifocal VF.

65 The mechanisms of alternans and EADs have been extensively studied under steady-state co

66 e to another, action potential alternans and EADs may occur during the transition between two periodi

67 amical mechanisms of transient alternans and EADs.

68 and a trigger (increased persistent INa and EADs) promotes reflection and arrhythmogenesis.

69 ular cleft can suppress APD prolongation and EADs in the presence of Na(+) channel mutations because

70 are sufficient to cause APD prolongation and EADs, the predominant characteristic of LQTs.

71 accompanied by aberrant Ca(2+) releases and EADs, which were abolished by inhibition of Ca(2+)/calmo

72 ipples, larger macroscopic Ca(2+) waves, and EADs.

73 of PRS, PNF, postreperfusion cardiac arrest, EAD, and AKI should be anticipated.

74 upling promotes complex EAD patterns such as EAD alternans that are not observed for solely voltage-d

75 tification of risk factors of IRI-associated EAD may guide patient management and possible timely gra

76 However, electrical mechanisms of atrial EADs, a potential cause of atrial fibrillation, are poor

77 Associations between EAD and recipient, donor, and transplant factors were ex

78 Genetic suppression of NCX reduces both EADs and DADs.

79 tes virtually all inward current elicited by EADs, and that this effect occurs at concentrations (40-

80 and the current paradigm holds that cardiac EAD dynamics are dominated by interaction between ICaL a

81 tual Ito-like current (n=1113 trials) caused EADs to reappear over a wide range of Ito conductance (0

82 aMKII activation were ineffective at causing EADs.

83 One of the major determinants of cellular EAD production and repolarization failure is the size of

84 Hence, cellular EADs have been implicated as a driver of potentially let

85 A key unanswered question is how cellular EADs partially synchronize in tissue, as is required for

86 showed that this bistable switch of cellular EADs provided both a trigger and a functional substrate

87 the Endoscopy Artefact Detection challenge (EAD).

88 cally homogeneous tissue models that chaotic EADs synchronize globally when the tissue is smaller tha

89 rcellular clefts, whereas for narrow clefts, EADs were suppressed.

90 ycling play a key role in generating complex EAD and DAD dynamics observed experimentally in cardiac

91 and 4) Ca-voltage coupling promotes complex EAD patterns such as EAD alternans that are not observed

92 recipients were monitored for complications, EAD (defined by postoperative day 7 bilirubin >10 mg/dL

93 However, in some countries EAD reach 0.5 to 1% of GDP annually, which is the same o

94 Global Expected Annual Damages (EAD) due to direct damage to road and railway assets ran

95 hypokalemia to induce bradycardia-dependent EADs at a long pacing cycle length of 6 s, when native r

96 Early after-depolarization (EAD), or abnormal depolarization during the plateau phas

97 tilide produced early after depolarizations (EADs) and arrhythmias, whereas verapamil, vanoxerine and

98 in the form of early after depolarizations (EADs).

99 atch leading to early after-depolarizations (EADs) and reflection of impulses in monolayers of well-p

100 ate to severe IRI, 42.9% of grafts developed EAD, and grafts with EAD had significantly inferior surv

101 tions were greater in patients who developed EAD compared with those without EAD (4720 [4374-5133] vs

102 isolated SHR ventricular myocytes developed EADs and triggered activity to the same extent as NR ven

103 Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive im

104 Further, simulations of a cell displaying EADs electrically connected to a cell with normal action

105 afts with entinostat, ATRA, and doxorubicin (EAD) resulted in significant tumor regression and restor

106 t are not observed for solely voltage-driven EADs.

107 nism that causes voltage oscillations during EADs, depending on the amplitude and kinetics of the L-t

108 ents undergoing early allograft dysfunction (EAD) (p < 0.05).

109 Early allograft dysfunction (EAD) after living donor liver transplantation (LDLT) has

110 the categorical early allograft dysfunction (EAD) classification, MEAF is a continuous score, based o

111 to a validated early allograft dysfunction (EAD) definition.

112 predictors for early allograft dysfunction (EAD) in human OLT patients.

113 d the impact of early allograft dysfunction (EAD) in IRI grafts are limited.

114 n of Sdc-1 with early allograft dysfunction (EAD), 1-year graft survival, and 1-year patient survival

115 day graft loss, early allograft dysfunction (EAD), L-GrAFT score, acute kidney injury, and comprehens

116 .0%; P = .003), early allograft dysfunction (EAD; 70.8% vs 45.6% and 8.3%; P = .02), and acute kidney

117 nonfunction (PNF), early graft dysfunction (EAD)].

118 fold more viral IE Zta and Rta and early (E) EAD protein than did cells infected with the parental wi

119 ; optical mapping revealed that the earliest EADs fired at the base.

120 How early (EADs) and delayed afterdepolarizations (DADs) overcome e

121 arging the size of the window region elicits EADs and why shrinking the window region can eliminate t

122 To examine EAD initiation, high-sensitivity intracellular Ca(2+) me

123 l number of cells that synchronously exhibit EADs are needed to result in arrhythmia triggers and sub

124 t influence membrane voltage (V) can explain EAD intermittency.

125 e identified as independent risk factors for EAD.

126 Factor V is an early marker for EAD and is a continuous predictor of short-term graft lo

127 t late Ca(2+) sparks provide a mechanism for EAD initiation.

128 urely voltage-dependent ionic mechanisms for EAD initiation.

129 nt (INa), but not late INa, are required for EAD initiation.

130 X current reversal as an indicator event for EADs, the model identified counterintuitive ionic change

131 molecular and biophysical and mechanism for EADs and impaired survival in adult cardiomyocytes.

132 still require synchronization mechanisms for EADs and DADs to overcome the robust protective effects

133 responsible for LQTS, and elevated risks for EADs may depend on genotypes, such as exercise in LQT1 v

134 ral heterogeneities provided a substrate for EADs, retrograde propagation along the same pathway (ref

135 tography-electroantennographic detection (GC-EAD) by orders of magnitude through a technique known as

136 circumstances a more sensitive and robust GC-EAD instrument will result from the application of this

137 polarization reserve was reduced to generate EADs and random ion channel or path cycle length fluctua

138 ly) and inactivation (positively), generated EADs (single, multiple or preceding repolarization failu

139 Global EAD are small relative to global GDP (~0.02%).

140 However, EADs are also frequent in the rapidly repolarizing mouse

141 However, EADs emerge upon simultaneous activation of both LCCs an

142 gional differences in I(Ca,L) density and in EAD susceptibility were analyzed in epicardial left vent

143 to be excessively covalently bound by HNE in EAD inferior parietal lobule (IPL) compared to age-relat

144 ssion of AD, and is the first to identify in EAD identical brain proteins previously identified as HN

145 The role of I(Ca,L) in EAD formation was directly assessed using the dynamic cl

146 gate excessively HNE-bound brain proteins in EAD compared to those in control.

147 into connecting HNE-bound brain proteins in EAD to those previously identified in MCI and AD, since

148 hat there is an overlap of brain proteins in EAD with previously identified oxidatively modified prot

149 trotonic effects may play a critical role in EAD-mediated arrhythmogenesis.

150 KII activation may be an important factor in EADs caused by oxidative stress.

151 previous study explains slow fluctuations in EADs, which may underlie intermittency of EAD trains and

152 t complex effects on EADs, but cannot induce EADs of significant amplitude without the participation

153 mol/L), or a combination were used to induce EADs, DADs, and triggered activity.

154 micromol/L, n=5), prevented H(2)O(2)-induced EADs and DADs, and the selective CaMKII peptide inhibito

155 sing Ca influx via I(Ca,L), H(2)O(2)-induced EADs were also frequently followed by DADs in response t

156 /L) for 5 to 15 minutes consistently induced EADs that were suppressed by the I(Na) blocker tetrodoto

157 g bradycardia, the emergence of H2O2-induced EADs was correlated with a shift in the timing of NCX cu

158 easured slow-rate dependence of H2O2-induced EADs.

159 the whole heart, suggesting that ISO-induced EADs are genotype specific.

160 der several experimental conditions inducing EADs, including oxidative stress with hydrogen peroxide,

161 Ca(2+) entry through Ca(V)1.2 and inhibiting EADs.

162 smic reticulum Ca(2+) release, and initiated EADs below the ICaL activation range (-47 +/- 0.7 mV).

163 t ventricular myocytes revealed intermittent EADs, with slow fluctuations between runs of APs with EA

164 ling and computer simulations to investigate EAD synchronization and arrhythmia induction in tissue m

165 riments in isolated myocytes, that irregular EAD behavior is dynamical chaos.

166 NR ventricular myocytes, except with larger EAD amplitude.

167 During 6-s pacing cycle length, EADs were blocked by the Ito blocker 4-aminopyridine, bu

168 tective negative feedback mechanism, masking EADs.

169 e H(2)O(2)) and suppressed H(2)O(2)-mediated EADs by reducing the number of foci, causing VF to termi

170 d PVT incidences by reducing Ca(2+)-mediated EADs and focal activity during isoproterenol perfusion (

171 interactions between coupled cells modulates EAD formation, cell connectivity was reduced by RNA sile

172 quilibrium reactivation of INa drives murine EADs.

173 This suggests that murine EADs exhibit unique dynamics, which are key for interpre

174 nonequilibrium INa dynamics underlie murine EADs.

175 though the uncoupled cells exhibit either no EAD or only a single EAD, when these cells are coupled t

176 ion with lower [K(+)](o), while there was no EAD formation in littermate control (LMC) or LQT1 myocyt

177 nously exhibit the same number of EADs or no EADs with a very small dispersion of refractoriness, or

178 Upon reducing I Kr, the APs without EADs (no-EAD response) showed gradual prolongation of AP duration

179 anscriptional silencing of RAR-beta Notably, EAD was the most effective combination in inducing diffe

180 e aimed to assess factor V as a biomarker of EAD and a predictor of graft loss after liver transplant

181 Among putative causes of EAD after LDLT are excessive portal pressure and/or flow

182 e might be at higher risk for development of EAD after OLT.

183 006) were associated with the development of EAD.

184 RI severity correlated with the incidence of EAD and graft survival at 6 months.

185 in EADs, which may underlie intermittency of EAD trains and consequent arrhythmias.

186 n model, factor V was a continuous marker of EAD (odds ratio [OR], 0.96; 95% confidence interval [CI]

187 the Hopf-homoclinic bifurcation mechanism of EAD-mediated triggered activity, and raise the possibili

188 Here we introduce a cell culture model of EAD propagation consisting of monolayers of cultured neo

189 Our objective was to evaluate patterns of EAD after LDLT.

190 PP and was the only independent predictor of EAD.

191 e no steatosis groups except for the rate of EAD (56.8% vs 45.6%; P = .04).

192 less concerning the possible relationship of EAD HNE-modified brain proteins with HNE-modified protei

193 Risk of EAD was associated with left lobe grafts, lower graft we

194 The symptoms of EAD mirror the disease advancement between the two phase

195 ransplant survival was compared with that of EAD in univariable and multivariable models by means of

196 an organizing center for different types of EAD dynamics.

197 tage oscillations that are characteristic of EADs.

198 al approach to investigate the dependence of EADs on the biophysical properties of the L-type Ca(2+)

199 We conclude that the irregular dynamics of EADs is intrinsically chaotic, with random fluctuations

200 as an important player in the generation of EADs.

201 PD prolongation and reduced the incidence of EADs in LQT2 myocytes.

202 may synchronously exhibit the same number of EADs or no EADs with a very small dispersion of refracto

203 igated, and mechanisms for the occurrence of EADs on a beat-to-beat basis have been proposed.

204 engthening AP duration and the occurrence of EADs promote DADs by increasing intracellular Ca loading

205 The occurrence of EADs was also drastically reduced in hetKO.

206 m leading to the concealing and revealing of EADs in LQT3 models.

207 a coupling strength-dependent suppression of EADs consistent with the experimental results.

208 n Scn5a+/Delta hearts through suppression of EADs.

209 states, forming a bistable on-off switch of EADs.

210 pathetic tone can be an effective trigger of EADs in LQT2 perfused hearts.

211 imulation demonstrated a high-risk window of EADs in LQT2 during ISO perfusion owing to mismatch in t

212 the effects of widening the window I(CaL) on EAD-propensity; and (iii) to test whether EADs from incr

213 tigate the effects of Ca-voltage coupling on EAD and DAD dynamics.

214 to accounts for these paradoxical effects on EADs by influencing the dynamic evolution of repolarizat

215 ous Ca waves also exhibit complex effects on EADs, but cannot induce EADs of significant amplitude wi

216 such as period 2 or chaos when alternans or EADs occur in pathological conditions.

217 MEAF outperformed EAD as predictor of transplant survival, either when use

218 er modeling revealed that I(NaL) potentiates EADs in the long QT syndrome type 2 setting through (1)

219 curve combining both lipid levels predicted EAD with 82% accuracy.

220 tion reserve in long QT syndrome and prevent EADs and PVTs.

221 Selective I(NaL) blockade by GS967 prevents EADs and abolishes PVT in long QT syndrome type 2 rabbit

222 agonists BayK8644 and isoproterenol produce EAD bursts that are suppressed by the LTCC blocker nitre

223 tion, is not by itself sufficient to produce EADs.

224 potential duration prolongation and produced EADs, in particular, at slow pacing rates.

225 ssociated mutant channels, myocytes produced EADs for wide intercellular clefts, whereas for narrow c

226 dening the I(CaL,D-C) window region produced EADs of various types, dependent on window width.

227 r example, a 15 mV activation shift produced EADs in nine of 17 (53%) human atrial myocytes vs. 0 of

228 Specifically, the model produces EADs in the morning, but not at other times of day.

229 e of intermediate Ito properties can promote EADs by influencing the temporal evolution of other curr

230 releases caused by RyR hyperactivity promote EADs and underlie the enhanced triggered activity throug

231 increased sodium current(INa) would promote EADs, we employed adenoviral transfer of Nav1.5 (Ad-Nav1

232 also impairs I(Na) inactivation and promotes EADs, we hypothesized that CaMKII activation may be an i

233 tions concur that I(Ca,L) elevation promotes EADs and is an important determinant of long QT type 2 a

234 pokalemia plays a critical role in promoting EAD-mediated arrhythmias by inducing a positive feedback

235 egional synchronization leads to propagating EADs, forming PVCs in tissue.

236 or global cellular CaMKII inhibition reduced EADs and improved cell survival to control levels in WT

237 Ca(2+) efflux from cytosol, thereby reducing EADs.

238 al properties of the native I(Ca,L) restored EAD occurrence in myocytes challenged by H(2)O(2) or hyp

239 The data show EAD formation in superfused canine pulmonary veins, enha

240 e previously identified in MCI and AD, since EAD is a transitional stage between MCI and late-stage A

241 cells exhibit either no EAD or only a single EAD, when these cells are coupled to form a tissue, more

242 er, only LQT2 myocytes developed spontaneous EADs following perfusion with lower [K(+)](o), while the

243 A stronger EAD-generating effect resulted from independently shifti

244 In summary, EAD formation is genotype specific, such that EADs can b

245 Whereas sufficiently large Ito can suppress EADs, a wide range of intermediate Ito properties can pr

246 se surrounding tissue to conduct or suppress EADs are poorly understood.

247 Pase activity can either promote or suppress EADs due to the complex effects of Ca on ionic current p

248 ation or larger pedestals tended to suppress EADs.

249 ese properties could be designed to suppress EADs.

250 owerful therapeutic strategy for suppressing EADs and EAD-mediated arrhythmias.

251 coupling can no longer globally synchronize EADs, resulting in regions of partial synchronization th

252 These regional partially synchronized EADs then form premature ventricular complexes that prop

253 uggests that the efficacy of drugs targeting EAD-mediated arrhythmias may depend on the time of day t

254 tion as the likely mechanism for terminating EAD bursts.

255 Computer modeling revealed that EAD generation by hypokalemia (with or without dofetilid

256 el in atrial cardiomyocytes, and showed that EADs of various types are generated by widening (particu

257 AD formation is genotype specific, such that EADs can be elicited in LQT2 myocytes simply by lowering

258 The EAD challenge promotes awareness of and addresses this k

259 The EAD is a physiological recording from the antenna of an

260 The EAD-like waveforms of Scn8a(N1768D/+) CA1 hippocampal ne

261 um reactivation of INa and thereby drive the EAD upstroke.

262 y inactive channels are recruited during the EAD upstroke, and that nonequilibrium INa dynamics under

263 Thus, the EAD-induced arrhythmias with repolarisation reserve atte

264 These EAD bursts exhibited a key dynamical signature of the du

265 These EADs were abolished by caffeine and tetrodotoxin (but no

266 I(CaL,D-C) window by ~10 mV abolished these EADs.

267 y that this mechanism may also contribute to EAD formation in clinical settings such as long QT syndr

268 enhanced cell differentiation in response to EAD triple therapy.

269 ne (0.05-3 muM) prolonged the AP, leading to EADs and reflection.

270 ch contributes to the enhanced propensity to EADs and TdP in female hearts.

271 l area of contiguous myocytes susceptible to EADs or DADs was surrounded by unsusceptible tissue.

272 mpared to results obtained using traditional EAD recording techniques.

273 different high-risk conditions that trigger EADs using transgenic rabbit models of LQT1 and LQT2, wh

274 depolarizing electrotonic current to trigger EADs and reflection.

275 prenaline (ISO) prolonged APDs and triggered EADs in LQT1 myocytes in the presence of lower [K(+)](o)

276 or of transplant loss than the commonly used EAD classification.

277 Ventricular EADs involve reactivation of a Ca(2+) current (I(CaL) )

278 The secondary outcome was EAD, as defined by Olthoff et al.

279 , 0.97; 95% CI, 0.94-0.99 per U/mL), whereas EAD was not significant when adjusted for factor V.

280 on EAD-propensity; and (iii) to test whether EADs from increased I(CaL) and AP duration are supressed

281 In 11 rabbit atrial myocytes in which EADs were generated either by increasing the conductance

282 Risk factors associated with EAD after LDLT include: graft type and size, preoperativ

283 he only factor independently associated with EAD was MaS (odds ratio, 5.44; confidence interval, 1.05

284 All PP except lactate correlated with EAD, 90-minute alanine aminotransferase showing the high

285 .9% of grafts developed EAD, and grafts with EAD had significantly inferior survival compared to graf

286 ays was 5.2 times higher for recipients with EAD versus those without EAD (P < 0.001).

287 teomics analysis of brain from subjects with EAD and even less concerning the possible relationship o

288 Simulations in 2-dimensional tissue with EAD-mediated multifocal VF showed progressive reduction

289 tatic cells also responded to treatment with EAD.

290 nihilation caused a transition to an AP with EADs as a new stable steady state.

291 h slow fluctuations between runs of APs with EADs present or absent.

292 pendent plateau oscillations consistent with EADs.

293 iations in action potential duration without EAD presence do not cause large dispersion of refractori

294 inferior survival compared to grafts without EAD.

295 ho developed EAD compared with those without EAD (4720 [4374-5133] vs 3838 [3202-4240] ng/mL, P = 0.0

296 for recipients with EAD versus those without EAD (P < 0.001).

297 ting in 2 stable AP states, with and without EADs (ie, bistability).

298 Upon reducing I Kr, the APs without EADs (no-EAD response) showed gradual prolongation of AP

299 n=7/12 and 100 nmol/L n=8/12 hearts without EADs and PVTs).

300 that propagate into recovered tissue without EADs.