ライフサイエンスコーパス: afterdepolarization

1 potential (without increasing the chance of afterdepolarization).

2 low-threshold burst firing driven by a spike afterdepolarization.

3 ane depolarization and the size of the spike afterdepolarization.

4 afterhyperpolarization and a longer-lasting afterdepolarization.

5 of both spontaneous Ca(2+) waves and delayed afterdepolarizations.

6 ntial duration (APD) and contribute to early afterdepolarizations.

7 reduced the occurrence of early and delayed afterdepolarizations.

8 the APD and reducing the frequency of early afterdepolarizations.

9 ch as early afterdepolarizations and delayed afterdepolarizations.

10 Ca(2+) stores in the pathogenesis of delayed afterdepolarizations.

11 ased susceptibility to arrhythmia-triggering afterdepolarizations.

12 s the heart from arrhythmias due to sporadic afterdepolarizations.

13 t of APD and suppresses development of early afterdepolarizations.

14 s triggered activity due to delayed or early afterdepolarizations.

15 isplayed prolonged repolarization with early afterdepolarizations.

16 rmalized the action potential, and prevented afterdepolarizations.

17 e by nonreentrant mechanisms such as delayed afterdepolarizations.

18 longation, increased I(Ca) facilitation, and afterdepolarizations.

19 ficant increase in the occurrence of delayed afterdepolarizations.

20 bility that resulted in formation of delayed afterdepolarizations.

21 tion and development of arrhythmogenic early afterdepolarizations.

22 tening, predisposing the myocardium to early afterdepolarizations.

23 f AP duration and provoked early and delayed afterdepolarizations.

24 hypokalemia, and quinidine resulted in early afterdepolarizations.

25 2 of the SCS occasionally resulted in early afterdepolarizations.

26 low heart rate triggers arrhythmogenic early afterdepolarizations.

27 ses the myocardium to arrhythmogenic delayed afterdepolarizations.

28 ay be due to triggered activity from delayed afterdepolarizations.

29 ariability of AP repolarization, and delayed afterdepolarizations.

30 longation and the induction of plateau early afterdepolarizations.

31 ) and generate triggered activity from early afterdepolarizations.

32 deling and an increased propensity for early afterdepolarizations.

33 ation), both lead to prolonged APs and early afterdepolarizations.

34 s of giant AnkG results in delayed and early afterdepolarizations.

35 olong the action potential and trigger early afterdepolarizations.

36 rane potential oscillations as early/delayed afterdepolarizations.

37 rrhythmia triggers such as early and delayed afterdepolarizations.

38 greater tendency for calcium-driven delayed afterdepolarizations.

39 romotion of arrhythmogenic waves and delayed afterdepolarizations.

40 (2+) waves underlying arrhythmogenic delayed afterdepolarizations.

41 ing to voltage instabilities through delayed afterdepolarizations.

42 carbon monoxide-induced proarrhythmic early afterdepolarizations.

43 loss led to altered LTCC function and early afterdepolarizations.

44 hich contributed to the development of early afterdepolarizations.

45 , which facilitates the formation of delayed afterdepolarizations.

46 ation of BFc inputs prolonged current-evoked afterdepolarizations.

47 action potential duration and arrhythmogenic afterdepolarizations.

48 (2+) exchanger activity and triggering early afterdepolarizations.

49 arization and vulnerability to phase 3 early afterdepolarizations.

50 e similarly demonstrated increased INa-L and afterdepolarizations.

51 he action potential, and occurrence of early afterdepolarizations.

52 ility of repolarization and suppressed early afterdepolarizations.

53 eading to the formation of early and delayed afterdepolarizations.

54 on potentials, calcium transients, and early afterdepolarizations.

55 L, abbreviated the APD, and suppressed early afterdepolarizations.

56 96 9 ms, n=81, P<0.01) and caused more early afterdepolarizations (11.7%) compared with isogenic cont

57 ic control (APD90: 618 8 ms, n=115 and early afterdepolarizations: 2.6%, P<0.05).

58 of 14.5 mV in abnormal APs exhibiting early afterdepolarizations (72.5% of the emulated APs were ali

59 or 2)-mediated store Ca(2+) leak and delayed afterdepolarizations, a known mechanism of Ca(2+)-mediat

60 ting neurons was paralleled by a gradient in afterdepolarization (ADP) amplitude.

61 as a bifurcation parameter that reduces the afterdepolarization (ADP) and decreases the slope (gain)

62 expresses a T-type calcium channel-mediated afterdepolarization (ADP) and shows rebound activity upo

63 ossy cells tested, and also produced a clear afterdepolarization (ADP) in nearly 100% of trials.

64 nderlying burst firing in these cells is the afterdepolarization (ADP) that follows each action poten

65 ifferent afferent input pathways, initiating afterdepolarization (ADP), and triggering burst firing.

66 set of these interneurons was replaced by an afterdepolarization (ADP), often of sufficient magnitude

67 ramidal neurons are typically followed by an afterdepolarization (ADP), which in many cells contribut

68 proximal Na+ channels and a prominent spike afterdepolarization (ADP).

69 imulus train gave rise to an NMDAR-dependent afterdepolarization (ADP).

70 ient to recruit K(V)4 channels and eliminate afterdepolarization (ADP).

71 opamine D2 receptor (D2R) activation elicits afterdepolarizations (ADPs) in subcortically projecting

72 ring frequency and produced large, sustained afterdepolarizations (ADPs) of stratum oriens-lacunosum

73 tween the afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs) that followed each action po

74 hat cause afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs).

75 e action potentials with large, long-lasting afterdepolarizations (ADPs).

76 Intracellular recordings revealed a slow afterdepolarization (AfD) that triggers myotonic action

77 on to NMDA receptors, the quinpirole-induced afterdepolarization also depended on L-type Ca(2+) chann

78 However, early afterdepolarizations also occurred in untubulated atrial

79 olarizing potential (AHP) and increased slow afterdepolarization amplitudes (ADP), and reduced I(AHP)

80 verted a medium afterhyperpolarization to an afterdepolarization and could convert tonic firing of si

81 ropagating action potential to attenuate the afterdepolarization and repetitive firing, axonal K(v)7

82 The spike-afterdepolarization and the generation of action potenti

83 xposure to the drug generated arrhythmogenic afterdepolarizations and >/=15-fold increases in INa-L.

84 We found that CsCl induced larger early afterdepolarizations and a greater prevalence of VT in d

85 Ca2+ overload occurring in ischemia leads to afterdepolarizations and aftercontractions that are resp

86 uM) increased the frequency and magnitude of afterdepolarizations and also led to development of trig

87 p the [Ca]SR below the threshold for delayed afterdepolarizations and arrhythmia.

88 sing Mg(2+) or flecainide eliminated delayed afterdepolarizations and decreased BVR independent of ef

89 on of drug-induced arrhythmias such as early afterdepolarizations and delayed afterdepolarizations.

90 respectively, compared with negligible early afterdepolarizations and ectopic beats in untreated cont

91 published studies using animal models, early afterdepolarizations and ectopic beats were observed in

92 inhibitor, did not reduce SCaEs and delayed afterdepolarizations and failed to prevent AF.

93 rdiomyocyte interior and also caused delayed afterdepolarizations and later cardiomyocyte death, both

94 ation endows DRG neurons with multiple early afterdepolarizations and leads to substantial prolongati

95 nce, we observed significantly more cellular afterdepolarizations and more severe premature atrial co

96 ibited reduced excitability with fewer early afterdepolarizations and narrower action potentials afte

97 p to suppress arrhythmias initiated by early afterdepolarizations and premature beats in the ventricl

98 ced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias.

99 ous SR Ca release events, triggering delayed afterdepolarizations and spontaneous beats.

100 nificant reduction of arrhythmogenic delayed afterdepolarizations and spontaneous Ca(2+) waves in iso

101 ate the susceptibility threshold for delayed afterdepolarizations and the aftercontraction wave propa

102 t genetic inhibition of NCX protects against afterdepolarizations and to investigate the underlying m

103 l opening furthermore contributed to delayed afterdepolarizations and triggered action potentials.

104 ly (1) reduced isoproterenol-induced delayed afterdepolarizations and triggered activity in infected

105 Early afterdepolarizations and triggered activity occurred spo

106 1), which predisposes HF myocytes to delayed afterdepolarizations and triggered activity.

107 marked arrhythmogenicity manifested by early afterdepolarizations and triggered arrhythmias, and redu

108 conditions may potentiate Ca waves and thus afterdepolarizations and triggered arrhythmias.

109 ction potential duration, and caused delayed afterdepolarizations and triggered beats in intact cardi

110 +/-28.9 ms (chronic; P<0.001), and generated afterdepolarizations and/or triggered activity in drug-t

111 synaptic spikes are followed by a pronounced afterdepolarization, and are broadened by pharmacologica

112 ecrease the input resistance, shorten the AP afterdepolarization, and generate inhibitory postsynapti

113 de and faster AP rise rate, larger postspike afterdepolarization, and reduced membrane time constant.

114 action potential duration, spontaneous early afterdepolarizations, and 2:1 atrioventricular block in

115 ent (for a given SR Ca(2+) release), delayed afterdepolarizations, and nonreentrant initiation of ven

116 duced the incidence of Ca(2+) waves, delayed afterdepolarizations, and spontaneous action potentials.

117 ith postpause action potential prolongation, afterdepolarizations, and triggered activity.

118 Afterdepolarizations apparently represent recurrent GABA

119 How delayed afterdepolarizations are synchronized to overcome the so

120 Delayed afterdepolarizations are thought to be due to spontaneou

121 Exposure to CO causes early afterdepolarization arrhythmias.

122 sed oxidative stress, CaMKII activation, and afterdepolarizations as triggers of lethal ventricular a

123 release have been shown to activate delayed afterdepolarizations as well as some cardiac arrhythmias

124 on potential duration and late phase 3 early afterdepolarizations associated with reduced sodium curr

125 polarization response and augmentation of an afterdepolarization, both triggered by pirenzepine-sensi

126 Ca(2+) has been implicated in the genesis of afterdepolarizations, but pretreatment with high-dose W-

127 To confirm that D2Rs can elicit this afterdepolarization by enhancing Ca(2+) (and Ca(2+)-depe

128 This indicates that during delayed afterdepolarizations, Ca release units (CRUs) interact w

129 ch-release to trigger suprathreshold delayed afterdepolarizations can be affected by heterogeneity in

130 ntricle model, demonstrating that such early afterdepolarizations can propagate and initiate reentran

131 higher mean diastolic potential, and delayed afterdepolarizations compared with controls.

132 Early afterdepolarizations, considered cellular substrates for

133 Delayed afterdepolarizations could be induced easily and reversi

134 Phase 2 or 3 early afterdepolarizations could be induced easily by Bay K864

135 g early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is unknown.

136 s sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) f

137 CR) from the sarcoplasmic reticulum, delayed-afterdepolarizations (DAD), and triggered activity.

138 ion of ISO in vivo, the incidence of delayed afterdepolarizations (DADs) and beat-to-beat variability

139 the peri-infarct zone is a source of delayed afterdepolarizations (DADs) and has a high beat-to-beat

140 arly afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltage oscillations kno

141 Delayed afterdepolarizations (DADs) carried by Na(+)-Ca(2+)-exch

142 holine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atrial myocytes.

143 How early (EADs) and delayed afterdepolarizations (DADs) overcome electrotonic source

144 ) waves in cardiac myocytes underlie delayed afterdepolarizations (DADs) that trigger cardiac arrhyth

145 reticulum (SR) Ca(2+) release causes delayed afterdepolarizations (DADs) via Ca(2+)-induced transient

146 Females were more prone to delayed afterdepolarizations (DADs), whereas males were more sus

147 a(+)/Ca(2+)-exchanger activation and delayed afterdepolarizations (DADs).

148 -sensitive inward currents to induce delayed afterdepolarizations (DADs).

149 ding to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).

150 In conclusion, H(2)O(2)-induced afterdepolarizations depend on both impaired I(Na) inact

151 atrial myocytes additionally exhibited early afterdepolarizations during hypokalemia, associated with

152 reatment also lowered the incidence of early afterdepolarizations during isoproterenol; an effect par

153 ranolazine on late phase 3 early and delayed afterdepolarization (EAD and DAD)-induced triggered acti

154 his study examined the role of phase 2 early afterdepolarization (EAD) in producing a trigger to init

155 proarrhythmic effect, ie, by promoting early afterdepolarization (EAD) or delayed afterdepolarization

156 midal neurons in brain slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1 but n

157 Exposure to H(2)O(2) initiated early afterdepolarization (EAD)-mediated triggered activity th

158 hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activity.

159 Early afterdepolarizations (EADs) and delayed afterdepolarizat

160 sudden cardiac death likely caused by early afterdepolarizations (EADs) and polymorphic ventricular

161 lazine (5 to 20 micromol/L) suppressed early afterdepolarizations (EADs) and reduced the increase in

162 (3) Frequent epicardial early afterdepolarizations (EADs) and spontaneous ventricular

163 nous H(2)O(2) has been shown to induce early afterdepolarizations (EADs) and triggered activity by im

164 ated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by

165 Spontaneous early afterdepolarizations (EADs) and ventricular tachycardia/

166 Pathologies that result in early afterdepolarizations (EADs) are a known trigger for tach

167 Early-afterdepolarizations (EADs) are abnormal action potentia

168 Early afterdepolarizations (EADs) are abnormal depolarizations

169 Early afterdepolarizations (EADs) are linked to both triggered

170 Cardiac action potential alternans and early afterdepolarizations (EADs) are linked to cardiac arrhyt

171 , but it is unclear how arrhythmogenic early afterdepolarizations (EADs) are triggered in failing hea

172 Early afterdepolarizations (EADs) are triggers of cardiac arrh

173 Early afterdepolarizations (EADs) are voltage oscillations tha

174 ecursor of lethal cardiac arrhythmias, early afterdepolarizations (EADs) during action potentials(APs

175 Irregularly occurring early afterdepolarizations (EADs) in cardiac myocytes are trad

176 Dofetilide (an IKr blocker) induced early afterdepolarizations (EADs) in female base myocytes cult

177 s to the development of arrhythmogenic early afterdepolarizations (EADs) in isolated cells and poorly

178 ation (APD) prolongation and prominent early afterdepolarizations (EADs) in neonatal cardiomyocytes e

179 Atrial early-afterdepolarizations (EADs) may contribute to atrial fib

180 tential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat chang

181 n further by small oscillations called early afterdepolarizations (EADs) that can occur either during

182 ted both to suppress and to facilitate early afterdepolarizations (EADs) when repolarization reserve

183 ce, and TG cardiomyocytes had frequent early afterdepolarizations (EADs), a hypothesized mechanism fo

184 membrane potential oscillations called early afterdepolarizations (EADs), and premature death in pace

185 n potential duration, Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointes.

186 Epicardial early afterdepolarizations (EADs), often accompanied by sponta

187 tracellular Ca2+ (Ca2+i) in triggering early afterdepolarizations (EADs), the origins of EADs and the

188 circadian pattern in the occurrence of early afterdepolarizations (EADs), which are abnormal depolari

189 ormal electrical oscillations, such as early afterdepolarizations (EADs), which are associated with l

190 f the cardiac action potential causing early afterdepolarizations (EADs).

191 h in turn could promote delayed and/or early afterdepolarizations (EADs).

192 d beat-to-beat variability, leading to early afterdepolarizations (EADs).

193 tened susceptibility to arrhythmogenic early afterdepolarizations (EADs).

194 and late sodium current that produces early afterdepolarizations (EADs).

195 ion (APD) and triggering proarrhythmic early afterdepolarizations (EADs).

196 lihood of cellular arrhythmias such as early afterdepolarizations (EADs).

197 rolongation of APD and an incidence of early afterdepolarization equal to values previously reported

198 nd increases the propensity to develop early afterdepolarizations, especially in Endo.

199 cardiomyocyte action potentials and delayed afterdepolarizations, factors that increase risk of arrh

200 to trigger an action potential and the fast afterdepolarization following action potentials graduall

201 GABAergic and generate large I(CAN)-mediated afterdepolarizations following bursts of action potentia

202 Notably, we could still elicit this afterdepolarization for some time after the cessation of

203 Single-cell behavior showed early afterdepolarizations for increases in TRPM4 channel expr

204 ed action potential duration, enhanced early afterdepolarization formation, and facilitated triggered

205 ing [Na(+)]i monotonically increased delayed afterdepolarization frequency.

206 gene expression, and an increase in delayed afterdepolarizations from 0/min to 12/min.

207 more generally to suppress delayed or early afterdepolarizations from any cause by overexpressing th

208 troke velocity, greater incidence of delayed afterdepolarizations, greater contraction force, and alt

209 hythmic substrate and triggers such as early afterdepolarization in experimental models.

210 The depolarization and slow afterdepolarization in GCs were blocked by the alpha1A-a

211 ings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-CMs compa

212 0.001 and P<0.01, respectively) and elicited afterdepolarizations in 8/16 SY/YY cells but only in 1/1

213 The mechanisms leading to delayed afterdepolarizations in AF patients have not been define

214 ous Ca2+ release events that lead to delayed afterdepolarizations in affected patients.

215 frequency and amplitude of SCaEs and delayed afterdepolarizations in atrial myocytes and intact atria

216 f AF by promoting regional SCaEs and delayed afterdepolarizations in atrial tissue, which can be prev

217 prolongation and depressed early and delayed afterdepolarizations in cardiomyocytes isolated from MI

218 dofetilide to increase APD and induce early afterdepolarizations in females.

219 , CORM-2-prolonged the APs and induced early afterdepolarizations in guinea pig myocytes.

220 ent is known to mediate arrhythmogenic early afterdepolarizations in heart, and these were similarly

221 entials and to a higher probability of early afterdepolarizations in MLP-/- than in control myocytes.

222 reticulum Ca(2+) release events and delayed afterdepolarizations in NPR-B(+/-) atrial myocytes.

223 d an increased risk of proarrhythmic delayed afterdepolarizations in POAF subjects in response to int

224 hypokalemia in the long term, or by delayed afterdepolarizations in the short term.

225 uM) and thapsigargin (10 muM) eliminated all afterdepolarizations in these cells.

226 Na(+) current-driven early afterdepolarizations in untubulated atrial cells were en

227 ect to increase APD diminished, as did early afterdepolarization incidence.

228 or AP firing, increased incidence of delayed afterdepolarizations, increased calcium transient durati

229 nsistent with the greater incidence of early afterdepolarizations induced in this region by dofetilid

230 M cells and Purkinje fibers to develop early afterdepolarization-induced extrasystoles, which are tho

231 Our data suggest delayed afterdepolarization-induced extrasystolic activity serve

232 /RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity at lower

233 se results support the hypothesis that early afterdepolarization-induced triggered activity in Purkin

234 esting that they might be initiated by early afterdepolarization-induced triggered activity in Purkin

235 This study sought to determine whether early afterdepolarization-induced triggered activity is respon

236 Delayed afterdepolarization-induced triggered beats that origina

237 Although it is widely accepted that afterdepolarizations initiate arrhythmias when action po

238 These ECG analyses suggest that early afterdepolarizations initiate TdP and, if present, may h

239 the inward aftercurrent underlying the slow afterdepolarization is inhibited by expression of a Galp

240 Surprisingly, this afterdepolarization is masked in quiescent brain slices,

241 We have shown previously that the muscarinic afterdepolarization is mediated by a calcium-activated n

242 ; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher sarcoplas

243 ggered activity (apparently induced by early afterdepolarizations) is observed.

244 tation induced QT prolongation and transient afterdepolarizations, known cellular mechanisms for arrh

245 Mechanically induced delayed afterdepolarization-like events contributed to the forma

246 to PV BCs, CCK BCs exhibited a mAChR-induced afterdepolarization (mADP) that was frequency and activi

247 Moreover, the cholinergic engagement of afterdepolarizations may contribute to the formation of

248 at the onset of focal activity showed early afterdepolarization-mediated triggered activity that led

249 ontaneous VF arising from the RV by an early afterdepolarization-mediated triggered activity.

250 ly coupled action potentials consistent with afterdepolarization-mediated triggered beats were readil

251 rats and 2 of 9 normal rats (P<0.05); early afterdepolarization occurred in two CKD rats but not nor

252 hat were responsible for the prominent spike afterdepolarization of CA3 pyramids.

253 ntial duration and a high incidence of early afterdepolarizations on 1-Hz electric point stimulation,

254 ibers attributable to abnormal automaticity, afterdepolarizations, or reentry.

255 K(V)4 channels regulates the duration of the afterdepolarization over more than one order of magnitud

256 ontaneous Ca(2+)-releases and arrhythmogenic afterdepolarizations, particularly upon exposure to infl

257 mulation induces a long-lasting subthreshold afterdepolarization, persistent firing, or prolonged pla

258 ncreased the amplitude of the postburst slow afterdepolarization potential (sADP) at the soma of both

259 hmogenic cells to generate delayed and early afterdepolarizations-related arrhythmias.

260 It is clear that delayed afterdepolarization resulting from abnormal activation o

261 motoneurons displayed a characteristic slow afterdepolarization (sADP).

262 mediate the muscarinic receptor-induced slow afterdepolarization seen in pyramidal cells of the cereb

263 nce of beta stimulation, we observed delayed afterdepolarizations, suggesting that accelerated recove

264 bral cortex induces the appearance of a slow afterdepolarization that can sustain autonomous spiking

265 obust excitatory effect that included a slow afterdepolarization that followed a train of action pote

266 application of TRH prominently enhanced the afterdepolarization that follows rebound Ca2+ spikes, su

267 , the D2R agonist quinpirole elicits a novel afterdepolarization that generates voltage fluctuations

268 , D2Rs can elicit a Ca(2+)-channel-dependent afterdepolarization that powerfully modulates activity i

269 ction potential repolarization to produce an afterdepolarization that triggers subsequent action pote

270 4) have a propensity to develop phase 2 to 4 afterdepolarizations that can elicit triggered beats; an

271 potentials evoked from rest have large, long afterdepolarizations that disappear with pre-spike hyper

272 The afterdepolarizations that initiate TdP are facilitated b

273 to contribute to the arrhythmogenic delayed afterdepolarizations that occur in Ca2+-overloaded cells

274 ed frequent spontaneous development of early afterdepolarizations that occurred at phase 3 of action

275 /Ca(2+) exchange current inducing a "delayed afterdepolarization" that can in turn trigger an action

276 s, in turn, is accompanied by arrhythmogenic afterdepolarizations thought to trigger torsades de poin

277 -clamp and Ca(2+) imaging, early and delayed afterdepolarizations trailed spontaneous Ca(2+) release

278 leading to increased vulnerability to early afterdepolarization, triggered activity, and ventricular

279 ing gain, causes AF-promoting atrial delayed afterdepolarizations/triggered activity in cAF patients.

280 panied by inward I(NCX) currents and delayed afterdepolarizations/triggered activity occurred more of

281 hat lead to focal ectopic firing via delayed afterdepolarizations/triggered activity.

282 -function increased [Ca2+]i and caused early afterdepolarizations under adrenergic stress, as observe

283 s underlying the muscarinic receptor-induced afterdepolarization using molecular biological and elect

284 the post-burst afterhyperpolarization to an afterdepolarization via a rapidly reversible upregulatio

285 The afterdepolarization was dependent on elevations in intra

286 -6) mol/L dofetilide, the incidence of early afterdepolarizations was 28% in DHT-treated and 55% in n

287 cle length=1 second), the incidence of early afterdepolarizations was: female, 67%; ORCH, 56%; male,

288 Early afterdepolarizations were more frequent in DHF than in c

289 Early afterdepolarizations were not accompanied by Ca(2+) wave

290 Early afterdepolarizations were observed after application of

291 ged significantly; and, in some cells, early afterdepolarizations were observed.

292 These phase-3 early afterdepolarizations were rather linked to reactivation

293 ction-potential (AP) durations after delayed afterdepolarizations were significantly prolonged.

294 s increased excitability and increased spike afterdepolarization, were affected by the training.

295 the RyR increased the probability of delayed afterdepolarizations when heart failure was simulated.

296 nd membrane potential, with signs of delayed afterdepolarizations when undergoing periodic pacing and

297 pontaneous Ca elevations (SCaEs) and delayed afterdepolarizations whenever the pacing train failed to

298 ent firing ability are due to changes to the afterdepolarization, which may in turn be modulated by t

299 pression, where high [Na(+)]i causes delayed afterdepolarizations, which can be prevented by imposing

300 he elevated [Na(+)]i of PCs promoted delayed afterdepolarizations, which were always preceded by spon