ライフサイエンスコーパス: pacemaker

1 s-LNvs) unique characteristics as the master pacemaker.

2 of circadian phase of the brain's circadian pacemaker.

3 r (right ventricle) active fixation leadless pacemaker.

4 rons rather than controlling their molecular pacemaker.

5 ary catheter, and early removal of temporary pacemaker.

6 iasmatic nucleus (SCN), the master circadian pacemaker.

7 inability of light to reset their circadian pacemaker.

8 nction of the s-LNvs as the master circadian pacemaker.

9 all absolute increase in needing a permanent pacemaker.

10 into host myocardium and create a biological pacemaker.

11 come data are yet available for the leadless pacemakers.

12 te, with the recent introduction of leadless pacemakers.

13 ional transvenous single-chamber ventricular pacemakers.

14 other novel technologies, including leadless pacemakers.

15 puts from a network of synchronous molecular pacemakers.

16 s identified from interrogation of permanent pacemakers.

17 ative management among patients with cardiac pacemakers.

18 ble cardioverter defibrillators or permanent pacemakers.

19 less pacemakers versus 4.1% for conventional pacemakers.

20 .6%, and 3.8%; P < .001), need for permanent pacemaker (10.0%, 13.8%, and 8.9%; P < .001), and bleedi

21 0 patients have a single chamber ventricular pacemaker, 14 a dual chamber pacemaker, 3 a biventricula

22 ber ventricular pacemaker, 14 a dual chamber pacemaker, 3 a biventricular pacemaker, and 1 has a sing

23 ngth of 1.5 Tesla in 1509 patients who had a pacemaker (58%) or an implantable cardioverter-defibrill

24 ired in 3 out of 35 patients without a prior pacemaker (8.6%).

25 lation of IKACh prevented dysfunction of SAN pacemaker activity by allowing net inward current to flo

26 their contribution to sinoatrial node (SAN) pacemaker activity has been investigated.

27 of SK channels could explain arrhythmic SAN pacemaker activity in the atrial-specific Na(+) /Ca(2+)

28 otide-modulated ion channel (HCN) drives the pacemaker activity in the heart, and its malfunction can

29 Dysfunction of pacemaker activity in the sinoatrial node (SAN) underlie

30 native ion-channel Kv4.3 and accelerate the pacemaker activity of rodent dopamine neurons.

31 r Ca(2+) accumulation during spontaneous SAN pacemaker activity produces intermittent hyperactivation

32 ICC pacemaker activity results from their ability to generat

33 the external globus pallidus (GPe) generate pacemaker activity that controls basal ganglia, circuitr

34 uctal gray neurons indicated the presence of pacemaker activity within neonatal lamina I projection n

35 Ca efflux results in intermittent bursts of pacemaker activity, reminiscent of human sinus node dysf

36 rain continuously generate a slow endogenous pacemaker activity, the mechanism of which is still deba

37 ries to cardiac and venous structures during pacemaker and defibrillator lead extraction are serious

38 munication and coupling between this central pacemaker and downstream clusters are not fully elucidat

39 formed in 1000 cases in which patients had a pacemaker and in 500 cases in which patients had an ICD.

40 A mathematical model of the circadian pacemaker and its response to light was used to demonstr

41 ral neurons (s-LNvs) acting as the circadian pacemaker and large ventral-lateral neurons (l-LNvs) reg

42 , misalignment between the central circadian pacemaker and the behavioral cycle) has not been systema

43 These devices included 37 pacemakers and 47 defibrillators.

44 ion (AT/AF) of any duration in patients with pacemakers and implantable cardioverter defibrillators (

45 atrial fibrillation (SCAF) in patients with pacemakers and patients with cryptogenic stroke.

46 on pacemakers, we present recent advances in pacemakers and preview future developments.

47 a dual chamber pacemaker, 3 a biventricular pacemaker, and 1 has a single chamber implantable cardio

48 34% per neutron-producing course for CIEDs, pacemakers, and implantable cardioverter-defibrillators,

49 were immunosuppressed, instrumented with VVI pacemakers, and injected subepicardially into the antero

50 een viewed as unlikely because the circadian pacemaker appears capable only of small, incremental res

51 Cardiac pacemakers are limited by device-related complications,

52 Although current leadless pacemakers are limited to right ventricular pacing, futu

53 rs is determined downstream of the molecular pacemakers are not yet well understood.

54 in their design, conventional (transvenous) pacemakers are prone to multiple potential short- and lo

55 ed lamina I neurons, thereby confirming that pacemakers are synaptically coupled to motor networks in

56 No patients had active pacemakers at the time of their anesthetics.

57 cturer analyses revealed a case of premature pacemaker battery depletion, as well as a hard reset in

58 of various Pu materials (Pu powder, cardiac pacemaker battery, (242)Cm heat source, etc.) was develo

59 te that expression of an important circadian pacemaker, BMAL1, decreases during osteoarthritis progre

60 Our results provide the first description of pacemaker bursting properties in embryonic preBotC neuro

61 cles, in phase with that of PDF, in the same pacemakers, but does not cycle in large LNv.

62 Specific regions acted as pacemakers by initiating calcium wave propagation.

63 hmicity in responsiveness to PDF in critical pacemakers called small LNvs.

64 und the SAN artery with Connexin 43-negative pacemaker cardiomyocytes visualized in Masson's trichrom

65 sarcoplasmic reticulum (SR) regulate cardiac pacemaker cell function by activation of electrogenic Na

66 s and Ca transient decay to insure fail-safe pacemaker cell operation within a wide range of rates.

67 A single isolated sinoatrial pacemaker cell presents intrinsic interbeat interval (IB

68 esponsiveness reflects the properties of the pacemaker cell type, not the receptor.

69 Sinoatrial node myocytes act as cardiac pacemaker cells by generating spontaneous action potenti

70 of the hypothalamus are described as master pacemaker cells for biological rhythms.

71 ural and technological systems, from cardiac pacemaker cells to coupled lasers.

72 In cardiac pacemaker cells, hetero-tetramer GIRK1/4 channels and ho

73 of rhythmic activity in cardiac and neuronal pacemaker cells.

74 ides a new perspective on the concept of SCN pacemaker cells.

75 rrent fluctuations on the IBIs of sinoatrial pacemaker cells.

76 bited Kv1.1; neither form regulated the HCN1 pacemaker channel.

77 mechanisms underpinning ligand regulation of pacemaker channels, and is generally applicable to weak-

78 index, cardiopulmonary disease, alcohol use, pacemaker, cholesterol, cardiac medications, and alterna

79 adian locomotor behaviour is controlled by a pacemaker circuit composed of clock-containing neurons.

80 ATEMENT Circadian behavior is generated by a pacemaker circuit comprising diverse classes of pacemake

81 to the operation of the Drosophila circadian pacemaker circuit, we established new fluorescent circad

82 important for the operation of the circadian pacemaker circuit.

83 rences in the molecular clockwork within the pacemaker circuit.SIGNIFICANCE STATEMENT Circadian behav

84 of vascular complications, bleeding, and new pacemaker/defibrillator implantation demonstrated no sig

85 to deactivation of cardiac devices, such as pacemakers, defibrillators, and mechanical circulatory s

86 ed as a pulse generator, mimicking a cardiac pacemaker delivering pulses of 10muA for 0.5ms at a freq

87 lanted medical devices, including catheters, pacemakers, dentures, and prosthetic joints, which provi

88 certain, especially in light of irreversible pacemaker dependence.

89 hnology has been the development of leadless pacemaker devices, and on the horizon is the development

90 le of a mutant G-protein in the nonsyndromic pacemaker disease because of GIRK channel activation.

91 the period and phase of the neural circadian pacemakers driving locomotor rhythms are unaffected.

92 eview of available clinical data on leadless pacemakers, early results with leadless devices are comp

93 heart chamber-specific (atrial, ventricular, pacemaker) electrophysiological phenotypes based on acti

94 a, our algorithm is capable of identifying a pacemaker even when a weak signal is present in the data

95 Pacemakers exhibited daily rhythmic changes in intracell

96 A suite of Atlantic Pacemaker experiments successfully reproduces the WTP mu

97 urons allows the network to sustain rhythmic pacemaker firing at swimming frequencies following brief

98 cally with nicotine exhibited enhanced basal pacemaker firing but a blunted nicotine-induced firing r

99 Pacemaker firing regularity was disrupted in MitoPark mi

100 ium channel membrane density, re-establishes pacemaker firing.

101 ng hindbrain population (HBO) that acts as a pacemaker for ocular saccades and controls the orientati

102 uggest that the Atlantic Ocean acts as a key pacemaker for the western Pacific decadal climate variab

103 rol cohort of 2667 patients with transvenous pacemakers from six previously published studies.

104 We now report pacemaker function of iPSC-CMs in a canine model.

105 comotor behavior without affecting circadian pacemaker function.

106 d WC-2 drives transcription of the circadian pacemaker gene frequency (frq), whose gene product, FRQ,

107 asmatic nucleus (SCN), the brain's circadian pacemaker, governs daily rhythms in behaviour and physio

108 Ca(2+) rhythms displayed by pacemaker groups that were associated with the morning o

109 was 94%: for patients whose leadless cardiac pacemaker had been implanted for <6 weeks (acute retriev

110 in 25 patients, patients with transcatheter pacemakers had significantly fewer major complications t

111 Leadless cardiac pacemakers have emerged as a safe and effective alternat

112 Pacemakers have existed for decades as a means to restor

113 nter trials, who received a leadless cardiac pacemaker implant and who subsequently underwent a devic

114 er next-generation implant materials such as pacemakers, implantable sensors, or prosthetic devices i

115 oronary interventions (1.0 to 2.4 per 1000), pacemaker/implantable cardioverter-defibrillator inserti

116 scans of the chest, nuclear procedures, and pacemaker/implantable cardioverter-defibrillator inserti

117 ever, BAV was associated with lower rates of pacemaker implantation (2.9% versus 8.0%; P<0.001) and b

118 . transfemoral approach), need for permanent pacemaker implantation (p = 0.02), and post-implant peri

119 orrhage requiring transfusion, and permanent pacemaker implantation (P<0.001).

120 eft bundle branch block (LBBB) and permanent pacemaker implantation (PPI) after transcatheter aortic

121 isk of conduction disturbances and permanent pacemaker implantation after TAVR, with prior right bund

122 In patients who needed permanent pacemaker implantation after the procedure (n=35), 31.4%

123 nced an increased risk of new-onset HF after pacemaker implantation compared with those without AVB.

124 ence and time course for developing HF after pacemaker implantation for cAVB.

125 identified patients undergoing dual-chamber pacemaker implantation from 2008 to 2014.

126 usion in 17.5%, clinical stroke in 1.8%, and pacemaker implantation in 3.0%.

127 ated with (1) total death, sudden death, and pacemaker implantation in a model, including CTG expansi

128 leads led our unit to undertake transvenous pacemaker implantation in neonates and infants from 1987

129 Epicardial pacemaker implantation is the favored approach in childr

130 ndle-branch block and the need for permanent pacemaker implantation may have a significant detrimenta

131 fe-threatening bleeding of 5%, and post-TAVI pacemaker implantation of 12%.

132 complications (2.2% versus 6.5%), as well as pacemaker implantation rate (12.0% versus 15.2%), were s

133 time, whereas rates of cardiac tamponade and pacemaker implantation significantly increased.

134 Permanent pacemaker implantation was required in 3 out of 35 patie

135 Need for permanent pacemaker implantation was significantly higher with the

136 Rate of pacemaker implantation was significantly higher with the

137 node dysfunction scheduled for dual-chamber pacemaker implantation were prospectively enrolled.

138 ent (but had higher prevalence of stroke and pacemaker implantation) and had worse health-related qua

139 had more conduction abnormalities requiring pacemaker implantation, larger improvement in effective

140 Cardiac tamponade, permanent pacemaker implantation, major vascular damage, and moder

141 d atrioventricular block requiring permanent pacemaker implantation, remain the most common complicat

142 brillation was lower with TAVI, but risk for pacemaker implantation, vascular complications, and para

143 Two patients have required pacemaker implantation, whereas the rest are in sinus rh

144 After pacemaker implantation, younger patients (</=55 years of

145 lable therapy for SSS consists of electronic pacemaker implantation.

146 major bleeding, sinus node dysfunction, and pacemaker implantation.

147 pileptic drug changes, epilepsy surgery, and pacemaker implantation.

148 tentially life-threatening complications and pacemaker implantation.

149 nd chronic (6 months to 4 years) phases post-pacemaker implantation.

150 f residual aortic regurgitation and need for pacemaker implantation.

151 ard lowering the rate of reinterventions and pacemaker implantations following ASA because, in this a

152 r interest is the low incidence of permanent pacemaker implantations.

153 There were no deaths, strokes, or permanent pacemaker implantations.

154 f-contained right ventricular single-chamber pacemakers implanted by using a femoral percutaneous app

155 retrieval (>6 weeks) of the leadless cardiac pacemaker in humans.

156 The master circadian pacemaker in mammals is located in the suprachiasmatic n

157 ctional tests demonstrate a normal circadian pacemaker in mir-124 mutants, indicating this miRNA regu

158 Moreover, the phase of the circadian pacemaker in the clock neurons that control rhythmic loc

159 IV lipid-emulsion therapy (2D), and using a pacemaker in the presence of unstable bradycardia or hig

160 ficant cardiogenic component (2D), and using pacemaker in the presence of unstable bradycardia or hig

161 proaches have been used to create biological pacemakers in animal models, induced pluripotent stem ce

162 ntegrate spatial signals and theta frequency pacemaker inputs, they generate phase precessing action

163 Atrioventricular node ablation with pacemaker insertion for rate control should be used as a

164 However, 30-day post-procedure pacemaker insertion increased from 8.8% in 2013 to 12.0%

165 s 0.6%, coronary occlusion was 0.8%, and new pacemaker insertion was 1.9%.

166 The most common reoperations were pacemaker insertion/revision in 212 patients (20%), Font

167 How the circadian pacemaker interacts with the genetic factors associated

168 ucleotide-binding domains (CNBDs) from human pacemaker ion channels critical for heart and brain func

169 Nevertheless, as the central pacemaker is functional in these mutants, miR-124 regula

170 the results suggest that the existence of a pacemaker is highly significant.

171 an algorithm to determine whether a genomic pacemaker is in effect (i.e rates of change vary with ag

172 The complication rate of the leadless pacemakers is influenced by the implanter learning curve

173 s, notably infection and problems related to pacemaker leads.

174 espond to sodium deficiency with spontaneous pacemaker-like activity-the consequence of "cardiac" HCN

175 r computational model reproduced the regular pacemaker-like spiking pattern, action potential shape,

176 on downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarc

177 heterotrimer action in GIRK-channel induced pacemaker membrane hyperpolarization.

178 The leadless cardiac pacemaker met prespecified pacing and sensing requiremen

179 storical comparison study, the transcatheter pacemaker met the prespecified safety and efficacy goals

180 h neurons fire in a similar regular and slow pacemaker mode, this firing activity is supported by dif

181 factors affecting the identification of the pacemaker model.

182 We enrolled 5379 patients with pacemakers (N=3141) or ICDs (N=2238) at 225 US sites (me

183 omatic implantable defibrillator [n = 11] or pacemaker [n = 19]).

184 N-dependent mechanism at E16.5 to a combined pacemaker/network-driven process at E18.5.

185 derlies the functional differences among the pacemaker neuron subgroups.

186 ment-dispersing factor (PDF), which mediates pacemaker neuron synchrony and output, is eliminated in

187 We also found pacemaker neuron-dependent activity rhythms in a second

188 e the proper tempo and sequence of circadian pacemaker neuronal activities.

189 normally operate in approximately 150 brain pacemaker neurons and in many peripheral tissues in the

190 Clk-GFP transgene was used to mark when late pacemaker neurons begin to develop.

191 dicate how selectivity of ethanol effects on pacemaker neurons can occur, and enhance our understandi

192 These results suggest that most late pacemaker neurons develop days before novel factors acti

193 In Drosophila, for example, brain pacemaker neurons dictate that flies are mostly active a

194 Five major groups of pacemaker neurons display synchronized molecular clocks,

195 Pacemaker neurons exert powerful control over brain circ

196 Our experiments revealed that pacemaker neurons impose rhythmic activity and excitabil

197 erences in the molecular clockwork among the pacemaker neurons in Drosophila Here, we identified the

198 otic temporal dynamics are known to occur in pacemaker neurons in molluscs, but there have been no st

199 t entrainment pathway is mediated by central pacemaker neurons in the brain.

200 to circadian light entrainment by circadian pacemaker neurons in the brain.

201 ormed brainwide calcium imaging of groups of pacemaker neurons in vivo for 24 hours.

202 rstood how the activity of a small number of pacemaker neurons is translated into rhythmic behavior o

203 model of 30 electrically-coupled conditional pacemaker neurons on one side of the tadpole hindbrain a

204 model of neural circuits consisting of four pacemaker neurons representing left and right, flexor an

205 emonstration that Rh7 functions in circadian pacemaker neurons represents, to our knowledge, the firs

206 The pacemaker neurons respond to violet light, and this resp

207 This LK/LK-R circuit connects pacemaker neurons to brain areas that regulate locomotor

208 rojections from small ventral lateral (sLNv) pacemaker neurons whenLarexpression is knocked down duri

209 Pacemaker neurons with an intrinsic ability to generate

210 emaker circuit comprising diverse classes of pacemaker neurons, each of which contains a molecular cl

211 However, the only known light sensor in pacemaker neurons, the flavoprotein cryptochrome (Cry),

212 x-containing clock gene promoters within key pacemaker neurons.

213 e of PDF in controlling the synchrony of the pacemaker neurons.

214 rhythmic behavior through a network of ~150 pacemaker neurons.

215 rties and the biophysical characteristics of pacemaker neurons.

216 isrupting the timekeeping mechanism in brain pacemaker neurons.

217 vior are organized by a network of circadian pacemaker neurons.

218 s an additional light-sensing pathway in fly pacemaker neurons.

219 hin the pigment dispersing factor (PDF) cell-pacemaker neurons; only mir-92a peaks during the night.

220 he suprachiasmatic nucleus (SCN), the master pacemaker of circadian physiology.

221 hanism to suggest that the Atlantic is a key pacemaker of the biennial variability in the Pacific inc

222 The principal pacemaker of the circadian clock of the cyanobacterium S

223 istics distinguishing the s-LNvs, the master pacemaker of the locomotor rhythms, from other clock neu

224 The circadian pacemaker of the Madeira cockroach, Rhyparobia (Leucopha

225 Cav3 T-type channels, which serve as pacemakers of the mammalian brain and heart, lack a C-te

226 n 79% patients using echocardiography-guided pacemaker optimization (2.21 L/min [+/- 0.97] and 1.2 L/

227 Echocardiography-guided pacemaker optimization is used in the outpatient setting

228 Echocardiography-guided pacemaker optimization of cardiac output is a feasible b

229 no reports relating to the effectiveness of pacemaker optimization on cardiac output in critically i

230 ressors were discontinued within 12 hours of pacemaker optimization on cardiac output, and all patien

231 therapy (CRT) receive either a biventricular pacemaker or a biventricular pacemaker with an implantab

232 protocol, in 1509 patients who had a legacy pacemaker or a legacy implantable cardioverter-defibrill

233 n the role of nonselective post-mortem CIED (pacemaker or defibrillator) analysis in this setting are

234 ur in any patient with a non-MRI-conditional pacemaker or ICD who underwent clinically indicated nont

235 strength of 1.5 tesla for patients who had a pacemaker or implantable cardioverter-defibrillator (ICD

236 Patients who have pacemakers or defibrillators are often denied the opport

237 ing to reveal the existence of heterogeneous pacemaker oscillatory properties relying on distinct com

238 en deaths (p < 0.001), defibrillators versus pacemakers (p < 0.005), and cardiac versus noncardiac ca

239 art Rate Limitation on Exercise Tolerance in Pacemaker Patients [TREPPE]; NCT02247245).

240 thout to have short AT/AF (5.1% vs. 7.9% for pacemaker patients and 11.5% vs. 10.4% for ICD patients;

241 t episodes of AT/AF were documented in 9% of pacemaker patients and 16% of ICD patients.

242 hout to have long AT/AF (31.9% vs. 22.1% for pacemaker patients and 28.7% vs. 20.2% for ICD patients;

243 (cAVB) on heart failure (HF) development in pacemaker patients has not been well characterized.

244 dopamine neurons fire action potentials in a pacemaker pattern in the absence of synaptic input, the

245 We explored this in the pacemaker PD neurons of the crab pyloric network.

246 The most common operations were pacemaker placement and Fontan revision.

247 Risk factors for pacemaker placement included systemic left ventricle (ha

248 em has been designed to avoid the need for a pacemaker pocket and transvenous lead.

249 ve replacement and often result in permanent pacemaker (PPM) implantation.

250 peutic isradipine concentrations reduced the pacemaker precision of adult mouse SN DA neurons but did

251 uropeptide sNPF, released from s-LNv and LNd pacemakers, produces Ca(2+) activation in the DN1 group

252 This finding has widespread implications for pacemaker programming and the use of heart-rate lowering

253 own regarding inspiratory neurons expressing pacemaker properties at embryonic stages.

254 e genetic programs that abnormally reinforce pacemaker properties at these sites and how this relates

255 slowed diastolic depolarization and reduced pacemaker rate in isolated SAN cells and intact tissue.

256 re matching, and mean and maximal biological pacemaker rates were 45 and 75 beats per minute.

257 ications, basic function/programming, common pacemaker-related issues, and remote monitoring, which a

258 development, rate and rhythm of the iPSC-CMs pacemakers remain to be optimized.

259 The PaceMaker results also suggest a decay in the rate of ch

260 The overall leadless pacemaker retrieval success rate was 94%: for patients w

261 maker to its 24.84-h rhythm and altering the pacemaker's phase-relationship to sleep in a manner that

262 Patients with pacemaker set by the treating anesthesiologist using hem

263 Both presently manufactured leadless pacemakers show similar complications, which are mostly

264 with conventional transvenous single-chamber pacemakers, slightly higher short-term complication rate

265 tive proportion of the different inspiratory pacemaker subtypes changes during prenatal development.

266 The central circadian pacemaker (Suprachiasmatic Nuclei, SCN) maintains the ph

267 enced abnormal chest ticking consistent with pacemaker syndrome, and 1 developed congestive heart fai

268 tween oscillator components in the circadian pacemaker system (retina, pineal, hypothalamus) as well

269 tor circuitry thus constitutes a stop-and-go pacemaker system for the whole-body coordination of cili

270 P as a promising alternative to conventional pacemaker systems.

271 A paradigm shift in pacemaker technology has been the development of leadles

272 ate the coupling between cells of a neuronal pacemaker that determines circadian period.

273 iological dissection of the master circadian pacemaker, the suprachiasmatic nuclei (SCN).

274 ocytes within the mammalian master circadian pacemaker, the suprachiasmatic nucleus (SCN), determine

275 gene Bmal1 into the brain's master circadian pacemaker, the suprachiasmatic nucleus (SCN).

276 ession of an underlying infradian affective "pacemaker." The authors attempted to determine which con

277 A new technology, leadless pacemaker therapy, was recently introduced clinically to

278 ed complications in conventional transvenous pacemaker therapy.

279 d by a change in the period of the circadian pacemaker, this is not the case in miR-124(KO) flies.

280 es, by periodically entraining the circadian pacemaker to its 24.84-h rhythm and altering the pacemak

281 nal neurons connect to the central circadian pacemaker to synchronize endogenous circadian clocks wit

282 role in synchronizing the central circadian pacemaker to the astronomical day by conveying informati

283 ntrast, in this study we apply the Universal PaceMaker (UPM) model to investigate changes in DNA meth

284 tic valve gradients, prior stroke, diabetes, pacemaker use, atrial fibrillation, slow gait speed, and

285 y lowering baseline and peak HR by adjusting pacemaker variables in conjunction with a single dose of

286 rates have been observed: 4.8% for leadless pacemakers versus 4.1% for conventional pacemakers.

287 The pacemaker was epicardially tested in a euthanized pig at

288 A pacemaker was implanted in 17.5% of patients.

289 A new permanent pacemaker was implanted in 4.5% of patients receiving th

290 nter study without controls, a transcatheter pacemaker was implanted in patients who had guideline-ba

291 The leadless pacemaker was successfully implanted in 504 of the 526 p

292 s to the functioning of the circadian master pacemaker, we identified UNF target genes using chromati

293 In the second part of this 2-part series on pacemakers, we present recent advances in pacemakers and

294 up and 4 control subjects (p = 0.038), and 6 pacemakers were implanted (all in the GP group; p = 0.01

295 r tachyarrhythmias in 17 (2%), and permanent pacemakers were implanted in 181 (21%).

296 acute renal failure, and need for permanent pacemaker) were examined.

297 34 patients with paroxysmal AF and implanted pacemakers where AF burden (AFB) could be continuously a

298 a biventricular pacemaker or a biventricular pacemaker with an implantable cardioverter-defibrillator

299 In one case, a pacemaker with less than 1 month left of battery life re

300 sNPF suppress basal Ca(2+) levels in target pacemakers with long durations by cell-autonomous action