ライフサイエンスコーパス: sinus node

1 he corresponding ionic current, I(f), in the sinus node.

2 injection into the artery that perfused the sinus node.

3 different connexin phenotypes in the intact sinus node.

4 nique to study the I(f) pacemaker current in sinus node.

5 mans and mice, with strong expression in the sinus node.

6 ion of I(f), and bradycardia in the isolated sinus node.

7 uding slices obtained from the region of the sinus node.

8 ntrinsic electrophysiological changes in the sinus node.

9 vivo in mice and in vitro in the denervated sinus node.

10 bundle on the spread of activation from the sinus node.

11 ifferent aspects of autonomic effects on the sinus node.

12 emature cessation of exercise before maximal sinus node activation.

13 Senescence and dysfunction of the sinus node affects many people later in life, causing ph

14 ression of key transcriptional regulators of sinus node and atrial conduction, including Nkx2-5 (NK2

15 RATIONALE: Familial sinus node and atrioventricular conduction dysfunction i

16 stores HCN4 mRNA and protein and I(f) in the sinus node and blunts the sinus bradycardia.

17 postulated, including surgical trauma to the sinus node and its blood supply.

18 represent vagal activity at the level of the sinus node and may not accurately reflect efferent vagal

19 metry, we here quantify >7,000 proteins from sinus node and neighbouring atrial muscle.

20 pping for radiofrequency modification of the sinus node and the long-term success rate of the procedu

21 diary sites of impulse generation within the sinus node and/or atrium in patients with inappropriate

22 Surgical trauma to the donor sinus node and/or its blood supply is a significant caus

23 of the net effects of autonomic tone on the sinus node, and carries prognostic significance.

24 have structurally normal atria and preserved sinus node architecture, but expression of key transcrip

25 BP-C(t/+) mice have normal ECG intervals and sinus node, atrial, and ventricular conduction and refra

26 ycardia may result from abnormalities of the sinus node, atrioventricular node, or the His-Purkinje s

27 commonly occurring in these patients affect sinus node beating rate and could be responsible for sev

28 y, peak HR remained low, suggesting impaired sinus node beta-receptor function may not fully account

29 performing single-nucleus RNA sequencing of sinus node biopsies, we attribute measured protein abund

30 d in 88% (N=71) of EBW, as opposed to 21% of sinus node breakthrough waves (N=5; P<0.001).

31 EBW were referred to as sinus node breakthrough waves if they were the earliest

32 A total of 218 EBW and 57 sinus node breakthrough waves were observed in 168 patie

33 nel regulation in the heart's pacemaker, the sinus node, by the autonomic nervous system, we investig

34 computational model of human sinus node cells to account for the dynamic intracellula

35 ively attenuate the high discharge rate from sinus node cells, causing inappropriate sinus tachycardi

36 dependent changes in the architecture of the sinus node comprise an increasing ratio between fibrobla

37 ng, responses of the donor sinus node (DSN) (sinus node controlling heart rate) and recipient sinus n

38 In immunostained sections of intact sinus node, Cx43- and Cx45-positive cells were limited i

39 Sinus node damage may lead to bradycardia.

40 ncy of occurrence of this current within the sinus node decrease, as does its contribution to automat

41 2 late transplant recipients with persistent sinus node denervation.

42 Sinus node development was mostly unaffected in all muta

43 illation (VF), and conduction abnormality as sinus node disease (SND), atrioventricular (AV) block or

44 sights into the complex relationship between sinus node disease and atrial arrhythmias.

45 th human cardiovascular phenotypes including sinus node disease, atrial fibrillation, ventricular tac

46 er implantation (atrio-ventricular blocks-5; sinus node disease-2), 3 patients developed atrial fibri

47 ge is discussed as a potential mechanism for sinus node disease.

48 We randomly assigned 1065 patients with sinus-node disease, intact atrioventricular conduction,

49 risk of atrial fibrillation in patients with sinus-node disease.

50 sistent atrial fibrillation in patients with sinus-node disease.

51 minal reflex testing, responses of the donor sinus node (DSN) (sinus node controlling heart rate) and

52 odds ratio [OR], 1.90 [95% CI, 1.36-2.67]), sinus node dysfunction (1 point; OR, 1.84 [95% CI, 1.04-

53 I (hazard ratio, 4.0; P=0.04), and previous sinus node dysfunction (hazard ratio, 8.0; 95% confidenc

54 ofosbuvir and daclatasvir, he had an extreme sinus node dysfunction (heart rate of 27beats/min).

55 and 7 of these patients also had evidence of sinus node dysfunction (P < .005).

56 Although sinus node dysfunction (SND) and atrial arrhythmias freq

57 ration family (n=25) with autosomal dominant sinus node dysfunction (SND) and atrioventricular block

58 ut genetic overlap has not been reported for sinus node dysfunction (SND) and noncompaction cardiomyo

59 Inherited forms of sinus node dysfunction (SND) clinically include bradycar

60 ildren experienced more frequent episodes of sinus node dysfunction (SND) compared with older subject

61 Sinus node dysfunction (SND) is a major clinically relev

62 Sinus node dysfunction (SND) is a major public health pr

63 Sinus node dysfunction (SND) is often associated with at

64 nt burden testing in 460,000 individuals for sinus node dysfunction (SND), distal conduction disease

65 ) compared with ventricular (VVIR) pacing in sinus node dysfunction (SND).

66 ndomized trial of DDDR versus VVIR pacing in sinus node dysfunction (SND).

67 of pacemaker activity, reminiscent of human sinus node dysfunction and "tachy-brady" syndrome.

68 All 11 patients presented with sinus node dysfunction and 10 had atrial arrhythmias.

69 parasympathetic influence has been linked to sinus node dysfunction and arrhythmia.

70 Respective subdomain sizes and severity of sinus node dysfunction and atrial arrhythmia susceptibil

71 c variation-driven ectopic PITX2 expression, sinus node dysfunction and atrial arrhythmogenesis, illu

72 or gene (PITX2), identified in patients with sinus node dysfunction and atrial fibrillation and model

73 than the broad categories and indications of sinus node dysfunction and atrioventricular block.

74 cribes an arrhythmia phenotype attributed to sinus node dysfunction and diagnosed by electrocardiogra

75 Following that operation she developed sinus node dysfunction and had a permanent epicardial du

76 We sought to eliminate sinus node dysfunction and postoperative bradyarrhythmia

77 t loss of an RE at the HCN4 locus results in sinus node dysfunction and reduced gene expression.

78 rmal SAN function and the pathophysiology of sinus node dysfunction and suggest new potential targets

79 more likely to occur in patients with early sinus node dysfunction and those with longer follow-up.

80 Bradycardia and sinus node dysfunction are common causes of early postop

81 pacing on subsequent stroke in patients with sinus node dysfunction are not known.

82 ant and persistent atrioventricular block or sinus node dysfunction can occur and indicate a need for

83 The most common bradyarrhythmia was sinus node dysfunction followed by high-grade atrioventr

84 iciency in mice may cause the stress-induced sinus node dysfunction found in many aged individuals an

85 Sinus node dysfunction has been previously reported to o

86 stroke in a population of patients paced for sinus node dysfunction in a large prospective clinical t

87 CPVT, such as the pathophysiological role of sinus node dysfunction in CPVT, and whether the arrhythm

88 Unlike sinus node dysfunction in nontransplanted patients, whic

89 o determine the early and late incidences of sinus node dysfunction in patients systematically and un

90 node function between the 2 stages, 23% had sinus node dysfunction in the early postoperative period

91 r its blood supply is a significant cause of sinus node dysfunction in the orthotopic heart transplan

92 Because sinus node dysfunction in the transplanted heart does no

93 patients, which typically worsens with time, sinus node dysfunction in the transplanted heart usually

94 uld be a therapeutic target for pathological sinus node dysfunction in veteran athletes.

95 Perioperative sinus node dysfunction is common after both the hemi-Fon

96 nus node function between the 2 stages, late sinus node dysfunction is common and more likely to occu

97 Sinus node dysfunction is increasingly common with longe

98 Sinus node dysfunction is the most common indication for

99 tained atrial tachyarrhythmia, implying that sinus node dysfunction is unlikely to be the dominant me

100 ity, spontaneous type I ECG, and presence of sinus node dysfunction might be considered as risk facto

101 Sinus node dysfunction occurred in 12 patients in the GP

102 Sinus node dysfunction occurs commonly after orthotopic

103 Bradycardia, due to sinus node dysfunction or atrioventricular (AV) block, w

104 nical trials in patients with pacemakers for sinus node dysfunction or atrioventricular block (AVB) a

105 eatment for patients with bradycardia due to sinus node dysfunction or atrioventricular block.

106 Ten patients with sinus node dysfunction scheduled for dual-chamber pacema

107 cardiac arrhythmia syndrome associated with sinus node dysfunction that is distinct from long QT syn

108 tment of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based (V

109 ain containing 1 (Popdc1) or Popdc2 leads to sinus node dysfunction under stressed conditions in aged

110 , whereas observed survival of patients with sinus node dysfunction was not significantly different f

111 Sinus node dysfunction was present in 7% of the patients

112 A total of 2,010 patients with sinus node dysfunction were randomized to ventricular or

113 ECG analysis revealed severe sinus node dysfunction when freely roaming mutant animal

114 art failure hospitalization in patients with sinus node dysfunction who require pacemaker therapy is

115 -venetoclax (cardiac failure, pneumonia, and sinus node dysfunction) and in one patient receiving chl

116 At follow-up, 7 (6%) of 108 patients had sinus node dysfunction, a permanent pacemaker, or both,

117 iminished P-wave amplitude characteristic of sinus node dysfunction, an AF risk factor in human patie

118 econd-degree atrioventricular blocks, 4 with sinus node dysfunction, and 5 sudden cardiac deaths.

119 s more major adverse events, major bleeding, sinus node dysfunction, and pacemaker implantation.

120 gous for the RE deletion showed bradycardia, sinus node dysfunction, and selective loss of Hcn4 expre

121 cardiac conduction disorder associated with sinus node dysfunction, arrhythmia, and right and occasi

122 conduction, and human SCN5A mutations cause sinus node dysfunction, atrial fibrillation, conductiona

123 Indications for HBP were sinus node dysfunction, atrioventricular conduction dise

124 ies with a phenotypic spectrum consisting of sinus node dysfunction, AV conduction defects, and hyper

125 nd at 6 months, decreased R wave amplitudes, sinus node dysfunction, cardiac hypertrophy, interstitia

126 r groups, affected individuals mainly showed sinus node dysfunction, conduction defects, and atrial a

127 cing (DDDR) and ventricular pacing (VVIR) in sinus node dysfunction, demonstrated no difference in de

128 To determine the early incidence of sinus node dysfunction, hospital records and perioperati

129 ficant clinical manifestation of progressive sinus node dysfunction, is the most frequent indication

130 ulmonary connection may increase the risk of sinus node dysfunction, previous studies have not report

131 Pacing-induced chronic AF induces sinus node dysfunction, prolongs intra-atrial conduction

132 of atrial fibrillation and in patients with sinus node dysfunction, reduces heart failure symptoms w

133 we studied a family with DCM associated with sinus node dysfunction, supraventricular tachyarrhythmia

134 Even after appropriate pacing for sinus node dysfunction, the sinus node may recover and p

135 ich reduced Na+ channel function might cause sinus node dysfunction.

136 vent diseases such as atrial fibrillation or sinus node dysfunction.

137 closely resemble those observed in clinical sinus node dysfunction.

138 d risk of death during pacemaker therapy for sinus node dysfunction.

139 with subsequent stroke in patients paced for sinus node dysfunction.

140 med SAN at birth, the mutant mice manifested sinus node dysfunction.

141 and exhibited ventricular preexcitation and sinus node dysfunction.

142 nts (92%) to determine the late incidence of sinus node dysfunction.

143 4 years after the Fontan operation, 44% had sinus node dysfunction.

144 high-grade atrioventricular block and 1 for sinus node dysfunction.

145 , atrial standstill, conduction disease, and sinus node dysfunction.

146 r (DDDR) versus ventricular (VVIR) pacing in sinus node dysfunction.

147 of dual-chamber versus ventricular pacing in sinus node dysfunction.

148 g the 300 patients enrolled, 190 (63.3%) had sinus-node dysfunction and 100 (33.3%) had atrioventricu

149 ing are alternative treatment approaches for sinus-node dysfunction that causes clinically significan

150 domly assigned a total of 2010 patients with sinus-node dysfunction to dual-chamber pacing (1014 pati

151 hamber pacing were observed in patients with sinus-node dysfunction, but not in those with atrioventr

152 Patients with sinus-node dysfunction, but not those with atrioventricu

153 In sinus-node dysfunction, dual-chamber pacing does not imp

154 stro-esophageal reflux, retinal disease, and sinus-node dysfunction, whereas related heterozygotes ha

155 principally in the subgroup of patients with sinus-node dysfunction.

156 cemaker cardiomyocytes in the embryonic delB sinus node ectopically express PITX2 at physiological do

157 There was extensive sinus node fibrosis.

158 eous depolarization of cardiomyocytes in the sinus node forming the primary natural pacemaker.

159 The prenatal delB sinus node forms discrete subdomains showing PITX2 dosag

160 ts underwent electrophysiological testing of sinus node function a mean of 9 +/- 3 days after surgery

161 Sinus node function and AF inducibility observed in the

162 ss the effects of reduced Cx40 expression on sinus node function and conduction velocity at different

163 Although most patients (81%) regained normal sinus node function between the 2 stages, 23% had sinus

164 Although many patients regain sinus node function between the 2 stages, late sinus nod

165 fitness and genetic variation contribute to sinus node function in endurance athletes.

166 nt to a highly conserved role of K(Ca)1.1 in sinus node function in humans, mice, zebrafish, and fly

167 Abnormalities of sinus node function were present in 14 of 33 patients (4

168 We observed no differences between groups in sinus node function, and ventricular arrhythmias were no

169 -induced chronic atrial fibrillation (AF) on sinus node function, intra-atrial conduction, and atrial

170 nctions appears to play an important role in sinus node function.

171 litates AV nodal conduction without altering sinus node function.

172 e at the SVC-Ao fat pad (a few fibers to the sinus node go directly to the RPV fat pad) before projec

173 nd ventricular muscle, its expression in the sinus node has been a subject of controversy.

174 developmental requirement for Cx40 in normal sinus node impulse initiation at 15.5 days postcoitus.

175 Additionally, sinus node impulse initiation was found to be ectopic in

176 with beta-blockers and even more so when the sinus node inhibitor ivabradine also is added.

177 The sinus node inhibitor ivabradine was approved for patient

178 sis (20.8% versus 6%; P=0.003) and transient sinus node injury (18.8% versus 0%; P=0.001) compared wi

179 The sinus node is a collection of highly specialised cells c

180 uggest that sympathetic reinnervation of the sinus node is accompanied by partial restoration of norm

181 Cardiac pacemaking initiated by the sinus node is attributable to the interplay of several m

182 pe Ca(2+) channels in pacemaking outside the sinus node is unknown.

183 effects of PTH and PTHrP on isolated rabbit sinus node, isolated canine Purkinje fibers, and disaggr

184 n potential model result in pacemaking and a sinus node-like action potential.

185 Sinus node maximum diastolic potential, activation volta

186 riate pacing for sinus node dysfunction, the sinus node may recover and permanent pacing may be disco

187 theter- or surgically- based right atrial or sinus node modification may be helpful, but even this is

188 re to determine whether Cx43 is expressed by sinus node myocytes, to characterize the spectrum of con

189 ng, we estimate ion channel copy numbers for sinus node myocytes.

190 ne Purkinje fibers, and disaggregated rabbit sinus node myocytes.

191 Further experiments showed that in the sinus node of swim-trained mice, upregulation of miR-423

192 in reaction showed remodeling of miRs in the sinus node of swim-trained mice.

193 d be considered for patients with underlying sinus node or atrioventricular conduction disturbances,

194 ritory infarcted and whether it includes the sinus node or AV node or important neuroreceptors; wheth

195 pectrum of connexin expression phenotypes in sinus node pacemaker cells, and to define the spatial di

196 or stress are initiated by a small number of sinus node pacemaker cells.

197 rate, associated with a higher incidence of sinus node (pacemaker) disease and electronic pacemaker

198 orary review summarizes current knowledge on sinus node pathophysiology with the broader goal of yiel

199 nd may serve as disease models to understand sinus node physiology and impulse generation.

200 series who were documented to have a normal sinus node preoperatively, only 1 patient required a per

201 Analysis of disaggregated sinus node preparations revealed three populations of pa

202 mical analysis of disaggregated adult canine sinus node preparations.

203 Abnormalities of the sinus node, prolongation of conduction times or inducibl

204 In group 1 (n=9 dogs), corrected sinus node recovery time (CSNRT), P-wave duration, 24-ho

205 At EPS-2, corrected sinus node recovery time and P-wave duration were prolon

206 vo, SND was demonstrated by ~63% increase in sinus node recovery time compared with wild type.

207 cept for a significant decrease in corrected sinus node recovery time in Tx mice.

208 Corrected sinus node recovery time, P-wave duration, 24-hour Holte

209 Heart rate, sinus node recovery time, Wenckebach cycle length, and a

210 tricular conduction properties and prolonged sinus node recovery time; and (c) inducible ventricular

211 They had similar corrected sinus node recovery times at 90 bpm (388+/-554 versus 37

212 e are summarized, including determination of sinus node recovery times, AV conduction properties, and

213 These results indicate that cells of the sinus node region exhibit a substantial TTX-sensitive cu

214 Single cells were isolated from the sinus node region of rabbits (2 days old to adult) to st

215 eactive signal was widely distributed in the sinus node region.

216 nK (-/-) hearts is highly restricted, to the sinus-node region, caudal atrial septum, and proximal co

217 We hypothesized that sinus node reinnervation would partially restore normal

218 e caused by surgical trauma, ischemia to the sinus node, rejection, drug therapy and increasing donor

219 endurance athletes, primarily attributed to sinus node remodeling or increased vagal modulation.

220 We used laser capture microdissection on a sinus node reporter mouse line to isolate RNA from PCs f

221 s node controlling heart rate) and recipient sinus node (RSN) in the innervated remnant right atrium

222 Sinus node (SAN) dysfunction (SND) manifests as low hear

223 The sinus node (SAN) is the primary pacemaker of the human h

224 ared to the shift documented with successful sinus node (SN) modification.

225 The sinus node (SN) serves as the primary pacemaker of the h

226 In right atrial preparations, sinus node (SN) was dominant and AVRs displayed 1:1 impu

227 Recent advances in catheter and surgical sinus node sparing ablation techniques have led to impro

228 rst of SGNA that resulted in tachycardia and sinus node suppression.

229 Sinus node sympathetic reinnervation was determined by h

230 hemical studies on sections of intact canine sinus node tissue.

231 images showed activation spreading from the sinus node to the rest of the atria, ending at the left

232 RNAseq revealed that ~ 44% of the sinus node transcriptome (7134 of 16,387 transcripts) ha

233 tion of the exciting discovery of the AV and sinus nodes, truly landmarks in our understanding of car

234 Potential mechanisms such as effects on the sinus node, ventricular efficiency, or autonomic functio

235 In all three hearts, the sinus node was nearly destroyed by a noninflammatory deg

236 Sinus node was successfully modified in all patients.

237 of connexins could create regions within the sinus node with different conduction properties, thereby