ライフサイエンスコーパス: sinus node

1 injection into the artery that perfused the sinus node.

2 different connexin phenotypes in the intact sinus node.

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

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

5 ntrinsic electrophysiological changes in the sinus node.

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

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

8 ifferent aspects of autonomic effects on the sinus node.

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

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

11 RATIONALE: Familial sinus node and atrioventricular conduction dysfunction i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 2 late transplant recipients with persistent sinus node denervation.

30 Sinus node development was mostly unaffected in all muta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 We sought to eliminate sinus node dysfunction and postoperative bradyarrhythmia

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

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

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

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

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

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

62 Sinus node dysfunction has been previously reported to o

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

64 Unlike sinus node dysfunction in nontransplanted patients, whic

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

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

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

68 Because sinus node dysfunction in the transplanted heart does no

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

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

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

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

73 Sinus node dysfunction is increasingly common with longe

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

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

76 Sinus node dysfunction occurred in 12 patients in the GP

77 Sinus node dysfunction occurs commonly after orthotopic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 4 years after the Fontan operation, 44% had sinus node dysfunction.

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

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

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

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

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

111 closely resemble those observed in clinical sinus node dysfunction.

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

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

114 and exhibited ventricular preexcitation and sinus node dysfunction.

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

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

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

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

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

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

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

122 There was extensive sinus node fibrosis.

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

124 Sinus node function and AF inducibility observed in the

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

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

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

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

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

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

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

132 litates AV nodal conduction without altering sinus node function.

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

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

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

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

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

138 The sinus node inhibitor ivabradine was approved for patient

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

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

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

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

143 Sinus node maximum diastolic potential, activation volta

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 mical analysis of disaggregated adult canine sinus node preparations.

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

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

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

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

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

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

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

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

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

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

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

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

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

172 We hypothesized that sinus node reinnervation would partially restore normal

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

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

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

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

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

178 Sinus node sympathetic reinnervation was determined by h

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

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

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

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

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

184 Sinus node was successfully modified in all patients.

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