ライフサイエンスコーパス: AV node

1 are the result of a morphologically atrophic AV node.

2 l lambs at 80% gestation by cryoablating the AV node.

3 ng myocardial cells and connexin 30.2 in the AV node.

4 roper AV junction development, including the AV node.

5 ea of isolated atrial tissue surrounding the AV node.

6 r junction that histologically resembled the AV node.

7 dependent negative dromotropic effect on the AV node.

8 ent with anterograde conduction block in the AV node.

9 is consistent with a left-sided input to the AV node.

10 proceeding from the left atrium reaches the AV node.

11 us provides a left atrial input to the human AV node.

12 ntrol reflecting a synergistic effect on the AV node.

13 an anterior to a posterior entry site to the AV node.

14 the vagal fibers to the atria and sinus and AV nodes.

15 patterns, fibrosis of the AV node, and twin AV nodes.

16 y vagally denervated the atria and sinus and AV nodes.

17 quency modification of the atrioventricular (AV) node.

18 ches provide inputs to the atrioventricular (AV) node.

19 elay characteristic of the atrioventricular (AV) node.

20 l myocardium and sinus and atrioventricular (AV) nodes.

21 brillation who underwent modification of the AV node ($13 109+/-2002) and 14 similar patients who und

22 s did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/-

23 odification are significantly lower than for AV node ablation in patients with chronic atrial fibrill

24 procedure and that the recurrence rate after AV node ablation would be 2%.

25 4 consecutive patients with AF who underwent AV node ablation, nine had sudden death after the ablati

26 tors of sudden death after atrioventricular (AV) node ablation and pacemaker implantation.

27 Atrioventricular (AV) node ablation and pacing has become accepted therapy

28 put rather than direct damage to the compact AV node accounts for the decrease in ventricular rate af

29 hether a separate atrial input site into the AV node actually exists in patients with dual anterograd

30 Vagal fibers to the sinus and AV nodes also converge at the SVC-Ao fat pad (a few fibe

31 n block occurred at the junction between the AV node and its input pathways.

32 al block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask

33 had radiofrequency catheter ablation of the AV node and pacemaker implantation for rate control of m

34 fter radiofrequency catheter ablation of the AV node and pacemaker implantation in patients with atri

35 small area of atrial tissue surrounding the AV node and the His bundle was isolated using sequential

36 Selective vagal denervation of the sinus and AV nodes and atria decreased HRV and eliminated BRS whil

37 al fat pads vagally denervated the sinus and AV nodes and atria without affecting vagal innervation o

38 mice display a hypoplastic atrioventricular (AV) node and then develop selective dropout of these con

39 ral pathways connecting LA GPs with the PVs, AV node, and SA node.

40 FP stimulation had a selective effect on the AV node, and slowed the ventricular rate during postoper

41 ricular activation patterns, fibrosis of the AV node, and twin AV nodes.

42 g that neural pathways between LAGPs and the AV node are via the right lower GP.

43 -type Ca2+ channels in the atrioventricular (AV) node are essential for AV conduction.

44 tients with normal hearts and no evidence of AV node arrhythmias.

45 oventricular delay before development of the AV node, as rapid ventricular activation occurs after ac

46 on over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients w

47 planes) has shown that the atrioventricular (AV) node (AVN) is continuous with only specialized myoca

48 ttempt at radiofrequency modification of the AV node because of symptomatic, drug-refractory atrial f

49 operties, which is gradually silenced as the AV node becomes matured.

50 calization to the cell-cell junctions of the AV node but preservation of connexin 40 and 43 in contra

51 vagal denervation of the atria and sinus and AV nodes can be produced by RFCA of these fat pads and r

52 thermore, localization of connexin 45 at the AV-node cell-cell junction and of beta-catenin and ZO-1

53 The frequency of AV node conduction and morphological abnormalities incre

54 The effect on AV node conduction is substantially enhanced by pretreat

55 e that CAR expression is required for normal AV-node conduction and cardiac function.

56 hort ventriculo-atrial interval and apparent AV node dependence.

57 ed effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without

58 y electrophysiology of the atrioventricular (AV) node during normal conduction and reentry.

59 subsequent development of atrioventricular (AV) node dysfunction, rate-responsive atrial pacing shou

60 dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the ad

61 These findings suggest that AV node electrophysiology undergoes maturational changes

62 netic protein signaling also plays a role in AV node formation, we investigated conduction system fun

63 AV node function was assessed at baseline and after 4 we

64 lation lines, the tricuspid annulus, and the AV node-His bundle.

65 incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine

66 trograde properties of the atrioventricular (AV) node in children and to determine the presence of ve

67 cation and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrill

68 small area of atrial tissue surrounding the AV node is feasible by transcatheter radiofrequency abla

69 The atrioventricular (AV) node is essential for the sequential excitation and

70 The atrioventricular (AV) node is insensitive to changes in extracellular pota

71 orting the premise that the pathways contain AV node-like tissue.

72 The initial charges generated by AV node modification are significantly lower than for AV

73 investigated conduction system function and AV node morphology in adult mice with conditional deleti

74 revealed increased AC(VI) expression in the AV node of transgenic mice versus controls.

75 mmunofluorescence staining for AC(VI) in the AV node of transgenic mice.

76 ed and whether it includes the sinus node or AV node or important neuroreceptors; whether many small

77 elative refractoriness and conduction of the AV node or to differences in autonomic input into the AV

78 Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the

79 In 10 patients with dual AV node pathway physiology, atrial pacing at three chose

80 low pathway does exist in patients with dual AV node pathway physiology.

81 lly exists in patients with dual anterograde AV node pathway physiology.

82 erior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separat

83 In most patients with dual AV node pathways and typical AV node reentrant tachycard

84 fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycard

85 The incidence of dual AV node pathways and VA conduction in the pediatric popu

86 The incidence of dual AV node pathways in group I was 15% and 44% in group II

87 to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV

88 Functionally fast AV node pathways may be located in the posteroseptal rig

89 Because dual AV node pathways serve as the substrate for AV node reen

90 The location of fast and slow AV node pathways was determined by atrial activation map

91 All evidence of dual AV node pathways was eliminated in six patients, and dua

92 t noinducible PSVT who have evidence of dual AV node pathways.

93 of ventriculoatrial (VA) conduction and dual AV node pathways.

94 nsitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in p

95 present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may particip

96 who have evidence of dual atrioventricular (AV) node pathways.

97 his "AV connecting system" originated in the AV node, penetrated the septum as the His bundle, and th

98 Sixteen patients with dual AV node physiology and typical AV node reentrant tachyca

99 documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beat

100 ays was eliminated in six patients, and dual AV node physiology remained present in one patient.

101 and PR interval changes consistent with dual AV node physiology were studied.

102 In 14 of 16 patients with dual-AV node physiology, administration of small doses of ade

103 ways in patients with dual atrioventricular (AV) node physiology.

104 tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant ta

105 AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the s

106 nts with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients we

107 Seven patients with AV node reentrant tachycardia had evidence of a posterio

108 ients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been st

109 The increase in AV node reentrant tachycardia in adults may relate to ch

110 sm of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophys

111 The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%.

112 potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infra

113 In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bund

114 ients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more

115 In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV b

116 n of low dose adenosine led to initiation of AV node reentrant tachycardia.

117 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia.

118 ferred therapeutic approach in patients with AV node reentrant tachycardia.

119 doses of adenosine in patients with typical AV node reentrant tachycardia.

120 Although AV node reentry is common in adults, it accounts for 13%

121 rial reentry tachycardia, 3/3 having typical AV node reentry tachycardia, and 2/2 having focal atrial

122 terior exit sites may participate in typical AV node reentry.

123 ting posteroseptal ablation in patients with AV node reentry.

124 eciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid

125 and 3) typical variety of atrioventricular (AV) node reentry tachycardia: combined electrographic an

126 t; in the third heart, only fragments of the AV node remained.

127 lar rate, radiofrequency modification of the AV node results in excellent long-term control of the ve

128 cal delivery of Gem to the atrioventricular (AV) node significantly slowed AV nodal conduction (prolo

129 r to differences in autonomic input into the AV node that allow dual pathway physiology to progress t

130 e is known to depress conduction through the AV node, the relative sensitivity to adenosine of the an

131 slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rap

132 (n=4) or abrupt conduction delay within the AV node through the FP (n=2).

133 conduction abnormalities extends beyond the AV node to also affect the SA node.

134 to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP throug

135 f excitation from the atrioventricular node (AV node) to ventricular myocardium [1].

136 ioventricular (AV) connection apart from the AV node, using programmed stimulation.

137 In two of the three hearts, the AV node was absent; in the third heart, only fragments o

138 +/- 13 versus 91 +/- 9 ms, P < 0.01), and of AV node Wenckebach cycle length (230 +/- 19 versus 213 +

139 AV node Wenckebach cycle length prolonged from 270+/-33

140 The age-related changes in the AV node with development are poorly understood.

141 eloping myocardium resulted in a hypoplastic AV node, with specific loss of slow-conducting cells exp