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1 l lambs at 80% gestation by cryoablating the AV node.
2 ng myocardial cells and connexin 30.2 in the AV node.
3 roper AV junction development, including the AV node.
4 ea of isolated atrial tissue surrounding the AV node.
5 r junction that histologically resembled the AV node.
6 dependent negative dromotropic effect on the AV node.
7 ent with anterograde conduction block in the AV node.
8 on in regulating the expression of NaV1.5 in 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 are the result of a morphologically atrophic AV node.
15 y vagally denervated the atria and sinus and AV nodes.
16  the vagal fibers to the atria and sinus and AV nodes.
17  patterns, fibrosis of the AV node, and twin AV nodes.
18 quency modification of the atrioventricular (AV) node.
19 elay characteristic of the atrioventricular (AV) node.
20 ches provide inputs to the atrioventricular (AV) node.
21 l myocardium and sinus and atrioventricular (AV) nodes.
22 brillation who underwent modification of the AV node ($13 109+/-2002) and 14 similar patients who und
23 s did the effective refractory period of the AV node (279 +/- 60 versus 304 +/- 67 ms versus 372 +/-
24 In protocol B, PICM was established by using AV node ablation and 4 weeks of electronic RV pacing, at
25 odification are significantly lower than for AV node ablation in patients with chronic atrial fibrill
26 procedure and that the recurrence rate after AV node ablation would be 2%.
27 r construct green fluorescent protein) after AV node ablation, and observed the animals for 8 weeks.
28 4 consecutive patients with AF who underwent AV node ablation, nine had sudden death after the ablati
29 tors of sudden death after atrioventricular (AV) node ablation and pacemaker implantation.
30                            Atrioventricular (AV) node ablation and pacing has become accepted therapy
31 put rather than direct damage to the compact AV node accounts for the decrease in ventricular rate af
32 hms in sinoatrial (SA) and atrioventricular (AV) node activity, and impose a time-of-day dependent su
33 hether a separate atrial input site into the AV node actually exists in patients with dual anterograd
34                Vagal fibers to the sinus and AV nodes also converge at the SVC-Ao fat pad (a few fibe
35 at ZO-1 is abundantly expressed in the human AV node and colocalizes with Cx40.
36 n block occurred at the junction between the AV node and its input pathways.
37 al block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask
38  had radiofrequency catheter ablation of the AV node and pacemaker implantation for rate control of m
39 fter radiofrequency catheter ablation of the AV node and pacemaker implantation in patients with atri
40  small area of atrial tissue surrounding the AV node and the His bundle was isolated using sequential
41 ggesting ZO-1 is differentially required for AV node and ventricular conduction.
42 Selective vagal denervation of the sinus and AV nodes and atria decreased HRV and eliminated BRS whil
43 al fat pads vagally denervated the sinus and AV nodes and atria without affecting vagal innervation o
44 mice display a hypoplastic atrioventricular (AV) node and then develop selective dropout of these con
45 ral pathways connecting LA GPs with the PVs, AV node, and SA node.
46 FP stimulation had a selective effect on the AV node, and slowed the ventricular rate during postoper
47 ricular activation patterns, fibrosis of the AV node, and twin AV nodes.
48 g that neural pathways between LAGPs and the AV node are via the right lower GP.
49 -type Ca2+ channels in the atrioventricular (AV) node are essential for AV conduction.
50 tients with normal hearts and no evidence of AV node arrhythmias.
51 oventricular delay before development of the AV node, as rapid ventricular activation occurs after ac
52 n of POPDC1 and POPDC2 was most prevalent in AV node, AV node pacemaker, and AV bundle cells.
53 on over an accessory AV pathway (AP) and the AV node (AVN) may be difficult, especially in patients w
54 ods that utilize sharp needle entry into the AV node (AVN) region, the modified method resulted in a
55 planes) has shown that the atrioventricular (AV) node (AVN) is continuous with only specialized myoca
56 ttempt at radiofrequency modification of the AV node because of symptomatic, drug-refractory atrial f
57 operties, which is gradually silenced as the AV node becomes matured.
58 calization to the cell-cell junctions of the AV node but preservation of connexin 40 and 43 in contra
59 vagal denervation of the atria and sinus and AV nodes can be produced by RFCA of these fat pads and r
60 thermore, localization of connexin 45 at the AV-node cell-cell junction and of beta-catenin and ZO-1
61                             The frequency of AV node conduction and morphological abnormalities incre
62                                The effect on AV node conduction is substantially enhanced by pretreat
63 tein responsible for maintaining appropriate AV node conduction through maintaining gap junction prot
64 e that CAR expression is required for normal AV-node conduction and cardiac function.
65 hort ventriculo-atrial interval and apparent AV node dependence.
66 ed effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without
67 system and cardiomyocyte clock to the SA and AV nodes differ, and this renders the cardiac conduction
68 y electrophysiology of the atrioventricular (AV) node during normal conduction and reentry.
69  subsequent development of atrioventricular (AV) node dysfunction, rate-responsive atrial pacing shou
70  dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the ad
71                  These findings suggest that AV node electrophysiology undergoes maturational changes
72 netic protein signaling also plays a role in AV node formation, we investigated conduction system fun
73                                              AV node function was assessed at baseline and after 4 we
74 lation lines, the tricuspid annulus, and the AV node-His bundle.
75  incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine
76 trograde properties of the atrioventricular (AV) node in children and to determine the presence of ve
77 cation and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrill
78  small area of atrial tissue surrounding the AV node is feasible by transcatheter radiofrequency abla
79                        The atrioventricular (AV) node is essential for the sequential excitation and
80                        The atrioventricular (AV) node is insensitive to changes in extracellular pota
81 orting the premise that the pathways contain AV node-like tissue.
82             The initial charges generated by AV node modification are significantly lower than for AV
83  investigated conduction system function and AV node morphology in adult mice with conditional deleti
84  revealed increased AC(VI) expression in the AV node of transgenic mice versus controls.
85 mmunofluorescence staining for AC(VI) in the AV node of transgenic mice.
86 ed and whether it includes the sinus node or AV node or important neuroreceptors; whether many small
87 elative refractoriness and conduction of the AV node or to differences in autonomic input into the AV
88 C1 and POPDC2 was most prevalent in AV node, AV node pacemaker, and AV bundle cells.
89                Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the
90                     In 10 patients with dual AV node pathway physiology, atrial pacing at three chose
91 low pathway does exist in patients with dual AV node pathway physiology.
92 lly exists in patients with dual anterograde AV node pathway physiology.
93 erior exit site exists for a retrograde slow AV node pathway, it remains unresolved whether a separat
94                   In most patients with dual AV node pathways and typical AV node reentrant tachycard
95 fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycard
96                        The incidence of dual AV node pathways and VA conduction in the pediatric popu
97                        The incidence of dual AV node pathways in group I was 15% and 44% in group II
98  to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV
99                            Functionally fast AV node pathways may be located in the posteroseptal rig
100                                 Because dual AV node pathways serve as the substrate for AV node reen
101                The location of fast and slow AV node pathways was determined by atrial activation map
102                         All evidence of dual AV node pathways was eliminated in six patients, and dua
103 of ventriculoatrial (VA) conduction and dual AV node pathways.
104 t noinducible PSVT who have evidence of dual AV node pathways.
105 nsitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in p
106 present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may particip
107  who have evidence of dual atrioventricular (AV) node pathways.
108 his "AV connecting system" originated in the AV node, penetrated the septum as the His bundle, and th
109                   Sixteen patients with dual AV node physiology and typical AV node reentrant tachyca
110  documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beat
111 ays was eliminated in six patients, and dual AV node physiology remained present in one patient.
112 and PR interval changes consistent with dual AV node physiology were studied.
113               In 14 of 16 patients with dual-AV node physiology, administration of small doses of ade
114 ways in patients with dual atrioventricular (AV) node physiology.
115 tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant ta
116  AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the s
117 nts with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients we
118                          Seven patients with AV node reentrant tachycardia had evidence of a posterio
119 ients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been st
120                              The increase in AV node reentrant tachycardia in adults may relate to ch
121 sm of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophys
122 The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%.
123 potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infra
124         In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bund
125 ients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more
126                 In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV b
127  doses of adenosine in patients with typical AV node reentrant tachycardia.
128 n of low dose adenosine led to initiation of AV node reentrant tachycardia.
129 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia.
130 ferred therapeutic approach in patients with AV node reentrant tachycardia.
131                                     Although AV node reentry is common in adults, it accounts for 13%
132 rial reentry tachycardia, 3/3 having typical AV node reentry tachycardia, and 2/2 having focal atrial
133 terior exit sites may participate in typical AV node reentry.
134 ting posteroseptal ablation in patients with AV node reentry.
135 eciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid
136  and 3) typical variety of atrioventricular (AV) node reentry tachycardia: combined electrographic an
137 t; in the third heart, only fragments of the AV node remained.
138 lar rate, radiofrequency modification of the AV node results in excellent long-term control of the ve
139  Western blot and immunostaining analyses of AV nodes showed that ZO-1 loss decreased Cx (connexin) 4
140 cal delivery of Gem to the atrioventricular (AV) node significantly slowed AV nodal conduction (prolo
141 r to differences in autonomic input into the AV node that allow dual pathway physiology to progress t
142 e is known to depress conduction through the AV node, the relative sensitivity to adenosine of the an
143  slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rap
144  (n=4) or abrupt conduction delay within the AV node through the FP (n=2).
145 uction system deletion of Tjp1 distal to the AV node (Tjp1(fl/fl); Kcne1(CreERt2)) did not demonstrat
146  conduction abnormalities extends beyond the AV node to also affect the SA node.
147 to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP throug
148 f excitation from the atrioventricular node (AV node) to ventricular myocardium [1].
149 ioventricular (AV) connection apart from the AV node, using programmed stimulation.
150              In two of the three hearts, the AV node was absent; in the third heart, only fragments o
151 +/- 13 versus 91 +/- 9 ms, P < 0.01), and of AV node Wenckebach cycle length (230 +/- 19 versus 213 +
152                                              AV node Wenckebach cycle length prolonged from 270+/-33
153               The age-related changes in the AV node with development are poorly understood.
154 eloping myocardium resulted in a hypoplastic AV node, with specific loss of slow-conducting cells exp

 
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