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1 nce interval, 2.14-5.81 for intraventricular conduction defect).
2 a-TcD) are believed to represent interatrial conduction defect.
3 (fl/fl); Kcne1(CreERt2)) did not demonstrate conduction defects.
4 n using Paclitaxel improved intraventricular conduction defects.
5 VES and CAP2 murine knockouts caused cardiac conduction defects.
6 e key DM1 phenotypes of myotonia and cardiac conduction defects.
7 ults in adult late-onset cardiomyopathy with conduction defects.
8 ith unknown ingestions or those with cardiac conduction defects.
9  cardiac hypertrophy and cardiomyopathy with conduction defects.
10 alvular defects were present in 42%; 75% had conduction defects.
11 tients with congenital atrioventricular (AV) conduction defects.
12  weeks after birth, most likely from cardiac conduction defects.
13 abolic dysfunction is an important driver of conduction defects.
14 m the immunized group had varying degrees of conduction defects.
15 ystrophy and myotonia, cataracts and cardiac conduction defects.
16  an equal number of GUSTO-I patients without conduction defects.
17 pment of heart failure including ventricular conduction defects.
18 (13% versus 7%, P:=0.013), and postoperative conduction defects (21.6% versus 12.4%, P:=0.001).
19 eft bundle branch block 17, intraventricular conduction defect 5, and right ventricular pacing 5) ref
20  associated with 63% prevention of the nerve conduction defect and complete prevention of structural
21 -L-carnitine resulted in 76% recovery of the conduction defect and corrected neuropathologic changes
22 ltage and are influenced by intraventricular conduction defects and acute myocardial infarction.
23                                      Cardiac conduction defects and atrial arrhythmia are common to b
24  neonatal lupus, comprising atrioventricular conduction defects and cardiomyopathy, occur in fetuses
25 characterized by persistent atrioventricular conduction defects and contractile dysfunction.
26  that PKC inhibition ameliorated the cardiac conduction defects and contraction abnormalities found i
27 ve neuropathy in Lewis rats characterized by conduction defects and demyelination in spinal nerves.
28 mery-Dreifuss muscular dystrophy (EDMD) with conduction defects and dilated cardiomyopathy (DCM).
29 resulted in progressive and profound cardiac conduction defects and heart failure.
30 een found in patients with DCM with familial conduction defects and muscular dystrophy, but the clini
31  investigated familial clustering of cardiac conduction defects and pacemaker insertion in the FHS (F
32  relevant role in myotonic dystrophy cardiac conduction defects and pathology.
33 ults in adult late-onset cardiomyopathy with conduction defects and up-regulation of mXinbeta.
34                       LBBB, intraventricular conduction defect, and RBBB combined with left anterior
35 iduals mainly showed sinus node dysfunction, conduction defects, and atrial arrhythmias, with infrequ
36 tricular preexcitation, atrial fibrillation, conduction defects, and cardiac hypertrophy.
37 hmias, atrial fibrillation, atrioventricular conduction defects, and death by 4 months of age.
38 rum consisting of sinus node dysfunction, AV conduction defects, and hypertrophic cardiomyopathy.
39 of sex, including corrected QT prolongation, conduction defects, and increased arrhythmia susceptibil
40 nsorimotor and autonomic neuropathy, cardiac conduction defects, and infiltrative cardiomyopathy.
41 ment depression, T-wave changes, ventricular conduction defects, and left ventricular hypertrophy bas
42 ever, since few patients had baseline severe conduction defects before paclitaxel treatment, the safe
43                    Hop-/- adult mice display conduction defects below the atrioventricular node (AVN)
44 e deficient in Etv1 exhibited marked cardiac conduction defects coupled with developmental abnormalit
45 trophy (CMD) and dilated cardiomyopathy with conduction defects (DCM-CD), respectively.
46  level leads to cardiac dysfunction, such as conduction defect, DCM, and heart failure, remains uncle
47 kyphoscoliosis, muscle pathology and cardiac conduction defects develop.
48 Cx46 mutant revealed the presence of cardiac conduction defects frequently associated with human hear
49 duals with at least 1 affected parent with a conduction defect had a 1.65-fold odds (odds ratio, 95%
50    Heterogeneous Cx43 expression resulted in conduction defects, however, as well as markedly depress
51 3243A>G variant (HR: 4.3; 95% CI: 1.8-10.1), conduction defects (HR: 3.0; 95% CI: 1.3-6.9), left vent
52 mtDNA deletions (HR: 4.3; 95% CI: 1.7-10.4), conduction defects (HR: 6.8; 95% CI: 3.0-15.4), and LV e
53 c pathway for progressive cardiomyopathy and conduction defects in congenital heart disease.
54 ctor and microRNA activities-induces cardiac conduction defects in DM1 individuals.
55 ription factor Nkx2-5 cause atrioventricular conduction defects in humans by unknown mechanisms.
56 ntractility and ameliorated intraventricular conduction defects in LmnaH222P/H222P mice, which was as
57 ted in diverse congenital heart diseases and conduction defects in mouse models and humans.
58                                    Postnatal conduction defects in Nkx2-5 mutation may result at leas
59  represent the first direct demonstration of conduction defects in the specialized conduction system
60 c heart, which may contribute in part to the conduction defects in the transgenic mice.
61 ransgenic heart, which may contribute to the conduction defects in the transgenic mice.
62 ilar mouse model, which reported only subtle conduction defects in their nervous system.
63                                              Conduction defects in these tissues produce a disproport
64  and Tbx5 deficiency in the adult VCS led to conduction defects, including prolonged PR and QRS inter
65     Transgene expression resulted in cardiac conduction defects, increased expression of the cardiac-
66  is associated with total and sudden deaths, conduction defects, left ventricular dysfunction, and su
67 ions that cause isolated progressive cardiac conduction defect (Lenegre syndrome), long-QT syndrome (
68  alterations of muscle excitability, cardiac conduction defects, mental retardation, and cognitive de
69  associated with the presence at baseline of conduction defects on the ECG and left ventricular systo
70  least 1 parent had any electrocardiographic conduction defect or pacemaker insertion, the offspring
71 tem, but its absence does not cause baseline conduction defects or arrhythmias in the adult mouse.
72 1), supraventricular arrhythmia (p = 0.003), conduction defects (p = 0.01), and "mildly" DCM (p = 0.0
73 -type BBBs (LBBB, RBBB, and intraventricular conduction defect, respectively).
74 in AF patients, including arrhythmia, atrial conduction defects, sarcomere disassembly, and altered c
75 +/- mice develop first-degree heart block, a conduction defect strikingly similar to that observed in
76                   The range and frequency of conduction defects suggest that additional factors promo
77 d by a chronotropic incompetence and cardiac conduction defects, thus increasing the susceptibility t
78 in mice leads to severe cardiac dysfunction, conduction defect, ventricular arrhythmias, fibrosis, ap
79 kx2-5 lead to progressive cardiomyopathy and conduction defects via unknown mechanisms.
80                 In the prevention study, the conduction defect was 73% prevented and structural abnor
81                                              Conduction defect was accompanied by reduction in ventri
82 story of sudden death or progressive cardiac conduction defect was found in 1.4% and 11.1%, respectiv
83 tion, splicing defects, myotonia and cardiac conduction defects, we find that MBNL1 overexpression di
84 omen with no BBB, LBBB, and intraventricular conduction defect were strong predictors of incident HF
85                                        These conduction defects were accompanied by overt mislocaliza
86                                              Conduction defects were correlated with dephosphorylatio
87                 DMPK-/- mice develop cardiac conduction defects which include first-, second-, and th
88 rface and ambulatory ECGs documented cardiac conduction defects, which were further confirmed by elec
89 rstitial and focal replacement fibrosis, and conduction defects with altered connexin 43 distribution
90 excitable cells and tissues can repair large conduction defects within primary 2- and 3-dimensional c