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1 conduction velocities across the atrial and ventricular myocardium.
2 heart failure, with reduced proliferation of ventricular myocardium.
3 ulate a crucial proliferation signal for the ventricular myocardium.
4 c, high level BMP-10 expression in the adult ventricular myocardium.
5 he muscular interventricular septum, and the ventricular myocardium.
6 through a thoracotomy directly into the left ventricular myocardium.
7 the pathological changes of noncompaction of ventricular myocardium.
8 transgenic mice developed tumors within the ventricular myocardium.
9 electrical heterogeneities intrinsic to the ventricular myocardium.
10 mal model with targeted activation of JNK in ventricular myocardium.
11 epicardial space and subsequently invade the ventricular myocardium.
12 of percutaneous myocardial GTx to human left ventricular myocardium.
13 a neurohormone synthesized predominantly in ventricular myocardium.
14 titution of the right and rarely of the left ventricular myocardium.
15 but also on transverse-tubular membranes in ventricular myocardium.
16 Irx4 expression is found exclusively in the ventricular myocardium.
17 zed by fibro-fatty infiltration of the right-ventricular myocardium.
18 on of ET and Ang II in plasma and atrial and ventricular myocardium.
19 ber of proliferating cardiac myocytes in the ventricular myocardium.
20 racteristics is an important property of the ventricular myocardium.
21 ractile proteins is faster in atrial than in ventricular myocardium.
22 enital heart disorder, noncompaction of left ventricular myocardium.
23 es in levels between failing and non-failing ventricular myocardium.
24 sing a porphyrinic sensor placed in the left ventricular myocardium.
25 ated with muscarinic receptor stimulation in ventricular myocardium.
26 ted to cells within the compact layer of the ventricular myocardium.
27 nol can predictably ablate a large volume of ventricular myocardium.
28 al staining is observed in the failing human ventricular myocardium.
29 vely stunned or, more likely, remodeled left ventricular myocardium.
30 and right ventricular cavities and the left ventricular myocardium.
31 c branches of the ANS on the cardiac SAN and ventricular myocardium.
32 ly leads to morphological alterations of the ventricular myocardium.
33 d an mean (SD) burden of 5.9% (7.3%) of left ventricular myocardium.
34 f arrhythmic substrate ablation in the thick ventricular myocardium.
35 e point of the mitral valve annulus from the ventricular myocardium.
36 .003; d=0.82) compared to corresponding left ventricular myocardium.
37 essential for synchronous activation of the ventricular myocardium.
38 lerosis, with downstream effects on the left ventricular myocardium.
39 s is feasible without instrumenting the left ventricular myocardium.
40 at ventricular myocytes and in mouse and rat ventricular myocardium.
41 ived from unipolar electrograms sampling the ventricular myocardium.
42 electrical and contractile activities in the ventricular myocardium.
43 ricular and atrial septal defects and a thin ventricular myocardium.
44 , while it was almost undetectable in canine ventricular myocardium.
45 ncorporated it into permeabilized human left ventricular myocardium.
46 modulating collagen deposition in mouse left ventricular myocardium.
47 lular sources and strategies to generate new ventricular myocardium.
48 dimensional (3D) electric propagation within ventricular myocardium.
49 haviour of transmurally intact, viable right-ventricular myocardium.
50 S) genes Tbx5, Cx40, and Cx43 throughout the ventricular myocardium.
51 isolated from different regions of the left ventricular myocardium.
52 gnaling and thereby promote expansion of the ventricular myocardium.
53 elerate the kinetics of force development in ventricular myocardium.
54 ive late gadolinium enhancement (LGE) in the ventricular myocardium.
55 omyocyte lateral membranes in failing canine ventricular myocardium.
56 hat activates Ca(2+) homeostatic proteins in ventricular myocardium.
57 on was mapped propagating from PF to working ventricular myocardium.
58 ngiogenesis, and inflammation in postinfarct ventricular myocardium.
59 ent for pacemaking when administered to left ventricular myocardium.
60 ardium and myocardium resulting in a thinned ventricular myocardium.
61 nsequence of premature stretch activation of ventricular myocardium.
63 9+/-178.3 mm(3); P=0.023) and infarcted left ventricular myocardium (1052.3+/-543.0 versus 340.3+/-16
65 ibrofatty replacement of primarily the right ventricular myocardium, a substrate for life-threatening
66 reatment of wild-type and cTnI(ala2) skinned ventricular myocardium accelerated stretch activation su
70 ncement was no longer detectable in the left ventricular myocardium, although persistent elevations i
72 were performed using the SUVmean of the left ventricular myocardium and blood pool and calculation of
73 trophysiology differently in left atrial vs. ventricular myocardium and causes extensive atrial fibro
74 e is synthesized primarily in the atrial and ventricular myocardium and constitutes the mature biolog
75 trioventricular canal characteristics in the ventricular myocardium and endocardium, indicating a rol
76 express 50% of the normal amount of Cx43 in ventricular myocardium and exhibit marked slowing of ven
77 and1 expression is restricted to the ventral ventricular myocardium and extends along the entire leng
78 PP6-L was dominantly expressed in both mouse ventricular myocardium and hiPSC-CMs, while it was almos
79 YDGF protein abundance increased in the left ventricular myocardium and in blood plasma of pressure-o
80 ta (beta-MyHC) is primarily expressed in the ventricular myocardium and in slow-twitch muscle fibers,
81 cells were identified in SHF-derived distal ventricular myocardium and in three lineages in the outf
82 day 13.5 and exhibit hypoplasia of the right ventricular myocardium and interventricular septum and d
83 sulates the AVCS from surrounding atrial and ventricular myocardium and may enhance the efficacy and
84 diac failure because of noncompaction of the ventricular myocardium and resultant ventricular dilatat
85 he predominant isoform expressed in both the ventricular myocardium and slow skeletal muscle fibres s
86 haMyHC mRNA is expressed in nonfailing human ventricular myocardium and that alphaMyHC mRNA expressio
87 3) is abundantly expressed in the atrial and ventricular myocardium and the rapid ventricular conduct
88 dy characterized the cellular composition of ventricular myocardium and validated the GeoMx platform'
89 tructures (atrioventricular junction or left ventricular myocardium) and organs at risk were contoure
90 tion (APD90) in atria, no effect on APD90 in ventricular myocardium, and an abbreviation of APD90 in
91 e outlet right ventricle (DORV), hypoplastic ventricular myocardium, and normal coronary vasculature.
93 yHC), alpha and beta, exist in the mammalian ventricular myocardium, and their relative expression is
94 ic lesions predominantly present in the left ventricular myocardium, and vasculatures in these lesion
96 cytes isolated from different regions of the ventricular myocardium are known to vary significantly.
98 changes parallel the changes found in human ventricular myocardium at the receptor level, suggesting
99 cardiomyopathy and in guinea-pig atrial and ventricular myocardium before and during pharmacological
100 tion from beat to beat, with the majority of ventricular myocardium being activated in a centrifugal
102 myocytes and fibrofatty replacement of right ventricular myocardium; biventricular involvement is oft
103 ddition, CGRP receptors were not observed in ventricular myocardium but were prominent in coronary ar
104 ates cardiogenesis and growth of the compact ventricular myocardium by modulating the cardiomyocyte c
107 c those in cells isolated from failing human ventricular myocardium, canine pacing-induced cardiomyop
108 We examined cTnI phosphorylation in left ventricular myocardium collected from failing hearts at
109 ith a cardiac defect characterized by a thin ventricular myocardium, common atrioventricular canal, a
111 al pole of the heart is the region where the ventricular myocardium continues as the vascular smooth
113 nts with isolated non-compaction of the left ventricular myocardium, dilated cardiomyopathy (DCM) and
114 ities by E10.5, with hyperplasia of the left ventricular myocardium, distention of the cardinal veins
115 ntricular septum, atrioventricular cushions, ventricular myocardium, dorsal mesenchymal protrusion, p
117 coronary artery disease by imaging the left ventricular myocardium during a first-pass contrast bolu
119 Hdac3 overexpression produces thickening of ventricular myocardium, especially the interventricular
120 embryos display pronounced hypoplasia of the ventricular myocardium essentially identical to the "thi
122 /=5 segments ( approximately 25% of the left ventricular myocardium) exhibited a blood flow/metabolis
123 ) both nonfailing intact and explanted human ventricular myocardium expressed substantial amounts of
124 with [13N]-ammonia for delineating the left ventricular myocardium, followed by imaging the expressi
125 and small nucleolar RNAs (snoRNAs) in right ventricular myocardium from 16 infants with nonsyndromic
126 Clark-type oxygen electrode in isolated left ventricular myocardium from 26 explanted failing human h
128 d the stretch activation response in skinned ventricular myocardium from both wild-type (WT) and cMyB
130 nal neural network (CNN) for segmenting left ventricular myocardium from CE-CT was developed, trained
131 myofilament localization was reduced in left ventricular myocardium from failing human hearts, which
132 te-specific GSK-3beta knockout mice and left ventricular myocardium from nonfailing and failing human
134 tients with nonischemic cardiomyopathy, left ventricular myocardium from patients with DoxCM exhibite
136 and microelectrode techniques in human left ventricular myocardium from patients with hypertrophic c
137 esults were compared with data from the left ventricular myocardium from similar sized normal (contro
138 hree predominant cell types that make up the ventricular myocardium, giving rise to transmural voltag
139 mages revealed uniform opacification of left ventricular myocardium greater than that of the cavity,
140 hydrogel derived from decellularized porcine ventricular myocardium has been shown to halt the post-i
141 s (AT1 and AT2) in chronically failing human ventricular myocardium has not been previously examined.
144 the increase in cardiac lactate to the left ventricular myocardium, implying a direct myocardial eff
154 dly decrease the inotropic state of the left ventricular myocardium independent of its bradycardic ef
155 activity in atrial myocardium compared with ventricular myocardium, indicating regional differences
158 d collagen content throughout right and left ventricular myocardium, irrespective of sampling locatio
159 of transcription (STAT)5 activation in left ventricular myocardium is associated with RIPC s cardiop
160 s and measurements of conduction velocity in ventricular myocardium is complicated by the fact that t
161 We suggest that the proper development of ventricular myocardium is dependent on the invasion of u
164 erging that gene expression profiles of left ventricular myocardium isolated from failing versus nonf
165 mechanical synchrony between left and right ventricular myocardium isolated from the same heart, in
166 direct cytopathic effects on the atrial and ventricular myocardium, later stages of progressive deco
167 lthough the systolic loading sequence of the ventricular myocardium likely affects its coupling with
168 zed, enzymatically digested and fractionated ventricular myocardium, localizes to injured tissues by
169 ricular cardiomyocytes to divide and replace ventricular myocardium lost from ischaemia-induced infar
170 ary performance in health and disease, right ventricular myocardium mechanical behaviour has received
171 Cs was slower when compared with normal left ventricular myocardium (median, 54 [interquartile range,
174 restimation resulted from inclusion of right ventricular myocardium (n=37; 38.1%), LV trabeculations
175 as cross-sectional percentage of viable left ventricular myocardium, n=9; 0.87%+/-1.4% versus n=6; 14
176 edle was advanced percutaneously to the left ventricular myocardium of 6 patients with chronic myocar
177 of A1-AdoR and A1-AdoR/G protein coupling in ventricular myocardium of 6- to 24-month-old Fischer 344
178 amounts of collagen were determined in left ventricular myocardium of 65 F2-mice and combined with g
180 lactosidase gene were identified in the left ventricular myocardium of adult female nude mice 6 weeks
181 lactosidase gene (Ad beta-gal) into the left ventricular myocardium of athymic nude rats (NDRs) versu
182 10(3) myocytes were in mitosis in the entire ventricular myocardium of control hearts and hearts affe
183 es of cardiocyte apoptosis exist in the left ventricular myocardium of dogs with chronic heart failur
184 hat autonomic conditions directly affect the ventricular myocardium of healthy subjects, causing diff
185 phosphorylation of phospholamban in the left ventricular myocardium of HF patients in atrial fibrilla
187 ssion of IL-13 was induced in left and right ventricular myocardium of WT mice within days in respons
188 tricular myocardium versus 20.4+/-10.6% left ventricular myocardium, P<0.0001) and corresponded to th
189 PLB) were determined in explanted human left ventricular myocardium (pediatric n=41; adult n=88).
190 leads to non-physiological activation of the ventricular myocardium, reducing global cardiac performa
192 Western blot analyses were performed on left ventricular myocardium remote from the infarct zone in l
193 techniques, we found that uncoupling of the ventricular myocardium results in ectopic sites of ventr
194 Mechanical experiments with skinned left ventricular myocardium revealed that PKCalpha significan
195 mputed tomography (CE-CT) images with expert ventricular myocardium segmentations were acquired from
197 embrane potential (DeltaV(m)) in the bulk of ventricular myocardium (so-called virtual electrodes), b
199 aximal standardized uptake value of the left ventricular myocardium (SUV(Myo)) as well as the average
200 analyzed inducible NOS (iNOS) expression in ventricular myocardium taken from 11 control subjects (w
201 2 subtypes of the angiotensin II receptor in ventricular myocardium taken from 9 donor hearts before
203 us to derive an immortal cell line from the ventricular myocardium that could be controllably withdr
207 ce-tip catheter to normal or scarred porcine ventricular myocardium, thereby setting the stage for fu
208 art disease resulting in large scale loss of ventricular myocardium through both apoptotic and necrot
212 n to retrograde propagation from the working ventricular myocardium to PFs, antegrade propagation occ
213 Cell-specific depletion of over 60% of the ventricular myocardium triggered signs of cardiac failur
215 RNA beta 1 species that are expressed in rat ventricular myocardium under basal conditions, and deter
216 ters and lesion formation characteristics in ventricular myocardium using a novel temperature-control
217 of electrical coupling across the developing ventricular myocardium using high-speed optical mapping
218 zed by progressive degeneration of the right ventricular myocardium, ventricular arrhythmias, fibrous
219 linium enhancement extent (33.2+/-16.2% left ventricular myocardium versus 20.4+/-10.6% left ventricu
220 virus containing the human beta(2)AR cDNA to ventricular myocardium via catheter-mediated subselectiv
222 intracellular compartment of guinea pig left ventricular myocardium was measured at 20 degrees C and
224 splantation, more than one-third of the left ventricular myocardium was replaced by fibrosis, mainly
226 ract myocardium specification, whereas right ventricular myocardium was specified but failed to prope
227 lagen are thought to affect the mechanics of ventricular myocardium, we investigated myocardial colla
228 ariations in T2 relaxation times of the left ventricular myocardium were assessed, and intrasession a
229 METHODS AND Paired biopsy samples of left ventricular myocardium were obtained from 9 patients wit
230 esent study, mitoK(ATP) channels from bovine ventricular myocardium were reconstituted using planar l
231 carbonate signal mainly confined to the left ventricular myocardium, whereas the [1-(13)C]lactate sig
232 an is expressed strongly in the trabeculated ventricular myocardium, whereas the compact proliferativ
233 grade propagation occurs from PFs to working ventricular myocardium, which suggests PFs are important
234 lts in ectopic activation of atrial genes in ventricular myocardium with an associated impairment of
236 , 20g, 40g, and 70g: (1) over left and right ventricular myocardium with or without fat, (2) either d
237 uate a technique for mapping and ablation of ventricular myocardium with the use of transcatheter sub
238 roperties compared to native adult rat right ventricular myocardium, with stiffnesses controlled by p
239 d looping, Lbh expression is confined to the ventricular myocardium, with the highest intensity in th