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1 ling can substitute for the influence of the outflow tract.
2 locity-time integral of the left ventricular outflow tract.
3  with a striking increase in the size of the outflow tract.
4 VEGF-C to stimulate vessel growth around the outflow tract.
5 V internal dimension were measured in the RV outflow tract.
6 ied the focal origin in the left ventricular outflow tract.
7 evelops from the slowly conducting embryonic outflow tract.
8  the AV endocardial cushions and the cardiac outflow tract.
9 ions in the pharyngeal apparatus and cardiac outflow tract.
10 particular, for the formation of the cardiac outflow tract.
11 ond heart field cells that contribute to the outflow tract.
12 r migration to the heart or septation of the outflow tract.
13 nd in the correct positioning of the cardiac outflow tract.
14 delay in the anterolateral right ventricular outflow tract.
15  displacement into the left ventricular (LV) outflow tract.
16 al arches and the septation of the heart and outflow tract.
17 ginally smaller in BAs than in WAs (proximal outflow tract, 30.9+/-5.5 versus 32.8+/-5.3 mm, P<0.001;
18 , we found aberrant myocardialization of the outflow tract, a process also known to be EMT dependent.
19 iagnosis for syndromic and nonsyndromic left outflow tract abnormalities and implications for at-risk
20 henotypes, including aortic arch and cardiac outflow tract abnormalities.
21  versus 0 mV); (2) delayed right ventricular outflow tract activation (82+/-18 versus 37+/-11 ms); (3
22 ryological context for understanding cardiac outflow tract alignment and membranous ventricular septa
23 lesion, supporting the idea that AHF-derived outflow tract alignment defects may constitute an embryo
24 function in the AHF results in a spectrum of outflow tract alignment defects ranging from overriding
25                Moreover, we found a range of outflow tract alignment defects resulting from a single
26 ng premature ventricular contractions of the outflow tract alternating with papillary muscle or fasci
27 entricular contractions originating from the outflow tract alternating with the papillary muscle or f
28 -CMR data analysis included left ventricular outflow tract and aortic valve segmentation, and extract
29 ht ventricular growth, and interventricular, outflow tract and aortico-pulmonary septation.
30 the second heart field, pharyngeal endoderm, outflow tract and atrioventricular endocardial cushions
31 ct was the most common CHD observed, whereas outflow tract and atrioventricular septal defects were t
32  myocardial movements that are essential for outflow tract and atrioventricular septation.
33 sect Hand2-dependent defects specifically in outflow tract and cardiac cushion independent of Hand2 f
34 uber ciliopathy syndromes, including cardiac outflow tract and cochlea defects associated with PCP pe
35 erning of structures formed from NCC such as outflow tract and cranial nerves.
36         Stenting of the systemic ventricular outflow tract and creation or enlargement of a ventricul
37  the outflow tract septum, migrated into the outflow tract and formed a septum.
38 xplants with isolated pharyngeal endoderm or outflow tract and found that outflow tract co-cultures p
39 acity, regulated by the neighbouring cardiac outflow tract and Hh signalling.
40 ritruncal blood vessels encircle the cardiac outflow tract and invade the aorta, but the underlying p
41 ngates the heart tube, and gives rise to the outflow tract and much of the right ventricle.
42 rise to three cardiovascular lineages in the outflow tract and myocardium in the distal ventricle.
43 preventing MV systolic displacement into the outflow tract and outflow obstruction.
44 participate in the remodeling of the cardiac outflow tract and pharyngeal arch arteries during cardio
45  scar most commonly in the right ventricular outflow tract and right ventricle basal regions.
46 age-sensitive role in the differentiation of outflow tract and right ventricle from progenitors of th
47 r region is known to be destined to form the outflow tract and right ventricle.
48  contributes to the septation of the cardiac outflow tract and the formation of aortic arches.
49  second heart field (AHF), gives rise to the outflow tract and the majority of the right ventricle an
50 regulates the signaling processes leading to outflow tract and valve morphogenesis and ventricular tr
51 tal heart disease through failure of cardiac outflow tract and ventricular septation.
52 nd the most common areas are the ventricular outflow tracts and left ventricular fascicles.
53 tracellular matrix homeostasis in HDAC3-null outflow tracts and semilunar valves, and pharmacological
54 genetic silencing of Tgf-beta1 in HDAC3-null outflow tracts and semilunar valves.
55 hose that affect the proper alignment of the outflow tracts and septation of the ventricles are a hig
56 ns (3087 [50%] ventricular bodies, 756 [12%] outflow tract, and 162 [3%] epicardial).
57 1 syndromes, including craniofacial, cardiac outflow tract, and aortic arch malformations.
58 om the epicardial right ventricular apex, RV outflow tract, and LV free wall, as well as premature at
59 tis, in situ stents in the right ventricular outflow tract, and presence of outflow tract irregularit
60  valve disease, area of the left ventricular outflow tract, and tricuspid annular geometry.
61 pression with simultaneous right ventricular outflow tract angioplasty and CA angiography.
62                                              Outflow tract anomalies identified by micro-CT included
63 l was used for soft tissue structures of the outflow tract, aortic root, and noncalcified valve cusps
64 tive primary repair; their right ventricular outflow tracts are characterized by mild residual obstru
65 tants are of aberrant shape, and the cardiac outflow tracts are short and malformed.
66                                           LV outflow tract area, indexed stroke volume, and AVA corre
67       Thirty-two patients with idiopathic RV outflow tract arrhythmias and 32 control subjects, match
68 nts with ARVC compared with patients with RV outflow tract arrhythmias and controls.
69 teria can help distinguish right ventricular outflow tract arrhythmias originating from ARVD/C compar
70 -24 versus 7+/-5 ms/cm) at right ventricular outflow tract borders.
71 s in lower vertebrates contain a rudimentary outflow tract but not a right ventricle, the existence a
72 y run in parallel along the left ventricular outflow tract, but in the Nkx2-5(+/-)/Sspn(KO) mutant th
73                                         Left outflow tract cardiac anomalies in children present as a
74 eal endoderm or outflow tract and found that outflow tract co-cultures prevented SAG-induced prolifer
75  arteriosus in basal actinopterygians, to an outflow tract commanded by the non-valved, elastic, bulb
76 o difference in E12 in the right ventricular outflow tract compared with the right-left ventricular o
77           In patients with right ventricular outflow tract conduit dysfunction, TPV replacement is as
78 ed as a viable therapy for right ventricular outflow tract conduit dysfunction.
79  function in patients with right ventricular outflow tract conduit dysfunction; the impact of this te
80 median age, 19 years) with right ventricular outflow tract conduit obstruction or regurgitation.
81 implantation in obstructed right ventricular outflow tract conduits in 2010 after a multicenter trial
82 treatment of dysfunctional right ventricular outflow tract conduits in patients >/=30 kg.
83 apy for dysfunctional right ventricular (RV) outflow tract conduits.
84 placement in dysfunctional right ventricular outflow tract conduits.
85 5 mutation is strongly associated with human outflow tract congenital heart disease (OFT CHD).
86 misalignment of the aortic arch arteries and outflow tract, contributing to development of double out
87 ects including pharyngeal arch artery (PAA), outflow tract, craniofacial and thymic abnormalities.
88                   Surgical right ventricular outflow tract cryoablation was performed in 22 patients
89 oppler gradient across the right ventricular outflow tract decreased from 41.9 +/- 27.9 mm Hg to 19.1
90 sistent truncus arteriosus, a severe cardiac outflow tract defect also seen in human congenital heart
91 ma, inner and outer ear malformations, heart outflow tract defects and craniofacial defects.
92 ls that some Isl1 derivatives in the cardiac outflow tract derive from Wnt1-expressing neural crest p
93                                          All outflow tract-destined cells are intermingled with those
94 es of cardiac progenitor differentiation and outflow tract development and has implications for under
95 e myocyte cell-cell adhesions during cardiac outflow tract development contributes to impaired outflo
96 hich is required for aortic arch and cardiac outflow tract development, and is a known genetic intera
97 TOF in 22q11.2DS and may function in cardiac outflow tract development.
98 (HR, 0.94 per 1%; P=0.02), right ventricular outflow tract diameter (HR, 1.08 per 1 mm; P=0.01), mitr
99                  A ratio of AML length to LV outflow tract diameter of >2.0 was associated with subao
100 a mean (SD) follow-up of 6.4 (2.5) years, RV outflow tract dimension increased from 35 mm (interquart
101             The RV size was determined by RV outflow tract dimension, and RV and left ventricular (LV
102 utflow obstruction in combination with small outflow tract dimension.
103 myofibres and collagen fibres to the apex-to-outflow-tract direction was consistent with this also be
104 tics of both syndromic and nonsyndromic left outflow tract disorders is hoped to lead to improved ide
105 ution involves the transition from a cardiac outflow tract dominated by a multi-valved conus arterios
106 nsformative technology for right ventricular outflow tract dysfunction with the potential to expand t
107 treatment of postoperative right ventricular outflow tract dysfunction.
108  disease patient with right ventricular (RV) outflow tract dysfunction.
109 lation without wall motion abnormalities; RV outflow tract ectopy; and exercise-induced T-wave pseudo
110 eir migration to the proximal aspects of the outflow tract endocardial cushions, resulting in the fai
111 inding EGF-like growth factor to Jag1-mutant outflow tract explant cultures rescued the hyperprolifer
112         Very few Islet-1(+) cells within the outflow tract expressed the cardiomyocyte marker alpha-a
113 gle device or with strategies to prepare the outflow tract for subsequent device deployment.
114  in gestation and display defects in cardiac outflow tract formation, atrial and ventricular septatio
115 ate atrioventricular canal morphogenesis and outflow tract formation.
116  cells required for proper patterning of the outflow tract, generation of the appropriate number of n
117 gitation, and 4 had a mean right ventricular outflow tract gradient >/=30 mm Hg.
118              A preoperative left ventricular outflow tract gradient >/=80 mm Hg was a predictor for p
119 ficacy of both SA and SM in left ventricular outflow tract gradient (LVOTG) reduction seems comparabl
120 essure ratio (P<0.001) and right ventricular outflow tract gradient (P=0.004) than those with no tear
121           RV T1 correlated inversely with RV outflow tract gradient (r=-0.28, P=0.02).
122                    Residual left ventricular outflow tract gradient after ablation was an independent
123 h significant reduction in right ventricular outflow tract gradient and the RV:Ao ratio when compared
124 g patients with significant (>/=30 mm Hg) RV outflow tract gradient and/or other residual hemodynamic
125                   A higher right ventricular outflow tract gradient at discharge (P=0.003) and younge
126      The peak instantaneous left ventricular outflow tract gradient decreased from 75.7+/-28.0 mm Hg
127 ce interval, 1.02-2.30) and left ventricular outflow tract gradient progression (hazard ratio, 1.45;
128     IVSd was not related to left ventricular outflow tract gradient reduction at rest (P=0.883) or du
129              Over time, the left ventricular outflow tract gradient slowly increases and mild aortic
130            The median peak right ventricular outflow tract gradient was 37 mm Hg before implantation
131 estent and lower discharge right ventricular outflow tract gradient were associated with longer freed
132 athy (HCM) exhibit elevated left ventricular outflow tract gradients (LVOTGs) and appear to have a wo
133 zation data in 162 consecutive patients with outflow tract gradients (median [interquartile range], 9
134 ressure ratio (P=0.02) and right ventricular outflow tract gradients (P</=0.001).
135    ASA had equal effects on left ventricular outflow tract gradients and symptoms throughout the spec
136                             Left ventricular outflow tract gradients are absent in an important propo
137 iomyopathy was frequently observed (proximal outflow tract &gt;/=32 mm; 45.0% of BAs, 58.5% of WAs).
138 the anterior subepicardial right ventricular outflow tract in 11 patients (group B).
139 446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 co
140 the derived, monovalvar, bulbar state of the outflow tract in modern actinopterygians.
141 rograms recorded in the epicardium of the RV outflow tract in patients with BrS.
142             However, this septum divided the outflow tract into two unequal sized vessels and effecti
143 t ventricular outflow tract, and presence of outflow tract irregularities at the implant site were as
144 enting of the ventricular septum or systemic outflow tract is feasible and effective in the short ter
145            As an additional consequence, the outflow tract is misspecified along its proximal-distal
146 ant mice, this latter process fails, and the outflow tract is shortened and misaligned as a result.
147      As a result, full blood momentum in the outflow tract is used to facilitate early ejection.
148 initial SHF population incorporates into the outflow tract, it is replenished from the surrounding pr
149                           Pacing from the RV outflow tract/lateral RV predicted significantly decreas
150 lmonary left ventricle, and left ventricular outflow tract (LVOT) conduit dysfunction has not been st
151                     Cardiac left ventricular outflow tract (LVOT) defects represent a common but hete
152 criteria for distinguishing left ventricular outflow tract (LVOT) from right ventricular outflow trac
153 e mitral valve could reduce left ventricular outflow tract (LVOT) obstruction and associated mitral r
154 rtrophic cardiomyopathy and left ventricular outflow tract (LVOT) obstruction, but without basal sept
155  (VAs) originating from the left ventricular outflow tract (LVOT) sometimes require catheter ablation
156  (VAs) originating from the left ventricular outflow tract (LVOT) sometimes require catheter ablation
157  (VAs) originating from the left ventricular outflow tract (LVOT), an alternative approach from the a
158 ve patients who experienced left ventricular outflow tract (LVOT)/annular/aortic contained/noncontain
159 associated with ascending aortic dilatation, outflow tract malrotation, overriding aorta, double outl
160 activity in the epicardial right ventricular outflow tract may be beneficial in patients with Brugada
161 results indicate that BMP signaling from the outflow tract modulates hedgehog-induced proliferation i
162 ar genetics of neural crest contributions to outflow tract morphogenesis and cell differentiation.
163 r the control of Bmp signaling that promotes outflow tract myocardial differentiation from cardiac pr
164 ow tract development contributes to impaired outflow tract myocardialization and displacement of the
165 ore, impaired NMII-B motor activity inhibits outflow tract myocardialization, leading to mislocalizat
166             BMP2 is made and secreted by the outflow tract myocardium.
167  the free wall of the right ventricular (RV) outflow tract (n=8), lateral RV (n=44), RV apex (n=61),
168 . 24 +/- 6 mm; p < 0.001) and less prevalent outflow tract obstruction (19% vs. 34%; p = 0.015); 2) h
169 thy with severe symptomatic left ventricular outflow tract obstruction (47+/-11 years, 63% male) intr
170                    However, left ventricular outflow tract obstruction (LVOTO) has been traditionally
171 y, there was mild residual right ventricular outflow tract obstruction (mean gradient, 24+/-13 mm Hg)
172 tions, including relief of right ventricular outflow tract obstruction (n=5), pulmonary arterioplasty
173  the use of paroxetine and right ventricular outflow tract obstruction (relative risk, 1.07; 95% CI,
174 between paroxetine use and right ventricular outflow tract obstruction and between sertraline use and
175 ntly accompanied by dynamic left ventricular outflow tract obstruction and symptoms of dyspnea, angin
176 sk of Ebstein's anomaly (a right ventricular outflow tract obstruction defect) in infants and overall
177          The prevalence of right ventricular outflow tract obstruction defects was 0.60% among lithiu
178        Patients with severe left ventricular outflow tract obstruction had a bisferiens pressure wave
179 g surgery for the relief of left ventricular outflow tract obstruction have low event rates during lo
180 ssociation of symptoms with left ventricular outflow tract obstruction in HCM, there exist paradoxica
181 ulmonary regurgitation and right ventricular outflow tract obstruction in selected patients.
182 tral valve was discovered as the cause of LV outflow tract obstruction in the M-mode echocardiography
183  whereas proximally, severe left ventricular outflow tract obstruction is associated with an addition
184                             Left ventricular outflow tract obstruction is present at rest in about on
185 ern was evident, which is associated with LV outflow tract obstruction loss and right ventricle systo
186 mic pulmonary hypertension, left ventricular outflow tract obstruction or dilated cardiomyopathy.
187 ands were younger with less left ventricular outflow tract obstruction than G- probands, however, had
188 .9 years) with significant right ventricular outflow tract obstruction underwent BMS followed by PPVI
189 ntry, including 249 in whom left ventricular outflow tract obstruction was absent both at rest and fo
190 remia and flow reserve in our study, whereas outflow tract obstruction was not an independent determi
191 rated vigorous left ventricular function, no outflow tract obstruction, and no aortic valve insuffici
192 ns in this series were for right ventricular outflow tract obstruction, highlighting the importance o
193 ly seen in association with left ventricular outflow tract obstruction, itself part of a spectrum of
194 ansvalvular gradient and no left ventricular outflow tract obstruction.
195  for right ventricular dilation and residual outflow tract obstruction.
196  for the surgical relief of left ventricular outflow tract obstruction.
197 dergoing surgical relief of left ventricular outflow tract obstruction.
198 ce of death due to electric abnormalities or outflow tract obstruction.
199 iograms were evaluated for right ventricular outflow tract obstruction.
200 tructive cardiomyopathy patients with severe outflow tract obstruction.
201  95% CI 3.60-25.91%), while left ventricular outflow tract obstruction/mid-ventricular obstruction (L
202        Associations between left ventricular outflow tract obstructions and nitrogen dioxide and betw
203  strategy consisting of relief of inflow and outflow tract obstructions, resection of endocardial fib
204 l defects, conotruncal, and left ventricular outflow tract obstructive lesions are underway.
205 ization are present in the right ventricular outflow tract of BrS patients.
206 labeled cells were detected in the atria and outflow tract of the developing heart.
207 he current knowledge of the genetics of left outflow tract of the heart, including the aortic stenosi
208 ally as the floor of the mandibular arch and outflow tract of the heart.
209 niofacial structures, pigment cells, and the outflow tract of the heart.
210 red for patterning of the great arteries and outflow tract of the heart.
211  branchiomeric muscles and the cells for the outflow tract of the heart.
212  neural crest cells arise, which pattern the outflow tract of the heart.
213 d connect the dorsal head vasculature to the outflow tract of the heart.
214 ifferentiation, cardiomyocyte proliferation, outflow tract (OFT) and atrioventricular septation, and
215 dial cells to mesenchymal cells (EMT) at the outflow tract (OFT) but not atrioventricular canal (AVC)
216 uding cells in the atrioventricular (AV) and outflow tract (OFT) cushions.
217 play key roles in development of the cardiac outflow tract (OFT) for establishment of completely sepa
218 vious genetic studies in mice indicated that outflow tract (OFT) formation requires Dvl1 and 2, but i
219                               Defects of the outflow tract (OFT) make up a large percentage of human
220                                              Outflow tract (OFT) malformation accounts for approximat
221 ecades, the mechanisms underlying RA-induced outflow tract (OFT) malformations are not understood.
222                              In mammals, the outflow tract (OFT) of the developing heart septates int
223 pharyngeal arch arteries (PAAs). and cardiac outflow tract (OFT) requires multipotent neural crest ce
224  mouse identifies common progenitors for the outflow tract (OFT), LV, atrium and SV but not the right
225 ular myocardium and in three lineages in the outflow tract (OFT).
226  signaling axis impairs morphogenesis of the outflow tract (OFT).
227 ve rise to the right ventricle and primitive outflow tract (OFT).
228                    Flow velocities in the LV outflow tract on the pre-SAM frame 1 and 2 mm from the t
229  PC-CMR of aortic valve and left ventricular outflow tract on the same day.
230                         The proximity of the outflow tracts (OTs) frequently results in an overlap in
231 ght ventricle (P=0.037) and left ventricular outflow tract (P<0.001) and higher in left ventricle-rig
232 act compared with the right-left ventricular outflow tract (P=0.75) pairs.
233 plified continuity equation=left ventricular outflow tract peak flow rate/aortic peak velocity.
234 00 ventricular extrasystoles (or >500 non-RV outflow tract) per 24 h; and symptoms, ventricular tachy
235 lve replacement in dilated right ventricular outflow tracts, permitting lower risk, nonsurgical pulmo
236 ignaling is required for EMT in the proximal outflow tract (pOFT) but not atrioventricular canal (AVC
237      In patients referred for left ventricle outflow tract premature ventricular contraction ablation
238 ght consecutive patients with left ventricle outflow tract premature ventricular contraction were inc
239 s (mean age 44 +/- 14 years, 21 female) with outflow tract premature ventricular contractions (PVCs)/
240 d October 2008, 64 patients who underwent RV outflow tract procedures in early childhood had more tha
241    Cranial pSHF cells also contribute to the outflow tract: proximal and distal at 4 somites, and dis
242 perior imaging of the right ventricular (RV) outflow tract, pulmonary arteries, aorta, and aortopulmo
243 n evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed long, and var
244 ects in children requiring right ventricular outflow tract reconstruction typically involves multiple
245                             Within the heart outflow tract, reduced proliferation of myocardial and e
246  conduction slowing in the right ventricular outflow tract region.
247 rs), 32 patients underwent right ventricular outflow tract reintervention for obstruction (n=27, with
248 ntractions originating in the left ventricle outflow tract represent a significant subgroup of patien
249 f the Melody TPV to patients with nonconduit outflow tracts (right ventricular outflow tract [RVOT])
250                               In hearts with outflow tract rotation defects, misplaced stems were ass
251 n of the aortic arch, right ventricular (RV) outflow tract (RVOT) and pulmonary arteries.
252 placed epicardially on the right ventricular outflow tract (RVOT) before video-assisted thoracoscopic
253           Due to recurrent right ventricular outflow tract (RVOT) dysfunction, patients with complex
254               The shape of right ventricular outflow tract (RVOT) has been assumed to be circular.
255 es have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electro
256 atients with postoperative right ventricular outflow tract (RVOT) obstruction or pulmonary regurgitat
257  outflow tract (LVOT) from right ventricular outflow tract (RVOT) origin in patients with idiopathic
258 siological sequelae of the right ventricular outflow tract (RVOT) reconstruction.
259 and cardiomyopathy-related right ventricular outflow tract (RVOT) ventricular arrhythmias (VAs) is cr
260 he anterolateral region, 8 (17.7%) in the RV outflow tract (RVOT), and 8 (17.7%) in the apex.
261 imings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were calculated
262 e usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valv
263 nonconduit outflow tracts (right ventricular outflow tract [RVOT]) has the potential to vastly expand
264  an isolated subepicardial right ventricular outflow tract scar serving as a substrate for fast VT in
265                       Larger preoperative RV outflow tract scar was associated with a smaller improve
266 aniofacial cartilaginous structures, cardiac outflow tract septation and thymic and dorsal root gangl
267 on of the second heart field (SHF) and heart outflow tract septation defects are combined, although t
268 modeling of the pharyngeal arch arteries and outflow tract septation during heart development, but th
269 haryngeal arch artery remodeling and cardiac outflow tract septation during vertebrate development.
270 ng of pharyngeal arch arteries and defective outflow tract septation resulting in the formation of a
271 c neural crest-derived cells, which form the outflow tract septum, migrated into the outflow tract an
272                                       The RV outflow tract, septum, and apex were mapped during left
273 diac phenotype (119-113 Ma) and suggest that outflow tract simplification in actinopterygians is comp
274  defects that are preceded by a reduction in outflow tract size and loss of caudal pharyngeal arch ar
275 or early primary repair by right ventricular outflow tract stenting (stent).
276                            Right ventricular outflow tract stenting of symptomatic tetralogy of Fallo
277 ) (r = 0.880; p < 0.0001), right ventricular outflow tract stroke volume (r = 0.660; p < 0.0001), and
278 y (ARVD/C) from those with right ventricular outflow tract tachycardia (RVOT-VT).
279  were placed into the right ventricular apex/outflow tract through a subclavian vein puncture with a
280 ng the left ventricle is reversed toward the outflow tract through rotating reversal flow around the
281 la: LVEI=indexed LV end-systolic diameter/LV outflow tract time-velocity integral.
282 the ventricular septum or subvalvar systemic outflow tract, using 1 of the following 3 delivery appro
283 as ([LA emptying fraction x left ventricular outflow tract-velocity time integral] / [indexed LA end-
284 ct (RVOT) origin in patients with idiopathic outflow tract ventricular tachycardia (OTVT) and lead V(
285 dle branch block excluding right ventricular outflow tract ventricular tachycardia.
286 uctural heart disease, most left ventricular outflow tract ventricular tachycardias (VTs) have a foca
287 ent of specific anatomical structures (e.g., outflow tract, ventricular septum, and atrial septum) th
288 ultiple cardiovascular defects affecting the outflow tract, ventricular septum, atrioventricular cush
289 irect transcriptional target of MEF2C in the outflow tract via an AHF-restricted Tdgf1 enhancer.
290 maximal Doppler velocity in left ventricular outflow tract (VmaxAo) measured using either approach, a
291 hologies (MMs) of inducible left ventricular outflow tract VT may indicate a scar-related VT that can
292  patients referred for ablation of sustained outflow tract VT without overt structural heart disease,
293 tural heart disease, 24 had left ventricular outflow tract VT, 10 had MM VT, and 14 had a single VT (
294 l pole morphogenesis, identifying defects in outflow tract wall and cushion morphology that preceded
295 terior right free wall and right ventricular outflow tract, which increased after flecainide from 17.
296 erved that VEGF-C is widely expressed in the outflow tract, while cardiomyocytes develop specifically
297 that CXCL12 is present at high levels in the outflow tract, while peritruncal endothelial cells (ECs)
298 bserved exclusively in the right ventricular outflow tract with the following properties (in comparis
299 ection flow velocity in the left ventricular outflow tract, with consequent loss of flow momentum.
300  (SHF) gives rise to the right ventricle and outflow tract, yet its evolutionary origins are unclear.

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