ライフサイエンスコーパス: right ventricle

1 and 22 (81%) had no antegrade flow from the right ventricle.

2 ion in demembranated trabeculae from the rat right ventricle.

3 y well suited for noninvasive imaging of the right ventricle.

4 d in 69% and 84%, respectively, covering the right ventricle.

5 -attenuation lesion at the inner wall of the right ventricle.

6 as open under water and air escaped from the right ventricle.

7 KE was quantified in the left and right ventricle.

8 raordinary endurance exercise may injure the right ventricle.

9 1 in the anterior SHF results in hypoplastic right ventricle.

10 ion increases myocyte number in the neonatal right ventricle.

11 xercise training seem to injure the systemic right ventricle.

12 ventricular septal defect, and double outlet right ventricle.

13 care must be taken to support the unassisted right ventricle.

14 t ventricle but less well for lesions in the right ventricle.

15 and misaligned, resulting in a double outlet right ventricle.

16 ization and displacement of the aorta to the right ventricle.

17 mmatory foci, that is, at the surface of the right ventricle.

18 oventricular valve defects and double outlet right ventricle.

19 d by ventricular arrhythmias and an abnormal right ventricle.

20 ventricular drain that was inserted into the right ventricle.

21 to be destined to form the outflow tract and right ventricle.

22 oss and fibrofatty tissue replacement of the right ventricle.

23 es rise to the outflow tract and much of the right ventricle.

24 mon atrioventricular canal and double outlet right ventricle.

25 , resulting in a common trunk overriding the right ventricle.

26 teins, is fibroadipocytic replacement of the right ventricle.

27 of preload, and progressive dilation of the right ventricle.

28 consecutive patients with VA origins in the right ventricle.

29 ietal band is one of the muscle bands in the right ventricle.

30 t may benefit lung vessels and the remodeled right ventricle.

31 ubule network integrity in both the left and right ventricles.

32 nce interval, -0.58 to -0.31); double-outlet right ventricle, -0.48 (95% confidence interval, -0.87 t

33 eft ventricle (124+/-27 vs 79+/-12 mL/m(2)), right ventricle (127+/-28 vs 83+/-14 mL/m(2)), left atri

34 ns were delivered to 3 separate sites in the right ventricle (30 W, 60 seconds, 17 mL/min irrigation)

35 um (39.7+/-4.2 to 42.3+/-4.3 ms; P=0.01) and right ventricle (48.1+/-2.5 to 53.3+/-5.3 ms; P<0.01).

36 lation comprised more patients with dominant right ventricle (66% vs. 36%) and hypoplastic left heart

37 not yet well established, mainly because the right ventricle, a common target of the disease, present

38 s derived from neonatal mouse heart left and right ventricles, a total of 45 167 unique transcripts w

39 malrotation, overriding aorta, double outlet right ventricle, aberrant semilunar valve development, b

40 quality in 74% of left ventricle and 84% of right ventricle acquisitions and performs better than SS

41 ving a chronically implanted single-chamber (right ventricle) active fixation leadless pacemaker.

42 Rather, the right ventricle actively contributes to venous return du

43 In pulmonary hypertension, the right ventricle adapts to the increasing vascular load b

44 This physiological mechanism protects the right ventricle against acute changes in preload, and it

45 mediated deletion resulted in double outlet right ventricle alignment heart defects.

46 The healthy right ventricle also demonstrates marked augmentation in

47 were included in this analysis (3501 for the right ventricle analysis).

48 ut was ultimately contraindicated because of right ventricle anatomy.

49 gene expressed in the cardiac outflow tract, right ventricle and atrium, pharyngeal mesoderm, periphe

50 derivation cohort, cardiac MRI mPAP model 1 (right ventricle and black blood) was defined as follows:

51 nging from overriding aorta to double-outlet right ventricle and dextro-transposition of the great ar

52 There is reliable remodeling of the excluded right ventricle and good function of the left ventricle.

53 y vascular resistance (PVR), effects reverse right ventricle and left ventricle remodeling, improves

54 defined as the angle between the base of the right ventricle and LV free wall, using the crest of the

55 s are incorporated into the cardiac outflow (right ventricle and outflow tract).

56 e second heart field (SHF) gives rise to the right ventricle and outflow tract, yet its evolutionary

57 he second heart field (SHF) give rise to the right ventricle and primitive outflow tract (OFT).

58 to the outflow tract and the majority of the right ventricle and provides an embryological context fo

59 in D2, cyclin A2, and Cdk4 expression in the right ventricle and that the Cyclin D2 and Cdk4 promoter

60 y), right atrium (synchrony), or for 2 weeks right ventricle and then 2 weeks normal sinus (resynchro

61 to be primarily determined by factors in the right ventricle and tricuspid valve and not the timing o

62 poorly looped hearts with aberrantly formed right ventricles and defective atrioventricular cushion

63 e imaging for the assessment of the left and right ventricles and of indexes of aortic function.

64 ing ventricular noncompaction, double outlet right ventricles and ventricular septal defects.

65 tricular septal defect, double outlet of the right ventricle) and brain defects but not midline fusio

66 ac function, maintenance of perfusion to the right ventricle, and correction of any physiologically d

67 ulmonic infundibulum associated with a small right ventricle, and increased OFT mesenchyme with failu

68 efects such as tetralogy of Fallot, systemic right ventricle, and univentricular hearts.

69 ype B, aortic arch hypoplasia, double-outlet right ventricle, and ventricular septal defect.

70 ts in decreased myocyte proliferation in the right ventricle, and we identified numerous cell cycle g

71 The median right ventricle:aortic pressure ratio after repair was 0

72 egments sensed from a conventional pacemaker right ventricle apical lead, and alerted patients to det

73 s to identify which patients with a systemic right ventricle are at risk for clinical events.

74 the basis for predominant involvement of the right ventricle are unknown.

75 a broad spectrum of CHD, including systemic right ventricles, are similar to those in ischemic heart

76 xtensive surgery in the atria and leaves the right ventricle as the systemic ventricle.

77 ies of the pulmonary vascular system and the right ventricle, as well as their coupling, as important

78 ld (SHF) contribute to the outflow tract and right ventricle, as well as to parts of the left ventric

79 esults in tricuspid atresia with hypoplastic right ventricle associated with the loss of AVC myocardi

80 ansposition of great arteries, double-outlet right ventricle, atrioventricular septal defects, and ca

81 y in the right ventricular outflow tract and right ventricle basal regions.

82 Some emphasized right ventricle-based shunts as a 'cause' of improving r

83 (univentricular heart with a right atrial to right ventricle bioprosthesis in 3, Ebstein's anomaly of

84 Electroanatomic mapping of the right ventricle, both endocardially and epicardially, an

85 ralogy of Fallot focuses on isthmuses in the right ventricle but may be hampered by hypertrophied myo

86 he disease has an early predilection for the right ventricle, but recognition of left-dominant and bi

87 endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magn

88 the left ventricular cavity, myocardium, and right ventricle by processing an incoming time series of

89 a; airway fibrosis; vascular remodeling; and right ventricle cardiac hypertrophy.

90 rized by echocardiography and left ventricle/right ventricle catheter-derived variables.

91 red with placebo in patients with a systemic right ventricle caused by congenitally or surgically cor

92 paration; isolated lung, upper torso, direct right ventricle contrast injection, and whole body with

93 physiological studies on cardiomyocytes from right ventricle demonstrated a shorter action potential

94 mutation embryos disrupted cardiac looping, right ventricle development, and ablated IKr activity at

95 The primary endpoint was right ventricle diameter at the third rhythm analysis: 3

96 This study aimed to compare right ventricle diameter during resuscitation from cardi

97 nography were able to detect a difference in right ventricle diameter of approximately 10 mm with a s

98 related (rho=0.378, P<.01) with the ratio of right ventricle diameter to left ventricle diameter (RV/

99 rd rhythm analysis during resuscitation, the right ventricle diameter was 32 mm (95% CI, 29-35) in th

100 The right ventricle diameter was measured.

101 During induction of cardiac arrest, the right ventricle dilated in all groups (p < 0.01 for all)

102 These findings indicate that right ventricle dilation may be inherent to cardiac arre

103 sinus diverticulum and one a right atrium to right ventricle diverticulum.

104 contributing to development of double outlet right ventricle (DORV) and ventricular septal defects (V

105 icular septal defect (VSD) and double-outlet right ventricle (DORV).

106 , and heart defects, including double-outlet right ventricle (DORV).

107 Dilation of the right ventricle during cardiac arrest and resuscitation

108 hat occur in the heart and in particular the right ventricle during WLS, and give an indication of th

109 Pressure-volume analysis of the right ventricle, during invasive cardiopulmonary exercis

110 impairment may be a relevant contribution to right ventricle dysfunction in pulmonary hypertension.

111 ical studies have mostly focused on modeling right ventricle dysfunction or failure and pulmonary art

112 function, followed by 4 weeks pacing at the right ventricle (dyssynchrony), right atrium (synchrony)

113 Preterm birth was associated with a small right ventricle (end diastolic volume, 79.8+/-13.2 versu

114 lume, 156+/-26 versus 172+/-28 mL, P<0.001), right ventricle (end-diastolic area=27.0+/-4.8 versus 28

115 Right ventricle enlargement and dysfunction were found i

116 ubstrate identification consisted in mapping right ventricle epicardial surface before and after flec

117 ada syndrome, AES is commonly located in the right ventricle epicardium and ajmaline exposes its exte

118 Extensive areas of AES were found in the right ventricle epicardium, which were wider in group 1

119 se in pulmonary arterial pressure leading to right ventricle failure caused sudden death.

120 However, right ventricle failure is a major predictor of outcomes

121 cord, with abnormal mucosa also seen in the right ventricle (Fig 1).

122 exercise group and control group (change in right ventricle free wall peak velocity E' exercise grou

123 t reduction of right ventricular diameter as right ventricle free wall thickness was increased and an

124 in the differentiation of outflow tract and right ventricle from progenitors of the second heart fie

125 onary arterial hypertension and in lungs and right ventricles from rats exposed to hypoxia.

126 f circulating histones on left ventricle and right ventricle function at clinically relevant concentr

127 proposed to use these agents to support the right ventricle function in pulmonary hypertension.

128 lmonary arterial pressure and improvement of right ventricle function.

129 Patients with a systemic right ventricle had elevated BNP levels, and positive co

130 graphic assessment of diseases affecting the right ventricle has lagged behind that of the left ventr

131 eceptor blockers in patients with a systemic right ventricle has not been elucidated.

132 ion of the great arteries (TGA) and systemic right ventricles have premature congestive heart failure

133 veolar counts, pulmonary vessel density, and right ventricle hypertrophy (RVH).Measurements and Main

134 ed, right ventricle pressures increased, and right ventricle hypertrophy and pulmonary changes occurr

135 ived to adulthood with spontaneous eccentric right ventricle hypertrophy.

136 the right ventricular systolic pressure and right ventricle hypertrophy.

137 Deletion of Hand2 in mice results in right ventricle hypoplasia and embryonic lethality.

138 ntified: 1) scars involving the subtricuspid right ventricle in 46 patients (group A); and 2) scars r

139 es that IUGR also leads to impairment of the right ventricle in addition to the left ventricle classi

140 explains the predominant involvement of the right ventricle in ARVC.

141 raction (EF), were measured for the left and right ventricle in both end-expiration and end-inspirati

142 derlying molecular mechanisms of the failing right ventricle in PAH?

143 urrently no approved therapies targeting the right ventricle in pulmonary hypertension.

144 tionated electrical activity recorded in the right ventricle in the setting of BrS.

145 w presents new insights into the role of the right ventricle independently and in conjunction with th

146 3.65 m s(-1)) were identified in the left or right ventricle initially with mechanical stimulation an

147 on cardiovascular magnetic resonance at the right ventricle insertion site.

148 he great arteries, worsening of the systemic right ventricle is accompanied by clinical events such a

149 is study was to test the hypothesis that the right ventricle is more dilated during resuscitation fro

150 In pulmonary hypertension, the status of the right ventricle is one of the most important predictors

151 iables that differentiated these groups were right ventricle:left ventricle inflow angle, LV width/LV

152 Samples of left and right ventricle (LV and RV) free wall collected from 32

153 The angle of right ventricle/LV inflow and other surrogates of inflow

154 ariable between the 3 cluster groups was the right ventricle:LV inflow angle (partial R(2)=0.86), def

155 The resultant increased work of the right ventricle may cause right heart failure and liver

156 Monophasic APs were recorded in the right ventricle (n = 62) and/or left ventricle (n = 9) a

157 dentified by micro-CT included double outlet right ventricle (n=36), transposition of the great arter

158 ified in the right atrium (n=25) than in the right ventricle (n=5).

159 rvival, yet eventual failure of the systemic right ventricle necessitates cardiac transplantation in

160 argeted to the right atrium, His bundle, and right ventricle of 10 mongrel dogs (23 to 32 kg) via a 1

161 atriuretic peptide B is also observed in the right ventricle of AC patients.

162 d, respectively, into the left ventricle and right ventricle of dogs to record endocardial activation

163 ygen consumption (MVO2) of the hypertrophied right ventricle of IPAH patients can be measured using P

164 s whether MVO2 can also be determined in the right ventricle of IPAH patients from the clearance of (

165 ilure may be defined as the inability of the right ventricle of the heart to provide adequate blood f

166 The right ventricle of the mammal heart is highly sensitive

167 yte diameters are significantly increased in right ventricles of AC patients.

168 entricular septal defects with double outlet right ventricle or overriding aorta.

169 tients, especially in patients with systemic right ventricles or single ventricle physiology.

170 , ventricular arrhythmias originate from the right ventricle outflow tract (RVOT).

171 At cardiac repair, a transannular patch for right ventricle outlet reconstruction was required in 44

172 e early and late remodelling of the left and right ventricle over the course of monocrotaline-induced

173 left ventricle, E12 values were lower in the right ventricle (P=0.037) and left ventricular outflow t

174 tract (P<0.001) and higher in left ventricle-right ventricle pairs (P=0.021) and left ventricular epi

175 eplacement of myocytes, predominantly in the right ventricle.Phenotypic expression of ARVC is variabl

176 Although structural abnormalities of the right ventricle predominate, it is well recognized that

177 resistance 1.5[2.2, 0.9] WU, and transmural right ventricle pressure 10[15, 6] mmHg during exhalatio

178 laterals unifocalized, and higher postrepair right ventricle pressure.

179 equently, endothelin-1 production increased, right ventricle pressures increased, and right ventricle

180 A second model, cardiac MRI mPAP model 2 (right ventricle pulmonary artery), which excludes the bl

181 logy, previous intracardiac repair, systemic right ventricle, pulmonary hypertension, pulmonary regur

182 The right ventricle-pulmonary artery (RVPA) shunt may improv

183 domized to modified Blalock-Taussig shunt or right ventricle-pulmonary artery shunt (RVPAS) found bet

184 the Norwood procedure (hazard ratio, 2.0 for right ventricle-pulmonary artery shunt versus modified B

185 ure to a modified Blalock-Taussig shunt or a right ventricle-pulmonary artery shunt.

186 H is determined largely by the status of the right ventricle, rather than the levels of pulmonary art

187 unctional consequences on left ventricle and right ventricle remain unclear.

188 function is dependent on LV health, the IUGR right ventricle remains poorly studied.

189 ental arrest and latent myopathy of left and right ventricles, respectively.

190 In contrast, the right ventricle responds to endurance training with ecce

191 croarray-based gene ontology analysis of the right ventricle revealed that a number of MCT-altered ge

192 These patients had mildly dilated right ventricles (right ventricular end-diastolic volume

193 e English language by using the search words right ventricle, right ventricular failure, pulmonary hy

194 [IQR: 14.4 to 103.8 pmol/l]) and a systemic right ventricle (RV) (31.1 pmol/l [IQR: 21.8 to 56.0 pmo

195 These patients have a systemic right ventricle (RV) and are at risk of arrhythmia, prem

196 The geometry of the right ventricle (RV) and left ventricle (LV) may alter t

197 F progenitor pool leads to an underdeveloped right ventricle (RV) and outflow tract (OFT).

198 T, and was associated with distension of the right ventricle (RV) and reduced cardiac output.

199 rt size and function in children with single right ventricle (RV) anomalies may be influenced by shun

200 intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and lef

201 Outcomes after right ventricle (RV) decompression in infants with pulmo

202 essential for normal outflow tract (OFT) and right ventricle (RV) development.

203 The failing right ventricle (RV) does not respond like the left vent

204 enetic protein receptor type 2 (BMPR2) gene, right ventricle (RV) dysfunction is associated with RV l

205 l deterioration, specifically a reduction in right ventricle (RV) ejection fraction and stroke volume

206 incorporated into a patient-specific silicon right ventricle (RV) emulating severe FTR, on which Kay

207 Until recently, the right ventricle (RV) has often been viewed as less impor

208 t with digoxin attenuated the development of right ventricle (RV) hypertrophy and prevented the pulmo

209 asing recognition of the crucial role of the right ventricle (RV) in determining functional status an

210 The systemic right ventricle (RV) in HLHS is subject to significant c

211 te the recognition of a critical role of the right ventricle (RV) in many aspects of cardiovascular m

212 less, gradual dysfunction and failure of the right ventricle (RV) in the systemic circulation remain

213 herosclerosis) performed cMRIs with complete right ventricle (RV) interpretation on 4,062 participant

214 However, the management of the borderline right ventricle (RV) is controversial, and there may be

215 The right ventricle (RV) is involved in systemic circulation

216 The right ventricle (RV) is of lesser importance in acquired

217 such as those with tetralogy of Fallot, the right ventricle (RV) is subject to pressure overload str

218 The right ventricle (RV) is the major determinant of functio

219 Rationale: Remodeling and fibrosis of the right ventricle (RV) may cause RV dysfunction and poor s

220 cial to confirm HB capture/exclude that only right ventricle (RV) myocardial septal pacing is present

221 rial function and structure were assessed in right ventricle (RV) myocardium collected from patients

222 have been identified at early stages in the right ventricle (RV) of infants with HLHS, although the

223 The right ventricle (RV) of the mammal heart is highly sensi

224 Right ventricle (RV) systolic performance at 24 hours wa

225 ere is minimal data on the adaptation of the right ventricle (RV) to pressure and volume overload and

226 Speckle-derived strain of the right ventricle (RV) was utilized to detect occult abnor

227 d along 4 anatomic axes: left ventricle (LV)-right ventricle (RV), LV:apico-basal, LV:anterior-poster

228 by remodelling of the pulmonary arteries and right ventricle (RV), which leads to functional decline

229 y showed a filling defect at the apex of the right ventricle (RV).

230 ng left ventricular pacing varies within the right ventricle (RV).

231 volumes for the left ventricle (LV) and the right ventricle (RV).

232 w tract (OFT), LV, atrium and SV but not the right ventricle (RV).

233 s such as main pulmonary artery diameter and right ventricle (RV)/left ventricle (LV) ratio.

234 dilation, with consequent compression of the right ventricle (RV); hydrops and low cardiac output are

235 le of the human left ventricle (LV, n=4) and right ventricle (RV, n=4) after 0, 4, and 8 hours of col

236 evels (P < .001), larger left (P = .023) and right ventricles (RV; P = .002), and worse RV function (

237 n (SVR) trial randomized infants with single right ventricles (RVs) undergoing a Norwood procedure to

238 Patients with systemic morphological right ventricles (RVs), including congenitally corrected

239 ay ventricular septal defects, double outlet right ventricle, semilunar valve hyperplasia and aortic

240 Studies of longitudinal axis function of the right ventricle show that contractile function improveme

241 Entrainment from the right ventricle showed ventricular fusion in 4 out of 5

242 f SSFP and TSE BB images of the left and the right ventricles showed a significant improvement with r

243 s increasingly shifted opinion away from the right ventricle shunt as a 'cause' of improved results.

244 The survival of the right ventricle shunt group is slightly higher at 3 year

245 , identifying this as a marker of a systemic right ventricle (SRV) that may most tolerate (and possib

246 great arteries (TGA) patients with systemic right ventricles (SRVs).

247 omyopathy phenotype, involving both left and right ventricles, suggesting that loss of the VIP gene o

248 ategies based on staged procedures, with the right ventricle supporting both systemic and pulmonary c

249 d with LV outflow tract obstruction loss and right ventricle systolic impairment.

250 The changes are greater in the right ventricle than previously observed in the left ven

251 ventricle exerts biomechanical stress on the right ventricle that can progress into heart failure.

252 xpression of structural abnormalities in the right ventricle that may have genetic, infective, or inf

253 ndary at the future junction of the left and right ventricles that arises prior to morphogenesis.

254 ontain a rudimentary outflow tract but not a right ventricle, the existence and function of SHF-like

255 2+)), and cell contractility specific to the right ventricle; these changes could explain the lower c

256 d upregulation of Gremlin 1 mRNA in lung and right ventricle tissue compared with normoxic controls.

257 trum of septation defects from double outlet right ventricle to common arterial trunk in mutants.

258 he native positive inotropic response of the right ventricle to increased afterload.

259 The median right ventricle to left ventricle diameter ratio was 1.3

260 l have been demonstrated with the use of the right ventricle to pulmonary artery (RV-PA) conduit comp

261 lody TPVR within the Contegra conduit in the right ventricle to pulmonary artery position.

262 the modified Blalock-Taussig shunt (MBTS) or right ventricle to pulmonary artery shunt (RVPAS).

263 allot is determined by the adaptation of the right ventricle to the physiological sequelae of the rig

264 tern of LGE localized at the junction of the right ventricle to the septum was respectively observed

265 Angioplasty and stent placement in right ventricle-to-pulmonary artery (RV-PA) conduits hav

266 Eligible patients with dysfunctional right ventricle-to-pulmonary artery conduits were screen

267 and effective in patients with dysfunctional right ventricle-to-pulmonary artery conduits.

268 Following Melody valve implant, the peak right ventricle-to-pulmonary artery gradient decreased f

269 al was better for the Norwood procedure with right ventricle-to-pulmonary artery shunt (RVPAS) compar

270 hybrid palliation (Blalock-Tausig shunt 591, right ventricle-to-pulmonary artery shunt 640, and hybri

271 nificant change is a renewed interest in the right ventricle-to-pulmonary artery shunt as the source

272 odel, whereas a 5-mm conduit was used in the right ventricle-to-pulmonary artery shunt model.

273 operation with a modified Blalock-Tausig or right ventricle-to-pulmonary artery shunt.

274 e with modified Blalock-Taussig shunt versus right-ventricle-to-pulmonary-artery shunt, 14-month neur

275 omparing outcomes in 549 infants with single right ventricle undergoing a Norwood procedure randomize

276 SVR) trial randomized subjects with a single right ventricle undergoing a Norwood procedure to a modi

277 ited cardiac defects including double-outlet right ventricle, ventricular septal defect (VSD), atriov

278 ld (SHF) led to trabeculation defects in the right ventricle, ventricular septal defect, persistent t

279 ds for better image quality were greater for right ventricle versus left ventricle (odds ratio, 1.8;

280 In the mouse studies, both the left and right ventricle walls were clearly observable, as were t

281 The right ventricle was dilated during resuscitation from ca

282 The right ventricle was dilated without evidence of right ve

283 However, the right ventricle was dilated, irrespective of the cause o

284 ing groups at the third rhythm analysis, the right ventricle was larger for hypovolemia than for prim

285 The right ventricle was more dilated during resuscitation wh

286 drogenase activity, left ventricular weight, right ventricle weight, and left ventricular mass after

287 cines and full-volume 3DTTE data sets of the right ventricle were used to measure end-diastolic volum

288 e significantly reduced the size of left and right ventricles, whereas that of DN-Lats2 caused hypert

289 er exercise training might injure a systemic right ventricle which is loaded with every heartbeat.

290 he left ventricle to contract later than the right ventricle, which in turn affects synchronized cont

291 y, it had multiple beneficial effects on the right ventricle, which included suppression of pathologi

292 and cardiomyocyte loss predominantly in the right ventricle, which is associated with life-threateni

293 nt state of three-dimensional imaging of the right ventricle will be highlighted along with the chall

294 highly penetrant phenotype of double outlet right ventricle with a concurrent ventricular septal def

295 3.86 m s(-1)) were identified in the left or right ventricle with a stimulating electrode.

296 We examined the right ventricle with cardiac magnetic resonance imaging

297 (RCM) is characterized by nondilated left or right ventricle with diastolic dysfunction.

298 maker that is nonsurgically implanted in the right ventricle with the use of a catheter.

299 rdium versus subendocardium in both left and right ventricles, with lower levels in Hey2(+/-) mice co

300 h block had delayed activation in the entire right ventricle, without ST-segment elevation, fractiona