ライフサイエンスコーパス: ventricular

1 imaging identified significantly higher left ventricular (18)F-FDG accumulation in TAC mice than in s

2 on that blocks Kv11.1 channels lengthens the ventricular action potential and causes cardiac arrhythm

3 The cardiac ventricular action potential depends on several voltage-

4 n voltage-gated ion channels involved in the ventricular action potential.

5 bundle pacing (HBP) results in physiological ventricular activation and has generated tremendous rese

6 inical outcomes compared with dyssynchronous ventricular activation with RV apical pacing.

7 etwork directly, HBP results in synchronized ventricular activation, which might translate into impro

8 associated with a steady reduction of right ventricular and pulmonary arterial pressures, toward nor

9 llary artery pseudoaneurysm (n = 1/24), left ventricular aneurysms (n = 3/24), pulmonary arteriovenou

10 We prospectively obtained paired left ventricular apical myocardial tissue from nonfailing don

11 This study determined ventricular arrhythmia prevalence, severity, phenotypica

12 Presence of ventricular arrhythmia was associated with male sex, bil

13 Severe ventricular arrhythmia was independently associated with

14 rget for preventing heart failure-associated ventricular arrhythmia.

15 ital mortality and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained vent

16 4.9% vs 44.5%, p = 0.023), and more pre-LVAD ventricular arrhythmias (VA) (77% vs 60%, p = 0.048).

17 short QT syndromes associated with malignant ventricular arrhythmias and sudden cardiac death.

18 ure ventricular complexes and pacing-induced ventricular arrhythmias at ZT14, and the hearts at ZT14

19 ion <55% was strongly associated with severe ventricular arrhythmias for DSP cases (P<0.001, sensitiv

20 pulation; the composite of ICD implantation, ventricular arrhythmias, and cardiac arrest: 0.96% (95%

21 nt morbidity and death from heart failure or ventricular arrhythmias.

22 lausible molecular mechanism for some lethal ventricular arrhythmias.

23 diac action potential that can trigger fatal ventricular arrhythmias.

24 plained by QT prolongation leading to lethal ventricular arrhythmias.

25 PDE9a inhibition increased the ventricular-arterial coupling ratio, reflecting impaired

26 ntractile and lusitropic reserve, as well as ventricular-arterial coupling, in the healthy heart duri

27 RT management following continuous flow Left Ventricular Assist Device (LVAD) implant vary: some cent

28 of major morbidity and mortality after left ventricular assist device (LVAD) implantation.

29 vascular aortic aneurysm repair (EVAR), left ventricular assist device (LVAD), and transcatheter aort

30 ilure (termed responders [R]) following left ventricular assist device (LVAD)-induced mechanical unlo

31 ained before and after (median=82 days) left ventricular assist device implantation (stage D; primary

32 er the ACA is also associated with increased ventricular assist device implantation in blacks.

33 tes that long-term support using a HeartWare ventricular assist device system offers survival of 51%

34 normal, failed and partially recovered (left ventricular assist device treatment) adult human hearts.

35 art failure, heart transplantation, and left ventricular assist device.

36 -0.88]; P<0.0001) and the composite of death/ventricular assist device/heart transplantation (hazard

37 Although intravascular microaxial left ventricular assist devices (LVADs) provide greater hemod

38 te increases over time in patients with left ventricular assist devices and is lowered by ablation.

39 ced heart failure, heart transplant and left ventricular assist devices have been the mainstay of tre

40 such as use of a percutaneous extracorporeal ventricular assist system, extracorporeal membrane oxyge

41 a observed in experiments on both atrial and ventricular cardiac cells.

42 Here, we review the major hallmarks of ventricular cardiomyocyte maturation and summarize key r

43 hysiology, and contractility of neonatal rat ventricular cardiomyocytes (NRVCMs) cultured on these sh

44 ilencing of CYP2J2 expression in human adult ventricular cardiomyocytes and interrogated whole genome

45 widespread alterations in gene expression of ventricular cardiomyocytes and leads to the activation o

46 contractility) and SERCA2a downregulation in ventricular cardiomyocytes from C-dnO1 mice, associated

47 cation in shaping action potentials (APs) in ventricular cardiomyocytes under beta-adrenergic stimula

48 Neonatal rat ventricular cardiomyocytes were infected with adenovirus

49 WT) and CryAB(R120G)-expressing neonatal rat ventricular cardiomyocytes.

50 ia (CPVT) (n = 9 [8%]), arrhythmogenic right ventricular cardiomyopathy (ARVC) (n = 9 [8%]), and dila

51 Arrhythmogenic right ventricular cardiomyopathy (ARVC), with skin manifestati

52 Task Force Criteria for arrhythmogenic right ventricular cardiomyopathy diagnosis and data regarding

53 nal Task Force Criteria arrhythmogenic right ventricular cardiomyopathy diagnosis was reached only in

54 Arrhythmogenic right ventricular cardiomyopathy diagnostic criteria had poor

55 iants that cause either arrhythmogenic right ventricular cardiomyopathy or dilated cardiomyopathy.

56 (CNN) model was trained to segment the left ventricular cavity, myocardium, and right ventricle by p

57 Ventricular cells subjected to hypokalemia exhibited Ca(

58 In this study, we assessed the levels of ventricular cerebrospinal fluid-cfmtDNA (vCSF-cfmtDNA) i

59 ZO-2 protein was increased significantly in ventricular CM in a presumed compensatory manner but was

60 rs, only 4 (younger age, male sex, premature ventricular complex count, and number of leads with T-wa

61 a trend for decreased spontaneous premature ventricular complexes and pacing-induced ventricular arr

62 atterning of the CCS into atrial node versus ventricular conduction system (VCS) components with dist

63 revealed a markedly enhanced homogeneity in ventricular conduction.

64 max is not a load-independent marker of left ventricular contractility and should be not used to trac

65 at in humans with stable heart failure, left ventricular contractility could be accentuated without a

66 modulate the cardiac nerve plexus to enhance ventricular contractility.

67 gnificance of neural remodeling in premature ventricular contraction-induced cardiomyopathy (PVC-CM)

68 ents (62%), whereas 6 patients had premature ventricular contraction-induced ventricular fibrillation

69 in lumbar CSF translated to the post-mortem ventricular CSF.

70 sites on Drd1 mimicked the cilia-beating and ventricular deficits.

71 Prolongation of ventricular depolarization is concentration-dependent wi

72 here was also significant reduction of right ventricular diameter as right ventricle free wall thickn

73 symptomatic PE and right ventricular to left ventricular diameter ratio >=0.9 as documented by comput

74 icant reduction in right ventricular to left ventricular diameter ratio and thrombus burden.

75 phic-measured right ventricular (RV)-to-left ventricular diameter ratio in massive and submassive pul

76 s, global left ventricular dysfunction, left ventricular diastolic dysfunction grade II or III, right

77 no significant change in heart rate or left ventricular diastolic pressure.

78 dulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial i

79 sitivity in detecting active subarachnoid or ventricular disease in symptomatic patients was 100% in

80 les taken from patients with subarachnoid or ventricular disease using quantitative polymerase chain

81 diastolic dysfunction grade II or III, right ventricular dysfunction and pericardial effusions.

82 as associated with oxidative stress and left ventricular dysfunction assessed by electron spin resona

83 We have learned that right ventricular dysfunction may be a predictor of survival b

84 udies had fewer comorbidities, had less left ventricular dysfunction, and received more inappropriate

85 cular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysf

86 LVEF, independent from the severity of left ventricular dysfunction.

87 ties, left ventricular hypertrophy, and left ventricular dysfunctions were demonstrated in Group OSAH

88 MR left ventricular eccentricity index (EI), main pulmonary arte

89 s (p = 0.028), with a reduction in number of ventricular ectopic beats during the ischaemic phase com

90 a lateral e'-wave greater than 8 (for a left ventricular ejection fraction >= 45%) or an E/A ratio le

91 ratio less than or equal to 1.5 (for a left ventricular ejection fraction < 45%).

92 This were consistent for left ventricular ejection fraction < 50% or >= 50%.

93 lation (HR, 2.6 [95% CI, 1.7-3.5]), and left ventricular ejection fraction <35% (HR, 2.0 [95% CI, 1.3

94 tion (HFrEF; heart failure with reduced left ventricular ejection fraction <40%) referred for stress

95 n functional class II or greater with a left ventricular ejection fraction <=40% and a modest elevati

96 Hg increase; 95% CI, 1.05 to 1.28), and left ventricular ejection fraction (aOR, 1.07 per 5% increase

97 Left ventricular ejection fraction (EF) recovery is associate

98 ion and on discharge in patients with a left ventricular ejection fraction (LVEF) >= 40%.

99 t Association functional class II/III), left ventricular ejection fraction (LVEF) >=55%, and N-termin

100 We evaluated the utility of left ventricular ejection fraction (LVEF) by echocardiography

101 Age, symptoms, left ventricular ejection fraction (LVEF), LV end-systolic di

102 rillation (AF) in patients with reduced left ventricular ejection fraction (LVEF).

103 3 acute kidney injury were preoperative left ventricular ejection fraction (odds ratio, 1.03 [95% CI,

104 , 1.89 [95% CI, 1.04-3.44]; P=0.04) and left ventricular ejection fraction (per 10% decrement from le

105 bjects, 88% male, 66+/-9 years old with left ventricular ejection fraction 34+/-6% were included.

106 of 789 patients with chronic HFpEF and left ventricular ejection fraction 45% or higher with New Yor

107 patients (age 51 +/- 14 years, 91% men, left ventricular ejection fraction 52% +/- 9%) had history of

108 ntly in men and women and patients with left ventricular ejection fraction above or below the median

109 ed consistent performance to detect low left ventricular ejection fraction across a range of racial/e

110 patients with chronic HF with a reduced left ventricular ejection fraction from 34 Dutch outpatient H

111 ith congestive heart failure or reduced left ventricular ejection fraction had a higher risk of nonar

112 Left ventricular ejection fraction has conventionally been us

113 Left ventricular ejection fraction increased >=10% in 46.5% o

114 ction (LVSD), defined as occurring when left ventricular ejection fraction is <50%.

115 Of these, 96 correlated with left ventricular ejection fraction measured at 4 months post-

116 We then correlated plasma proteins with left ventricular ejection fraction measured at 4 months post-

117 aortic stenosis (AS) despite preserved left ventricular ejection fraction remains challenging.

118 age was 61 years, 86% were men, median left ventricular ejection fraction was 20%, 81% had ischemic

119 wall thickness was 22.9 +/- 8.7 mm and left ventricular ejection fraction was 53.4 +/- 6.6%.

120 lar wall thickness was 18 +/- 8 mm, and left ventricular ejection fraction was 61 +/- 12%.

121 ection fraction (per 10% decrement from left ventricular ejection fraction, 50%; hazard ratio, 1.63 [

122 ion and subgroup analyses revealed that left ventricular ejection fraction, not the extent of left ve

123 ical and imaging covariates, including right ventricular ejection fraction.

124 Three of 170 patients (2%) had abnormal left ventricular ejection fraction.

125 ts are most prominent in patients whose left ventricular end-diastolic dimension Z score before inter

126 lic volume index threshold of 227% or a left ventricular end-diastolic volume index of 58 ml/m(2) ide

127 atrial area, left atrial volume index, left ventricular end-diastolic volume index, peak E wave, and

128 unction (MAD), a larger left atrium and left ventricular end-systolic diameter, and T-wave inversion/

129 Percentage-predicted right ventricular end-systolic volume index can identify a hig

130 e remodeling, defined as an increase in left ventricular end-systolic volume index of >15% at 24 mont

131 d Main Results: A percentage-predicted right ventricular end-systolic volume index threshold of 227%

132 ration of ciliary motility and age-dependent ventricular enlargement in 22q11DS.

133 on external CT scans and scans demonstrating ventricular enlargement.

134 rve density was reduced in the anterior left ventricular epicardium of DBH-Sap hearts compared to con

135 e genes and biological mechanisms underlying ventricular excitability.

136 ter was essential for prenatal and postnatal ventricular expression of Nppa and Nppb but not of any o

137 Right ventricular failure (RVF) is a cause of major morbidity

138 tion, more than half present with refractory ventricular fibrillation unresponsive to initial standar

139 ined or sustained ventricular tachycardia or ventricular fibrillation).

140 th out-of-hospital cardiac arrest (OHCA) and ventricular fibrillation, more than half present with re

141 eatment in patients with OHCA and refractory ventricular fibrillation.

142 ventions terminating ventricular tachycardia/ventricular fibrillation.

143 ospital cardiac arrest from shock-refractory ventricular fibrillation/pulseless ventricular tachycard

144 ad premature ventricular contraction-induced ventricular fibrillation/VT (29%), and VT could not be i

145 ntricular block or complete heart block; (3) ventricular fibrillation; (4) ventricular tachycardia (>

146 ed without an increase in heart rate or left ventricular filling pressures.

147 Despite growing interest in right ventricular form and function in diseased states, there

148 d annular plane systolic excursion and right ventricular free wall strain).

149 cases of acute myocardial injury with normal ventricular function (4/5, 80% with late gadolinium enha

150 spid regurgitation velocity; and worse right ventricular function (tricuspid annular plane systolic e

151 y of data regarding characteristics of right ventricular function - namely contractile and lusitropic

152 gns of abnormal diastolic and systolic right ventricular function and compression of the atrioventric

153 Left ventricular function and New York Heart Association clas

154 C) developed cardiac hypertrophy and reduced ventricular function associated with increased Orai1 exp

155 Symptoms and left ventricular function at 2 years did not differ significa

156 We evaluated left ventricular function at rest, maximal aerobic capacity (

157 to further improvement in management of left ventricular function in patients with diabetes.

158 mild symptoms, a low PVC burden, and normal ventricular function may be best served with simple reas

159 it (7.6% vs. 9.0%, P < 0.01) strains but not ventricular function or myocardial damage.

160 ne on the vasculature and its effects on the ventricular function using wave intensity analysis.

161 (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiolog

162 smaller infarct size and preserved long-term ventricular function.

163 perimental MI had significantly reduced left ventricular function.

164 Left ventricular functional parameters, especially ventricula

165 Entrainment from the right ventricle showed ventricular fusion in 4 out of 5 cases.

166 The left ventricular global longitudinal strain was higher in the

167 impedance (Z(va)), which reflects total left ventricular hemodynamic burden, was lower with TAVR than

168 measure the concentrations of eight MMPs in ventricular human CSF.

169 Individuals with left ventricular hypertrophy (LVH) and elevated cardiac bioma

170 phenotypic information about high-risk left ventricular hypertrophy (LVH) embedded in CAC-CT.

171 evaluated with respect to diagnosis of left ventricular hypertrophy (LVH), eligibility for disease-s

172 lar counts (RACs), vessel density, and right ventricular hypertrophy (RVH).

173 % CI: 0.94 to 0.97) among patients with left ventricular hypertrophy by ECG criteria and 0.95 (95% CI

174 Left ventricular hypertrophy was present in 19 individuals (8

175 Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfunctio

176 Cardiac structural abnormalities, left ventricular hypertrophy, or concentric geometry, were hi

177 f these anomalies are partially due to right ventricular insufficiency, recent data support a mechani

178 e mouse and chick models to show that dorsal ventricular layer (dVL) cells adjacent to dorsal midline

179 ncompletely understood, we investigated left ventricular (LV) and left atrial (LA) pathophysiological

180 aortic stenosis (ModAS) (n=13), SevAS, left ventricular (LV) ejection fraction >=55% (SevAS-preserve

181 y hypothesized that a relatively larger left ventricular (LV) electrical dyssynchrony in smaller hear

182 (oHCM) is characterized by unexplained left ventricular (LV) hypertrophy associated with dynamic LV

183 pressure was significantly elevated and left ventricular (LV) hypertrophy was evident by a 50% increa

184 continue CRT while others turn off the left ventricular (LV) lead at LVAD implant.

185 for changes in prognostically important left ventricular (LV) parameters.

186 Left ventricular (LV) wall thickness and LV mass were greater

187 tion with incident HF and HF phenotype (left ventricular [LV] ejection fraction [LVEF] >= or < 50%) i

188 ion at submaximal and maximal exercise, left ventricular mass and compliance, and blood volume compar

189 Greater early left ventricular mass index (LVMi) regression is associated w

190 The main outcome was left ventricular mass index by cardiac magnetic resonance ima

191 ration of 135 mmol/L did not change the left ventricular mass index, despite significant reductions a

192 ate sodium of 135 mmol/L did not reduce left ventricular mass relative to control, despite improving

193 scular obstruction (MVO) (percentage of left ventricular mass) quantified by cardiac magnetic resonan

194 Patients with extensive LGE (>=15% of left ventricular mass) were at highest risk (HR, 12; 95% CI:

195 agnetic resonance imaging (MRI)-derived left ventricular measurements in 36,041 UK Biobank participan

196 9+/-178.3 mm(3); P=0.023) and infarcted left ventricular myocardium (1052.3+/-543.0 versus 340.3+/-16

197 the atrioventricular junction (n=5) and left ventricular myocardium (n=20) of intact animals.

198 Adult rat ventricular myocytes expressing wild-type SERCA2b or a r

199 TV1 RNA sequencing dataset from neonatal rat ventricular myocytes transduced with Etv1 showed recipro

200 Primary adult rat ventricular myocytes, adeno-associated virus (AAV)-media

201 latter effect is more potent in atrial than ventricular myocytes, and this could be explained by our

202 3-dimensional nanostructure of TT in rabbit ventricular myocytes, preserved at different stages of t

203 o be absent in tubulated atrial myocytes and ventricular myocytes.

204 I < 2) were more likely to have dynamic left ventricular outflow tract (LVOT) obstruction (63.3% vs 3

205 thy, and a major determinant of dynamic left ventricular outflow tract (LVOT) obstruction.

206 ) has become an important treatment of right ventricular outflow tract dysfunction.

207 The 3-year mean right ventricular outflow tract echocardiographic gradient was

208 ore, left atrial diameter z score, peak left ventricular outflow tract gradient, and presence of a pa

209 crease in velocity-time integral of the left ventricular outflow tract greater than or equal to 10% d

210 One delayed left ventricular outflow tract obstruction required elective

211 s, assess for presence and mechanism of left ventricular outflow tract obstruction, and risk stratifi

212 egurgitation in patients with repaired right ventricular outflow tracts.

213 aphy imaging of the appendage from the right ventricular outflow.

214 , resting HR, HRV, and atrial (p = 0.03) and ventricular (p = 0.03) proarrhythmia persisted.

215 dogs had atrioventricular-node ablation and ventricular pacemakers at 80 beats/min to control ventri

216 sis is the gold standard metric of assessing ventricular performance.

217 ained syncope, septal diameter z-score, left ventricular posterior wall diameter z score, left atrial

218 the human disease, including increased right ventricular pressures, medial thickening, neointimal les

219 portant trigger and substrate for atrial and ventricular proarrhythmia.

220 icular pacemakers at 80 beats/min to control ventricular rate.

221 pulmonary artery systolic pressure, RV/left ventricular ratio, and RV fractional area change.

222 ich 2 subsequent MIs affected different left ventricular regions in the same mouse.

223 At rest, GLI slowed left ventricular relaxation (2.11 +/- 0.59 vs. 1.70 +/- 0.23

224 A clinical score (RAISE) that used left ventricular remodeling (hypertrophy/diastolic dysfunctio

225 o-fibrotic signaling pathways before adverse ventricular remodeling and progression of HF.

226 study was to define CF heterogeneity during ventricular remodeling and the underlying mechanisms tha

227 Study of Biomarkers, Symptom Improvement and Ventricular Remodeling During Entresto Therapy for Heart

228 The only predictor of left ventricular remodeling was treatment with sonothrombolys

229 ontrol group was more likely to exhibit left ventricular remodeling with an odds ratio of 2.79 ([95%

230 reduce weight, have salutary effects on left ventricular remodeling, and reduce hospitalization for H

231 ocyte contractility and reduction in adverse ventricular remodeling.

232 ed whether HIV serostatus is associated with ventricular repolarization lability by using the QT vari

233 e effects on atrioventricular conduction and ventricular repolarization.

234 5 beats); (5) atrial fibrillation with rapid ventricular response; (6) supraventricular tachycardia (

235 ation in exercise capacity and promotes left ventricular reverse remodeling in asymptomatic or minima

236 s in baseline clinical characteristics, left ventricular reverse remodeling, or outcomes on multivari

237 69%) patients with LVSD had evidence of left ventricular reverse remodeling.

238 orts have shown that the avian visual dorsal ventricular ridge (DVR) is organized as a trilayered com

239 approach) alone or in combination with right ventricular (RV) (LVs+RV), BiV, and HB pacing was perfor

240 g structural changes of arrhythmogenic right ventricular (RV) cardiomyopathy are limited.

241 Knowledge of right ventricular (RV) function has lagged behind that of the

242 egative in 14 patients (10%), isolated right ventricular (RV) involvement was found in 58 (41%), bive

243 Controls had advanced liver disease, right ventricular (RV) systolic pressure <40 mm Hg, and normal

244 ort-term computed tomographic-measured right ventricular (RV)-to-left ventricular diameter ratio in m

245 tem consists of 3 steps: (1) localization of ventricular segment based on population templates, (2) p

246 Fully automated ventricular segmentation by the tested algorithm provide

247 Ventricular segmentation, radiomics features extraction,

248 Atrial and ventricular sensing, lead impedance, and capture thresho

249 We evaluated left ventricular shape, including a novel measure of maximal

250 ay matter structures, 81 fiber tracts, and 8 ventricular structures.

251 eural differentiation in the young postnatal ventricular-subventricular zone (V-SVZ), in which neural

252 We focus on developmental changes in the ventricular system and CSF sources (including neural pro

253 oxel-wise as a function of distance from the ventricular system.

254 hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as occu

255 el activator of cardiac myosin-improves left ventricular systolic function and remodeling and reduces

256 for at-risk individuals with preserved left ventricular systolic function is unclear.

257 are reasonable drugs in patients with normal ventricular systolic function.

258 95% CI: 1.12 to 2.51; p = 0.012), and right ventricular systolic pressure >=50 mm Hg (HR: 2.27; 95%

259 ricular volumes (p = 0.005) and higher right ventricular systolic pressure (p < 0.0001).

260 Secondary outcomes included sustained ventricular tachyarrhythmia and appropriate ICD therapy.

261 s, which may underlie a circadian pattern of ventricular tachyarrhythmia/sudden cardiac death.

262 Ventricular tachyarrhythmias and sudden cardiac death sh

263 effectively suppressed catecholamine-induced ventricular tachyarrhythmias in Casq2-/- mice, whereas N

264 art block; (3) ventricular fibrillation; (4) ventricular tachycardia (>15 beats); (5) atrial fibrilla

265 n = 16 [14%]), catecholaminergic polymorphic ventricular tachycardia (CPVT) (n = 9 [8%]), arrhythmoge

266 red tetralogy of Fallot die prematurely from ventricular tachycardia (VT) and sudden cardiac death.

267 luding 104 patients who underwent epicardial ventricular tachycardia ablation and Lariat left atrial

268 t QT syndrome, catecholaminergic polymorphic ventricular tachycardia and Brugada syndrome.

269 ion, as in the catecholaminergic polymorphic ventricular tachycardia mice studies, or more generally

270 ias, including catecholaminergic polymorphic ventricular tachycardia or long QT syndrome and sudden c

271 ular arrhythmias (non-sustained or sustained ventricular tachycardia or ventricular fibrillation).

272 , resuscitated cardiac arrest, and sustained ventricular tachycardia).

273 origin of the arrhythmic beats that initiate ventricular tachycardia, and regarding optimal therapeut

274 ed age at diagnosis, documented nonsustained ventricular tachycardia, unexplained syncope, septal dia

275 ception is the catecholaminergic polymorphic ventricular tachycardia-causing N53I substitution, which

276 efractory ventricular fibrillation/pulseless ventricular tachycardia.

277 ion (14%), torsades de pointe or polymorphic ventricular tachycardia/fibrillation (6% [sustained 3%,

278 Susceptibility to VT/VF (ventricular tachycardia/fibrillation) is difficult to pr

279 ienced appropriate interventions terminating ventricular tachycardia/ventricular fibrillation.

280 garding the prognosis and management of left ventricular thrombus (LVT).

281 ory effects of periodontitis on cardiac left ventricular tissue and the therapeutic activity of melat

282 Microarray analysis of ventricular tissue revealed that miR-21 and miR-221, 2 a

283 Patients with symptomatic PE and right ventricular to left ventricular diameter ratio >=0.9 as

284 events and a significant reduction in right ventricular to left ventricular diameter ratio and throm

285 ar ejection fraction, not the extent of left ventricular trabeculation, had an important influence on

286 nternational, multicenter cohort study, left ventricular unloading was associated with lower mortalit

287 severe MR (p = 0.0005) despite smaller left ventricular volumes (p = 0.005) and higher right ventric

288 -resolved low-resolution images yielded left ventricular volumes comparable to those from full-resolu

289 y the tested algorithm provides contours and ventricular volumes that could be used to aid expert seg

290 For evaluation of clinical performance, left ventricular volumes were measured, and statistical signi

291 Left ventricular volumes, ejection fraction, risk area (befor

292 Left ventricular vorticity metrics were observed to be higher

293 rdiographic abnormalities that included left ventricular wall motion abnormalities, global left ventr

294 Maximum left ventricular wall thickness was 18 +/- 8 mm, and left ven

295 The maximum left ventricular wall thickness was 22.9 +/- 8.7 mm and left

296 entricular functional parameters, especially ventricular work and reserve, provided the best estimati

297 ave unique transcriptional signatures in LGE ventricular zone (VZ) cells.

298 rom the nucleus at the apical surface of the ventricular zone of the cerebral cortex(5-8).

299 adial glia-like neural stem cells within the ventricular zone of the medial ganglionic eminence.

300 oepithelia of the retina and cerebrocortical ventricular zones provide a platform for progenitor cell