ライフサイエンスコーパス: ventricular

1 Ventricular abnormalities, namely ependymitis and choroi

2 0 healthy controls, ARVC patients had longer ventricular activation duration (median, 52 versus 42 ms

3 Ventricular activation was prolonged in old Scn5a+/Delta

4 After aortic valve replacement, left ventricular afterload is often characterized by the resi

5 Lastly, we demonstrate that SHF ventricular and OFT progenitors exhibit unique sensitivi

6 trial fibrillation (AF) risk, including left ventricular and pulmonary pathology, systemic inflammati

7 Blinded quantification of left ventricular and right ventricular (RV) volumes was perfo

8 The median ventricular arrhythmia score during exercise was signifi

9 utcome was defined as all-cause mortality or ventricular arrhythmia, defined as aborted cardiac arres

10 ciated with greater adjusted odds of serious ventricular arrhythmias (OR, 31.8; 95% CI, 4.3-236.3) an

11 In patients with A-HF, ventricular arrhythmias (VAs) are common.

12 ntable cardioverter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutan

13 od1(-/-)-PMI mice showed significantly fewer ventricular arrhythmias and lower mortality after isopro

14 CRT reduced the rate of onset of new ventricular arrhythmias detected by ICDs in patients wit

15 deaths, lead failures, losses of capture, or ventricular arrhythmias occurred during MRI.

16 criptional control of the Cspg4 locus led to ventricular arrhythmias, atrial fibrillation, atrioventr

17 llator (S-ICD) was developed to defibrillate ventricular arrhythmias, avoiding drawbacks of transveno

18 regarding the composite end point (malignant ventricular arrhythmias, end-stage heart failure, or dea

19 ongation, a risk factor for life-threatening ventricular arrhythmias, is a potential side effect of m

20 y with dilated cardiomyopathy and atrial and ventricular arrhythmias.

21 re were 11 278 appropriate ICD detections of ventricular arrhythmias.

22 turbance, atrial fibrillation, and malignant ventricular arrhythmias.

23 ICDs in patients without a history of prior ventricular arrhythmias.

24 n a large Spanish family with inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and

25 Changes in volumes, strain, and ventricular-arterial coupling were consistently associat

26 splasia develops during continuous-flow left ventricular assist device (LVAD) support.

27 ced heart failure patients selected for left ventricular assist device (LVAD) were more likely to be

28 ity in patients with end-stage HF after left ventricular assist device (LVAD)-induced remodeling to i

29 interval, 4.19-8.61; P<0.001), need for left ventricular assist device (odds ratio, 3.48; 95% confide

30 ssment and Comparative Effectiveness of Left Ventricular Assist Device and Medical Management) demons

31 sies of multiple HF patients undergoing left ventricular assist device implantation surgery.

32 accounting for the competing risk of death, ventricular assist device implantation, or cardiac trans

33 e surgical procedures, may be unsuitable for ventricular assist device implantation.

34 t in an adult or pediatric patient who has a ventricular assist device or total artificial heart.

35 e analysis evaluated 51 continuous-flow left ventricular assist device patients who received secondar

36 Patients with continuous-flow left ventricular assist device receiving secondary prophylaxi

37 Left ventricular assist device-supported patients are usually

38 Improved safety of left ventricular assist devices means that these are becoming

39 lure receiving mechanical unloading via left ventricular assist devices show increased CTCF abundance

40 ctional counterpart of transient apical left ventricular ballooning.

41 Left ventricular biopsies were obtained from 5 donors and 26

42 ion correlated with cardiac fibrosis on left ventricular biopsy (P=0.63; P<0.01).

43 In ventricular cardiac myocytes (VCM), Gbeta5 deficiency pr

44 cterized human pluripotent stem-cell-derived ventricular cardiomyocytes are strategically aligned to

45 ial network formation and fusion activity in ventricular cardiomyocytes.

46 omyopathy, specifically arrhythmogenic right ventricular cardiomyopathy (ARVC).

47 diomyopathy and none to arrhythmogenic right ventricular cardiomyopathy.

48 lure (HF) prevalence in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) varies dep

49 patients with inherited arrhythmogenic right ventricular cardiomyopathy/dysplasia, although their cel

50 thway for MP biogenesis in mammalian cardiac ventricular cells, identifying elements of a pathway by

51 sticity and to preserve the integrity of the ventricular chamber.

52 Ventricular tachycardia and premature ventricular complexes (PVCs) most frequently occur in th

53 gesting their role in the development of the ventricular conduction system and that electrical propag

54 tes gap junctions and delays both atrial and ventricular conduction.

55 d for left ventricle outflow tract premature ventricular contraction ablation, an aortic valve closur

56 Premature ventricular contraction rate increased with exercise, an

57 with left ventricle outflow tract premature ventricular contraction were included.

58 In contrast, VT or premature ventricular contractions in the setting of a structurall

59 Premature ventricular contractions originating in the left ventric

60 ophy is also frequently associated with left ventricular diastolic dysfunction.

61 c left ventricular remodeling, greater right ventricular dilatation (base, 34+/-7 versus 31+/-6 and 3

62 D4(+) T cells and prevented progressive left ventricular dilatation and hypertrophy, whereas adoptive

63 Left ventricular dilation and loss of heart function was prec

64 , congestive heart failure, and greater left ventricular dilation at diagnosis were independently ass

65 Trpc6 deletion also ameliorated left ventricular dilation, improved cardiac function, and ten

66 at 12, 24, 48, 72 hours and before external ventricular drain removal.

67 t successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >/=4 d

68 ed the interferon response and improved left ventricular dysfunction and survival.

69 ocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, whereas genetic knockdo

70 ary embolism using imaging presence of right ventricular dysfunction is essential for triage; however

71 ass, use of multiple inotropes, severe right ventricular dysfunction on echocardiography, ratio of ri

72 intracoronary infusion in patients with left ventricular dysfunction post STEMI.

73 om donor mice with HF induced long-term left ventricular dysfunction, fibrosis, and hypertrophy in na

74 61+/-7 and 61+/-7 mm, P<0.0001), more right ventricular dysfunction, increased epicardial fat thickn

75 tly higher in patients with HF-PH with right ventricular dysfunction, pulmonary vascular remodeling w

76 nerally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the territ

77 icular transmural pressure, and greater left ventricular eccentricity index (1.10+/-0.19 versus 0.99+

78 ociation class II to IV symptoms, and a left ventricular EF of 40% or less to treatment with enalapri

79 fects were found on secondary outcomes: left ventricular EF, peak aerobic exercise capacity, and N-te

80 troke volume changes little while preserving ventricular efficiency.

81 In HFpEF, defined as left ventricular ejection fraction >/=40%, we derived propens

82 Two hundred sixty-one patients with left ventricular ejection fraction </=35% and New York Heart

83 tients with coronary artery disease and left ventricular ejection fraction </=40%.

84 (63+/-14 years, 60% men) with preserved left ventricular ejection fraction (>60%) and chronic moderat

85 V, 72 patients undergoing ViR had lower left ventricular ejection fraction (45.6 +/- 17.4% vs. 55.3 +

86 SE=0.23), % females (B=-0.38, SE=0.04), left ventricular ejection fraction (B=-0.81, SE=0.20), and bo

87 Improvement in left ventricular ejection fraction (EF) to >35% occurs in man

88 atients with heart failure with reduced left ventricular ejection fraction (HFrEF) and is an independ

89 ination of left ventricular volumes and left ventricular ejection fraction (LVEF).

90 d to compacted myocardium (P<0.001) and left ventricular ejection fraction (P=0.01).

91 elative area change was associated with left ventricular ejection fraction (P=0.045) and ventricular-

92 spectively enrolled (age 62+/-11 years, left ventricular ejection fraction 27+/-7%).

93 ents (39%; 73% men; age, 41+/-25 years; left ventricular ejection fraction 49+/-16%) with high incide

94 reduced LV systolic function (mean+/-SD left ventricular ejection fraction = 52+/-11% versus 63+/-8%;

95 identified 472 donor hearts with LVSD (left ventricular ejection fraction [LVEF] </=40%) on initial

96 CCC with either a preserved or reduced left ventricular ejection fraction [LVEF]).

97 bserved with echocardiography (baseline left ventricular ejection fraction [LVEF], 61%; global longit

98 gnificantly with MR imaging measures of left ventricular ejection fraction and end-systolic volume, b

99 d the incremental value of considering right ventricular ejection fraction for the prediction of futu

100 ], P=0.02) and no significant change of left ventricular ejection fraction in the cell group.

101 fety of levosimendan in patients with a left ventricular ejection fraction of 35% or less who were un

102 was 32+/-12% (range, 6-54%) with mean right ventricular ejection fraction of 48+/-15% (range, 7-78%)

103 owever, PPM is associated with impaired left ventricular ejection fraction recovery post-transcathete

104 hemic dilated cardiomyopathy), the mean left ventricular ejection fraction was 32+/-12% (range, 6-54%

105 The left ventricular ejection fraction was consistently decreased

106 equency methods can be used to document left ventricular ejection fraction with accuracy comparable w

107 ive relationships with age, female sex, left ventricular ejection fraction, and body mass index.

108 Ivabradine treatment improved left ventricular ejection fraction, and clinical status and Q

109 ccurrence of atrial arrhythmias and low left ventricular ejection fraction, as estimated using multiv

110 raditional cardiovascular risk factors, left ventricular ejection fraction, myocardial scar and ische

111 ent were increasing age, lower baseline left ventricular ejection fraction, worse post-procedural mit

112 stion, but no significant difference in left ventricular ejection fraction.

113 al, 1.09-2.07), but not with decline in left ventricular ejection fraction.

114 atients with heart failure with reduced left ventricular ejection fraction.

115 an age=49-80 years, sex=0%-92% females, left ventricular ejection fraction=26%-61%).

116 e gadolinium enhancement, and left and right ventricular ejection fractions.

117 al function (ejection fraction [EF] and left ventricular end-diastolic pressure) was assessed at days

118 congestive heart failure, and increased left ventricular end-systolic dimension zscore at diagnosis w

119 ated with the right atrial volume than right ventricular end-systolic volume in AF-TR (P<0.001).

120 cle-right ventricle pairs (P=0.021) and left ventricular epicardium (P=0.08).

121 if patient survival and mechanisms of right ventricular failure in pulmonary hypertension could be p

122 d a better survival than those in refractory ventricular fibrillation (p = 0.017).

123 ving documented ventricular tachycardia (VT)/ventricular fibrillation (VF) and Brugada syndrome-relat

124 After defibrillation of initial ventricular fibrillation (VF), it is crucial to prevent

125 atients with refractory out-of-hospital (OH) ventricular fibrillation (VF)/ventricular tachycardia (V

126 ral highly dangerous heart diseases, such as ventricular fibrillation and congestive heart failure.

127 ined as aborted cardiac arrest or documented ventricular fibrillation and ventricular tachycardia (la

128 ents with repetitive ventricular tachycardia/ventricular fibrillation episodes alternating with perio

129 ts the recurrence of ventricular tachycardia/ventricular fibrillation in such patients.

130 Detection was set to ventricular fibrillation number of intervals to detect=2

131 ifekalant (NIF) are used in the treatment of ventricular fibrillation or tachycardia; however, only f

132 lantable cardiac defibrillator discharge for ventricular fibrillation or ventricular tachycardia >240

133 adjusted) in the VT zone, and 6 of 10 in the ventricular fibrillation zone.

134 aventricular tachycardias converted to VT or ventricular fibrillation.

135 first recurrence of ventricular tachycardia/ventricular fibrillation.

136 ion MI, and 8.9% had ventricular tachycardia/ventricular fibrillation.

137 ersion of induced ventricular tachycardia or ventricular fibrillation.

138 d late gadolinium enhancement, indicative of ventricular fibrosis, before randomization to either CA

139 t strain correlated with the volume of early ventricular filling (r=0.67; P<0.01), but not LV stiffne

140 Optimal thresholds for ventricular function (RV EF <30%: hazard ratio, 3.90; 95

141 iPSC-EV-treated mice exhibited improved left ventricular function at 35 d after myocardial infarction

142 stablishes coronary blood flow, and improves ventricular function following an AMI.

143 n and CVB3 copy number, and an improved left ventricular function in NOD2(-/-) CVB3 mice compared wit

144 myopathy characterized by impaired diastolic ventricular function resulting in a poor clinical progno

145 matic severe aortic stenosis and normal left ventricular function, current practice guidelines empiri

146 Improvements in left ventricular function, functional status, and quality of

147 r cardiac repair in vivo with regard to left ventricular function, vascularization, and amelioration

148 blood pressure, systolic, or diastolic left ventricular function.

149 and functional remodeling and improves left ventricular functional reserve.

150 tinct MEF2A co-regulators for the atrial and ventricular gene sets, and a subset of these was found t

151 ynamic in nature and sensitive to changes in ventricular geometry and loading, current therapy is mai

152 Left ventricular global longitudinal strain (GLS) and left at

153 e-permeabilized cardiomyocytes in human left ventricular heart tissue.

154 Ventricular hemodynamics are then quantified by numerica

155 hic (ECG) criteria for the diagnosis of left ventricular hypertrophy (LVH) have low sensitivity.

156 ld lead to more lowering of the risk of left ventricular hypertrophy (LVH) in patients with hypertens

157 on, has been inconsistently linked with left ventricular hypertrophy.

158 Echocardiography showed left ventricular hypokinesis.

159 s than 1 month left of battery life reset to ventricular inhibited pacing and could not be reprogramm

160 greater pericardial restraint and heightened ventricular interdependence, reflected by increased rati

161 predominate, it is well recognized that left ventricular involvement is common, particularly in advan

162 rdioprotective gene networks to prevent left ventricular (LV) adverse remodeling.

163 toring forces are known determinants of left ventricular (LV) diastolic function.

164 ne models recapitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left atri

165 148 mL/m(2)) volumes, and lower RV and left ventricular (LV) ejection fractions compared with contro

166 ejection fraction develop increases in left ventricular (LV) end-diastolic pressures during exercise

167 exposure was positively associated with left ventricular (LV) fractional shortening (z-score for diff

168 Left ventricular (LV) global longitudinal strain (GLS) is a m

169 Left ventricular (LV) hypertrophy and abnormal myocardial str

170 Left ventricular (LV) morphology and systolic and diastolic f

171 l implications beyond the reflection of left ventricular (LV) pathology are not well understood.

172 The analysis included 16 traits of left ventricular (LV) structure, and systolic and diastolic f

173 le, age 54 +/- 12 years) complicated by left ventricular (LV) systolic dysfunction; (2) an age- and s

174 RV outflow tract dimension, and RV and left ventricular (LV) systolic function were determined by RV

175 years; p = 0.002) and had lower indexed left ventricular mass (5.1 g/m(2) reduction; padjusted = 0.03

176 mpedance spectroscopy), 24-hour BP, and left ventricular mass (cardiac magnetic resonance imaging).

177 cular posterior wall, 11+/-4 [7-21] mm; left ventricular mass, 86+/-41 [46-195] g/m(2)) was progressi

178 red global longitudinal strain, indexed left ventricular mass, and indexed left atrial volume.

179 dary objective was to assess changes in left ventricular mass.

180 mpared with dimension and area methods, left ventricular measurements by volume method have the best

181 rolonged catecholamine infusion, use of left ventricular mechanical assist device, or renal replaceme

182 at Fontan 1, but it was not associated with ventricular morphology, the subject's age, or the type o

183 Fontan cohort was 90% and was independent of ventricular morphology.

184 ted the distribution characteristics of left-ventricular myocardial strain using a novel cine MRI bas

185 of transcription (STAT)5 activation in left ventricular myocardium is associated with RIPC s cardiop

186 In fixed ventricular myocardium, dual-axis electron tomography wa

187 but also on transverse-tubular membranes in ventricular myocardium.

188 lectrophysiological property of neonatal rat ventricular myocyte (NRVM) cultures.

189 report prospective markers of atrial versus ventricular myocyte formation from hPSCs and their use i

190 Using computer simulations of a ventricular myocyte model, we show that initiation and t

191 incorporated into a physiologically detailed ventricular myocyte model.

192 redictive in silico model of the adult human ventricular myocyte.

193 um (Ca(2+)) and transverse-tubule imaging of ventricular myocytes from MCM-Speg(fl/fl) mice post HF r

194 Our objective is to understand how adult ventricular myocytes regulate the IKs amplitudes under b

195 p to IKs amplitudes, in chronically stressed ventricular myocytes, and use COS-7 cell expression to p

196 in suppressed L-type Ca(++) currents (rabbit ventricular myocytes, IC50=66.5+/-4 mumol/L) and IK1 (HE

197 epending on initial ion circumstances within ventricular myocytes, these multi-stable AP states might

198 erformed using Fluo-3 in voltage clamped rat ventricular myocytes.

199 ated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a median separation of 20 nm in 2D

200 Left ventricular NOD2 mRNA expression was also induced in CVB

201 art defect (CTD) case-parent trios, 317 left ventricular obstructive tract defect (LVOTD) case-parent

202 er in the right ventricle (P=0.037) and left ventricular outflow tract (P<0.001) and higher in left v

203 ity were then evaluated in response to right ventricular outflow tract PVCs with fixed short, fixed l

204 bers normally run in parallel along the left ventricular outflow tract, but in the Nkx2-5(+/-)/Sspn(K

205 isk of developing HF in the setting of right ventricular pacing and to determine whether these patien

206 ositioned across the valve ring during rapid ventricular pacing.

207 ing, His bundle pacing, and endocardial left ventricular pacing.

208 c transplantation was associated with poorer ventricular performance and functional health status ass

209 relationships between laboratory measures of ventricular performance and functional status over time.

210 pansion during systole, which modulates left ventricular performance and impacts systemic hemodynamic

211 erventricular septum, 12+/-4 [7-23] mm; left ventricular posterior wall, 11+/-4 [7-21] mm; left ventr

212 rrhythmogenic cardiomyopathy, often of right ventricular predominance.

213 data on the clinical course of patients with ventricular preexcitation in the ECG originates from ter

214 s up-regulated in both ventricles with right ventricular preference.

215 Variations in the ventricular preload and afterload influence pulmonary ar

216 graphy (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, respect

217 maging, the rats were catheterized, and left ventricular pressures were recorded.

218 METHODS AND In a canine model (n=10), ventricular radiofrequency lesions were created using Th

219 nd reduced AF duration without affecting the ventricular refractoriness or blood pressure in pigs sub

220 Parameters of ventricular remodeling and modulation of cardio-renal sy

221 cardial cavity volumes at day 3, followed by ventricular remodeling at day 30, and recovery at day 60

222 cardiomyopathy, was the commonest pattern of ventricular remodeling in ATTR.

223 injury, and it is a strong predictor of left ventricular remodeling in ST-segment-elevation myocardia

224 IIT was not superior to MCT in changing left ventricular remodeling or aerobic capacity, and its feas

225 n was associated with significant atrial and ventricular remodeling, along with systolic dysfunction

226 80-3006 mL]; P<0.0001), more concentric left ventricular remodeling, greater right ventricular dilata

227 logical changes responsible for adverse left ventricular remodeling, the relationship between inflamm

228 g the hemodynamic consequences and extent of ventricular remodeling, which is an important predictor

229 ial injury and its predictive value for left ventricular remodeling.

230 regurgitation is indicated to avoid adverse ventricular remodeling.

231 xerted a sustained beneficial effect on left ventricular remodeling.

232 ed by increased cardiac output and a reduced ventricular response to stress, is present in up to 30%

233 e heart were determined from CT and the left ventricular ROI, and mean counts were calculated using E

234 mice producing GM-CSF can succumb from left ventricular rupture, a complication mitigated by anti-GM

235 may contribute to long-term pulmonary right ventricular (RV) dysfunction in patients after surgery f

236 d 13.0+/-2.9 years, had higher indexed right ventricular (RV) end-diastolic (range 85-326 mL/m(2), me

237 We report right ventricular (RV) filling and ejection abnormalities in I

238 p between parasympathetic activity and right ventricular (RV) function in patients with PAH, and the

239 Although it is known that right ventricular (RV) function is dependent on LV health, the

240 Right ventricular (RV) morphology has been associated with dri

241 quantification of left ventricular and right ventricular (RV) volumes was performed from standard cin

242 ients (71 with pulmonary atresia with intact ventricular septum and 28 with virtual atresia) underwen

243 Patients with pulmonary atresia with intact ventricular septum deemed suitable for RV decompression

244 Myofibers in the ventricular septum follow a stereotypical pattern that i

245 hocardiogram as normal or abnormal for right ventricular size and function in patients with acute pul

246 ervention occurs after deterioration of left ventricular size and function.

247 er, the mechanisms that direct atrial versus ventricular specification remain largely unknown.

248 Left ventricular structure and function and cardiac troponin-

249 al CVD was defined by 10-year change in left ventricular structure and function.

250 nd to analyze their clinical value for right ventricular substrate delineation.

251 The mammalian ventricular-subventricular zone (V-SVZ) presents the hig

252 Adult neural stem cells (NSCs) in the ventricular-subventricular zone (V-SVZ) produce diverse

253 upper cortical layers and accumulated at the ventricular/subventricular zones.

254 n the brain aqueduct as part of the internal ventricular system and in the spinal canal during respir

255 Atrial fibrillation (AF) and left ventricular systolic dysfunction (LVSD) frequently co-ex

256 lity in patients with AMI without HF or left ventricular systolic dysfunction (LVSD).

257 ents indicated modest increases in the right ventricular systolic pressure and right ventricle hypert

258 Society of Thoracic Surgeons score and right ventricular systolic pressure were 2+/-3 and 15+/-16 mm

259 structural heart disease (SHD) and recurrent ventricular tachyarrhythmias (VT).

260 by speckle-tracking echocardiography predict ventricular tachyarrhythmias and provide incremental pro

261 er lifetime in 166 patients (19%), sustained ventricular tachyarrhythmias in 17 (2%), and permanent p

262 echocardiographic risk factors in predicting ventricular tachyarrhythmias.

263 ined as appropriate ICD therapy or sustained ventricular tachyarrhythmias.

264 or discharge for ventricular fibrillation or ventricular tachycardia >240 bpm) and 36 nonsudden cardi

265 t or documented ventricular fibrillation and ventricular tachycardia (lasting >/=30 seconds or recurr

266 syncope, atrial fibrillation, non-sustained ventricular tachycardia (nsVT), maximum left ventricular

267 -hospital (OH) ventricular fibrillation (VF)/ventricular tachycardia (VT) cardiac arrest is unknown.

268 Catheter ablation of ventricular tachycardia (VT) is being increasingly perfo

269 Ventricular tachycardia (VT) radiofrequency ablation has

270 ere enrolled: 63 (group 1) having documented ventricular tachycardia (VT)/ventricular fibrillation (V

271 al aortic valves, who underwent scar-related ventricular tachycardia ablation, were analyzed to corre

272 Ventricular tachycardia and premature ventricular comple

273 atients meeting study criteria scheduled for ventricular tachycardia or PVC ablation over a 9-month p

274 ients had a successful conversion of induced ventricular tachycardia or ventricular fibrillation.

275 ek blanking period, there were 4 episodes of ventricular tachycardia over the next 46 patient-months,

276 CC causes a unique ventricular tachycardia substrate concentrated to the ba

277 15, five patients with high-risk, refractory ventricular tachycardia underwent treatment.

278 Of these, 177 (28.8%) had idiopathic ventricular tachycardia, 408 (66.5%) had symptomatic PVC

279 redistribution of gap junctions and promotes ventricular tachycardia, showing the functional signific

280 Nonsustained ventricular tachycardia, syncope, a family history of su

281 In idiopathic ventricular tachycardia, there was an increase in incide

282 Patients with repetitive ventricular tachycardia/ventricular fibrillation episode

283 strate reduces or prevents the recurrence of ventricular tachycardia/ventricular fibrillation in such

284 nd point was the time to first recurrence of ventricular tachycardia/ventricular fibrillation.

285 ad non-ST-segment elevation MI, and 8.9% had ventricular tachycardia/ventricular fibrillation.

286 iptional signatures closer to those of adult ventricular tissue, higher myofibril density and alignme

287 dolinium enhancement in phenotyping the left ventricular to identify those at highest risk for SCD.

288 diffraction from synchrotron light in intact ventricular trabeculae from the rat to measure the axial

289 r pulmonary venous pressure relative to left ventricular transmural pressure, and greater left ventri

290 ventricular ejection fraction (P=0.045) and ventricular-vascular coupling ratio (P=0.042).

291 before and after surgery, quantification of ventricular volume and function, stress imaging, shunt q

292 Average annualised per cent change in ventricular volume was computed as a measure of brain at

293 There was a significant reduction of left ventricular volumes (end-systolic volume: -4.3 [11.3] ve

294 post-cycle 17 for the determination of left ventricular volumes and left ventricular ejection fracti

295 ere implanted into the anterior-lateral left ventricular wall in C57BL/6J (allogeneic model, n = 17)

296 cterize microstructural dynamics during left ventricular wall thickening, and apply the technique in

297 ventricular tachycardia (nsVT), maximum left ventricular wall thickness and obstruction were signific

298 as trabecular and compact components of the ventricular wall.

299 ration of neural progenitor cells within the ventricular zone and is required for normal brain histog

300 the fraction of cells expressing Sox2 in the ventricular zone.