ライフサイエンスコーパス: left ventricular

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

2 new locus in chromosome 1 is associated with left ventricular adverse remodeling and clinical heart f

3 terial impedance (Zva) estimates the overall left ventricular afterload (valve and arterial component

4 mammillary artery pseudoaneurysm (n = 1/24), left ventricular aneurysms (n = 3/24), pulmonary arterio

5 s defined as one that was wrapped around the left ventricular apex.

6 We prospectively obtained paired left ventricular apical myocardial tissue from nonfailin

7 er, CRT management following continuous flow Left Ventricular Assist Device (LVAD) implant vary: some

8 serum creatinine (sCr) improves early after left ventricular assist device (LVAD) implantation but s

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

10 Left ventricular assist device (LVAD) therapy is an incr

11 Left ventricular assist device (LVAD) unloading and hemo

12 Endovascular aortic aneurysm repair (EVAR), left ventricular assist device (LVAD), and transcatheter

13 rt failure (termed responders [R]) following left ventricular assist device (LVAD)-induced mechanical

14 l-cause mortality, heart transplantation, or left ventricular assist device implant and a secondary a

15 e obtained before and after (median=82 days) left ventricular assist device implantation (stage D; pr

16 [n=128], cardiac transplantation [n=55], or left ventricular assist device implantation [n=9]).

17 w can one choose between transplantation and left ventricular assist device implantation if advanced

18 the longest multicenter follow-up of primary left ventricular assist device outcomes.

19 art transplant now require longer periods of left ventricular assist device support in patients.

20 from normal, failed and partially recovered (left ventricular assist device treatment) adult human he

21 th heart failure, heart transplantation, and left ventricular assist device.

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

23 ormed, 7,904 (32%) were bridged with durable left ventricular assist devices (LVADs), 177 (0.7%) with

24 art failure, but their role in patients with left ventricular assist devices and cardiac transplant i

25 VF rate increases over time in patients with left ventricular assist devices and is lowered by ablati

26 advanced heart failure, heart transplant and left ventricular assist devices have been the mainstay o

27 bserved in 8 of their 18 core proteins after left ventricular assist devices implantation.

28 ts had nonischemic cardiomyopathy, and 3 had left ventricular assist devices.

29 The Registry to Evaluate the HeartWare Left Ventricular Assist System was an investigator-initi

30 ate definition of the extent and severity of left-ventricular assist device (LVAD) infection may faci

31 A)-infected Hu-NSG mice can recapitulate key left ventricular cardiac deficits and pathophysiological

32 twork (CNN) model was trained to segment the left ventricular cavity, myocardium, and right ventricle

33 dP/dtmax is not a load-independent marker of left ventricular contractility and should be not used to

34 ed that in humans with stable heart failure, left ventricular contractility could be accentuated with

35 with symptomatic PE and right ventricular to left ventricular diameter ratio >=0.9 as documented by c

36 ignificant reduction in right ventricular to left ventricular diameter ratio and thrombus burden.

37 s post-BEC therapy, the right ventricular to left ventricular diameter ratio decreased from 1.52+/-0.

38 Mean RV-to-left ventricular diameter ratio decreased from baseline

39 mographic-measured right ventricular (RV)-to-left ventricular diameter ratio in massive and submassiv

40 arasternal short-axis views, EI and right-to-left ventricular diameter ratio were assessed.

41 Echocardiographic assessment included RV-to-left ventricular diameter ratio within 4 hours of treatm

42 lities, global left ventricular dysfunction, left ventricular diastolic dysfunction grade II or III,

43 e was no significant change in heart rate or left ventricular diastolic pressure.

44 0% or less and is accompanied by progressive left ventricular dilatation and adverse cardiac remodeli

45 ondrial CaMKII inhibition are protected from left ventricular dilation and dysfunction after MI.

46 calmodulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocard

47 C, C4KOs developed severe heart failure with left ventricular dilation, impaired cardiomyocyte growth

48 econsideration of discontinuing asymptomatic left ventricular dysfunction and HF screening in low-ris

49 -2 diet therapeutic approach also attenuated left ventricular dysfunction and remodeling post-MI (lef

50 reventive strategy attenuated development of left ventricular dysfunction and remodeling post-transve

51 ion was associated with oxidative stress and left ventricular dysfunction assessed by electron spin r

52 Left ventricular dysfunction improved significantly duri

53 CD studies had fewer comorbidities, had less left ventricular dysfunction, and received more inapprop

54 e units in 14 centers for cardiogenic shock, left ventricular dysfunction, and severe inflammatory st

55 Thus, in rats with left ventricular dysfunction, chronic RMH pacing improve

56 , inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmi

57 nced multidisciplinary heart team to prevent left ventricular dysfunction, heart failure, reduced qua

58 entricular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic

59 nt in LVEF, independent from the severity of left ventricular dysfunction.

60 nd cyclophosphamide are both associated with left ventricular dysfunction.

61 rmalities, left ventricular hypertrophy, and left ventricular dysfunctions were demonstrated in Group

62 MR left ventricular eccentricity index (EI), main pulmonary

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

64 n E/A ratio less than or equal to 1.5 (for a left ventricular ejection fraction < 45%).

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

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

67 fraction (HFrEF; heart failure with reduced left ventricular ejection fraction <40%) referred for st

68 cutive ischemic cardiomyopathy patients with left ventricular ejection fraction <=35% without prior h

69 iation functional class II or greater with a left ventricular ejection fraction <=40% and a modest el

70 Heart Association functional class II to IV, left ventricular ejection fraction <=40%, and elevated n

71 0-mm Hg increase; 95% CI, 1.05 to 1.28), and left ventricular ejection fraction (aOR, 1.07 per 5% inc

72 Left ventricular ejection fraction (EF) is an indicator

73 Left ventricular ejection fraction (EF) recovery is asso

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

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

76 sociated with significant improvement in the left ventricular ejection fraction (LVEF) (45.8 increasi

77 Left ventricular ejection fraction (LVEF) alone has not

78 We evaluated the utility of left ventricular ejection fraction (LVEF) by echocardiog

79 chemic or dilated cardiomyopathy and reduced left ventricular ejection fraction (LVEF) face a high ri

80 HFrEF occurs when the left ventricular ejection fraction (LVEF) is 40% or less

81 ) severe aortic stenosis (AS) with preserved left ventricular ejection fraction (LVEF) may have poore

82 Age, symptoms, left ventricular ejection fraction (LVEF), LV end-systol

83 ion informed etiology, functional class, and left ventricular ejection fraction (LVEF).

84 l fibrillation (AF) in patients with reduced left ventricular ejection fraction (LVEF).

85 included nonadherence (n=109, 89%), reduced left ventricular ejection fraction (n=104, 85%), coronar

86 tage 3 acute kidney injury were preoperative left ventricular ejection fraction (odds ratio, 1.03 [95

87 scular risk factors, but significantly lower left ventricular ejection fraction (p < 0.001) and lower

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

89 HR, 1.32 [95% CI, 1.19-1.46]; P<0.001), and left ventricular ejection fraction (per 10%: HR, 0.88 [9

90 ty subjects, 88% male, 66+/-9 years old with left ventricular ejection fraction 34+/-6% were included

91 (65+/-11 years, median [interquartile range] left ventricular ejection fraction 38.7% [37.2-39.0]), 1

92 trial of 789 patients with chronic HFpEF and left ventricular ejection fraction 45% or higher with Ne

93 ve patients (69% males, age 44 +/- 15 years, left ventricular ejection fraction 49 +/- 14%) with myoc

94 All patients (age 51 +/- 14 years, 91% men, left ventricular ejection fraction 52% +/- 9%) had histo

95 GH-ExS (N=493, age 56+/-15 years, 61% women, left ventricular ejection fraction 64+/-8%), higher VE/V

96 n (cardiac index 3 L/min per m(2) or less or left ventricular ejection fraction [LVEF] 35% or less) a

97 sistently in men and women and patients with left ventricular ejection fraction above or below the me

98 strated consistent performance to detect low left ventricular ejection fraction across a range of rac

99 with placebo, did not significantly improve left ventricular ejection fraction after 52 weeks.

100 5 patients with symptomatic HF with impaired left ventricular ejection fraction and 97 participants w

101 The primary outcome measure was left ventricular ejection fraction at 52 weeks, assessed

102 The mean left ventricular ejection fraction at baseline and at 52

103 e as good in the LG AS groups with preserved left ventricular ejection fraction compared with the HG

104 r reverse remodeling, there was a subsequent left ventricular ejection fraction decrement.

105 8246 patients with chronic HF with a reduced left ventricular ejection fraction from 34 Dutch outpati

106 convolutional neural network to predict low left ventricular ejection fraction from the ECG.

107 nts with congestive heart failure or reduced left ventricular ejection fraction had a higher risk of

108 Left ventricular ejection fraction has conventionally be

109 int was left ventricular reverse remodeling (left ventricular ejection fraction increase by >=10% or

110 Left ventricular ejection fraction increased >=10% in 46

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

112 Of these, 96 correlated with left ventricular ejection fraction measured at 4 months

113 We then correlated plasma proteins with left ventricular ejection fraction measured at 4 months

114 lammatory stage II-IIIC breast cancer, and a left ventricular ejection fraction of 55% or more were r

115 an eGFR <60 mL.min(-1).1.73 m(-2), a median left ventricular ejection fraction of 62%, and a median

116 In patients with iron deficiency, a left ventricular ejection fraction of less than 50%, and

117 with transferrin saturation <20%), and had a left ventricular ejection fraction of less than 50%.

118 disease, presence of valvular heart disease, left ventricular ejection fraction phenotype (heart fail

119 lure (HF) therapy in patients with a reduced left ventricular ejection fraction remain lower than gui

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

121 Left ventricular ejection fraction was <30% in one-third

122 edian age was 61 years, 86% were men, median left ventricular ejection fraction was 20%, 81% had isch

123 had symptomatic heart failure, and the mean left ventricular ejection fraction was 26.4+/-5.8%.

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

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

126 perative arterial diameter, systolic BP, and left ventricular ejection fraction was fairly predictive

127 ), with severe aortic stenosis and preserved left ventricular ejection fraction who underwent AVR.

128 ling post-transverse aortic constriction/MI (left ventricular ejection fraction+/-SD, 36+/-8 in vehic

129 tricular dysfunction and remodeling post-MI (left ventricular ejection fraction, 41+/-11 in MI-vehicl

130 ar ejection fraction (per 10% decrement from left ventricular ejection fraction, 50%; hazard ratio, 1

131 tension, coronary disease, left atrial size, left ventricular ejection fraction, and year of ablation

132 gression and subgroup analyses revealed that left ventricular ejection fraction, not the extent of le

133 systolic augmentation (absolute increase in left ventricular ejection fraction, obese +16+/-7% versu

134 lar intercalated disc and modestly decreased left ventricular ejection fraction, suggesting ZO-1 is d

135 treatment, despite no significant changes in left ventricular ejection fraction, the diastolic functi

136 Age, sex, body mass index, left ventricular ejection fraction, type 2 diabetes mell

137 l function, and body mass index but not with left ventricular ejection fraction.

138 cted coronary artery territory, and baseline left ventricular ejection fraction.

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

140 ients with HFrEF, mean age of 57 years, mean left-ventricular ejection fraction, 26%, and 12 (17%) wi

141 enefits are most prominent in patients whose left ventricular end-diastolic dimension Z score before

142 max, dlmean, pL and sgridAND correlated with left ventricular end-diastolic pressure across both grou

143 systolic volume index threshold of 227% or a left ventricular end-diastolic volume index of 58 ml/m(2

144 /left atrial area, left atrial volume index, left ventricular end-diastolic volume index, peak E wave

145 disjunction (MAD), a larger left atrium and left ventricular end-systolic diameter, and T-wave inver

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

147 ic nerve density was reduced in the anterior left ventricular epicardium of DBH-Sap hearts compared t

148 ntuated without an increase in heart rate or left ventricular filling pressures.

149 Left ventricular function and New York Heart Association

150 Symptoms and left ventricular function at 2 years did not differ sign

151 We evaluated left ventricular function at rest, maximal aerobic capac

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

153 Myocardial blush grade and left ventricular function were significantly lower in pa

154 bdominal, liver, and myocardial fat content, left ventricular function, and (31)P magnetic resonance

155 sease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aet

156 ystemic shunt (TIPS) creation, regardless of left ventricular function.

157 to experimental MI had significantly reduced left ventricular function.

158 Left-ventricular function did not change in any group.

159 Left ventricular functional parameters, especially ventr

160 Conclusion: TAC induces rapid changes in left ventricular geometry and contractile function, with

161 The left ventricular global longitudinal strain was higher i

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

163 Individuals with left ventricular hypertrophy (LVH) and elevated cardiac

164 Left ventricular hypertrophy (LVH) and late gadolinium e

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

166 Left ventricular hypertrophy (LVH) was present in 60 sub

167 s was evaluated with respect to diagnosis of left ventricular hypertrophy (LVH), eligibility for dise

168 Conclusion Cardiac MRI findings of left ventricular hypertrophy and late gadolinium enhance

169 5 (95% CI: 0.94 to 0.97) among patients with left ventricular hypertrophy by ECG criteria and 0.95 (9

170 In select carriers without left ventricular hypertrophy on echocardiogram, SCD occu

171 ties (long PR, complete bundle branch block, left ventricular hypertrophy voltage criteria, long QTc,

172 Left ventricular hypertrophy was present in 19 individua

173 Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfu

174 Cardiac structural abnormalities, left ventricular hypertrophy, or concentric geometry, we

175 re men, 31 had diabetes mellitus, and 59 had left ventricular hypertrophy.

176 n, progressive conduction system disease and left ventricular hypertrophy.

177 Left ventricular internal diameter during systole (LVIDs

178 In 40 left ventricular irradiated targets, all lesions were id

179 are incompletely understood, we investigated left ventricular (LV) and left atrial (LA) pathophysiolo

180 neonatal heart regeneration preserves native left ventricular (LV) biomechanical properties after MI.

181 positive relationship between heart rate and left ventricular (LV) contractility known as the force-f

182 elerations have shown to enable 3D CINE with left ventricular (LV) coverage in a single breath-hold.

183 Left ventricular (LV) diastolic dysfunction is recognize

184 Early detection of left ventricular (LV) dysfunction before the onset of ov

185 eptides may contribute to ECM remodeling and left ventricular (LV) dysfunction.

186 erate aortic stenosis (ModAS) (n=13), SevAS, left ventricular (LV) ejection fraction >=55% (SevAS-pre

187 Association functional class II to IV with a left ventricular (LV) ejection fraction <=40% and type 2

188 study hypothesized that a relatively larger left ventricular (LV) electrical dyssynchrony in smaller

189 of transvenous implantation of a lead at the left ventricular (LV) endocardial side of the interventr

190 Left ventricular (LV) epicardial pacing results in slowl

191 Left ventricular (LV) fibrosis was quantified by Picro S

192 : 0.06; p = 0.002) was associated with worse left ventricular (LV) global longitudinal strain (GLS).

193 pathy (oHCM) is characterized by unexplained left ventricular (LV) hypertrophy associated with dynami

194 lood pressure was significantly elevated and left ventricular (LV) hypertrophy was evident by a 50% i

195 Left ventricular (LV) hypertrophy was reported in 73% of

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

197 ardiac biomarkers would demonstrate elevated left ventricular (LV) myocardial stiffness in comparison

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

199 oarctation of aorta (COA) results in chronic left ventricular (LV) pressure overload and subsequently

200 to assess the potential mediation effect of left ventricular (LV) remodeling on the association betw

201 Left ventricular (LV) systolic function may be overestim

202 r cardiopulmonary bypass and reperfusion and left ventricular (LV) tissue from mice subjected to I/R

203 Left ventricular (LV) wall thickness and LV mass were gr

204 sociation with incident HF and HF phenotype (left ventricular [LV] ejection fraction [LVEF] >= or < 5

205 function at submaximal and maximal exercise, left ventricular mass and compliance, and blood volume c

206 ve a higher arterial afterload and increased left ventricular mass index (LVMI) compared with control

207 and ABP and evaluate their associations with left ventricular mass index (LVMI) in untreated persons.

208 Greater early left ventricular mass index (LVMi) regression is associa

209 The main outcome was left ventricular mass index by cardiac magnetic resonanc

210 ncentration of 135 mmol/L did not change the left ventricular mass index, despite significant reducti

211 fibrillation and changes in kidney function, left ventricular mass or BAD.

212 function was not secondary to a reduction in left ventricular mass or through modulation of the after

213 Left ventricular mass regression was better associated w

214 e of severe prosthesis-patient mismatch, and left ventricular mass regression were similar in TAVR an

215 ialysate sodium of 135 mmol/L did not reduce left ventricular mass relative to control, despite impro

216 crovascular obstruction (MVO) (percentage of left ventricular mass) quantified by cardiac magnetic re

217 MVO extent (% left ventricular mass) was determined by cardiovascular

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

219 iac magnetic resonance imaging (MRI)-derived left ventricular measurements in 36,041 UK Biobank parti

220 Results EI and right-to-left ventricular measures were significantly increased i

221 461.9+/-178.3 mm(3); P=0.023) and infarcted left ventricular myocardium (1052.3+/-543.0 versus 340.3

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

223 Structures (atrioventricular junction or left ventricular myocardium) and organs at risk were con

224 Although left ventricular noncompaction (LVNC) has been associate

225 ventricular tachycardia and his father with left ventricular noncompaction and catecholaminergic pol

226 for diastolic heart failure, her father with left ventricular noncompaction, and 2 fourth-degree rela

227 h MPRI < 2) were more likely to have dynamic left ventricular outflow tract (LVOT) obstruction (63.3%

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

229 DeltaMSID >=3 mm and the presence of left ventricular outflow tract calcifications under the

230 tors of 30-day pacemaker dependency included left ventricular outflow tract calcifications under the

231 z score, left atrial diameter z score, peak left ventricular outflow tract gradient, and presence of

232 of increase in velocity-time integral of the left ventricular outflow tract greater than or equal to

233 Left ventricular outflow tract obstruction occurred more

234 One delayed left ventricular outflow tract obstruction required elec

235 gnosis, assess for presence and mechanism of left ventricular outflow tract obstruction, and risk str

236 nexplained syncope, septal diameter z-score, left ventricular posterior wall diameter z score, left a

237 iovascular function in the form of right and left ventricular pressure-volume loops and ventricular p

238 om 60.6 +/- 14.2 to 33.8 +/- 10.7 mm Hg), RV/left ventricular ratio (from 1.19 +/- 0.33 to 0.87 +/- 0

239 with main pulmonary artery size and right-to-left ventricular ratio achieved the highest correlations

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

241 information, to automate the recognition of left ventricular regional wall motion abnormalities.

242 in which 2 subsequent MIs affected different left ventricular regions in the same mouse.

243 without HF followed for a mean of 3.5 years, left ventricular relative wall thickness and mean left v

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

245 A clinical score (RAISE) that used left ventricular remodeling (hypertrophy/diastolic dysfu

246 nfarction and is an independent predictor of left ventricular remodeling over time.

247 The only predictor of left ventricular remodeling was treatment with sonothrom

248 the control group was more likely to exhibit left ventricular remodeling with an odds ratio of 2.79 (

249 ure, reduce weight, have salutary effects on left ventricular remodeling, and reduce hospitalization

250 , as well as echocardiographic indicators of left ventricular remodeling, were associated with greatl

251 hocardiography and their value in preventing left ventricular remodeling.

252 e, mass, and function, the assessment of the left ventricular repercussions of AS by CMR is not routi

253 e to assess cardiac morphology and function, left ventricular replacement fibrosis, and pre-post cont

254 The secondary end point was left ventricular reverse remodeling (left ventricular ej

255 erioration in exercise capacity and promotes left ventricular reverse remodeling in asymptomatic or m

256 rences in baseline clinical characteristics, left ventricular reverse remodeling, or outcomes on mult

257 roup of 29 of 74 (39%) patients with initial left ventricular reverse remodeling, there was a subsequ

258 300 (69%) patients with LVSD had evidence of left ventricular reverse remodeling.

259 We evaluated left ventricular shape, including a novel measure of max

260 RNA and protein expression were confirmed in left ventricular specimens obtained from patients with t

261 Study outcomes were measures of left ventricular structure and function.

262 Low LVSWI, reflecting poor left ventricular systolic and diastolic performance, is

263 were to be withheld if there was evidence of left ventricular systolic dysfunction (LVSD) defined as

264 cribe hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as

265 fy patients presenting with dyspnea who have left ventricular systolic dysfunction (LVSD).

266 s study sought to evaluate the prevalence of left ventricular systolic dysfunction among patients who

267 ned by concurrent new-onset heart failure or left ventricular systolic dysfunction is more strongly a

268 es, and higher prevalence of moderate-severe left ventricular systolic dysfunction.

269 Most trials enrolled patients with preserved left ventricular systolic function and low symptom burde

270 a novel activator of cardiac myosin-improves left ventricular systolic function and remodeling and re

271 mitosis, sarcomere disassembly and improved left ventricular systolic function following myocardial

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

273 ng regarding the prognosis and management of left ventricular thrombus (LVT).

274 ammatory effects of periodontitis on cardiac left ventricular tissue and the therapeutic activity of

275 possible hypertrophic remodeling at cardiac left ventricular tissues provoked by periodontitis-relat

276 ricular ejection fraction, not the extent of left ventricular trabeculation, had an important influen

277 These findings support use of left ventricular unloading in patients with cardiogenic

278 This study aimed to evaluate whether left ventricular unloading in patients with cardiogenic

279 c shock treated with VA-ECMO with or without left ventricular unloading using an Impella at 16 tertia

280 In the matched cohort, left ventricular unloading was associated with lower 30-

281 his international, multicenter cohort study, left ventricular unloading was associated with lower mor

282 Left ventricular unloading was used in 337 of the 686 pa

283 ns occurred more frequently in patients with left ventricular unloading: severe bleeding in 98 (38.4%

284 nts, we performed quantitative assessment of left ventricular volume and mass, wall thickness, segmen

285 s undeniably the gold standard for assessing left ventricular volume, mass, and function, the assessm

286 more severe MR (p = 0.0005) despite smaller left ventricular volumes (p = 0.005) and higher right ve

287 Super-resolved low-resolution images yielded left ventricular volumes comparable to those from full-r

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

289 Fully automated and manual left ventricular volumes were strongly correlated for en

290 Left ventricular volumes, ejection fraction, risk area (

291 Secondary measures were left ventricular volumes, infarct size (assessed in a su

292 Left ventricular vorticity metrics were observed to be h

293 depth of ablated lesions reached 90% of the left ventricular wall in both normal and infarcted myoca

294 chocardiographic abnormalities that included left ventricular wall motion abnormalities, global left

295 Maximum left ventricular wall thickness was 18 +/- 8 mm, and lef

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

297 ventricular relative wall thickness and mean left ventricular wall thickness were independent predict

298 nted images to annotate the location of each left ventricular wall.

299 I3:p.R79C carriers had significantly thicker left ventricular walls compared with noncarriers while i

300 recordings of coronary perfused donor heart left ventricular wedge preparations (n=12), and adapted