ライフサイエンスコーパス: LV

1 LV full recovery was defined as LVEF >=55%.

2 LV GLS may therefore be useful in the risk stratificatio

3 LV mass and LV mass index of TEVAR patients increased fr

4 LV myocardial stiffness in patients with LVH and elevate

5 LV systolic dysfunction was reported in 40% of men (who

6 LV(EV), distal pulmonary venous blood volume for vessels

7 LV.InsB in combination with a suboptimal dose of anti-CD

8 LVs pacing provides short-term hemodynamic improvement a

9 lly significant (LV-LT: r = 0.785; P < .001; LV-LD: r = 0.696; P < .001; and LT-LD: r = 0.121; P = .0

10 We used 120 LV-only FE models for training LV stress predictions.

11 or pressure was 1.257 +/- 0.488 mmHg; for 20 LV FE test examples, the mean absolute errors were, resp

12 multivariate analysis, the LV involvement, a LV-dominant phenotype, and the 5-year ARVC risk score we

13 e in LV ejection fraction >=10% and absolute LV ejection fraction <=50%.

14 24.1%) achieved LVRR and 45 (22.6%) achieved LV full recovery.

15 p vein thrombosis, is more common, but acute LV systolic dysfunction was noted in ~20%.

16 se positron emission tomography scans, acute LV myocardial injury was associated with myocardial infl

17 nic fibroblasts, neonatal myocytes, or adult LV myocytes isolated from "redox dead" (Cys17Ser) PKARIa

18 s in LVEDV and LVESV <12%]; group 3: adverse LV remodeling with compensation [>=12% increase in LVEDV

19 ncrease in LVEDV only]; and group 4: adverse LV remodeling [>=12% increase in both LVESV and LVEDV])

20 ttenuated inflammation and abrogated adverse LV remodeling following I/R injury.

21 we show that Dysf(-/-) mice develop adverse LV remodeling following I/R injury secondary to the coll

22 ost-infarction significantly reduced adverse LV remodeling and the decline of cardiac function.

23 factors and diseases associated with adverse LV remodeling.

24 An LV stiffness index of > 0.11 ml(-1) was independently as

25 derwent heart transplantation or received an LV assist device.

26 nts with Duchenne muscular dystrophy with an LV ejection fraction >=55% on >=1 cardiac magnetic reson

27 On multivariable analysis, LV GLS <7.0% was associated with increased mortality (HR

28 in vs. placebo, respectively; p < 0.001) and LV end-systolic volume (-26.6 +/- 20.5 ml vs. -0.5 +/- 2

29 in vs. placebo, respectively; p < 0.001) and LV sphericity, and improvements in LV ejection fraction

30 Blood volume (mL kg(-1) ) and LV mass index (g m(-2) ) were larger in OT versus OU (~1

31 in 58 (41%), biventricular in 52 (37%), and LV dominant in 16 (12%).

32 leading cause of death (10 of 17; 59%), and LV systolic dysfunction predicted an adverse outcome.

33 ociation to prognostically relevant 6MWT and LV mass regression than echocardiography.

34 Compared with MB, LV-Co and LV-Cr significantly altered cellular stress and ATP path

35 amples that was suggestive of dysbiosis, and LV-Co increased the risk of association with this group.

36 values for LV end-diastolic volume index and LV end-systolic volume index were negligible (g<0.10).

37 fraction, LV end-diastolic volume index, and LV end-systolic volume index.

38 , the relationship between these indices and LV diastolic dysfunction and exertional symptoms has not

39 ation of biometric data could predict LD and LV.

40 terized by direct measurement of LT, LD, and LV, rather than making assumptions based on AL.

41 te was high, whereas frequencies of LVRR and LV full recovery were low.

42 LV mass and LV mass index of TEVAR patients increased from 138.5 +/-

43 an increased LV weight/body weight ratio and LV end diastolic volume (WT, 50.8 mul; CatA-TG, 61.9 mul

44 Blood volume (CO rebreathing) and LV mass (cardiac magnetic resonance imaging), plus invas

45 novel, biological difference between RV and LV fibroblasts that might underlie distinctions in patho

46 We examined associations between SDB and LV diastolic and systolic function using data from 1506

47 trium (LA), RV, interventricular septum, and LV posterior wall diameters at 18 months (P < .001).

48 for LV, LA, RV, interventricular septum, and LV posterior wall diameters increased over a relatively

49 EDV ratio on the association between sex and LV reverse remodeling (LV end-systolic volume change) an

50 Left ventricular (LV) wall thickness and LV mass were greater in men (P<0.001).

51 26 muVs and 31 +/- 7 ms; both p < 0.05) and LVs+RV pacing (to 108 +/- 37 muVs; p < 0.05; and 29 +/-

52 As LV diastolic dysfunction typically precede heart failure

53 m for the identification of LVSD (defined as LV ejection fraction <=35%) to a cohort of patients aged

54 the interventricular septum, referred to as LV septal (LVs) pacing, was demonstrated.

55 re cine imaging was performed in short-axis, LV outflow tract (LVOT), and two-, three-, and four-cham

56 ent of the lateral and postero-lateral basal LV and is associated mostly with variants in desmoplakin

57 As compared with baseline, LVs pacing resulted in a larger reduction in QRS area (t

58 However, the association between LV noncompaction (LVNC) phenotype and vigorous physical

59 o screen for pharmacological agents to blunt LV dysfunction and associated pathophysiologic causes re

60 (18)F-flurpiridaz PET MPI is not affected by LV size and is superior to SPECT MPI in patients with sm

61 ion deterioration (12 patients), followed by LV systolic and diastolic deterioration (in 5 patients).

62 life cognitive function was accounted for by LV mass index.

63 in older mice on FFD, and Shc inhibition by LV in older mice or hepatocyte-specific deletion resulte

64 with concentric LV remodeling and concentric LV hypertrophy, respectively.

65 and 136 (14.2%) individuals with concentric LV remodeling and concentric LV hypertrophy, respectivel

66 DBG/LV and DBG/HV presented almost no inflammatory cells.

67 Group DBG: CSD filled with a DBG; group DBG/LV: CSD filled by the combination of DBG and HA in a low

68 d in group DBG, which was not present in DBG/LV and DBG/HV as confirmed by the larger size of the par

69 To define LV pressure-volume relationships, right heart catheteriz

70 tion undergoing cardiac surgery and donating LV biopsy (non-pressure-loaded heart biopsy, n=7).

71 he increase in LVdP/dtmax was similar during LVs and BiV pacing (17 +/- 10% vs. 17 +/- 9%, respective

72 +/- 9%, respectively) and larger than during LVs+RV pacing (11 +/- 9%; p < 0.05).

73 lar (LV) hypertrophy associated with dynamic LV outflow tract obstruction.

74 Echocardiographic LV stiffness index was measured by a method previously v

75 s of infection, 33% of Hu-NSG mice exhibited LV dyskinesia and dyssynchrony.

76 male left ventricle (LV) than in the female LV.

77 tion) for LV blood cavity, 0.89 +/- 0.03 for LV myocardium, and 0.62 +/- 0.08 for LV trabeculation (m

78 .03 for LV myocardium, and 0.62 +/- 0.08 for LV trabeculation (mean absolute error, 3.63 g +/- 3.4).

79 ts of 0.96 +/- 0.01 (standard deviation) for LV blood cavity, 0.89 +/- 0.03 for LV myocardium, and 0.

80 ive, we sought to use deep learning (DL) for LV in-silico modeling.

81 For six test FE models, the DL error for LV volume was 1.599 +/- 1.227 ml, and the error for pres

82 2.25) independently determined the risk for LV full recovery.

83 Mean z scores for LV, LA, RV, interventricular septum, and LV posterior wa

84 was an overall increase in mean z scores for LV, left atrium (LA), RV, interventricular septum, and L

85 rences between groups in baseline values for LV end-diastolic volume index and LV end-systolic volume

86 standard was the manual segmentation of four LV anatomic structures performed on end-diastolic short-

87 d with improvements in LV ejection fraction, LV end-diastolic volume index, and LV end-systolic volum

88 function was reported in 40% of men (who had LV ejection fraction, 34+/-11%) and 59% of women (LV eje

89 [CI]: 0.59 to 3.14 ml; p = 0.004) and higher LV mass (beta = 0.81 g; 95% CI: 0.11 to 1.51 g; p = 0.02

90 med a significant association between higher LV mass and body mass index and, in men, associations wi

91 Compared to NF, LF severe AS had higher LV stiffness indices (>0.11 ml(-1) OR 3.067, 95% CI 1.82

92 lesterol was causally associated with higher LV end-diastolic volume (beta = 1.85 ml; 95% confidence

93 g; p = 0.023) and triglycerides with higher LV mass (beta = 1.37 g; 95% CI: 0.45 to 2.3 g; p = 0.004

94 ls were independently associated with higher LV mass, lower LV systolic function, and reduced left at

95 culiar biventricular adaptation, with higher LV/RV (1.41+/-0.16 versus 1.36+/-0.15, P<0.0001) and low

96 entions such as exercise training to improve LV compliance may prevent the full manifestation of the

97 abetic HFrEF patients significantly improves LV volumes, LV mass, LV systolic function, functional ca

98 The primary endpoint was change in LV end-diastolic and -systolic volume assessed by cardia

99 Secondary outcomes included changes in LV systolic function, peak oxygen consumption, and quali

100 cardiac magnetic resonance with a decline in LV ejection fraction >=10% and absolute LV ejection frac

101 and circumferential strains and declines in LV ejection fraction and fractional shortening were obse

102 There was no difference in LV global longitudinal strain.

103 ot demonstrate any significant difference in LV systolic function compared with patients with normal

104 was statistically significantly different in LV-HF versus LV-Control.

105 Although total improvement in LV measures was similar between groups, Black patients a

106 .001) and LV sphericity, and improvements in LV ejection fraction (6.0 +/- 4.2 vs. -0.1 +/- 3.9; p <

107 s (P<0.0001) associated with improvements in LV ejection fraction, LV end-diastolic volume index, and

108 A progressive increase in LV/RV dimensions was observed in women from those engage

109 Each g/m(2.7) increment in LV mass index was associated with a 0.03 standardized un

110 -21 and miR-221 in RV fibroblasts but not in LV fibroblasts nor cardiomyocytes of either ventricle.

111 settings were associated with a reduction in LV ejection fraction.

112 agliflozin was associated with reductions in LV mass (-17.8 +/- 31.9 g vs. 4.1 +/- 13.4 g, for empagl

113 m release from the sarcoplasmic reticulum in LV myocytes, without affecting intrinsic ryanodine recep

114 are required to maintain PROX1 expression in LVs and LVVs in response to VEGF-C signaling.

115 Analyses included LV ejection fraction (LVEF); global longitudinal strain

116 grafts stiffen the aorta and likely increase LV afterload.

117 Increased LV stiffness was related to LV concentric remodelling an

118 g in CatA-TG was accompanied by an increased LV weight/body weight ratio and LV end diastolic volume

119 nce measures (LV end-diastolic volume index, LV ejection fraction), diuretic intensification, symptom

120 eier analysis, patients with LV involvement (LV dominant and biventricular) had a worse prognosis tha

121 at compared with immediate reperfusion (IR), LV unloading before reperfusion improves myocardial ener

122 ation of a second potassium conductance, G(K(LV)) .

123 ller LVs (67% vs. 43%, P < 0.001) and larger LVs (76% vs. 61%, P < 0.001).

124 EDV of less than 113 mL (n = 369) and larger LVs defined as having an LVEDV of at least 113 mL (n = 3

125 area under the curve (AUC) of 0.75 in larger LVs to 0.67 in smaller LVs (P = 0.03), whereas PET perfo

126 ity improved in smaller compared with larger LVs (90% vs. 83%, P = 0.03), the PET specificity did not

127 We first engineered lentiviral (LV) and adeno-associated viral (AAV) vectors that prefer

128 rimary efficacy end point), quality of life, LV structural remodeling ( EF >5% and ESV 10%) and heart

129 dently associated with higher LV mass, lower LV systolic function, and reduced left atrial function o

130 , left ventricular ejection fraction (LVEF), LV end-systolic diameter-index (LVESDi), DBP, and RHR we

131 There was no difference in change in LVEF, LV end diastolic and end systolic diameters between the

132 Forty-six patients with LVH (LV septum >11 mm) and elevated cardiac biomarkers (N-ter

133 parted by palmitate helps explain maintained LV function and may contribute to designing novel therap

134 significantly improves LV volumes, LV mass, LV systolic function, functional capacity, and quality o

135 LV end-diastolic volume, LV myocardium mass, LV trabeculation, and trabeculation mass-to-total myocar

136 Compared with MB, LV-Co and LV-Cr significantly altered cellular stress an

137 %) diabetes and 23 (21.9%) prediabetes, mean LV ejection fraction 32.5% (9.8%), and 81 (77.1%) New Yo

138 cardiovascular magnetic resonance measures (LV end-diastolic volume index, LV ejection fraction), di

139 These findings suggest a new role for mEC LV as a bifurcation gate for feedforward (telencephalic)

140 ing of hippocampal output signals within mEC LV is asymmetric, favoring excitation of far projecting

141 In CatA-TG mice, LV interstitial fibrosis formation was enhanced by 19%,

142 In preclinical models, LV unloading reduced the expression of hypoxia-sensitive

143 he composite outcome of all-cause mortality, LV assist device implantation, or heart transplantation

144 In mouse LV cardiomyocytes, disulfide-containing PKARIalpha was n

145 n end-diastolic short-axis cine cardiac MRI: LV trabeculations, LV myocardium, LV papillary muscles,

146 rdiac MRI: LV trabeculations, LV myocardium, LV papillary muscles, and the LV blood cavity.

147 eling [>=12% decrease in LVESV]; group 2: no LV remodeling [changes in LVEDV and LVESV <12%]; group 3

148 nockdown significantly attenuated RV but not LV fibroblast proliferation.

149 ges were assessed as the first derivative of LV pressure (LVdP/dtmax).

150 s a possible but not uncommon determinant of LV hypertrabeculation in asymptomatic subjects.

151 The duration of LV unloading before reperfusion was inversely associated

152 To explore the effect of LV unloading duration on infarct size, we analyzed data

153 EMI-DTU) trial and then tested the effect of LV unloading on ischemia and reperfusion injury, cardiac

154 fraction [LVEF] >= or < 50%) independent of LV structure and function.

155 en VPA and LVNC phenotype was independent of LV volumes.

156 -invasive echocardiographic-derived index of LV stiffness may be important in LF AS.

157 ed a novel echocardiography-derived index of LV stiffness to compare between these groups.

158 th LV hypertrophy and subclinical markers of LV diastolic dysfunction.

159 ween SDB severity and subclinical markers of LV systolic function.

160 n nor ICAM-1 was associated with measures of LV diastolic function after multivariable adjustment.

161 at risk for developing DMDAC before onset of LV dysfunction and its clinical utility warrants further

162 e nucleotide polymorphism-based predictor of LV mass in 7,601 individuals with LV mass measurements m

163 clinical step for assessing the presence of LV dysfunction and may potentially aid in the early diag

164 Echocardiographic-derived profiling of LV forward flow, filling pressure, and RV function allow

165 Automatic quantification of LV end-diastolic volume, LV myocardium mass, LV trabecul

166 s associated with a significant reduction of LV end-diastolic volume (-25.1 +/- 26.0 ml vs. -1.5 +/-

167 However, the prognostic value of LV GLS in secondary MR has not been evaluated.

168 ought to demonstrate the prognostic value of LV GLS over LVEF in patients with secondary MR.

169 ctrophysiological and hemodynamic effects of LVs with BiV and His bundle (HB) pacing in CRT patients.

170 heart rate settings had no adverse effect on LV structure or function, whereas conventional settings

171 In early PAH LV myocardium proteins that may be linked to an increase

172 In particular, LV stiffness has not been compared between LF vs NF.

173 Pathological LV remodelling was evident by the re-expression of fetal

174 rdiomyocyte c-Kit signalling in pathological LV remodelling following pressure overload.

175 /- 10.28 g/m/yr, whereas in control patients LV characteristics did not change.

176 stic performance according to the median PET LV end-diastolic volume (LVEDV), with smaller LVs define

177 ry end points include change in postexercise LV outflow tract gradient, New York Heart Association cl

178 The preserved LV ejection fraction (EF) group in MIS-C showed diastoli

179 ary wedge pressure - right atrial pressure), LV myocardial stiffness was nearly 30% greater in LVH th

180 rmed a median of 2.1 years later to quantify LV diastolic function, systolic function, and structure.

181 ransporter 2 inhibitor empagliflozin reduced LV volumes in patients with HFrEF and type 2 diabetes or

182 The effect of reduced LV(EV) on mortality (hazard ratio: 1.07; 95% CI: 1.05, 1

183 urden and exercise capacity through reducing LV outflow tract obstruction.

184 ation between sex and LV reverse remodeling (LV end-systolic volume change) and sex and the composite

185 As a result, LV end-diastolic wall thickness-to-chamber radius (h/R)

186 is of the following groups (group 1: reverse LV remodeling [>=12% decrease in LVESV]; group 2: no LV

187 Favorable reverse LV remodeling may be a mechanism by which sodium-glucose

188 Expert Panel reviews the biology of reverse LV remodeling and the clinical course of patients with H

189 in combination with right ventricular (RV) (LVs+RV), BiV, and HB pacing was performed in 27 patients

190 sive or massive pulmonary embolism and an RV/LV diameter ratio >=0.9 on chest computed tomography.

191 r adjusting for age, gender, and baseline RV/LV ratio, pulmonary artery systolic pressure, and modifi

192 odel adjusted R(2) for absolute change in RV/LV ratio, pulmonary artery systolic pressure, modified M

193 entricular septum, referred to as LV septal (LVs) pacing, was demonstrated.

194 S-preserved ejection fraction, n=37), SevAS, LV ejection fraction <55% (SevAS-reduced ejection fracti

195 correlation between indices of COA severity, LV diastolic function (average e' and E/e'), and exertio

196 s dimensions were statistically significant (LV-LT: r = 0.785; P < .001; LV-LD: r = 0.696; P < .001;

197 erformance was similar in larger and smaller LVs (AUC, 0.79 vs. 0.77, P = 0.49).

198 igher sensitivity than SPECT in both smaller LVs (67% vs. 43%, P < 0.001) and larger LVs (76% vs. 61%

199 UC) of 0.75 in larger LVs to 0.67 in smaller LVs (P = 0.03), whereas PET performance was similar in l

200 Accordingly, in smaller LVs, PET had a higher AUC (0.77) than the SPECT AUC (0.6

201 In smaller LVs, there was a degradation of SPECT sensitivity that w

202 V end-diastolic volume (LVEDV), with smaller LVs defined as having an LVEDV of less than 113 mL (n =

203 perior to SPECT MPI in patients with smaller LVs, highlighting the importance of appropriate test sel

204 ~16%, respectively, both P <= 0.015) Static LV chamber compliance was greater in OT compared to both

205 ickness, LV mass, and diastolic and systolic LV function; and a standardized neurocognitive battery t

206 Temporary LVs pacing (transaortic approach) alone or in combinatio

207 In summary, these analyses show that LV mass-associated genetic variability associates with d

208 These results indicate that LVs pacing may serve as a valuable alternative for CRT.

209 The LV showed activation of genes related to inflammation an

210 The LV was less distensible in LVH than in controls (smaller

211 Although the LV myocardial stiffness of patients with LVH is greater

212 At multivariate analysis, the LV involvement, a LV-dominant phenotype, and the 5-year

213 LV myocardium, LV papillary muscles, and the LV blood cavity.

214 uantitative metrics or visual grades and the LV mass index (LVMI) (indexed to body surface area on ec

215 With increasing preservation duration, the LV showed an increase in nuclear translocation of NFkapp

216 he myocardium and time were features for the LV pressure and volume training, and passive material pr

217 antification and visualization of EVV in the LV is feasible and may provide further insight into the

218 xpression and increased CatA activity in the LV of transgenic mice (CatA-TG) reduced EC-SOD protein l

219 rtrophy was evident by a 50% increase in the LV weight-to-tibia length ratio due to cardiomyocyte hyp

220 rk starts by an accurate localization of the LV blood pool center-point using a fully convolutional n

221 ed ROIs are used for the segmentation of the LV cavity and myocardium via a novel FCN architecture.

222 del predicted the quantitative values of the LV relaxation velocities (e') measured by echocardiograp

223 nt centroid coordinates were features of the LV stress prediction models.

224 n to determine the clinical relevance of the LV(EV) in multivariable models, including sex and anthro

225 Children completed 2 questionnaires, the LV Prasad Functional Vision Questionnaire-II (LVP-FVQ-II

226 Our results demonstrated that the LV and RV of human donor hearts have distinct responses

227 corrected QRS area for heart size using the LV end-diastolic volume (QRSarea/LVEDV).

228 ous vascular volume, and sarcopenia with the LV epicardial volume (LV(EV)) (myocardium and chamber) e

229 e 29 clinical phenotypes associated with the LV mass genetic predictor at FDR q < 0.05.

230 ography to quantify relative wall thickness, LV mass, and diastolic and systolic LV function; and a s

231 icant change in PET sensitivity according to LV size (P = 0.07).

232 o improve exercise time and limit changes to LV function in people with HFrEF and cardiac implantable

233 but less is known about its contribution to LV size.

234 pressure overload and subsequently leads to LV diastolic dysfunction and heart failure over time.

235 Increased LV stiffness was related to LV concentric remodelling and diastolic dysfunction, and

236 e and function, in particular in relation to LV mass.

237 Taken together, LV-Co resuscitation exacerbated the loss of bacterial di

238 rt-axis cine cardiac MRI: LV trabeculations, LV myocardium, LV papillary muscles, and the LV blood ca

239 We used 120 LV-only FE models for training LV stress predictions.

240 hese data suggest that SBP may underestimate LV afterload in this population.

241 ed that a polygenic discovery approach using LV mass measurements made in a clinical population would

242 condary mitral regurgitation (MR) when using LV ejection fraction (EF).

243 emory-associated activity back into layer V (LV).

244 ment of lymphatic vessels, lymphatic valves (LVs) and lymphovenous valves (LVVs).

245 ng anterior chamber depth (ACD), lens vault (LV), iris curvature (IC), anterior chamber width, lens t

246 an, at least in part, offset left ventricle (LV) dysfunction in hearts from diabetic mice, improving

247 piridaz PET MPI according to left ventricle (LV) size.

248 ificantly higher in the male left ventricle (LV) than in the female LV.

249 V) does not respond like the left ventricle (LV) to guideline-directed medical therapy of heart failu

250 ptional profile of the human left ventricle (LV, n=4) and right ventricle (RV, n=4) after 0, 4, and 8

251 nderstood, we investigated left ventricular (LV) and left atrial (LA) pathophysiological changes and

252 d to cardiomyocytes of the left ventricular (LV) apex.

253 eneration preserves native left ventricular (LV) biomechanical properties after MI.

254 hip between heart rate and left ventricular (LV) contractility known as the force-frequency relations

255 own to enable 3D CINE with left ventricular (LV) coverage in a single breath-hold.

256 Left ventricular (LV) diastolic dysfunction is recognized as playing a maj

257 Early detection of left ventricular (LV) dysfunction before the onset of overt Duchenne muscu

258 bute to ECM remodeling and left ventricular (LV) dysfunction.

259 sis (ModAS) (n=13), SevAS, left ventricular (LV) ejection fraction >=55% (SevAS-preserved ejection fr

260 onal class II to IV with a left ventricular (LV) ejection fraction <=40% and type 2 diabetes or predi

261 d that a relatively larger left ventricular (LV) electrical dyssynchrony in smaller hearts contribute

262 lantation of a lead at the left ventricular (LV) endocardial side of the interventricular septum, ref

263 Left ventricular (LV) epicardial pacing results in slowly propagating pace

264 Left ventricular (LV) fibrosis was quantified by Picro Sirius Red and gene

265 was associated with worse left ventricular (LV) global longitudinal strain (GLS).

266 aracterized by unexplained left ventricular (LV) hypertrophy associated with dynamic LV outflow tract

267 significantly elevated and left ventricular (LV) hypertrophy was evident by a 50% increase in the LV

268 Left ventricular (LV) hypertrophy was reported in 73% of male and 74% of f

269 while others turn off the left ventricular (LV) lead at LVAD implant.

270 would demonstrate elevated left ventricular (LV) myocardial stiffness in comparison with healthy cont

271 n prognostically important left ventricular (LV) parameters.

272 a (COA) results in chronic left ventricular (LV) pressure overload and subsequently leads to LV diast

273 ential mediation effect of left ventricular (LV) remodeling on the association between lifetime systo

274 Left ventricular (LV) systolic function may be overestimated in patients w

275 bypass and reperfusion and left ventricular (LV) tissue from mice subjected to I/R or sham surgery we

276 Left ventricular (LV) wall thickness and LV mass were greater in men (P<0.

277 ident HF and HF phenotype (left ventricular [LV] ejection fraction [LVEF] >= or < 50%) independent of

278 ally significantly different in LV-HF versus LV-Control.

279 nd sarcopenia with the LV epicardial volume (LV(EV)) (myocardium and chamber) estimated from chest CT

280 s (LT), lens diameter (LD), and lens volume (LV) were measured intraoperatively using SD-OCT in 293 e

281 c quantification of LV end-diastolic volume, LV myocardium mass, LV trabeculation, and trabeculation

282 patients significantly improves LV volumes, LV mass, LV systolic function, functional capacity, and

283 ced earlier, at the moderate AS stage, where LV function remains preserved.

284 We aimed to assess whether LV strain will predict those who develop DMDAC.

285 While LV tissue modulus for P1 MI and sham mice were similar (

286 ble analyses, female sex was associated with LV end-systolic volume change (beta=0.12; P=0.003) and a

287 Greater SDB severity was associated with LV hypertrophy and subclinical markers of LV diastolic d

288 s with DSP and were strongly associated with LV late gadolinium enhancement (90%), even in cases of a

289 othesis that trauma TEVAR is associated with LV mass increase and adverse off-target aortic remodelin

290 ies have identified few SNPs associated with LV mass.

291 03), the PET specificity did not change with LV size (76% vs. 76%, P = 0.9).

292 edictor of LV mass in 7,601 individuals with LV mass measurements made during routine clinical care.

293 At Kaplan-Meier analysis, patients with LV involvement (LV dominant and biventricular) had a wor

294 ommunity structure were most pronounced with LV-Co, and correlated with biomarkers of hepatocellular

295 .268; P < .001), it was not significant with LV (r = 0.084; P = .15).

296 al load indices correlate more strongly with LV hypertrophy.

297 RV but underestimated the risk in those with LV involvement.

298 ection fraction, 34+/-11%) and 59% of women (LV ejection fraction, 28+/-13%).

299 To handle the increased workload, LV growth greatly outpaces that of the RV during postnat

300 ere also independently associated with worse LV GLS.