ライフサイエンスコーパス: LV

1 LV early filling was determined from LV volume-time curv

2 LV ejection fraction (LVEF) less than 50% (P < .001) and

3 LV ejection fraction is robustly preserved in at least t

4 LV ejection fraction recovered in 80% of survivors with

5 LV function was assessed by serial echocardiography, 2,3

6 LV global longitudinal strain was measured using speckle

7 LV mass was negatively associated with any HAART exposur

8 LV mass, however, is overestimated with SSIR.

9 LV systolic function is enhanced in cirrhosis due to aug

10 LV T1 correlated with RV T1 (r=0.45, P<0.001), cardiopul

11 LV twist and apical rotation were not altered from basel

12 LV twist mechanics are reduced in males compared to fema

13 LV-GLS was measured on 2-, 3-, and 4-chamber views using

14 LV-mediated GT allowed immunologic reconstitution, altho

15 right ventricular myocardium (n=37; 38.1%), LV trabeculations (n=5; 5.2%), papillary muscle (n=3; 3.

16 and 4 months post-treatment, we measured (1) LV global longitudinal strain, twisting, and percent dif

17 infarct size (6% LV; IQR: 2% to 18% vs. 13% LV; IQR: 7% to 23%; p = 0.006; and p for interaction = 0

18 ejection fraction </=47%, infarct size >/=19%LV, and microvascular obstruction >/=1.4%LV were identif

19 in control mice with large infarcts (>/=25% LV).

20 =19%LV, and microvascular obstruction >/=1.4%LV were identified as the best cutoff values for MACE pr

21 stenting reduced the final infarct size (6% LV; IQR: 2% to 18% vs. 13% LV; IQR: 7% to 23%; p = 0.006

22 itudinal strain (25% versus 17% versus 6%,), LV twist (27% versus 17% versus 1%), %untwMVO (31% versu

23 At 2 years (n=85), LV ejection fraction was similar in the bone marrow mono

24 Abnormal LV structure, systolic function (based on LV ejection fr

25 In addition, LV-V5 seemed to be a better predictor for ACEs than MHD.

26 Adverse LV remodeling and deteriorating LV ejection fraction occ

27 arct size, LV ejection fraction, and adverse LV remodeling, changes associated with decreased neutrop

28 Obese patients demonstrate greater adverse LV remodeling and more impaired LV deformation after STE

29 ced recovery of LV function, greater adverse LV remodeling, and more device implantations.

30 questionnaires by telephone before and after LV treatment.

31 pressure overloaded hearts revealed that all LV parameters (LV end-diastolic and -systolic dimensions

32 Although LV ejection fraction was comparable between groups, long

33 onventional CRT underwent implantation of an LV endocardial pacing electrode and a subcutaneous pulse

34 cs and phosphoproteomics approach to analyze LV biopsies from patients undergoing CABG and from pigs

35 ratio, 3.90; 95% CI, 1.84-8.26; P < .001 and LV EF <45%: hazard ratio, 3.23; 95% CI, 1.57-6.65; P = .

36 no significant change in cACD (P = .190) and LV (P = .430) in fellow eyes.

37 tic valve area between 1.0 and 1.5 cm(2) and LV systolic dysfunction defined as LV ejection fraction

38 The quantified thresholds (RV EF <30% and LV EF <45%) may be implemented in noninvasive risk strat

39 Patients with NFLG had less severe AS and LV remodeling than patients with normal-flow high-gradie

40 Patients with concomitant moderate AS and LV systolic dysfunction are at high risk for clinical ev

41 of patients with concomitant moderate AS and LV systolic dysfunction.

42 ness were lower whereas LV contractility and LV fractional shortening were higher when compared to th

43 ed by RV fractional area change (RV-FAC) and LV ejection fraction (LVEF), respectively.

44 prove survival compared with standard FU and LV before and after radiotherapy.

45 (P = .003) and ACA (P < .001) increased and LV (P = .002) decreased in APAC eyes.

46 onance scans were performed to define LA and LV remodeling and ischemic MR, and were correlated with

47 -up, in the HAART-exposed group, LV mass and LV end-diastolic septal thickness were lower whereas LV

48 oncentric hypertrophy (increased LV mass and LV mass/volume(0.67)) with change in LVEDV.

49 ted hemodynamic load, cardiac mechanics, and LV remodeling in an elderly community-based population.

50 hronized LV pacing, multisite LV pacing, and LV endocardial pacing offer promise as novel pacing opti

51 P = 0.06, <0.01 and 0.08, respectively) and LV ejection fraction (AUC = 0.56, 0.69 and 0.69; all P >

52 clusion exhibited increased infarct size and LV macrophage content after 24-48 h reperfusion compared

53 Low-vision devices without therapy and LV devices with therapy.

54 deterioration in LV end-diastolic volume and LV end-systolic volume.

55 cm(2) and LV systolic dysfunction defined as LV ejection fraction <50%.

56 tracking echocardiography was used to assess LV structure and function at baseline, during PEI and fo

57 prosthetic PAS undergoing redo AVR, baseline LV-GLS provides incremental prognostic use over establis

58 s confirmed the predictive value of baseline LV SUV for subsequent cardiac abnormalities.

59 Basic LV services may be sufficient for most LV patients with

60 d (2) to investigate the correlation between LV wall thickness (LVWT) and other disease features in m

61 During beta1 -AR blockade, LV volumes were unchanged but blood pressure and heart r

62 during beta1 -adrenergic receptor blockade, LV apical rotation, twist and untwisting velocity were r

63 longer term in STEMI patients complicated by LV dysfunction.

64 iding left ventricular (LV) stroke volume by LV myocardial volume, and long-axis strain (LAS) was cal

65 In the derivation cohort, LV ejection fraction </=47%, infarct size >/=19%LV, and

66 eaflets of intraluminal valves in collecting LVs.

67 s (changes on electrocardiography; decreased LV systolic, diastolic diameter, or septal E' velocity;

68 Adverse LV remodeling and deteriorating LV ejection fraction occurred in control mice with large

69 predictors (age, body mass index, diabetes, LV end-diastolic volume index, LGE, EF) (hazard ratio =

70 interval cardiovascular events and a dilated LV (increased LV end-diastolic volume [EDV] indexed to b

71 al, and few participants developed a dilated LV.

72 ransseptal activation with absence of direct LV Purkinje activity; (3) homogeneous propagation within

73 tolic diameter, and higher echocardiographic LV ejection fraction than controls.

74 Children after rTOF do not have elevated LV native T1 or LV extracellular volume, but show eviden

75 The most common indications for endocardial LV pacing were difficult CS anatomy (n =12), failure to

76 e infarcted myocardium of mice and evaluated LV remodeling and function 28 days after myocardial infa

77 Underestimation was because of focal LV hypertrophy (n=10; 10.3%) or poor acoustic windows (n

78 93-0.99) and non-BH SSIR (r = 0.92-0.98) for LV ejection fraction (EF), volume, and mass (P < .0001 f

79 at ages 3 to 18 years and were evaluated for LV structure and function 31 years later.

80 2 +/- 3 years) were specifically matched for LV length (males: 8.5 +/- 0.5 cm, females: 8.2 +/- 0.6 c

81 nction (left ventricular ejection fraction), LV diastolic function (early relaxation velocity), and c

82 LV early filling was determined from LV volume-time curves as derived from cardiac magnetic r

83 Full LV coverage T1 and T2 mapping are more accurate than a 3

84 e with MSI < 0.50 and we would advocate full LV coverage in future studies.

85 r coronary heart disease, underlying greater LV diffuse fibrosis is associated with lower QRS voltage

86 nction was worse in individuals with greater LV trabeculation, supporting the concept of hypertrabecu

87 rs of follow-up, in the HAART-exposed group, LV mass and LV end-diastolic septal thickness were lower

88 oup had a greater extent of LGE and a higher LV end-diastolic volume index than other groups, but lev

89 to determine the ability to detect impaired LV function.

90 ater adverse LV remodeling and more impaired LV deformation after STEMI compared with those with norm

91 ese patients had significantly more impaired LV global longitudinal strain (-13.7+/-3.8 versus -15.0+

92 SCs from LVD and sham hearts did not improve LV remodeling and function, cardiac MSCs from LVD exacer

93 and in ischemic cardiomyopathy, they improve LV function, effects apparently modulated in part by sys

94 s, reduces myocardial fibrosis, and improves LV function in the setting of HF.

95 in LV structure (volume) with alterations in LV functional characteristics (strain, ) into a -volume

96 T (req) may be associated with changes in LV function in the longer term in STEMI patients complic

97 ilatation and inflammation; these changes in LV function related to cirrhosis can be assessed using r

98 ion measures were associated with changes in LV geometry and function by multivariable-adjusted linea

99 We used CMR to consider changes in LV mass, myocardial strain and T1 mapping.

100 Our findings indicate that changes in LV morphology and function depend on the type of body ma

101 this study, we combined temporal changes in LV structure (volume) with alterations in LV functional

102 Secondary end points included changes in LV volumes, infarct size, and major adverse cardiac even

103 eliminated the progressive deterioration in LV end-diastolic volume and LV end-systolic volume.

104 n attenuate the progressive deterioration in LV function and adverse remodeling in mice with large in

105 er, it is unknown whether sex differences in LV mechanics are fundamentally regulated by differences

106 tudy aimed to investigate sex differences in LV mechanics with altered adrenergic stimulation achieve

107 utaneous approach mitigates the elevation in LV filling pressures with volume loading in both normal

108 arance with persistent activation of FPR2 in LV.

109 Improvements in LV function were accompanied by significant elevations i

110 hs of HD was associated with improvements in LV mass, strain and troponin.

111 hic CRT response (>/=5% absolute increase in LV ejection fraction).

112 dial approach would mitigate the increase in LV end-diastolic pressure that develops during volume lo

113 dogs, pericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while en

114 le enhancing the saline-mediated increase in LV end-diastolic volume.

115 with a greater probability of an increase in LV mass >12% (highest category versus <limit of detectio

116 tence of an additional mechanism involved in LV filling, namely, a hydraulic force contributing to th

117 levation myocardial infarctions resulting in LV dysfunction.

118 tients with recent STEMI exhibited increased LV wall active tension when normalized by SBP.

119 ciation of concentric hypertrophy (increased LV mass and LV mass/volume(0.67)) with change in LVEDV.

120 ovascular events and a dilated LV (increased LV end-diastolic volume [EDV] indexed to body surface ar

121 Low family SES was associated with increased LV mass and impaired diastolic performance more than 3 d

122 Doxorubicin dose-dependently increases LV MRGlu, particularly in the presence of low baseline (

123 substrate concentrated to the basal lateral LV, with marked epicardial predominance.

124 d (4) latest activation at the basal lateral LV.

125 with bolus fluorouracil (FU) and leucovorin (LV) compared with surgery alone.

126 sus 0.40+/-0.08 cm(2)/m(2); P<0.0001), lower LV mass index (74+/-18 versus 90+/-26 g/m(2); P=0.01), b

127 lling forces are more orthogonal to the main LV flow direction in heart failure patients with LBBB co

128 The groups had similar mean LV ejection fraction at diagnosis (29.6 with versus 27.3

129 Women with preeclampsia had smaller mean LV end-diastolic diameters (5.2 versus 6.0 cm; P=0.001),

130 Optical APs were mapped when measuring LV developed pressure (LVDP), coronary flow rate and oxy

131 city and regenerative potential of meningeal LVs should allow manipulation of cerebrospinal fluid dra

132 We show here that meningeal LVs develop postnatally, appearing first around the fora

133 min, a drug associated with improved post-MI LV function in experimental studies.

134 les related to factors that regulate post-MI LV remodeling and repair.

135 In mice given CMCs 2 days after MI, LV ejection fraction 28 days later was significantly inc

136 Basic LV services may be sufficient for most LV patients with mild visual impairment.

137 Synchronized LV pacing, multisite LV pacing, and LV endocardial pacing offer promise as no

138 nd sex differences were found for normalized LV wall thickening and normalized myocardial mass, witho

139 entricular filling (r=0.67; P<0.01), but not LV stiffness constant beta (-0.34; P=0.051) or relaxatio

140 RV, but not LV, T1 were higher in patients than in controls (1031+/-

141 Addition of LV-GLS to the clinical model increased the C statistic s

142 Quantitative analysis of LV function and mass was performed.

143 lso were associated with distinct aspects of LV mechanical function.

144 its were associated with distinct aspects of LV mechanics, underscoring potential differential effect

145 ergoing cardiac MR imaging for assessment of LV dysfunction with EF less than 50%.

146 Conclusion Assessment of LV function with SSIR at 3.0 T is noninferior to the sta

147 Because SMR is an intrinsic consequence of LV dysfunction, causality between SMR and mortality shou

148 tion probability model for ACEs consisted of LV-V5, age, and weighted ACE risk score per patient (c-s

149 However, the degree of LV enlargement was minimal, and few participants develop

150 n abnormality the greater the discordance of LV filling force with the predominant LV flow direction

151 ibited significantly increased expression of LV pro-inflammatory and pro-fibrotic genes and collagen

152 The incidence of LV thrombus was as follows: (a) nonanterior infarction,

153 predictor for VO2max even after inclusion of LV stiffness and relaxation time (beta=0.80; P<0.01).

154 a distinct feature of HFpEF, independent of LV stiffness and relaxation.

155 Rasa1 gene in adult mice resulted in loss of LV endothelial cells (LECs) specifically from the leafle

156 body mass index with subclinical measures of LV mechanical function.

157 od socioeconomic status (SES) on measures of LV structure and function are lacking.

158 For predicting the occurrence of LV thrombus, a multiple regression model was applied.

159 dity and mortality and different patterns of LV remodeling and recovery of LV function when compared

160 1% [7.4%] vs 10.0% [6.2%] as a percentage of LV mass; P = .001).

161 s administration did not improve recovery of LV function over 2 years.

162 nt patterns of LV remodeling and recovery of LV function when compared with patients with PPCM that i

163 tion was associated with reduced recovery of LV function, greater adverse LV remodeling, and more dev

164 rdiac macrophages in peri-infarct regions of LV in T2DM mice.

165 iles and highlighted the prognostic value of LV remodeling and subclinical dysfunction.

166 those in control subjects (median number of LVs per bronchiole: 4.75 (BOS), 6.47 (RAS), 4.25 (contro

167 mon progenitors for the outflow tract (OFT), LV, atrium and SV but not the right ventricle (RV).

168 al LV structure, systolic function (based on LV ejection fraction and longitudinal strain), and diast

169 ht ventricular (RV) function is dependent on LV health, the IUGR right ventricle remains poorly studi

170 Volumes of interest were drawn on LV myocardium to quantify mean SUV.

171 How LBBB-related effects on LV diastolic function may contribute to those therapeuti

172 n multivariate Cox regression analysis, only LV ejection fraction (EF) and LAS independently indicate

173 er rTOF do not have elevated LV native T1 or LV extracellular volume, but show evidence of increased

174 se intolerance, arrhythmia, and native T1 or LV extracellular volume.

175 aded hearts revealed that all LV parameters (LV end-diastolic and -systolic dimensions, ejection frac

176 In HD patients, LV SUV showed a progressive increase during doxorubicin

177 During PEI, LV end-diastolic volume and stroke volume were increased

178 -free survival rates were 39% in the FU plus LV arm and 37% in the ECF arm ( Plogrank = .94; multivar

179 erall survival rates were 44% in the FU plus LV arm and 44% in the ECF arm ( Plogrank = .69; multivar

180 CI, 0.78 to 1.24 comparing ECF with FU plus LV).

181 tion (P = .008) independently helped predict LV thrombus.

182 nce of LV filling force with the predominant LV flow direction (r(2) = 0.49).

183 highlighting the burden of HF with preserved LV ejection fraction in the elderly.

184 severe aortic valve diseases (with preserved LV ejection fraction).

185 ortic valve diseases in those with preserved LV ejection fraction.

186 15-epi-LXA4 injected mice displayed reduced LV and lung mass to body weight ratios and improved ejec

187 s, AAS users demonstrated relatively reduced LV systolic function (mean+/-SD left ventricular ejectio

188 ts in both strains had significantly reduced LV fibrosis and improved vascular function.

189 aluation (N=58) showed significantly reduced LV systolic (left ventricular ejection fraction = 49+/-1

190 tinue inflammation post-MI, thereby reducing LV dysfunction.

191 Conclusion Average regional LV function was worse in individuals with greater LV tra

192 roups (51.6%) with no difference in regional LV function.

193 In 26 of 36 studies reporting LV function by SMR grade, increasing SMR severity was as

194 imal preparations, the pericardium restrains LV filling when central blood volume increases.

195 Severe LV dysfunction with a restrictive LV filling pattern was evident, which is associated with

196 Results LV thrombus was detected in 27 of 392 patients (7%): 18

197 ore than half of patients undergoing routine LV ablation procedures (predominately PVC ablations) exp

198 re was no association between progressive RV/LV structural disease and newly developed ECG TFC.

199 n fraction (EF) was 44% (10%), and mean (SD) LV EF was 53% (8%).

200 The SELECT-LV (Safety and Performance of Electrodes implanted in th

201 Severe LV dysfunction with a restrictive LV filling pattern was

202 ce implantation in patients with more severe LV dysfunction resulting in overestimation of clinical s

203 patients typically demonstrated (1) a single LV breakthrough at the septum (38+/-15 ms post-QRS onset

204 arction significantly improved infarct size, LV ejection fraction, and adverse LV remodeling, changes

205 ence between MI size3-slices and MI sizefull LV (P = 0.93) with an excellent correlation between the

206 rthermore, using AAR3-slices and MI sizefull LV resulted in 'negative' MSI in 7/48 patients.

207 All mutation carriers had smaller LV cavity, higher ratio of LVWT to diastolic diameter, a

208 Women showed smaller LV cavity size, greater concentricity, lower myocardial

209 otential differential effects along specific LV planes of deformation.

210 lume established short travel/low-volume (ST/LV) and long travel/high-volume (LT/HV) cohorts.

211 with changes in global longitudinal strain, LV twisting-untwisting (P<0.05).

212 Following RF-RDN in both strains, LV ejection fraction remained significantly above those

213 inal strain (GLS) is a marker of subclinical LV dysfunction.

214 e relationship between strain and subsequent LV outcomes, and (3) assessed the relationship between s

215 Additionally, patients with symptomatic LV dysfunction had higher odds of lateral precordial T-w

216 Synchronized LV pacing, multisite LV pacing, and LV endocardial pacin

217 Measures of systolic LV function such as the ejection intraventricular pressu

218 M, 6 F, mean 15.9 years) revealed long-term LV abnormalities in IUGR offspring.

219 ulation, providing preliminary evidence that LV twist mechanics may be more sensitive to adrenergic c

220 Our data show that LV-mediated GT for patients with OS significantly amelio

221 Moreover, we showed that LV-FKRP cells were driven to release exosomes carrying F

222 In stratified analyses, the LV rehabilitation group with BCDVAbetter-eye worse than

223 However, the LV rehabilitation group improved more in all visual func

224 and characterize PW1-expressing cells in the LV myocardium in normal and ischemic conditions 7 days a

225 a time-shift in microglial activation in the LV-wall adhesions between age-grouped PV-KO and wild-typ

226 TRAF3IP2 antisense oligonucleotides into the LV in a clinically relevant time frame significantly inh

227 stances between the epicardial border of the LV apex and the midpoint of a line connecting the origin

228 Systematic characterization of the LV epicardial/endocardial scar distribution and density

229 The findings demonstrate that the LV filling forces are more orthogonal to the main LV flo

230 63%) undergoing a retrograde approach to the LV developed at least 1 new brain lesion.

231 How RASA1 mutations lead to the LV leakage defects that occur in CM-AVM is not understoo

232 ontribute not only to the SV but also to the LV, atria and OFT and are found also in the dorsal splan

233 a greater extent in perfused hearts when the LV performs pressure-volume work.

234 vity; (3) homogeneous propagation within the LV cavity; and (4) latest activation at the basal latera

235 Surprisingly, in adult mice, the LVs showed regression after VEGF-C or VEGFR3 deletion, a

236 the-art self-inactivating lentiviral vector (LV-w1.6 WASp) has resulted in significant clinical benef

237 The lateral ventricle (LV) is a preferential location for brain tumor spread; h

238 ely evaluate the accuracy of left ventricle (LV) analysis with a two-dimensional real-time cine true

239 ibutors to remodeling of the left ventricle (LV) have been well studied in general population cohorts

240 Remodeling of the left ventricle (LV) in response to pressure overload leads to the re-exp

241 determine if excess greater left ventricle (LV) trabeculation is associated with decreased average r

242 hypertrophy, a thick-walled left ventricle (LV) ultimately transitions to a dilated cardiomyopathy.

243 nts because of dysfunctional left ventricle (LV).

244 Patients undergoing left ventricular (LV) ablation were compared with a control group of those

245 We sought to compare left ventricular (LV) activation patterns in heart failure patients with n

246 e gene networks to prevent left ventricular (LV) adverse remodeling.

247 In left ventricular (LV) biopsies from patients undergoing coronary artery by

248 Our left ventricular (LV) CMRI studies in IUGR baboons (8 M, 8 F, 5.7 years -

249 MAPKs and Akt occurred in left ventricular (LV) CMs, requiring both C5a receptors, C5aR1 and -2.

250 are known determinants of left ventricular (LV) diastolic function.

251 apitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left atrial infarction

252 Preserved left ventricular (LV) ejection fraction (EF) and reduced myocardial strain

253 rditis (AM) with preserved left ventricular (LV) ejection fraction (EF).

254 respectively) and included left ventricular (LV) ejection fraction, infarct size, and microvascular o

255 volumes, and lower RV and left ventricular (LV) ejection fractions compared with controls.

256 ction develop increases in left ventricular (LV) end-diastolic pressures during exercise that contrib

257 positively associated with left ventricular (LV) fractional shortening (z-score for difference = 1.07

258 nt presenting with reduced left ventricular (LV) function following a recent MI.

259 rction affects recovery of left ventricular (LV) function.

260 right ventricular (RV) and left ventricular (LV) function.

261 ampsia impacts clinical or left ventricular (LV) functional outcomes.

262 Left ventricular (LV) global longitudinal strain (GLS) is a marker of subc

263 Left ventricular (LV) hypertrophy and abnormal myocardial strain predict m

264 mapping was used to assess left ventricular (LV) interstitial diffuse fibrosis.

265 value of a simple index of left ventricular (LV) long-axis function-lateral mitral annular plane syst

266 Increased left ventricular (LV) mass and diastolic dysfunction are associated with c

267 vascular risk factors, and left ventricular (LV) mass were performed to examine the association of lo

268 STRACT: Sex differences in left ventricular (LV) mechanics exist at rest and during acute physiologic

269 POINTS: Sex differences in left ventricular (LV) mechanics occur during acute physiological challenge

270 and afterward to estimate left ventricular (LV) metabolic rate of glucose (MRGlu).

271 Left ventricular (LV) morphology and systolic and diastolic function were

272 s beyond the reflection of left ventricular (LV) pathology are not well understood.

273 condition on preoperative left ventricular (LV) remodeling and myocardial fibrosis and postoperative

274 Advanced age is related to left ventricular (LV) remodeling.

275 this study was to examine left ventricular (LV) strain ()-volume loops to provide novel insight into

276 was calculated by dividing left ventricular (LV) stroke volume by LV myocardial volume, and long-axis

277 ysis included 16 traits of left ventricular (LV) structure, and systolic and diastolic function.

278 Left ventricular (LV) systolic dysfunction and moderate aortic stenosis (A

279 - 12 years) complicated by left ventricular (LV) systolic dysfunction; (2) an age- and sex- matched h

280 primary outcome measures: left ventricular (LV) systolic function (left ventricular ejection fractio

281 ic indices to characterize left ventricular (LV) systolic function and its relationship to activation

282 ract dimension, and RV and left ventricular (LV) systolic function were determined by RV fractional a

283 sought to compare maximal left ventricular (LV) wall thickness (WT) measurements as obtained by rout

284 es would be more severe in left ventricular (LV) working hearts (LWHs) than Langendorff (LANG) perfus

285 d they become darkly stained large vesicles (LVs) after release from the Golgi.

286 on (CM-AVM) is a blood and lymphatic vessel (LV) disorder that is caused by inherited inactivating mu

287 nt discovery of meningeal lymphatic vessels (LVs) has raised interest in their possible involvement i

288 iastolic septal thickness were lower whereas LV contractility and LV fractional shortening were highe

289 ing redo AVR, we sought to determine whether LV-GLS provides incremental prognostic use.

290 eover, an increase in FM was associated with LV concentric remodeling and impairment of systolic and

291 ereas an increase in FFM was associated with LV eccentric remodeling and improved systolic and diasto

292 attern was evident, which is associated with LV outflow tract obstruction loss and right ventricle sy

293 banalyses, the associations of DeltaLAV with LV mass parameters were driven by associations with base

294 HCM patients with LV apical aneurysms are at high risk for arrhythmic sudd

295 dent predictor of mortality in patients with LV dysfunction, incremental to common clinical and cardi

296 Patients with LV thrombus at 6 months were restudied at 1 year.

297 ollow-up of 181 weeks +/- 168, patients with LV thrombus displayed a very low rate of stroke (0%), pe

298 own SES in adulthood, the relationship with LV mass (differences [95% CI], 1.5 [0.2 to 2.8] for low

299 asing SMR severity was associated with worse LV function.

300 er body mass index was associated with worse LV longitudinal strain, radial strain (apical view), and