ライフサイエンスコーパス: left ventricular

1 vaging jeopardized myocardium and preventing left ventricular adverse remodeling and functional deter

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

3 pulmonary artery diameter z score, the right/left ventricular and pulmonary artery/ascending aorta di

4 of atrial fibrillation (AF) risk, including left ventricular and pulmonary pathology, systemic infla

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

6 Asp in a large Spanish family with inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia

7 p.Glu401Asp mutation as a cause of inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia

8 Timing of left ventricular assist device (LVAD) implantation in ad

9 tive of mortality after continuous flow (CF) left ventricular assist device (LVAD) implantation.

10 Mechanical circulatory support with a left ventricular assist device (LVAD) is an established

11 tribute to positive or negative outcomes for left ventricular assist device (LVAD) patients remains u

12 giodysplasia develops during continuous-flow left ventricular assist device (LVAD) support.

13 advanced heart failure patients selected for left ventricular assist device (LVAD) were more likely t

14 activity in patients with end-stage HF after left ventricular assist device (LVAD)-induced remodeling

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

16 Assessment and Comparative Effectiveness of Left Ventricular Assist Device and Medical Management) d

17 biopsies of multiple HF patients undergoing left ventricular assist device implantation surgery.

18 t common complications after continuous-flow left ventricular assist device implantation.

19 ective analysis evaluated 51 continuous-flow left ventricular assist device patients who received sec

20 rs had a previous GI bleeding history before left ventricular assist device placement (33% versus 5%;

21 Patients with continuous-flow left ventricular assist device receiving secondary proph

22 Left ventricular assist device-supported patients are us

23 routinely discarded during implantation of a left ventricular assist device.

24 overy in response to mechanical unloading by left ventricular assist devices (LVADs) has been demonst

25 Left ventricular assist devices (LVADs) have been used a

26 Continuous-flow left ventricular assist devices (LVADs) have revolutioni

27 Improved safety of left ventricular assist devices means that these are bec

28 t failure receiving mechanical unloading via left ventricular assist devices show increased CTCF abun

29 The HeartMate 3 (HM3) Left Ventricular Assist System (LVAS) (Abbott) is a cent

30 a functional counterpart of transient apical left ventricular ballooning.

31 RNA-146a levels were moderately increased in left ventricular biopsies of patients with aortic stenos

32 Left ventricular biopsies were obtained from 5 donors an

33 epigenome-wide mapping of DNA methylation in left-ventricular biopsies and whole peripheral blood of

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

35 lar capture threshold (4%), and increases in left ventricular capture threshold (3%).

36 pertrophy is also frequently associated with left ventricular diastolic dysfunction.

37 Although age-associated changes in left ventricular diastolic function are well recognized,

38 of CD4(+) T cells and prevented progressive left ventricular dilatation and hypertrophy, whereas ado

39 Left ventricular dilation and loss of heart function was

40 r age, congestive heart failure, and greater left ventricular dilation at diagnosis were independentl

41 Trpc6 deletion also ameliorated left ventricular dilation, improved cardiac function, an

42 ction fraction, left ventricular mass index, left ventricular dimension, deceleration time, left atri

43 y was associated with larger left atrial and left ventricular dimensions (p < 0.05).

44 Mean heart doses and mean left ventricular doses (MLVD) were estimated by reconstr

45 erwent successful stenting for STEMI and had left ventricular dysfunction (ejection fraction</=48%) >

46 y the potential negative interaction between left ventricular dysfunction (LVD) and MSC activation.

47 ablated the interferon response and improved left ventricular dysfunction and survival.

48 diomyocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, whereas genetic kn

49 fety and potential efficacy in patients with left ventricular dysfunction post STEMI who are at risk

50 S10) intracoronary infusion in patients with left ventricular dysfunction post STEMI.

51 s) from donor mice with HF induced long-term left ventricular dysfunction, fibrosis, and hypertrophy

52 Left ventricular dysfunction, mediated by ventricular in

53 ve generally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the t

54 occurs in the myocardium and correlates with left ventricular dysfunction.

55 rget DLST are important metabolic players in left ventricular dysfunction.

56 yocardial infarction characterized by severe left ventricular dysfunction.

57 include progressive heart failure and severe left ventricular dysfunction.

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

59 t Association class II to IV symptoms, and a left ventricular EF of 40% or less to treatment with ena

60 nt effects were found on secondary outcomes: left ventricular EF, peak aerobic exercise capacity, and

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

62 Among those with a left ventricular ejection fraction >35% (N=121; mean lef

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

64 atment and control groups in HFrEF patients (left ventricular ejection fraction </=40%).

65 in patients with coronary artery disease and left ventricular ejection fraction </=40%.

66 We studied patients with systolic HF (left ventricular ejection fraction </=45%) and mild to m

67 e Registry and divided them into SHIFT type (left ventricular ejection fraction <40%, New York Heart

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

69 ng ViV, 72 patients undergoing ViR had lower left ventricular ejection fraction (45.6 +/- 17.4% vs. 5

70 .14, SE=0.23), % females (B=-0.38, SE=0.04), left ventricular ejection fraction (B=-0.81, SE=0.20), a

71 Improvement in left ventricular ejection fraction (EF) to >35% occurs i

72 of patients with heart failure with reduced left ventricular ejection fraction (HFrEF) and is an ind

73 f sudden cardiac death (SCD) in those with a left ventricular ejection fraction (LVEF) <35%.

74 terial coupling, and their associations with left ventricular ejection fraction (LVEF) and heart fail

75 etermination of left ventricular volumes and left ventricular ejection fraction (LVEF).

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

77 tic relative area change was associated with left ventricular ejection fraction (P=0.045) and ventric

78 e prospectively enrolled (age 62+/-11 years, left ventricular ejection fraction 27+/-7%).

79 patients (121 men), aged 67.4+/-11.9 years, left ventricular ejection fraction 33.1+/-13.6% (n=137),

80 patients (39%; 73% men; age, 41+/-25 years; left ventricular ejection fraction 49+/-16%) with high i

81 8) showed significantly reduced LV systolic (left ventricular ejection fraction = 49+/-10% versus 58+

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

83 , and identified 472 donor hearts with LVSD (left ventricular ejection fraction [LVEF] </=40%) on ini

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

85 was observed with echocardiography (baseline left ventricular ejection fraction [LVEF], 61%; global l

86 ed significantly with MR imaging measures of left ventricular ejection fraction and end-systolic volu

87 who would otherwise benefit on the basis of left ventricular ejection fraction and heart failure sym

88 Despite normal left ventricular ejection fraction and serum biomarkers,

89 group exhibited significant improvements in left ventricular ejection fraction at 3, 6, and 12 month

90 Echocardiographic left ventricular ejection fraction change from baseline

91 nd provides incremental value in addition to left ventricular ejection fraction for the prediction of

92 the trastuzumab group had a > 10% decline in left ventricular ejection fraction from baseline to a va

93 20% of patients with severe AS and preserved left ventricular ejection fraction have Vmax in this ran

94 ng revealed a significantly decreased global left ventricular ejection fraction in parallel with incr

95 d 12 months, there was a greater increase in left ventricular ejection fraction in patients taking iv

96 [15.8], P=0.02) and no significant change of left ventricular ejection fraction in the cell group.

97 Patients with a left ventricular ejection fraction less than or equal to

98 nd safety of levosimendan in patients with a left ventricular ejection fraction of 35% or less who we

99 However, PPM is associated with impaired left ventricular ejection fraction recovery post-transca

100 Left ventricular ejection fraction remains the primary r

101 onary disease and heart failure with reduced left ventricular ejection fraction undertook, after care

102 ; mean age was 64 years, 75% were male, mean left ventricular ejection fraction was 32%, and peak VO2

103 onischemic dilated cardiomyopathy), the mean left ventricular ejection fraction was 32+/-12% (range,

104 were of other race/ethnicity, and the median left ventricular ejection fraction was 34%.

105 The left ventricular ejection fraction was consistently decr

106 We observed that the improvement in left ventricular ejection fraction was significantly gre

107 ic frequency methods can be used to document left ventricular ejection fraction with accuracy compara

108 es: left ventricular (LV) systolic function (left ventricular ejection fraction), LV diastolic functi

109 tricular ejection fraction >35% (N=121; mean left ventricular ejection fraction, 45+/-6%), RV dysfunc

110 negative relationships with age, female sex, left ventricular ejection fraction, and body mass index.

111 Ivabradine treatment improved left ventricular ejection fraction, and clinical status

112 the occurrence of atrial arrhythmias and low left ventricular ejection fraction, as estimated using m

113 prediction algorithm composed of RBP4, TTR, left ventricular ejection fraction, interventricular sep

114 Although usually associated with reduced left ventricular ejection fraction, isolated RV systolic

115 rate, hypertension, systolic blood pressure, left ventricular ejection fraction, left ventricular mas

116 ond traditional cardiovascular risk factors, left ventricular ejection fraction, myocardial scar and

117 ation III/IV symptoms, transaortic gradient, left ventricular ejection fraction, or procedural charac

118 differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypoca

119 justment were increasing age, lower baseline left ventricular ejection fraction, worse post-procedura

120 ardiac arrest do not have a markedly reduced left ventricular ejection fraction.

121 which occur in the setting of more preserved left ventricular ejection fraction.

122 for patients with heart failure with reduced left ventricular ejection fraction.

123 particularly in those with severely reduced left ventricular ejection fraction.

124 congestion, but no significant difference in left ventricular ejection fraction.

125 nterval, 1.09-2.07), but not with decline in left ventricular ejection fraction.

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

127 f LVAD implantation predicted high post-LVAD left ventricular ejection fractions (P<0.01) and ejectio

128 oducibility were assessed on measurements of left ventricular end-diastolic dimension, area, and volu

129 pigs developed HF as evidenced by increased left ventricular end-diastolic pressure and left ventric

130 Although left ventricular end-diastolic pressure decreased in 45/

131 cardial function (ejection fraction [EF] and left ventricular end-diastolic pressure) was assessed at

132 ared with placebo, a significant decrease in left ventricular end-diastolic volume (-18 mL; P=0.009)

133 vated B-type natriuretic peptide, and larger left ventricular end-diastolic volume index.

134 age, congestive heart failure, and increased left ventricular end-systolic dimension zscore at diagno

135 METHOD AND In 7 sheep, left ventricular endocardial and transmural mapping was

136 entricle-right ventricle pairs (P=0.021) and left ventricular epicardium (P=0.08).

137 st serious side effects were exacerbation of left ventricular failure in patients with congestive hea

138 ot correlate with myocardial Gal-3 levels or left ventricular fibrosis, whereas a positive correlatio

139 Nitroprusside reduces afterload and left ventricular filling pressures in patients with LGSA

140 ersus 78%, P<0.001), had less-depressed mean left ventricular fractional shortening z scores (-7.85+/

141 33% vs. 14%; p = 0.0027, respectively), and left ventricular function </=35% (26% vs. 10%; p = 0.007

142 myocardial infarction complicated by reduced left ventricular function and HF.

143 ited more adverse cardiac remodeling, poorer left ventricular function and higher mortality by increa

144 and iPSC-EV-treated mice exhibited improved left ventricular function at 35 d after myocardial infar

145 ession and CVB3 copy number, and an improved left ventricular function in NOD2(-/-) CVB3 mice compare

146 icity, sex, comorbidities, insurance status, left ventricular function, and aortic stenosis severity

147 assessment reveals normal coronary arteries, left ventricular function, and resting ECG.

148 ymptomatic severe aortic stenosis and normal left ventricular function, current practice guidelines e

149 raphics, risk factors, coronary anatomy, and left ventricular function, end-systolic volume index and

150 Improvements in left ventricular function, functional status, and qualit

151 perior cardiac repair in vivo with regard to left ventricular function, vascularization, and ameliora

152 ffect blood pressure, systolic, or diastolic left ventricular function.

153 dity and mortality in patients with impaired left ventricular function.

154 ICD implantation on the basis of symptoms or left ventricular function.

155 tural and functional remodeling and improves left ventricular functional reserve.

156 Left ventricular global longitudinal strain (GLS) and le

157 mbrane-permeabilized cardiomyocytes in human left ventricular heart tissue.

158 Asymptomatic left ventricular hypertrabeculation, the mildest end of

159 n conclusion, we report the first example of left ventricular hypertrabeculation/LVNC with germline M

160 ystolic strain in hypertensive patients with left ventricular hypertrophy (HTN LVH) and hypertensive

161 1 in the DT (FGFR1(DT-cKO) mice) resulted in left ventricular hypertrophy (LVH) and decreased kidney

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

163 d would lead to more lowering of the risk of left ventricular hypertrophy (LVH) in patients with hype

164 rophic myocyte growth and the development of left ventricular hypertrophy (LVH) in rodents.

165 cardiac AL amyloidosis, asymmetrical septal left ventricular hypertrophy (LVH) was present in 79% of

166 RAF1 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced

167 associated with worse allograft function and left ventricular hypertrophy (LVH).

168 e free from CVD and underwent measurement of left ventricular hypertrophy by ECG, coronary artery cal

169 sure overload-induced cardiac stress induces left ventricular hypertrophy driven by increased cardiom

170 l of transverse aortic constriction in which left ventricular hypertrophy occurred by 2 weeks without

171 a genetic disorder that is characterized by left ventricular hypertrophy unexplained by secondary ca

172 conventional paradigm of the progression of left ventricular hypertrophy, a thick-walled left ventri

173 ic with structural abnormalities, defined as left ventricular hypertrophy, dilation or dysfunction, o

174 HRadjBMI and BMI were associated with higher left ventricular hypertrophy, glycemic traits, interleuk

175 mily A and family B men >30 years of age had left ventricular hypertrophy, which was mainly asymmetri

176 All patients showed asymmetrical left ventricular hypertrophy, with maximal left ventricu

177 cretion, has been inconsistently linked with left ventricular hypertrophy.

178 : vascular dysfunction; arterial stiffening; left ventricular hypertrophy; and worsened metrics of di

179 Echocardiography showed left ventricular hypokinesis.

180 An increase in left ventricular interstitial collagen deposition and a

181 icle predominate, it is well recognized that left ventricular involvement is common, particularly in

182 Our findings suggest that left ventricular longitudinal relaxation velocity declin

183 We sought to compare left ventricular (LV) activation patterns in heart failu

184 of cardioprotective gene networks to prevent left ventricular (LV) adverse remodeling.

185 In left ventricular (LV) biopsies from patients undergoing

186 Our left ventricular (LV) CMRI studies in IUGR baboons (8 M,

187 ogy, activation of MAPKs and Akt occurred in left ventricular (LV) CMs, requiring both C5a receptors,

188 d restoring forces are known determinants of left ventricular (LV) diastolic function.

189 I swine models recapitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left

190 Preserved left ventricular (LV) ejection fraction (EF) and reduced

191 ied in acute myocarditis (AM) with preserved left ventricular (LV) ejection fraction (EF).

192 d n=458 patients, respectively) and included left ventricular (LV) ejection fraction, infarct size, a

193 mean 148 mL/m(2)) volumes, and lower RV and left ventricular (LV) ejection fractions compared with c

194 erved ejection fraction develop increases in left ventricular (LV) end-diastolic pressures during exe

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

196 ained from a patient presenting with reduced left ventricular (LV) function following a recent MI.

197 on myocardial infarction affects recovery of left ventricular (LV) function.

198 ended to quantify right ventricular (RV) and left ventricular (LV) function.

199 own whether preeclampsia impacts clinical or left ventricular (LV) functional outcomes.

200 Left ventricular (LV) global longitudinal strain (GLS) i

201 Left ventricular (LV) hypertrophy and abnormal myocardia

202 ar (n = 1131), T1 mapping was used to assess left ventricular (LV) interstitial diffuse fibrosis.

203 te the prognostic value of a simple index of left ventricular (LV) long-axis function-lateral mitral

204 Increased left ventricular (LV) mass and diastolic dysfunction are

205 mographics, cardiovascular risk factors, and left ventricular (LV) mass were performed to examine the

206 KEY POINTS: Sex differences in left ventricular (LV) mechanics occur during acute physi

207 mal PET beforehand and afterward to estimate left ventricular (LV) metabolic rate of glucose (MRGlu).

208 Left ventricular (LV) morphology and systolic and diasto

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

210 the impact of NFLG condition on preoperative left ventricular (LV) remodeling and myocardial fibrosis

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

212 CT: The purpose of this study was to examine left ventricular (LV) strain ()-volume loops to provide

213 on fraction (MCF) was calculated by dividing left ventricular (LV) stroke volume by LV myocardial vol

214 The analysis included 16 traits of left ventricular (LV) structure, and systolic and diasto

215 3% male, age 54 +/- 12 years) complicated by left ventricular (LV) systolic dysfunction; (2) an age-

216 phy, we assessed 3 primary outcome measures: left ventricular (LV) systolic function (left ventricula

217 st echocardiographic indices to characterize left ventricular (LV) systolic function and its relation

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

219 We sought to compare maximal left ventricular (LV) wall thickness (WT) measurements a

220 that hypoxic changes would be more severe in left ventricular (LV) working hearts (LWHs) than Langend

221 sus 64%; P=0.99) and the proportion of total left ventricular mass (%late gadolinium enhancement; 10.

222 udinal strain (>15% improvement) and indexed left ventricular mass (>20% decrease) at 1 year occurred

223 54.1 years; p = 0.002) and had lower indexed left ventricular mass (5.1 g/m(2) reduction; padjusted =

224 (bioimpedance spectroscopy), 24-hour BP, and left ventricular mass (cardiac magnetic resonance imagin

225 uretic peptide, ejection fraction, E/E', and left ventricular mass (hazard ratio: 1.164; 95% confiden

226 The mean change in left ventricular mass index from randomization was simil

227 ressure, left ventricular ejection fraction, left ventricular mass index, left ventricular dimension,

228 agreement among the ECG criteria against the left ventricular mass index.

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

230 measured global longitudinal strain, indexed left ventricular mass, and indexed left atrial volume.

231 content is a strong explanatory variable for left ventricular mass, unaffected by BP and total body o

232 secondary objective was to assess changes in left ventricular mass.

233 f body composition and fat distribution, and left ventricular mass.

234 y, compared with dimension and area methods, left ventricular measurements by volume method have the

235 ours after study drug initiation, need for a left ventricular mechanical assist device or failure to

236 of prolonged catecholamine infusion, use of left ventricular mechanical assist device, or renal repl

237 stigated the distribution characteristics of left-ventricular myocardial strain using a novel cine MR

238 of variation measuring nonuniformity of the left ventricular myocardium activity distribution.

239 vator of transcription (STAT)5 activation in left ventricular myocardium is associated with RIPC s ca

240 Left ventricular NOD2 mRNA expression was also induced i

241 Left ventricular noncompaction (LVNC) can occur in isola

242 icular trabeculation satisfying criteria for left ventricular noncompaction (LVNC) on routine cardiac

243 In this review, left ventricular noncompaction cardiomyopathy, which is

244 al heart defect (CTD) case-parent trios, 317 left ventricular obstructive tract defect (LVOTD) case-p

245 cular arrhythmias (VAs) originating from the left ventricular outflow tract (LVOT), an alternative ap

246 e lower in the right ventricle (P=0.037) and left ventricular outflow tract (P<0.001) and higher in l

247 It is frequently accompanied by dynamic left ventricular outflow tract obstruction and symptoms

248 myofibers normally run in parallel along the left ventricular outflow tract, but in the Nkx2-5(+/-)/S

249 clusion on the velocity-time integral of the left ventricular outflow tract.

250 e pacing, His bundle pacing, and endocardial left ventricular pacing.

251 ter additional adjustment for the respective left ventricular parameter, higher RV ejection fraction

252 ic expansion during systole, which modulates left ventricular performance and impacts systemic hemody

253 (interventricular septum, 12+/-4 [7-23] mm; left ventricular posterior wall, 11+/-4 [7-21] mm; left

254 ardiography (n = 4 per group), and right and left ventricular pressure (n = 5 and n = 4 per group, re

255 We demonstrate that left ventricular pressure is closely linked to KATP chan

256 lenge (dobutamine 0.3-10 mug/kg/min) using a left ventricular pressure/volume catheter.

257 nce imaging, the rats were catheterized, and left ventricular pressures were recorded.

258 dial injury, and it is a strong predictor of left ventricular remodeling in ST-segment-elevation myoc

259 HIIT was not superior to MCT in changing left ventricular remodeling or aerobic capacity, and its

260 L [2380-3006 mL]; P<0.0001), more concentric left ventricular remodeling, greater right ventricular d

261 e biological changes responsible for adverse left ventricular remodeling, the relationship between in

262 and exerted a sustained beneficial effect on left ventricular remodeling.

263 ic myocardium and has been linked to adverse left ventricular remodeling.

264 ocardial injury and its predictive value for left ventricular remodeling.

265 of the heart were determined from CT and the left ventricular ROI, and mean counts were calculated us

266 ereas mice producing GM-CSF can succumb from left ventricular rupture, a complication mitigated by an

267 ), blood pressure (86% versus 39%; P<0.001), left ventricular size (96% versus 83%; P<0.001), right v

268 f intervention occurs after deterioration of left ventricular size and function.

269 chocardiographic methods are used to measure left ventricular size and function.

270 gional and chamber strains (namely segmental left ventricular strain, left atrial strain, and right v

271 , effective regurgitant orifice area [EROA], left ventricular stroke volume [LVSV]) and quality-of-li

272 he aortic forward flow volume from the total left ventricular stroke volume.

273 Left ventricular structure and function and cardiac trop

274 ion of Simple 7 metrics with incident HF and left ventricular structure and function by cardiac magne

275 linical CVD was defined by 10-year change in left ventricular structure and function.

276 , serological studies, socioeconomic status, left ventricular structure, and medications.

277 Left ventricular systolic dysfunction (LVSD) accounts fo

278 Atrial fibrillation (AF) and left ventricular systolic dysfunction (LVSD) frequently

279 mortality in patients with AMI without HF or left ventricular systolic dysfunction (LVSD).

280 dysfunction is more commonly associated with left ventricular systolic dysfunction, although isolated

281 t cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial in

282 aseline of conduction defects on the ECG and left ventricular systolic dysfunction.

283 fication and echocardiographic assessment of left ventricular systolic function were addressed at fol

284 eased myocardial fibrosis and improvement of left ventricular systolic function.

285 res termed sheetlets that reorientate during left ventricular thickening.

286 l left ventricular hypertrophy, with maximal left ventricular thickness in the basal septum (19-31 mm

287 Emc10 expression was also increased in left ventricular tissue samples from patients with acute

288 ha-smooth muscle actin or collagen 1alpha in left ventricular tissue sections of IL10KO chimeric mice

289 te gadolinium enhancement in phenotyping the left ventricular to identify those at highest risk for S

290 g negative correlation was found between the left ventricular total isovolumic time and stroke volume

291 Presence of prominent left ventricular trabeculation satisfying criteria for l

292 higher pulmonary venous pressure relative to left ventricular transmural pressure, and greater left v

293 at SRC-2 CKO mice exhibit markedly decreased left ventricular vasculature in response to transverse a

294 left ventricular end-diastolic pressure and left ventricular volume indexes.

295 There was a significant reduction of left ventricular volumes (end-systolic volume: -4.3 [11.

296 e and post-cycle 17 for the determination of left ventricular volumes and left ventricular ejection f

297 ng of these 2 groups were similar, including left ventricular volumes, mass, maximal wall thickness,

298 que were implanted into the anterior-lateral left ventricular wall in C57BL/6J (allogeneic model, n =

299 characterize microstructural dynamics during left ventricular wall thickening, and apply the techniqu

300 ined ventricular tachycardia (nsVT), maximum left ventricular wall thickness and obstruction were sig