ライフサイエンスコーパス: LVH

1 LVH classification was discordant between modalities in

2 LVH, elevated LV filling pressure, and abnormal myocardi

3 LVH- FD had lower stress MBF than controls (2.36 versus

4 8 years among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0

5 Treatment changed the prevalence of 4 LVH groups to 23%, 4%, 5%, and 7%; 62% had normal LVM af

6 H+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001).

7 us 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001).

8 Currently accepted LVH ECG criteria such as Cornell voltage and Sokolow-Lyo

9 arly cardiac involvement and distinguish AFD LVH from other causes.

10 cidence of HF or CV death over 8 years among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT

11 On multivariable analyses, LVH was predictive for higher 30-day mortality compared

12 he composite end point in adjusted analysis (LVH hazard ratio [HR], 3.0; 95% confidence interval [CI]

13 By multivariable analysis, LVH was associated with increased 30-day mortality for a

14 n LVH and cTnT (p(interaction) = 0.0005) and LVH and NT-proBNP (p(interaction) = 0.014) were highly s

15 VH (hazard ratio 1.25, 95% CI 1.19-1.31) and LVH (hazard ratio 1.35, 95% CI 1.29-1.42) were associate

16 us studies of the association between AF and LVH were based primarily on echocardiographic measures o

17 (Allopurinol in Patients with Diabetes and LVH; UKCRN 8766).

18 suggested as a promotor of hypertension and LVH.

19 dy was conducted in 66 patients with IHD and LVH, comparing 600 mg/day allopurinol versus placebo the

20 ndothelial function in patients with IHD and LVH.

21 ), and 7.8 (3.1-15.5) miles to HVH, IVH, and LVH, respectively.

22 associated with increased blood pressure and LVH.

23 flow response with blood pressure status and LVH.

24 regression of LVM in patients with T2DM and LVH.

25 y mortality was higher for all resections at LVH, but only for proctectomies at IVH.

26 h 41.5%, 7.2%, and 51.3% patients treated at LVH, MVH, and HVH, respectively.

27 ) normalized BP and significantly attenuated LVH in the Hyp mouse model of excess FGF-23, but did not

28 rly, among SPRINT participants with baseline LVH (n=605, 7.4%), those assigned to the intensive (vers

29 Among SPRINT participants without baseline LVH (n=7559), intensive (versus standard) BP lowering wa

30 The interaction between LVH, low but detectable cardiac troponin T (cTnT), and e

31 The interactions between LVH and cTnT (p(interaction) = 0.0005) and LVH and NT-pr

32 images are suboptimal or suggest borderline LVH.

33 In both LVH and sham hearts, all phosphorylation states were sig

34 ion states were significantly populated, but LVH hearts showed a significant decrease in U-PLB, with

35 CMR-LVH was defined as left ventricular mass >/=95th percent

36 Lyon voltage product after adjusting for CMR-LVH (HR: 1.83, 95% CI: 1.06 to 3.14, p = 0.02).

37 The associations with AF for CMR-LVH and Sokolow-Lyon voltage product were attenuated whe

38 prognostic signi fi cance independent of CMR-LVH.

39 n(-1).m(-)(0.92); P=6x10(-5)) and concentric LVH (log likelihood, -9.9; P=0.001), independently of kn

40 concentric LV remodelling (cLVR), concentric LVH (cLVH), and eccentric LVH (eLVH).

41 individuals (14%) exhibited mild concentric LVH mimicking physiological LVH.

42 e conventional gray zone of mild, concentric LVH.

43 nearly 30% greater in LVH than in controls (LVH stiffness constant, 0.053+/-0.027 versus controls, 0

44 was greater in participants with CMR-derived LVH (hazard ratio [HR]: 2.04, 95% confidence interval [C

45 AF was associated with ECG-derived LVH measure of Sokolow-Lyon voltage product after adjust

46 iovascular disease, both CMR and ECG-derived LVH were associated with incident AF.

47 sociated with a 46% lower risk of developing LVH (hazard ratio=0.54; 95% confidence interval, 0.43-0.

48 d and both concentric nondilated and dilated LVH had increased risks of all-cause or cardiovascular m

49 (cLVR), concentric LVH (cLVH), and eccentric LVH (eLVH).

50 ECG-LVH showed prognostic signi fi cance independent of CMR-

51 ECG-LVH was defined by Cornell voltage criteria.

52 ECG-LVH was present in 4.2% (N=312) of the participants, of

53 Concomitant presence of prolonged-QT and ECG-LVH carries a higher risk than either predictor alone.

54 as highest in the group with concomitant ECG-LVH and prolonged-QTa (hazard ratio, 1.63; 95% confidenc

55 Eleven ECG-LVH criteria were assessed.

56 e ECG with left ventricular hypertrophy (ECG-LVH).

57 terval, 1.12-2.36), followed by isolated ECG-LVH (1.48; 1.24-1.77), and then isolated prolonged-QTa (

58 se mortality for various combinations of ECG-LVH and prolonged-QTa.

59 n explain the prognostic significance of ECG-LVH, and whether prolonged-QT coexisting with ECG-LVH sh

60 considered as an innocent consequence of ECG-LVH.

61 In models with similar adjustment where ECG-LVH and prolonged-QTa were entered as 2 separate variabl

62 tic peptide) <100 pg/mL), and those with ECG-LVH and abnormal levels of either biomarker (malignant L

63 roups: those without ECG-LVH, those with ECG-LVH and normal biomarkers (hs-cTnT (high sensitivity car

64 t extent QT prolongation coexisting with ECG-LVH can explain the prognostic significance of ECG-LVH,

65 and whether prolonged-QT coexisting with ECG-LVH should be considered as an innocent consequence of E

66 odel and compared with the group without ECG-LVH or prolonged-QTa, mortality risk was highest in the

67 classified into 3 groups: those without ECG-LVH, those with ECG-LVH and normal biomarkers (hs-cTnT (

68 fic blockade of FGFR4 attenuates established LVH in the 5/6 nephrectomy rat model of CKD.

69 of regression of LVH in those with existing LVH.

70 Compared with LVH- FD, LVH+ FD had higher left ventricular ejection fraction (7

71 Adjustment for LVH as a time-varying covariate did not substantially at

72 , 0.65-0.91] before and after adjustment for LVH as a time-varying covariate, respectively).

73 was compared before and after adjustment for LVH as a time-varying covariate.

74 .0 +/- 7.7 versus 15.9 +/- 6.9 ml/kg/min for LVH (p < 0.0001).

75 n combined) was an independent predictor for LVH among patients not receiving antihypertensive treatm

76 xpression of the mutant gene is required for LVH or whether early gene expression acts as an immutabl

77 aging mice lacking FGFR4 are protected from LVH.

78 lar magnetic resonance was performed on 40 G+LVH- patients (33+/-15 years, 38% men), 67 patients with

79 Compared with controls, G+LVH- patients also had a higher frequency of clefts (28%

80 iers without left ventricular hypertrophy (G+LVH-) but are difficult to quantify.

81 In G+LVH+ and G-LVH+ cohorts, maximal apical fractal dimensio

82 In G+LVH- patients, apical left ventricular trabeculation was

83 magnetic resonance images are abnormal in G+LVH- patients, providing a preclinical marker of disease

84 s, 76% men; 31 with a pathogenic mutation [G+LVH+]), and 69 matched healthy volunteers (44+/-15 years

85 pre-LVH (genotype positive, LVH negative [G+LVH-]).

86 ls (P<0.0001) irrespective of gene status (G+LVH+: 1.370+/-0.08; G-LVH+: 1.380+/-0.09).

87 The G+LVH- sample (n=73) was 29 +/- 13 years old and 51% were

88 In this G+LVH- population, cardiac myosin-binding protein C mutati

89 G+/LVH- individuals demonstrated altered cardiac dimensions

90 [SD] age at baseline, 27 [14] years), 55 G+/LVH- (20 [10] years), and 42 G-/LVH- (18 [8] years).

91 rformed in 178 participants, including 81 G+/LVH+ (mean [SD] age at baseline, 27 [14] years), 55 G+/L

92 ed in patients with overt HCM, as well as G+/LVH- mutation carriers (ECV=0.36+/-0.01, 0.33+/-0.01, 0.

93 as having 74% accuracy in discriminating G+/LVH- participants from controls.

94 f overt patients with HCM but absent from G+/LVH- subjects.

95 as 4.9 (0.2) phenotypes per individual in G+/LVH+, 2.4 (0.2) in G+/LVH-, and 1.3 (0.2) in controls (P

96 =0.36+/-0.01, 0.33+/-0.01, 0.27+/-0.01 in G+/LVH+, G+/LVH-, controls, respectively; P</=0.001 for all

97 e systematically compared echo and CMR in G+/LVH- subjects.

98 s per individual in G+/LVH+, 2.4 (0.2) in G+/LVH-, and 1.3 (0.2) in controls (P < .001).

99 Mutation carriers with LVH (G+/LVH+), mutation carriers without LVH (G+/LVH-), and heal

100 Sarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), patients wi

101 imaging of mutation carriers without LVH (G+/LVH-) to monitor for phenotypic evolution, but the optim

102 (G+/LVH+), mutation carriers without LVH (G+/LVH-), and healthy related control individuals (G-/LVH-)

103 with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), patients with HCM without mutations (sarcom

104 .01, 0.33+/-0.01, 0.27+/-0.01 in G+/LVH+, G+/LVH-, controls, respectively; P</=0.001 for all comparis

105 tive of gene status (G+LVH+: 1.370+/-0.08; G-LVH+: 1.380+/-0.09).

106 In G+LVH+ and G-LVH+ cohorts, maximal apical fractal dimension was great

107 ears), 55 G+/LVH- (20 [10] years), and 42 G-/LVH- (18 [8] years).

108 and healthy related control individuals (G-/LVH-) were enrolled through HCMNet sites.

109 f subsequent adverse events in a new 4-group LVH classification based on LV dilatation (high LV end-d

110 he patients had masked hypertension, 32% had LVH, and 38% had estimated glomerular filtration rate le

111 At 20 mo, the SHR had LVH characterized by decreased LVEF and increased EDV, w

112 IQR: 2.3 to 13.9 years), 71% of subjects had LVH, 29% had AF, 21% required de novo pacemakers (median

113 abnormal in 40% of subjects who did not have LVH.

114 In athletes with HCM, LVH was frequently (36%) confined to the apex and only 1

115 y cohort were created: low-volume hospitals (LVH) for both PD and PAO, mixed-volume hospital (MVH) wi

116 spectrum of phenotypic manifestations or how LVH influences disease expression.

117 T1 mapping was performed in 13 HTN LVH (mean age, 56.23 +/- 3.30 years), 17 HTN non-LVH (me

118 ients with left ventricular hypertrophy (HTN LVH) and hypertensive patients without LVH (HTN non-LVH)

119 for the evaluation of fibrosis extent in HTN LVH and HTN non-LVH, while native T1 has limited value.

120 pertensive left ventricular hypertrophy (HTN-LVH) is a leading cause of heart failure.

121 RI was similar in HTN-LVH/low RI and heart failure with preserved ejection fra

122 9.5%), patients with HTN-LVH and low RI (HTN-LVH/low RI; n=15, 5.9%) had an amplified myocardial resp

123 d normal RI (n=50; 19.5%), patients with HTN-LVH and low RI (HTN-LVH/low RI; n=15, 5.9%) had an ampli

124 ithout LVH (n=191; 74.6%) and those with HTN-LVH and normal RI (n=50; 19.5%), patients with HTN-LVH a

125 t adequately risk-stratify patients with HTN-LVH.

126 Akt activation induces cardiac hypertrophy (LVH), which may lead to heart failure.

127 LV hypertrophy (LVH) is common in patients with IHD including normotensi

128 tions and left ventricular (LV) hypertrophy (LVH) are cardinal features of hypertrophic cardiomyopath

129 athological left ventricle (LV) hypertrophy (LVH) results in reactive and replacement fibrosis.

130 e) resulted in left ventricular hypertrophy (LVH) and decreased kidney expression of alpha-Klotho in

131 dividuals with left ventricular hypertrophy (LVH) and elevated cardiac biomarkers in middle age are a

132 as a model of left ventricular hypertrophy (LVH) and failure.

133 Left ventricular hypertrophy (LVH) and late gadolinium enhancement (LGE) were independ

134 rate or severe left ventricular hypertrophy (LVH) and paired measurements of LVMi at baseline and 1 y

135 capacity with left ventricular hypertrophy (LVH) and systolic/diastolic dysfunction in asymptomatic

136 ing idiopathic left ventricular hypertrophy (LVH) and/or fibrosis (n = 59, 16%); arrhythmogenic right

137 d pathological left ventricular hypertrophy (LVH) are of intense interest.

138 dividuals with left ventricular hypertrophy (LVH) at higher risk for heart failure (HF) and death.

139 ein genes, and left ventricular hypertrophy (LVH) develops as an adaptive response to sarcomere dysfu

140 changes before left ventricular hypertrophy (LVH) develops.

141 bout high-risk left ventricular hypertrophy (LVH) embedded in CAC-CT.

142 ubphenotype of left ventricular hypertrophy (LVH) has been described, in which minimal elevations in

143 e diagnosis of left ventricular hypertrophy (LVH) have low sensitivity.

144 of the risk of left ventricular hypertrophy (LVH) in patients with hypertension and whether reducing

145 development of left ventricular hypertrophy (LVH) in rodents.

146 th and without left ventricular hypertrophy (LVH) induced by aortic banding.

147 Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular disease,

148 Left ventricular hypertrophy (LVH) is common in T2DM and contributes to patients' high

149 disease (CAD), left ventricular hypertrophy (LVH) or stroke.

150 Left ventricular hypertrophy (LVH) typically manifests during or after adolescence in

151 Left ventricular hypertrophy (LVH) was present in 60 subjects (67%) at baseline.

152 etrical septal left ventricular hypertrophy (LVH) was present in 79% of patients with ATTR (70% sigmo

153 iation between left ventricular hypertrophy (LVH), de fi ned by cardiac magnetic resonance (CMR) and

154 o diagnosis of left ventricular hypertrophy (LVH), eligibility for disease-specific therapy, and prog

155 p pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1(L613V/+) knock-in mice

156 ortant role in left ventricular hypertrophy (LVH).

157 ations such as left ventricular hypertrophy (LVH).

158 physiological left ventricular hypertrophy (LVH).

159 anistically to left ventricular hypertrophy (LVH).

160 development of left ventricular hypertrophy (LVH).

161 that can cause left ventricular hypertrophy (LVH).

162 rriers without left ventricular hypertrophy (LVH).

163 ry patterns on left ventricular hypertrophy (LVH).

164 t function and left ventricular hypertrophy (LVH).

165 Left ventricular hypertrophy (LVH; high LV mass [LVM]) is traditionally classified as

166 24 [55%] with left ventricular hypertrophy [LVH]) and 27 healthy controls with multiparametric cardi

167 30-day mortality for PD was 5.6% in LVH, 3.2% in MVH, and 2.5% in HVH.

168 The LV was less distensible in LVH than in controls (smaller volume for the same fillin

169 ocardial stiffness was nearly 30% greater in LVH than in controls (LVH stiffness constant, 0.053+/-0.

170 Oxidative stress (OS) has been implicated in LVH development, and allopurinol has been previously sho

171 sion of BDNF, Ras, ERK1/2, and c-fox mRNA in LVH.

172 vestigation of potentially novel pathways in LVH and offers a freely accessible protocol for similar

173 any of the cardiac MRI parameters, including LVH (P = .15 for interaction term) and LGE (P = .38 for

174 reversible cardiomyocyte defects that induce LVH.

175 Akt activation induced LVH and progressive repression of mitochondrial fatty ac

176 idney expression of alpha-Klotho and induced LVH in mice.

177 Athletes with HCM exhibit less LVH, larger left ventricular cavities, and normal indice

178 from conception to 6 weeks had markedly less LVH and fibrosis at 40 weeks.

179 Five-year OS was consistently worse at local LVH and IVH.

180 %) at local IVH, and 20,171 (40.8%) at local LVH.

181 normal levels of either biomarker (malignant LVH).

182 ck men who developed HF, 30.8% had malignant LVH at baseline, with a corresponding population attribu

183 thesis that a higher prevalence of malignant LVH among blacks may contribute to racial disparities in

184 lained by the higher prevalence of malignant LVH in blacks.

185 A higher prevalence of malignant LVH may in part explain the higher risk of HF among blac

186 The prevalence of malignant LVH was 3-fold higher among black men and women versus w

187 .8 (95% CI, 2.1-3.5) in those with malignant LVH and 0.9 (95% CI, 0.6-1.5) in those with LVH and norm

188 or attenuate risk associated with malignant LVH should be investigated as a strategy to lower HF ris

189 F cases occurring among those with malignant LVH, and the corresponding population attributable fract

190 Hypertensive patients with relatively mild LVH without either increased LV volume or concentricity

191 rophic cardiomyopathy, including 1 with mild LVH by CMR at baseline.

192 %) exhibited T-wave inversion and had milder LVH (15.8+/-3.4 mm versus 19.7+/-6.5 mm, P<0.001), large

193 ome-wide expression arrays of in vivo murine LVH.

194 g) resulted in lower rates of developing new LVH in those without LVH and higher rates of regression

195 trical LVH was present in 18%, and 3% had no LVH.

196 ed all-cause death (aHR of severe LVH vs. no LVH: 1.71; 95% CI: 1.20 to 2.44; p = 0.003).

197 (mean age, 56.23 +/- 3.30 years), 17 HTN non-LVH (mean age, 56.41 +/- 2.78 years), and 12 normal cont

198 d hypertensive patients without LVH (HTN non-LVH) using cardiac diffusion-weighted imaging and T1 map

199 on of fibrosis extent in HTN LVH and HTN non-LVH, while native T1 has limited value.

200 based on the presence (+) or absence (-) of LVH and biomarker levels above (+) or below (-) the pred

201 ere mutation carriers even in the absence of LVH.

202 bined gene network and proteomic analysis of LVH reveals novel insights into the integrated pathomech

203 ful measurement in the imaging assessment of LVH and AFD.

204 hemodynamic stress modify the association of LVH with adverse outcomes, identifying a malignant subph

205 The association of LVH with incident AF was evaluated using multivariable C

206 nges appear to precede mechanical changes of LVH progression in the SHR model.

207 001), independently of known determinants of LVH, including body mass index.

208 Simultaneously to the development of LVH, adipose tissue (AT) lipolysis becomes elevated upon

209 single lead measurement for the diagnosis of LVH (AUC: 0.80; p < 0.001).

210 e proposed criteria for the ECG diagnosis of LVH improved the sensitivity and overall accuracy of the

211 lly significant with respect to diagnosis of LVH, prognosis, and treatment decisions.(C) RSNA, 2020.

212 patients with echocardiographic evidence of LVH.

213 ignalling might contribute to other forms of LVH.

214 d primarily on echocardiographic measures of LVH.

215 automatically detect high-risk phenotypes of LVH in participants undergoing CAC-CT, without the need

216 23 directly contributes to the high rates of LVH and cardiac death in CKD.

217 Progression and regression of LVH as defined by Cornell voltage criteria derived from

218 Regression of LVH has been shown previously to improve CV mortality an

219 ted whether allopurinol causes regression of LVH in patients with T2DM.

220 ithout LVH and higher rates of regression of LVH in those with existing LVH.

221 ypertension and whether reducing the risk of LVH explains the reported cardiovascular disease (CVD) b

222 mes, identifying a malignant subphenotype of LVH with high risk for progression to HF and CV death.

223 tor (CTGF) was overexpressed in all types of LVH.

224 s study aimed to observe effects of BSJYD on LVH in spontaneously hypertensive rats (SHRs) and explor

225 This favorable effect on LVH did not explain most of the reduction in CVD events

226 ) is less profibrotic than pressure overload LVH (POH).

227 Volume overload LVH (VOH) is less profibrotic than pressure overload LVH

228 uture lipid-based therapies for pathological LVH or heart failure.

229 to mitochondrial dysfunction in pathological LVH.

230 d extracellular subproteomes in pathological LVH.

231 M to study the reversibility of pathological LVH.

232 the adult heart contributes to pathological LVH in part by reducing mitochondrial oxidative capacity

233 t distinguish pathological and physiological LVH.

234 ient to differentiate HCM from physiological LVH and should be complemented by additional structural

235 y for differentiating HCM from physiological LVH: 13% had a left ventricular cavity >54 mm, 87% had a

236 mild concentric LVH mimicking physiological LVH.

237 c cardiomyopathy pre-LVH (genotype positive, LVH negative [G+LVH-]).

238 s in genetic hypertrophic cardiomyopathy pre-LVH (genotype positive, LVH negative [G+LVH-]).

239 ups (eg, pulmonary capillary wedge pressure: LVH, 13.4+/-2.7 versus control, 11.7+/-1.7 mm Hg, P<0.00

240 6 weeks reduced fibrosis but did not prevent LVH or functional changes.

241 Preventing LVH by inhibiting mTOR failed to prevent the decline in

242 erload in IHD and may therefore also regress LVH.

243 High-dose allopurinol regresses LVH, reduces LV end-systolic volume, and improves endoth

244 ling might protect from CKD- and age-related LVH.

245 tion methods were built to predict high-risk LVH based on CAC-CT radiomics, sex, height, and body sur

246 (95% CI, 0.66-0.80) for detecting high-risk LVH in a distinct validation subset of 395 participants.

247 dred twenty-four participants with high-risk LVH were identified by cardiac magnetic resonance.

248 Severe LVH at 1 year was observed in 39%, which was independent

249 ssical features of pre-excitation and severe LVH are not uniformly present, and diagnosis should be c

250 a greater risk factor burden and more severe LVH compared with those who were LVH+ biomarker- (p < 0.

251 ith increased all-cause death (aHR of severe LVH vs. no LVH: 1.71; 95% CI: 1.20 to 2.44; p = 0.003).

252 Among patients with moderate or severe LVH treated with TAVR who are alive at 1 year, greater L

253 Echo is unlikely to miss substantial LVH; however, CMR identified mild hypertrophy in approxi

254 reverse septal contour), whereas symmetrical LVH was present in 18%, and 3% had no LVH.

255 ducible Raf1(L613V) expression, we show that LVH results from the interplay of cardiac cell types.

256 ere 66% more likely to regress/improve their LVH (hazard ratio=1.66; 95% confidence interval, 1.31-2.

257 Those LVH+ and cTnT+ and/or NT-proBNP+ (n = 144) were older an

258 Subjects were stratified according to LVH and by detectable cTnT (>/=3 pg/ml) and increased NT

259 Time-varying LVH classes were tested for association with all-cause a

260 sus local intermediate (IVH) and low-volume (LVH) hospitals were identified.

261 Nine percent of participants were LVH+, 25% cTnT+, and 24% NT-proBNP+.

262 Individuals who were LVH+ and either cTnT+ or NT-proBNP+ remained at >4-fold

263 more severe LVH compared with those who were LVH+ biomarker- (p < 0.01 for each).

264 on, and LV mass compared with those who were LVH- biomarker-.

265 with LVH), healthy volunteers (n=67; 0% with LVH), patients with hypertension (n=41; 24% with LVH), p

266 hypertrophic cardiomyopathy (n=34; 100% with LVH), those with severe aortic stenosis (n=21; 81% with

267 in (AL) cardiac amyloidosis (n=20; 100% with LVH).

268 , patients with hypertension (n=41; 24% with LVH), patients with hypertrophic cardiomyopathy (n=34; 1

269 e studied: patients with AFD (n=44; 55% with LVH), healthy volunteers (n=67; 0% with LVH), patients w

270 with severe aortic stenosis (n=21; 81% with LVH), and patients with definite amyloid light-chain (AL

271 eric vascular dysfunction is associated with LVH and hypertension, independently of common risk facto

272 asked hypertension, and its association with LVH supports the case for routine ABPM and cardiac struc

273 Mutation carriers with LVH (G+/LVH+), mutation carriers without LVH (G+/LVH-),

274 Sarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), pat

275 Although prolonged-QT commonly coexists with LVH, both are independent markers of poor prognosis.

276 Compared with LVH- FD, LVH+ FD had higher left ventricular ejection fr

277 cardiac biomarkers identify individuals with LVH at high risk for developing heart failure (HF).

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

279 Patients with LVH (LVM/body surface area >/=116 and >/=96 g/m(2) in me

280 In patients with LVH (n=105), T1 discriminated completely between AFD and

281 LV myocardial stiffness in patients with LVH and elevated biomarkers (stage-B HFpEF) is greater t

282 We tested the hypothesis that patients with LVH and elevated cardiac biomarkers would demonstrate el

283 the LV myocardial stiffness of patients with LVH is greater than that of healthy controls at this ear

284 gnosis should be considered in patients with LVH who develop atrial fibrillation or require permanent

285 ul to reduce CV events in T2DM patients with LVH.

286 subendocardium with greater reductions with LVH, storage, edema, and scar.

287 LVH and 0.9 (95% CI, 0.6-1.5) in those with LVH and normal biomarkers, with similar findings in each

288 arriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), patients with HCM without mutations

289 ined normal in HCM mutation carriers without LVH (1.7 +/- 0.1; p = 0.61 vs. controls, p = 0.02 vs. ov

290 serial imaging of mutation carriers without LVH (G+/LVH-) to monitor for phenotypic evolution, but t

291 ith LVH (G+/LVH+), mutation carriers without LVH (G+/LVH-), and healthy related control individuals (

292 Interestingly, HCM mutation carriers without LVH also showed an impaired oxygenation response to aden

293 overt HCM, 10 HCM mutation carriers without LVH, 11 athletes, and 20 healthy controls underwent card

294 However, in HCM mutation carriers without LVH, only oxygenation is impaired.

295 thy sarcomere gene mutation carriers without LVH.

296 Perfusion is reduced even without LVH suggesting it is an early disease marker.

297 Compared with participants without LVH, the adjusted hazard ratio for HF was 2.8 (95% CI, 2

298 (HTN LVH) and hypertensive patients without LVH (HTN non-LVH) using cardiac diffusion-weighted imagi

299 Compared with hypertensive patients without LVH (n=191; 74.6%) and those with HTN-LVH and normal RI

300 rates of developing new LVH in those without LVH and higher rates of regression of LVH in those with