ライフサイエンスコーパス: LVH

1 LVH and diastolic dysfunction are associated with elevat

2 LVH was defined as the upper 95th percentile of indexed

3 LVH was more common in children with either confirmed (3

4 LVH, elevated LV filling pressure, and abnormal myocardi

5 8 years among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0

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

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

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

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

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

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

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

13 ve inversion in leads V(4) through V(6)) and LVH, assessed by Sokolow-Lyon voltage criteria (R(V5-6)+

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

15 rdiovascular events in patients with CKD and LVH.

16 group study in patients with stage 3 CKD and LVH.

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

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

19 ndothelial function in patients with IHD and LVH.

20 mice demonstrated elevated FGF23 levels and LVH.

21 ECG left ventricular strain and LVH were independently predictive of poor prognosis in p

22 regression of LVM in patients with T2DM and LVH.

23 SRL may be useful to attenuate LVH and improve cardiac allograft diastolic function.

24 ment with an FGF-receptor blocker attenuated LVH, although no change in blood pressure was observed.

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

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

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

28 Because LVH and endothelial dysfunction associate with prognosis

29 There was no significant association between LVH and kidney function.

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 WT-TAC mice developed relatively compensated LVH, despite reduced mitochondrial function and repressi

40 Elevated LVM index, concentric LVH, altered diastolic function, and cardiac workload si

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

42 e conventional gray zone of mild, concentric LVH.

43 ficantly worse in the presence of concentric LVH and eccentric LVH compared with the absence of LVH (

44 In conclusion, LVH is common and associates with poor outcomes among pa

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

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

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

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

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

50 the presence of concentric LVH and eccentric LVH compared with the absence of LVH (P = 0.0009 and P <

51 aggravate the adverse prognosis of eccentric LVH.

52 free survival in the subgroup with eccentric LVH at baseline (P = 0.034).

53 e of LVH at baseline was 47%, with eccentric LVH more frequent than concentric.

54 oth criteria predicted, compared with no ECG LVH, 5.8-fold higher risk of heart failure (95% confiden

55 Similarly, ECG LVH by both criteria predicted, compared with no ECG LVH

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

57 ECG-LVH was defined by Cornell voltage criteria.

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

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

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

61 Eleven ECG-LVH criteria were assessed.

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

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

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

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

66 considered as an innocent consequence of ECG-LVH.

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

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

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

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

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

72 of regression of LVH in those with existing LVH.

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

74 , 0.65-0.91] before and after adjustment for LVH as a time-varying covariate, respectively).

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

76 .0 +/- 7.7 versus 15.9 +/- 6.9 ml/kg/min for LVH (p < 0.0001).

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

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

79 aging mice lacking FGFR4 are protected from LVH.

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

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

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

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

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

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

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

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

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

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

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

91 G+/LVH- individuals demonstrated altered cardiac dimensions

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

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

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

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

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

97 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

98 =0.36+/-0.01, 0.33+/-0.01, 0.27+/-0.01 in G+/LVH+, G+/LVH-, controls, respectively; P</=0.001 for all

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

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

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

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

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

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

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

106 .01, 0.33+/-0.01, 0.27+/-0.01 in G+/LVH+, G+/LVH-, controls, respectively; P</=0.001 for all comparis

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

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

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

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

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

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

113 At baseline, 17% of children had LVH (11% eccentric and 6% concentric) and 9% had concent

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

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

116 Hispanic subgroups were more likely to have LVH than non-Hispanic whites after adjustment for hypert

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

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

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

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

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

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

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

124 9.5%), patients with HTN-LVH and low RI (HTN-LVH/low RI; n=15, 5.9%) had an amplified myocardial resp

125 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

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

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

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

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

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

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

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

133 Left ventricular hypertrophy (LVH) and diastolic dysfunction occur after cardiac trans

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

135 prevalence of left ventricular hypertrophy (LVH) and left ventricular (LV) remodeling patterns withi

136 vation (RD) on left ventricular hypertrophy (LVH) and systolic and diastolic function in patients wit

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

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

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

140 prevalence of left ventricular hypertrophy (LVH) assessed by echocardiography was 32%, 48%, 57%, and

141 Left ventricular hypertrophy (LVH) associates with increased risk for cardiovascular d

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

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

144 changes before left ventricular hypertrophy (LVH) develops.

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

146 of concentric left ventricular hypertrophy (LVH) improved from 28% at pre-operative to only 3% at fo

147 lar strain and left ventricular hypertrophy (LVH) in asymptomatic aortic stenosis is not well describ

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

149 in regressing left ventricular hypertrophy (LVH) in renal transplant recipients (RTRs) with chronic

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

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

152 Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease

153 Left ventricular hypertrophy (LVH) is associated with electric remodeling and increase

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

155 Left ventricular hypertrophy (LVH) is usually accompanied by intensive interstitial an

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

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

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

159 constriction (left ventricular hypertrophy (LVH)) or sham operation.

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

161 (CKD) reduces left ventricular hypertrophy (LVH), which is a risk factor for cardiovascular (CV) mor

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

163 development of left ventricular hypertrophy (LVH).

164 that can cause left ventricular hypertrophy (LVH).

165 rriers without left ventricular hypertrophy (LVH).

166 t also regress left ventricular hypertrophy (LVH).

167 t function and left ventricular hypertrophy (LVH).

168 ortant role in left ventricular hypertrophy (LVH).

169 ations such as left ventricular hypertrophy (LVH).

170 physiological left ventricular hypertrophy (LVH).

171 anistically to left ventricular hypertrophy (LVH).

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

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

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

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

176 nted the down-regulation of SERCA protein in LVH hearts, TG-LVH hearts showed no increase in inotropi

177 ction of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF

178 However, this advantage was not sustained in LVH hearts in which the energetic status was compromised

179 reversible cardiomyocyte defects that induce LVH.

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

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

182 n a mouse model of pressure overload-induced LVH, produced by transverse aortic constriction (TAC).

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

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

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

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

187 %) exhibited T-wave inversion and had milder LVH (15.8+/-3.4 mm versus 19.7+/-6.5 mm, P<0.001), large

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

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

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

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

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

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

194 d eccentric LVH compared with the absence of LVH (P = 0.0009 and P < or = 0.0001, respectively).

195 odeling according to the presence/absence of LVH and abnormal/normal LV mass to LV end-diastolic volu

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

197 ere mutation carriers even in the absence of LVH.

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

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

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

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

202 ary immunosuppression for the attenuation of LVH and diastolic dysfunction of the cardiac allograft.

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

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

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

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

207 ealed regional differences in the effects of LVH.

208 patients with echocardiographic evidence of LVH.

209 ignalling might contribute to other forms of LVH.

210 d primarily on echocardiographic measures of LVH.

211 g, we used a well-established mouse model of LVH (transverse aortic constriction [TAC]).

212 min per 1.73 m(2) had twofold higher odds of LVH (OR=2.20, 95% CI=1.40-3.40; P<0.001) relative to sub

213 causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels c

214 adults, but its role in the pathogenesis of LVH in children is not as well established.

215 LVMi were the only significant predictors of LVH regression according to a multivariate model that ex

216 were the strongest independent predictors of LVH.

217 are insufficient to predict the presence of LVH in children with CKD.

218 -origin Hispanics had a higher prevalence of LVH and abnormal LV remodeling compared with non-Hispani

219 A higher prevalence of LVH and abnormal LV remodeling was also observed among M

220 The prevalence of LVH at baseline was 47%, with eccentric LVH more frequen

221 23 directly contributes to the high rates of LVH and cardiac death in CKD.

222 levels contribute directly to high rates of LVH and mortality in individuals with CKD.

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

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

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

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

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

228 f FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether thes

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

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

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

232 nority in the U.S., but there are no data on LVH and LV geometry among Hispanic subgroups.

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

234 The effect of RD on LVH and LV function is unclear.

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

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

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

238 d extracellular subproteomes in pathological LVH.

239 to mitochondrial dysfunction in pathological LVH.

240 M to study the reversibility of pathological LVH.

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

242 t distinguish pathological and physiological LVH.

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

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

245 mild concentric LVH mimicking physiological LVH.

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

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

248 6 weeks reduced fibrosis but did not prevent LVH or functional changes.

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

250 Allopurinol significantly reduced LVH (P=0.036), improved endothelial function (P=0.009),

251 fferences among Hispanic subgroups regarding LVH and LV remodeling should be taken into account when

252 erload in IHD and may therefore also regress LVH.

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

254 ure CsA proved to be effective in regressing LVH in RTRs regardless of BP, mainly by reducing left ve

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

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

257 During the study, LVH prevalence and mean left ventricular mass index did

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

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

260 egulation of SERCA protein in LVH hearts, TG-LVH hearts showed no increase in inotropic response when

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

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

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

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

265 Hypertension leads to LVH in adults, but its role in the pathogenesis of LVH i

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

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

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

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

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

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

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

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

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

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

276 in was present in 340 patients (23.6%), with LVH by Sokolow-Lyon voltage in 260 (17.1%) and by Cornel

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

278 1.73 m(2) also significantly associated with LVH and abnormal LV geometry compared with eGFR>/=60 ml/

279 F23 levels are independently associated with LVH in a large, racially diverse CKD cohort.

280 ar mass and evaluate factors associated with LVH in children with stages 2 through 4 chronic kidney d

281 masked hypertension and its association with LVH supports early echocardiography and ambulatory BP mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 thy sarcomere gene mutation carriers without LVH.

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

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

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

300 in inotropic response when compared with WT-LVH hearts.