ライフサイエンスコーパス: ventricular hypertrophy

1 ts (sarcomere mutation carriers without left ventricular hypertrophy).

2 mere mutation carriers with and without left ventricular hypertrophy.

3 not be guided solely on the severity of left ventricular hypertrophy.

4 h raised pulmonary artery pressure and right ventricular hypertrophy.

5 with incident hypertension and risk of left ventricular hypertrophy.

6 es, pulmonary vascular remodeling, and right ventricular hypertrophy.

7 molecules are crucial to calcium cycling and ventricular hypertrophy.

8 er mean gradients, and comparable degrees of ventricular hypertrophy.

9 n, 31 had diabetes mellitus, and 59 had left ventricular hypertrophy.

10 individuals at risk for hypertension or left ventricular hypertrophy.

11 pressure (pulmonary hypertension) and right ventricular hypertrophy.

12 ogressive conduction system disease and left ventricular hypertrophy.

13 the onset of systemic hypertension and left ventricular hypertrophy.

14 ckle cell positive athlete who also had left ventricular hypertrophy.

15 mixed logistic model was used to assess left ventricular hypertrophy.

16 ats with established PAH and decreased right ventricular hypertrophy.

17 th HCTZ, CTDN was associated with lower left ventricular hypertrophy.

18 ing of the pulmonary artery media, and right ventricular hypertrophy.

19 regional wall motion abnormalities, and left-ventricular hypertrophy.

20 e in pulmonary vascular remodeling and right ventricular hypertrophy.

21 ting CA from other causes of concentric left ventricular hypertrophy.

22 ve aortic valve narrowing and secondary left ventricular hypertrophy.

23 8 children with normal echoes developed left ventricular hypertrophy.

24 of sudden cardiac death (SCD) and mild left ventricular hypertrophy.

25 factors, particularly hypertension and left ventricular hypertrophy.

26 aortic stenosis often have significant left ventricular hypertrophy.

27 f Tsc1c/cSM22cre+/- mice, with regression of ventricular hypertrophy.

28 of sarcomeric mutation carriers without left ventricular hypertrophy.

29 th isolated HCM and syndromes including left ventricular hypertrophy.

30 s definitively associated with isolated left ventricular hypertrophy.

31 on, has been inconsistently linked with left ventricular hypertrophy.

32 blood pressures, cardiac fibrosis, and left ventricular hypertrophy.

33 n of peripheral pulmonary arteries and right ventricular hypertrophy.

34 ence interval: 1.02, 1.21) and incident left ventricular hypertrophy (1.02, 95% confidence interval:

35 (6%), mitral valve abnormalities (51%), left ventricular hypertrophy (19%), and atrial fibrillation (

36 ncrease in the prevalence of concentric left ventricular hypertrophy (2 of 64 [3%] versus 20 of 64 [3

37 performed in 44 Fabry patients without left ventricular hypertrophy (35.7+/-14.5 years, 68.2% female

38 rt failure (43% versus 34%; P=0.04) and left ventricular hypertrophy (77% versus 58%; P=0.02) and a l

39 entional paradigm of the progression of left ventricular hypertrophy, a thick-walled left ventricle (

40 Left ventricular hypertrophy (adjusted hazard ratio, 1.52; 95

41 The decrease in the prevalence of left ventricular hypertrophy after renal transplantation is b

42 s significantly associated with greater left ventricular hypertrophy and a higher prevalence of left

43 NF-kappaB deletion promoted maladaptive left ventricular hypertrophy and accelerated progression towa

44 ommon genetic disorder characterized by left ventricular hypertrophy and cardiac hyper-contractility.

45 te atrial fibrillation (AF) by inducing left ventricular hypertrophy and diastolic and left atrial dy

46 pectively) with good discrimination for left ventricular hypertrophy and diastolic dysfunction as bin

47 induced significant, severity-dependent left ventricular hypertrophy and diastolic dysfunction compar

48 FHS diet-fed mice developed progressive left ventricular hypertrophy and diastolic dysfunction with p

49 erved FEV1/FVC ratio is associated with left ventricular hypertrophy and diastolic dysfunction.

50 nt with S17834 or resveratrol prevented left ventricular hypertrophy and diastolic dysfunction.

51 etabolic heart disease characterized by left ventricular hypertrophy and diastolic dysfunction.

52 tion of neonatal cardiomyoblasts resulted in ventricular hypertrophy and dilation, supporting a funct

53 arly markers of cardiomyopathy, such as left ventricular hypertrophy and dysfunction, and early marke

54 Indices of left ventricular hypertrophy and ejection fraction were simil

55 ln1(Tie2) mice exhibited unprecedented right ventricular hypertrophy and failure and progressive mort

56 ry, angioproliferative remodeling, and right ventricular hypertrophy and failure.

57 otensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in patients with hy

58 renin-angiotensin system contributes to left ventricular hypertrophy and fibrosis, a major determinan

59 Grx2(-/-) hearts also developed left ventricular hypertrophy and fibrosis, and mice became hy

60 of angiotensin II receptor blockers on left ventricular hypertrophy and fibrosis, which are predicti

61 ng miRNAs correlated with the degree of left ventricular hypertrophy and fibrosis.

62 ic dysfunction seen in conjunction with left ventricular hypertrophy and fibrosis.

63 veloped cardiomyopathy characterized by left ventricular hypertrophy and glycogen accumulation, with

64 r FGF23 in the kidney, which stimulates left ventricular hypertrophy and hepatic production of inflam

65 ver, only A-17 reduced hypoxia-induced right ventricular hypertrophy and improved pulmonary artery ac

66 ance, pulmonary artery remodeling, and right ventricular hypertrophy and improving functional capacit

67 Conclusion Cardiac MRI findings of left ventricular hypertrophy and late gadolinium enhancement

68 of structural heart disease, including left ventricular hypertrophy and left atrial enlargement, in

69 ic left ventricular dysfunction expressed as ventricular hypertrophy and left atrial enlargement.

70 Echocardiographic data showed left ventricular hypertrophy and lower fractional shortening

71 omere gene hypothesis, such as regional left ventricular hypertrophy and myocardial fibrosis, as well

72 There was also right ventricular hypertrophy and pathological evidence for pu

73 In the athymic rat, imatinib decreased right ventricular hypertrophy and pulmonary arteriolar muscula

74 ight ventricular systolic pressure and right ventricular hypertrophy and pulmonary vascular remodelin

75 ECG abnormalities were present in 87%, with ventricular hypertrophy and repolarization abnormalities

76 medial thickness, and echocardiographic left ventricular hypertrophy and systolic dysfunction.

77 ing demonstrated that KO mice developed less ventricular hypertrophy and that contractile function is

78 rbidity, impaired chronotropic reserve, left ventricular hypertrophy, and activation of inflammatory,

79 n treatment to minimize myocardial fibrosis, ventricular hypertrophy, and arrhythmias.

80 reased relative wall thickness or overt left ventricular hypertrophy, and associated diastolic dysfun

81 HFpEF mice developed hypertension, left ventricular hypertrophy, and diastolic dysfunction and h

82 ts develop renal failure, hypertension, left ventricular hypertrophy, and diastolic dysfunction, amon

83 mice developed HFpEF with hypertension, left ventricular hypertrophy, and diastolic dysfunction.

84 r 3 weeks dose-dependently reduced PH, right ventricular hypertrophy, and distal pulmonary artery mus

85 artery pressure, vascular remodeling, right ventricular hypertrophy, and fibrosis in comparison with

86 showed higher body weight, significant left ventricular hypertrophy, and impaired diastolic function

87 aptive concentrations, and then induces left ventricular hypertrophy, and is possibly implicated in t

88 Patients with increased age, left ventricular hypertrophy, and left atrial dilatation were

89 al fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch block we

90 , hypertension, cardiovascular disease, left ventricular hypertrophy, and left bundle-branch block pr

91 al infarction, lower ejection fraction, left ventricular hypertrophy, and left ventricular dilatation

92 Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfunctio

93 d right ventricular systolic pressure, right ventricular hypertrophy, and loss of small arteries.

94 ng cardiovascular complications such as left ventricular hypertrophy, and minimizing the use of corti

95 cell abnormalities in vascular injury, right ventricular hypertrophy, and morbidity associated with P

96 linked to CKD and greater risk of CVD, left ventricular hypertrophy, and mortality in dialysis patie

97 f systolic right ventricular pressure, right ventricular hypertrophy, and percentage of remodeled pul

98 hronic kidney disease, mild to moderate left ventricular hypertrophy, and preserved left ventricular

99 ricular systolic pressure measurement, right ventricular hypertrophy, and pulmonary distal arterial m

100 entricular systolic pressure increase, right ventricular hypertrophy, and pulmonary vessel wall thick

101 criteria for right ventricular (RV) or left ventricular hypertrophy, and symmetrical cardiac enlarge

102 and attenuated the development of PH, right ventricular hypertrophy, and vascular remodeling in both

103 uine prevented the development of PAH, right ventricular hypertrophy, and vascular remodelling after

104 ge B HF (normal exercise tolerance with left ventricular hypertrophy, and/or reduced global longitudi

105 cular dysfunction; arterial stiffening; left ventricular hypertrophy; and worsened metrics of diabete

106 ocity (CV) and conduction anisotropy in left ventricular hypertrophy are associated with topographica

107 le mechanistic role of exercise-induced left ventricular hypertrophy as the basis for J-point elevati

108 d right ventricular systolic pressure, right ventricular hypertrophy, as well as collagen deposition

109 yocardial and perivascular fibrosis and left ventricular hypertrophy associated with diastolic dysfun

110 on LVM was evident among patients with left ventricular hypertrophy at baseline.

111 tolic dysfunction pathway that includes left ventricular hypertrophy, atrial enlargement, and heart f

112 od pressure, current smoking, diabetes, left ventricular hypertrophy, atrial fibrillation, and previo

113 es, ventricular conduction defects, and left ventricular hypertrophy based on the Minnesota code.

114 exhibited a significant attenuation of left ventricular hypertrophy based on tissue weight assessmen

115 Left ventricular hypertrophy became less marked over time (ma

116 ly associated with HFpEF, and male sex, left ventricular hypertrophy, bundle branch block, previous m

117 High FGF-23 levels promote left ventricular hypertrophy but not coronary artery calcific

118 It is characterised by left ventricular hypertrophy but there is an important pre-hy

119 ATPase and phospholamban were normal in left ventricular hypertrophy, but decreased in failing hearts

120 Diabetic patients had more ventricular hypertrophy, but systolic and diastolic vent

121 tension is linked to the development of left ventricular hypertrophy, but whether this association ex

122 % CI: 0.94 to 0.97) among patients with left ventricular hypertrophy by ECG criteria and 0.95 (95% CI

123 e from CVD and underwent measurement of left ventricular hypertrophy by ECG, coronary artery calcium,

124 el multimodality testing strategy using left ventricular hypertrophy by ECG, coronary artery calcium,

125 also strongly associated with incident left ventricular hypertrophy by electrocardiography over 6 ye

126 tid intima-media thickness or stenosis, left ventricular hypertrophy [by ECG or echocardiography], le

127 g right ventricular systolic pressure, right ventricular hypertrophy, cardiac fibrosis, and vascular

128 elected areas, such as undifferentiated left ventricular hypertrophy, cardio-oncology, aortic stenosi

129 ion of MYK-461 suppresses the development of ventricular hypertrophy, cardiomyocyte disarray, and myo

130 y vascular remodeling, and reduces the right ventricular hypertrophy characteristic of PH.

131 ry vascular remodeling, and reduce the right ventricular hypertrophy characteristic of PH.

132 duals: sarcomere mutation carriers with left ventricular hypertrophy (clinical HCM; n=36), mutation c

133 uscularization but a similar degree of right ventricular hypertrophy compared with wild-type mice.

134 These changes resulted in right ventricular hypertrophy, confirming hemodynamically sign

135 ry hypertension that directly leads to right ventricular hypertrophy, decompensated right-sided heart

136 ver 4 years, the adjusted prevalence of left ventricular hypertrophy decreased from 15.3% to 12.6% in

137 onectin deficiency in HFpEF exacerbates left ventricular hypertrophy, diastolic dysfunction, and HF.

138 Uremic cardiomyopathy, characterized by left ventricular hypertrophy, diastolic dysfunction, and impa

139 in aldosterone-infused mice ameliorated left ventricular hypertrophy, diastolic dysfunction, lung con

140 th structural abnormalities, defined as left ventricular hypertrophy, dilation or dysfunction, or sig

141 kground lacked hallmarks of HCM such as left ventricular hypertrophy, disarray of myofibers, and inte

142 overload-induced cardiac stress induces left ventricular hypertrophy driven by increased cardiomyocyt

143 fasting, as well as patients diagnosed with ventricular hypertrophy due to valvular aortic stenosis,

144 ed risk of development of hypertension, left ventricular hypertrophy/dysfunction, vascular dysfunctio

145 ed-QT commonly coexists in the ECG with left ventricular hypertrophy (ECG-LVH).

146 ors, incident hypertension and incident left ventricular hypertrophy, estimated by complete-case anal

147 r density in nonfailing, hypertrophied (left ventricular hypertrophy), failing, and failing left vent

148 age-related cardiac changes in humans (left ventricular hypertrophy, fibrosis and diastolic dysfunct

149 Instead, our results suggest the ventricular hypertrophy for human R249Q mutation is a co

150 typically characterized by asymmetrical left ventricular hypertrophy, frequently is caused by mutatio

151 64% and a decrease in the prevalence of left ventricular hypertrophy from 66% to 56%.

152 be present in mutation carriers without left ventricular hypertrophy (G+LVH-) but are difficult to qu

153 BMI and BMI were associated with higher left ventricular hypertrophy, glycemic traits, interleukin 6,

154 oved left ventricular function, blunted left ventricular hypertrophy, greater preservation of viable

155 ation; 38 were clinically affected with left ventricular hypertrophy >/=13 mm.

156 Left ventricular hypertrophy has been identified as an indepe

157 ents with genetic mutations but without left-ventricular hypertrophy has emerged, with unresolved nat

158 ease (CKD) and strongly associated with left ventricular hypertrophy, heart failure, and death.

159 ffic-related air pollution is linked to left ventricular hypertrophy, heart failure, and death.

160 d glucose metabolism, renal impairment, left ventricular hypertrophy, heart failure, and others.

161 n fraction patients enrolled in TOPCAT, left ventricular hypertrophy, higher left ventricular filling

162 ic strain in hypertensive patients with left ventricular hypertrophy (HTN LVH) and hypertensive patie

163 Hypertensive left ventricular hypertrophy (HTN-LVH) is a leading cause of

164 nosis is based on otherwise unexplained left-ventricular hypertrophy identified by echocardiography o

165 olymorphisms in PPP3R1 to be associated with ventricular hypertrophy in AA hypertensive patients.

166 e, normalized sympathetic activity, and left ventricular hypertrophy in Ang II rats, as well as in th

167 e role of CLP-1 in vivo in induction of left ventricular hypertrophy in angiotensinogen-overexpressin

168 decline in BP may predict a decline in left ventricular hypertrophy in children with CKD and suggest

169 latory hormone that directly stimulates left ventricular hypertrophy in experimental models.

170 The pathogenesis of left ventricular hypertrophy in patients with CKD is incomple

171 ed with hypertensive heart disease with left ventricular hypertrophy in the absence of coronary arter

172 ditional investigation as predictors of left ventricular hypertrophy in these patients.

173 redistribution of LTCC were studied in left ventricular hypertrophy in vivo and in cultured adult fe

174 actile dysfunction in pressure-overload left ventricular hypertrophy in vivo.

175 on-AF cardiovascular diagnoses, such as left ventricular hypertrophy, in 28 participants (4.6%).

176 pressure (BP) is an important marker of left ventricular hypertrophy, incident hypertension, and futu

177 Predictors of left ventricular hypertrophy included systolic BP, female sex

178 The prevalence of hypertension and left ventricular hypertrophy increased with the degree of ane

179 istance, functional residual capacity, right ventricular hypertrophy index, and total cell count in B

180 uced pulmonary vascular remodeling and right ventricular hypertrophy indicating a role for Gremlin 1

181 a HFHS diet prevent the development of left ventricular hypertrophy, interstitial fibrosis, and dias

182 We hypothesized that athletic left ventricular hypertrophy is a consequence of increased my

183 Furthermore, despite the fact that ventricular hypertrophy is a well-established risk facto

184 Left ventricular hypertrophy is absent in the minority of adu

185 on is restricted to the right atrium, though ventricular hypertrophy is accompanied by increased BMP1

186 Left ventricular hypertrophy is an initial compensatory mecha

187 Left ventricular hypertrophy is rare in children with TNNT2 m

188 especially prevalent in late life (eg, left ventricular hypertrophy, ischemic heart disease, heart f

189 I HDAC inhibitor only modestly reduced right ventricular hypertrophy, it had multiple beneficial effe

190 ing and then examine the development of left ventricular hypertrophy, its subsequent decompensation,

191 rophy despite a lack of exercise and cardiac ventricular hypertrophy leading to premature death.

192 rosis, volume overload, and progressive left ventricular hypertrophy, leading to elevated N-terminal

193 characterized by diastolic dysfunction, left ventricular hypertrophy, left atrial dilatation, and int

194 eep disordered breathing, inflammation, left ventricular hypertrophy, left atrial enlargement, and su

195 Left ventricular hypertrophy, left atrial volume, AEVS, and n

196 ic model additionally included smoking, left ventricular hypertrophy, left bundle branch block, and d

197 probrain natriuretic peptide level and left ventricular hypertrophy, left ventricular systolic and d

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

199 Individuals with left ventricular hypertrophy (LVH) and elevated cardiac bioma

200 ly hypertensive rat (SHR) as a model of left ventricular hypertrophy (LVH) and failure.

201 Left ventricular hypertrophy (LVH) and late gadolinium enhanc

202 tients with baseline moderate or severe left ventricular hypertrophy (LVH) and paired measurements of

203 d renal sympathetic denervation (RD) on left ventricular hypertrophy (LVH) and systolic and diastolic

204 e association of exercise capacity with left ventricular hypertrophy (LVH) and systolic/diastolic dys

205 d in 40% of cases, including idiopathic left ventricular hypertrophy (LVH) and/or fibrosis (n = 59, 1

206 between physiological and pathological left ventricular hypertrophy (LVH) are of intense interest.

207 The prevalence of left ventricular hypertrophy (LVH) assessed by echocardiograp

208 identify asymptomatic individuals with left ventricular hypertrophy (LVH) at higher risk for heart f

209 tations in sarcomere protein genes, and left ventricular hypertrophy (LVH) develops as an adaptive re

210 em to induce profibrotic changes before left ventricular hypertrophy (LVH) develops.

211 phenotypic information about high-risk left ventricular hypertrophy (LVH) embedded in CAC-CT.

212 A malignant subphenotype of left ventricular hypertrophy (LVH) has been described, in whi

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

214 pact of ECG left ventricular strain and left ventricular hypertrophy (LVH) in asymptomatic aortic ste

215 ld lead to more lowering of the risk of left ventricular hypertrophy (LVH) in patients with hypertens

216 rs proved to be effective in regressing left ventricular hypertrophy (LVH) in renal transplant recipi

217 c myocyte growth and the development of left ventricular hypertrophy (LVH) in rodents.

218 in pig cardiac tissue, with and without left ventricular hypertrophy (LVH) induced by aortic banding.

219 Left ventricular hypertrophy (LVH) is a major risk factor for

220 Left ventricular hypertrophy (LVH) is an important mechanism

221 Left ventricular hypertrophy (LVH) is common in T2DM and cont

222 Left ventricular hypertrophy (LVH) is usually accompanied by

223 ncluding coronary artery disease (CAD), left ventricular hypertrophy (LVH) or stroke.

224 Left ventricular hypertrophy (LVH) typically manifests during

225 Left ventricular hypertrophy (LVH) was present in 60 subjects

226 iac AL amyloidosis, asymmetrical septal left ventricular hypertrophy (LVH) was present in 79% of pati

227 ks after ascending aortic constriction (left ventricular hypertrophy (LVH)) or sham operation.

228 ught to examine the association between left ventricular hypertrophy (LVH), de fi ned by cardiac magn

229 evaluated with respect to diagnosis of left ventricular hypertrophy (LVH), eligibility for disease-s

230 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Ra

231 adaptive cardiac modifications such as left ventricular hypertrophy (LVH).

232 ealthy athletes with mild physiological left ventricular hypertrophy (LVH).

233 D, it may contribute mechanistically to left ventricular hypertrophy (LVH).

234 tural changes before the development of left ventricular hypertrophy (LVH).

235 acellular lipid disorder that can cause left ventricular hypertrophy (LVH).

236 paired in HCM mutation carriers without left ventricular hypertrophy (LVH).

237 arterial compliance might also regress left ventricular hypertrophy (LVH).

238 about the effect of dietary patterns on left ventricular hypertrophy (LVH).

239 iated with worse allograft function and left ventricular hypertrophy (LVH).

240 ERK) pathway plays an important role in left ventricular hypertrophy (LVH).

241 Left ventricular hypertrophy (LVH; high LV mass [LVM]) is tra

242 ents (49 years, 43% male, 24 [55%] with left ventricular hypertrophy [LVH]) and 27 healthy controls w

243 Persistence of the left ventricular hypertrophy may result from the combined adv

244 Arterial stiffness and left ventricular hypertrophy may significantly influence the

245 tance, thus leading to hypertension and left ventricular hypertrophy, metabolic syndrome/diabetes mel

246 es of uncertain significance (n=41), such as ventricular hypertrophy, myocardial fibrosis, and minor

247 Compared with those without left ventricular hypertrophy (n=51) and left ventricular hype

248 table, treatment-naive patients (mainly left ventricular hypertrophy-negative); advanced disease cont

249 transverse aortic constriction in which left ventricular hypertrophy occurred by 2 weeks without func

250 Left ventricular hypertrophy on ECG was a strong predictor of

251 In select carriers without left ventricular hypertrophy on echocardiogram, SCD occurred,

252 t, it was independently associated with left ventricular hypertrophy only in women.

253 Left ventricular hypertrophy or concentric remodeling, LA enl

254 e muscle contraction was not altered in left ventricular hypertrophy or failing hearts.

255 Cardiac structural abnormalities, left ventricular hypertrophy, or concentric geometry, were hi

256 brosis in the absence of myocarditis or left ventricular hypertrophy, or other known pathogeneses, wa

257 Mutant mice display right ventricular hypertrophy, overriding aorta, ventricular s

258 However, correlation with left ventricular hypertrophy parameters holds true for only a

259 alyses we find association of NRG1 with left ventricular hypertrophy phenotypes, fibrinogen and urea

260 , ERI2, IL18RAP, IL23RAP and NRG1) with left ventricular hypertrophy phenotypes.

261 uretic peptide, which is induced during left ventricular hypertrophy, plays an anti-fibrogenic and an

262 After 1 year of ERT initiation, left ventricular hypertrophy-positive patients have a detecta

263 Twenty patients starting ERT (60% left ventricular hypertrophy-positive) were compared with 18

264 table, established ERT patients (mainly left ventricular hypertrophy-positive).

265 rtic dissection (3, 8%), and idiopathic left ventricular hypertrophy/possible hypertrophic cardiomyop

266 Rather than developing compensatory left ventricular hypertrophy, pressure overload in cardiomyoc

267 rmalities included voltage criteria for left ventricular hypertrophy, prolongation of the corrected Q

268 as assessed in mice via measurement of right ventricular hypertrophy, pulmonary vascular remodeling,

269 is (CA) from other causes of concentric left ventricular hypertrophy remains a clinical challenge, es

270 lectrocardiographic (ECG) criteria for right ventricular hypertrophy (RVH) measured by cardiac magnet

271 lar counts (RACs), vessel density, and right ventricular hypertrophy (RVH).

272 differentiated CA from other causes of left ventricular hypertrophy (sensitivity, 88%; specificity,

273 8 months enabled modeling of polygenic left ventricular hypertrophy starting from patient cells.

274 carriers of sarcomere mutation without left ventricular hypertrophy, suggesting that contractile abn

275 silent cTOD (i.e., myocardial ischemia, left ventricular hypertrophy, systolic dysfunction, diastolic

276 rigger, not the result, of pathological left ventricular hypertrophy through NF-kappaB-related pathwa

277 overload accelerates the progression of left ventricular hypertrophy to heart failure in mice.

278 ation product, and Sokolow-Lyon voltage left ventricular hypertrophy treated as time-varying covariat

279 netic disorder that is characterized by left ventricular hypertrophy unexplained by secondary causes

280 (long PR, complete bundle branch block, left ventricular hypertrophy voltage criteria, long QTc, and

281 risk of adverse outcome associated with left ventricular hypertrophy was additive to the risk associa

282 Extreme left ventricular hypertrophy was most frequently associated w

283 CI], -15.4 to -0.01), particularly when left ventricular hypertrophy was present (-18.6 g per square

284 Left ventricular hypertrophy was present in 144 athletes (27.

285 Left ventricular hypertrophy was present in 19 individuals (8

286 At month 24, left ventricular hypertrophy was present in 41.7% versus 37.7

287 Extreme left ventricular hypertrophy was the most common risk factor

288 Left ventricular hypertrophy was the most prevalent (29.7%) f

289 However, right ventricular hypertrophy was unchanged despite attenuated

290 assess the relationship between BP and left ventricular hypertrophy, we prospectively analyzed data

291 ular ejection fraction, and presence of left ventricular hypertrophy were associated with greater odd

292 nt for aortic stenosis with evidence of left ventricular hypertrophy were randomly assigned to GIK or

293 nd evidence on the electrocardiogram of left ventricular hypertrophy), which later formed the basis f

294 A and family B men >30 years of age had left ventricular hypertrophy, which was mainly asymmetrical,

295 sive patients with electrocardiographic left ventricular hypertrophy with no history of AF, in sinus

296 for SCD risk based on ECG criteria for left ventricular hypertrophy with repolarization abnormalitie

297 ECG left ventricular hypertrophy with strain is associated with a

298 All patients showed asymmetrical left ventricular hypertrophy, with maximal left ventricular t

299 However, ECG markers of left ventricular hypertrophy, with or without repolarization

300 left ventricular hypertrophy (n=51) and left ventricular hypertrophy without ECG strain (n=30), patie