ライフサイエンスコーパス: ventricular hypertrophy

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

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

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

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

5 ats with established PAH and decreased right ventricular hypertrophy.

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

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

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

9 e in pulmonary vascular remodeling and right ventricular hypertrophy.

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

11 ve aortic valve narrowing and secondary left ventricular hypertrophy.

12 8 children with normal echoes developed left ventricular hypertrophy.

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

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

15 factors, particularly hypertension and left ventricular hypertrophy.

16 aortic stenosis often have significant left ventricular hypertrophy.

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

18 allmark of mitochondrial dysfunction in left ventricular hypertrophy.

19 n none of the mutation carriers without left ventricular hypertrophy.

20 ine risk factors plus electrocardiogram left ventricular hypertrophy.

21 ertensive therapy and regression of ECG left ventricular hypertrophy.

22 e associated in a 7-yr study to reverse left ventricular hypertrophy.

23 None of the patients had ventricular hypertrophy.

24 and can predispose to hypertension and left ventricular hypertrophy.

25 blood pressure, diabetes, smoking, and left ventricular hypertrophy.

26 n of peripheral pulmonary arteries and right ventricular hypertrophy.

27 mere mutation carriers with and without left ventricular hypertrophy.

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

29 h raised pulmonary artery pressure and right ventricular hypertrophy.

30 with incident hypertension and risk of left ventricular hypertrophy.

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

32 molecules are crucial to calcium cycling and ventricular hypertrophy.

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

34 individuals at risk for hypertension or left ventricular hypertrophy.

35 pressure (pulmonary hypertension) and right ventricular hypertrophy.

36 ate the development of cardiac (specifically ventricular) hypertrophy.

37 (6%), mitral valve abnormalities (51%), left ventricular hypertrophy (19%), and atrial fibrillation (

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

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

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

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

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

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

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

45 systolic pressure >30 mm Hg exhibited right ventricular hypertrophy and an increase in the number an

46 scular disease and a high prevalence of left ventricular hypertrophy and arterial stiffness that conf

47 Extreme left ventricular hypertrophy and blunted blood pressure respo

48 heart against pressure overload-induced left ventricular hypertrophy and CHF.

49 , and the hearts were protected against left ventricular hypertrophy and CHF.

50 Left ventricular hypertrophy and coronary artery calcificatio

51 F-23 concentrations are associated with left ventricular hypertrophy and coronary artery calcificatio

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

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

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

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

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

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

58 nd Kir6.2 KO mice developed more severe left ventricular hypertrophy and dysfunction as compared with

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

60 Indices of left ventricular hypertrophy and ejection fraction were simil

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

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

63 arterial hypertension and pathological right ventricular hypertrophy and failure.

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

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

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

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

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

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

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

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

72 tly higher in mutation carriers without left ventricular hypertrophy and in subjects with overt hyper

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

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

75 Echocardiographic data showed left ventricular hypertrophy and lower fractional shortening

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

77 In addition, the ventricular hypertrophy and proximal aorta dilation obse

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

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

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

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

82 athy, 39 subjects with mutations but no left ventricular hypertrophy, and 30 controls who did not hav

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

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

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

86 ificant pulmonary vascular remodeling, right ventricular hypertrophy, and decreased lung alveolarizat

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

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

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

90 heart disease, valvular heart disease, left ventricular hypertrophy, and estimated glomerular filtra

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

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

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

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

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

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

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

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

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

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

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

102 ical stressors are at risk for hypertension, ventricular hypertrophy, and premature atherosclerosis;

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

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

105 ricular systolic pressure, significant right ventricular hypertrophy, and striking vascular remodelin

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

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

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

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

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

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

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

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

114 ophy, and also 2 survivors with extreme left ventricular hypertrophy at age 15 years.

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

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

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

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

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

120 CG (ST-segment or T-wave abnormalities, left ventricular hypertrophy, bundle branch block, or left-ax

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

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

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

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

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

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

127 wn predictive value of in-treatment ECG left ventricular hypertrophy by Cornell product and Sokolow-L

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

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

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

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

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

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

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

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

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

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

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

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

140 tion between the level of hypertension, left ventricular hypertrophy, deterioration of GFR, and the p

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

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

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

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

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

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

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

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

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

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

155 Left ventricular hypertrophy has been identified as an indepe

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

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

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

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

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

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

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

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

164 lmonary arterial pressure and inhibits right ventricular hypertrophy in a rat model of PAH.

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

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

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

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

169 ed with left ventricular mass index and left ventricular hypertrophy in patients with CKD.

170 in inhibiting tumor growth in mice and left-ventricular hypertrophy in rats and in the bovine cartil

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

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

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

176 Prevalence of left ventricular hypertrophy increased from 7.5% (95% CI, 6.4

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

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

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

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

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

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

183 Left ventricular hypertrophy is absent in the minority of adu

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

185 Left ventricular hypertrophy is an initial compensatory mecha

186 Left ventricular hypertrophy is rare in children with TNNT2 m

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

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

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

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

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

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

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

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

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

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

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

198 study was to examine the prevalence of left ventricular hypertrophy (LVH) and left ventricular (LV)

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

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

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

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

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

204 Left ventricular hypertrophy (LVH) associates with increased

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

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

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

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

209 Prevalence of concentric left ventricular hypertrophy (LVH) improved from 28% at pre-o

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

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

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

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

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

215 Left ventricular hypertrophy (LVH) is an important mechanism

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

217 Left ventricular hypertrophy (LVH) is usually accompanied by

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

219 Left ventricular hypertrophy (LVH) typically manifests during

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

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

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

223 th chronic kidney disease (CKD) reduces left ventricular hypertrophy (LVH), which is a risk factor fo

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

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

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

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

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

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

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

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

235 ccelerated coronary atherosclerosis and left ventricular hypertrophy manifest in the fourth decade; h

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

237 Arterial stiffness and left ventricular hypertrophy may significantly influence the

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

239 We analyzed data from a canine left ventricular hypertrophy model to determine how the energ

240 ze that altered metabolic properties in left ventricular hypertrophy modulate DeltaPsi(m) spatiotempo

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

242 ty of cardiac disease processes such as left ventricular hypertrophy, myocardial ischemia, and diabet

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

244 ender, hypertension, diabetes mellitus, left ventricular hypertrophy, obesity, serum total cholestero

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

246 ease in log FGF-23; P=0.01) and risk of left ventricular hypertrophy (odds ratio per 1-SD increase in

247 Left ventricular hypertrophy on ECG was a strong predictor of

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

249 Left ventricular hypertrophy or concentric remodeling, LA enl

250 ased TAC-induced mortality but did not alter ventricular hypertrophy or dysfunction compared with wil

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

252 rotic state preceded the development of left ventricular hypertrophy or fibrosis visible on MRI.

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

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

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

256 se in log FGF-23; P=0.01; odds ratio of left ventricular hypertrophy per 1-SD increase in log FGF-23,

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

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

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

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

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

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

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

264 A(3)R KO attenuated 5-week TAC-induced left ventricular hypertrophy (ratio of ventricular mass/body

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

266 decreased in pressure overload-induced left ventricular hypertrophy, resulting in action potential a

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

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

269 Autophagy is activated during ventricular hypertrophy, serving to maintain cellular ho

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

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

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

273 echanism in the transition from compensatory ventricular hypertrophy to heart failure.

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

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

276 and decreased pulmonary hypertension, right ventricular hypertrophy, vascular remodeling, vascular c

277 The OR for left ventricular hypertrophy was 4.8 in men (95% CI: 1.03 to

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

279 In contrast, adaptive right ventricular hypertrophy was less than anticipated.

280 Extreme left ventricular hypertrophy was most frequently associated w

281 Left ventricular hypertrophy was observed in LKB1-KO mice at

282 Left ventricular hypertrophy was particularly marked (maximum

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

286 Extreme left ventricular hypertrophy was the most common risk factor

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

288 However, right ventricular hypertrophy was unchanged despite attenuated

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

290 e to pulmonary vascular remodeling and right ventricular hypertrophy, we tested the hypothesis that b

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 Hypertension and left ventricular hypertrophy were the risk factors most stron

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

295 ght ventricular systolic pressures and right ventricular hypertrophy with corresponding pulmonary vas

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

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

300 Extreme left ventricular hypertrophy (z-score: >6) and an abnormal bl