ライフサイエンスコーパス: left ventricular hypertrophy

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

2 iated with incident hypertension and risk of left ventricular hypertrophy.

3 tify individuals at risk for hypertension or left ventricular hypertrophy.

4 re men, 31 had diabetes mellitus, and 59 had left ventricular hypertrophy.

5 n, progressive conduction system disease and left ventricular hypertrophy.

6 a sickle cell positive athlete who also had left ventricular hypertrophy.

7 from the onset of systemic hypertension and left ventricular hypertrophy.

8 nd a mixed logistic model was used to assess left ventricular hypertrophy.

9 ed with HCTZ, CTDN was associated with lower left ventricular hypertrophy.

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

11 ressive aortic valve narrowing and secondary left ventricular hypertrophy.

12 of 18 children with normal echoes developed left ventricular hypertrophy.

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

14 risk factors, particularly hypertension and left ventricular hypertrophy.

15 tical aortic stenosis often have significant left ventricular hypertrophy.

16 e a hallmark of mitochondrial dysfunction in left ventricular hypertrophy.

17 but in none of the mutation carriers without left ventricular hypertrophy.

18 baseline risk factors plus electrocardiogram left ventricular hypertrophy.

19 tihypertensive therapy and regression of ECG left ventricular hypertrophy.

20 Hg are associated in a 7-yr study to reverse left ventricular hypertrophy.

21 ystem and can predispose to hypertension and left ventricular hypertrophy.

22 tolic blood pressure, diabetes, smoking, and left ventricular hypertrophy.

23 ling cascades involved in the development of left ventricular hypertrophy.

24 hort of sarcomeric mutation carriers without left ventricular hypertrophy.

25 ns with isolated HCM and syndromes including left ventricular hypertrophy.

26 genes definitively associated with isolated left ventricular hypertrophy.

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

28 tolic blood pressures, cardiac fibrosis, and left ventricular hypertrophy.

29 sarcomere mutation carriers with and without left ventricular hypertrophy.

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

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

32 onfidence interval: 1.02, 1.21) and incident left ventricular hypertrophy (1.02, 95% confidence inter

33 ects (6%), mitral valve abnormalities (51%), left ventricular hypertrophy (19%), and atrial fibrillat

34 ant increase in the prevalence of concentric left ventricular hypertrophy (2 of 64 [3%] versus 20 of

35 were performed in 44 Fabry patients without left ventricular hypertrophy (35.7+/-14.5 years, 68.2% f

36 e heart failure (43% versus 34%; P=0.04) and left ventricular hypertrophy (77% versus 58%; P=0.02) an

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

38 Left ventricular hypertrophy (adjusted hazard ratio, 1.5

39 The decrease in the prevalence of left ventricular hypertrophy after renal transplantation

40 nd was significantly associated with greater left ventricular hypertrophy and a higher prevalence of

41 p65 NF-kappaB deletion promoted maladaptive left ventricular hypertrophy and accelerated progression

42 diovascular disease and a high prevalence of left ventricular hypertrophy and arterial stiffness that

43 Extreme left ventricular hypertrophy and blunted blood pressure

44 s a common genetic disorder characterized by left ventricular hypertrophy and cardiac hyper-contracti

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

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

47 Left ventricular hypertrophy and coronary artery calcifi

48 ed FGF-23 concentrations are associated with left ventricular hypertrophy and coronary artery calcifi

49 promote atrial fibrillation (AF) by inducing left ventricular hypertrophy and diastolic and left atri

50 , respectively) with good discrimination for left ventricular hypertrophy and diastolic dysfunction a

51 dels induced significant, severity-dependent left ventricular hypertrophy and diastolic dysfunction c

52 HFHS diet-fed mice developed progressive left ventricular hypertrophy and diastolic dysfunction w

53 preserved FEV1/FVC ratio is associated with left ventricular hypertrophy and diastolic dysfunction.

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

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

56 -tg and Kir6.2 KO mice developed more severe left ventricular hypertrophy and dysfunction as compared

57 Early markers of cardiomyopathy, such as left ventricular hypertrophy and dysfunction, and early

58 approach to treat pressure overload-induced left ventricular hypertrophy and dysfunction.

59 Indices of left ventricular hypertrophy and ejection fraction were

60 regression of target end organ effects like left ventricular hypertrophy and endothelial dysfunction

61 angiotensin II receptor blocker losartan on left ventricular hypertrophy and fibrosis in patients wi

62 the renin-angiotensin system contributes to left ventricular hypertrophy and fibrosis, a major deter

63 Grx2(-/-) hearts also developed left ventricular hypertrophy and fibrosis, and mice beca

64 fects of angiotensin II receptor blockers on left ventricular hypertrophy and fibrosis, which are pre

65 ulating miRNAs correlated with the degree of left ventricular hypertrophy and fibrosis.

66 astolic dysfunction seen in conjunction with left ventricular hypertrophy and fibrosis.

67 ce developed cardiomyopathy characterized by left ventricular hypertrophy and glycogen accumulation,

68 or for FGF23 in the kidney, which stimulates left ventricular hypertrophy and hepatic production of i

69 ficantly higher in mutation carriers without left ventricular hypertrophy and in subjects with overt

70 Conclusion Cardiac MRI findings of left ventricular hypertrophy and late gadolinium enhance

71 lence of structural heart disease, including left ventricular hypertrophy and left atrial enlargement

72 Echocardiographic data showed left ventricular hypertrophy and lower fractional shorte

73 sarcomere gene hypothesis, such as regional left ventricular hypertrophy and myocardial fibrosis, as

74 imal-medial thickness, and echocardiographic left ventricular hypertrophy and systolic dysfunction.

75 omyopathy, 39 subjects with mutations but no left ventricular hypertrophy, and 30 controls who did no

76 ltimorbidity, impaired chronotropic reserve, left ventricular hypertrophy, and activation of inflamma

77 n increased relative wall thickness or overt left ventricular hypertrophy, and associated diastolic d

78 HFpEF mice developed hypertension, left ventricular hypertrophy, and diastolic dysfunction

79 atients develop renal failure, hypertension, left ventricular hypertrophy, and diastolic dysfunction,

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

81 onary heart disease, valvular heart disease, left ventricular hypertrophy, and estimated glomerular f

82 rats showed higher body weight, significant left ventricular hypertrophy, and impaired diastolic fun

83 maladaptive concentrations, and then induces left ventricular hypertrophy, and is possibly implicated

84 djusted for risk factors including diabetes, left ventricular hypertrophy, and ischemia (adjusted haz

85 Patients with increased age, left ventricular hypertrophy, and left atrial dilatation

86 atrial fibrillation, myocardial infarction, left ventricular hypertrophy, and left bundle branch blo

87 rate, hypertension, cardiovascular disease, left ventricular hypertrophy, and left bundle-branch blo

88 cardial infarction, lower ejection fraction, left ventricular hypertrophy, and left ventricular dilat

89 Histological abnormalities, left ventricular hypertrophy, and left ventricular dysfu

90 versing cardiovascular complications such as left ventricular hypertrophy, and minimizing the use of

91 s are linked to CKD and greater risk of CVD, left ventricular hypertrophy, and mortality in dialysis

92 ith chronic kidney disease, mild to moderate left ventricular hypertrophy, and preserved left ventric

93 ltage criteria for right ventricular (RV) or left ventricular hypertrophy, and symmetrical cardiac en

94 h stage B HF (normal exercise tolerance with left ventricular hypertrophy, and/or reduced global long

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

96 n velocity (CV) and conduction anisotropy in left ventricular hypertrophy are associated with topogra

97 ossible mechanistic role of exercise-induced left ventricular hypertrophy as the basis for J-point el

98 ial myocardial and perivascular fibrosis and left ventricular hypertrophy associated with diastolic d

99 pertrophy, and also 2 survivors with extreme left ventricular hypertrophy at age 15 years.

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

101 diastolic dysfunction pathway that includes left ventricular hypertrophy, atrial enlargement, and he

102 c blood pressure, current smoking, diabetes, left ventricular hypertrophy, atrial fibrillation, and p

103 changes, ventricular conduction defects, and left ventricular hypertrophy based on the Minnesota code

104 GR-1 exhibited a significant attenuation of left ventricular hypertrophy based on tissue weight asse

105 Left ventricular hypertrophy became less marked over tim

106 ing ECG (ST-segment or T-wave abnormalities, left ventricular hypertrophy, bundle branch block, or le

107 trongly associated with HFpEF, and male sex, left ventricular hypertrophy, bundle branch block, previ

108 High FGF-23 levels promote left ventricular hypertrophy but not coronary artery cal

109 It is characterised by left ventricular hypertrophy but there is an important p

110 a(2+)ATPase and phospholamban were normal in left ventricular hypertrophy, but decreased in failing h

111 hypertension is linked to the development of left ventricular hypertrophy, but whether this associati

112 e known predictive value of in-treatment ECG left ventricular hypertrophy by Cornell product and Soko

113 5 (95% CI: 0.94 to 0.97) among patients with left ventricular hypertrophy by ECG criteria and 0.95 (9

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

115 a novel multimodality testing strategy using left ventricular hypertrophy by ECG, coronary artery cal

116 T was also strongly associated with incident left ventricular hypertrophy by electrocardiography over

117 carotid intima-media thickness or stenosis, left ventricular hypertrophy [by ECG or echocardiography

118 in selected areas, such as undifferentiated left ventricular hypertrophy, cardio-oncology, aortic st

119 ndividuals: sarcomere mutation carriers with left ventricular hypertrophy (clinical HCM; n=36), mutat

120 Over 4 years, the adjusted prevalence of left ventricular hypertrophy decreased from 15.3% to 12.

121 rrelation between the level of hypertension, left ventricular hypertrophy, deterioration of GFR, and

122 adiponectin deficiency in HFpEF exacerbates left ventricular hypertrophy, diastolic dysfunction, and

123 Uremic cardiomyopathy, characterized by left ventricular hypertrophy, diastolic dysfunction, and

124 sion in aldosterone-infused mice ameliorated left ventricular hypertrophy, diastolic dysfunction, lun

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

126 c background lacked hallmarks of HCM such as left ventricular hypertrophy, disarray of myofibers, and

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

128 creased risk of development of hypertension, left ventricular hypertrophy/dysfunction, vascular dysfu

129 olonged-QT commonly coexists in the ECG with left ventricular hypertrophy (ECG-LVH).

130 factors, incident hypertension and incident left ventricular hypertrophy, estimated by complete-case

131 ceptor density in nonfailing, hypertrophied (left ventricular hypertrophy), failing, and failing left

132 lates age-related cardiac changes in humans (left ventricular hypertrophy, fibrosis and diastolic dys

133 CM), typically characterized by asymmetrical left ventricular hypertrophy, frequently is caused by mu

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

135 may be present in mutation carriers without left ventricular hypertrophy (G+LVH-) but are difficult

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

137 improved left ventricular function, blunted left ventricular hypertrophy, greater preservation of vi

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

139 Left ventricular hypertrophy has been identified as an i

140 patients with genetic mutations but without left-ventricular hypertrophy has emerged, with unresolve

141 o traffic-related air pollution is linked to left ventricular hypertrophy, heart failure, and death.

142 y disease (CKD) and strongly associated with left ventricular hypertrophy, heart failure, and death.

143 paired glucose metabolism, renal impairment, left ventricular hypertrophy, heart failure, and others.

144 ection fraction patients enrolled in TOPCAT, left ventricular hypertrophy, higher left ventricular fi

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

146 Hypertensive left ventricular hypertrophy (HTN-LVH) is a leading caus

147 diagnosis is based on otherwise unexplained left-ventricular hypertrophy identified by echocardiogra

148 essure, normalized sympathetic activity, and left ventricular hypertrophy in Ang II rats, as well as

149 ed the role of CLP-1 in vivo in induction of left ventricular hypertrophy in angiotensinogen-overexpr

150 hat a decline in BP may predict a decline in left ventricular hypertrophy in children with CKD and su

151 regulatory hormone that directly stimulates left ventricular hypertrophy in experimental models.

152 The pathogenesis of left ventricular hypertrophy in patients with CKD is inc

153 ociated with left ventricular mass index and left ventricular hypertrophy in patients with CKD.

154 ociated with hypertensive heart disease with left ventricular hypertrophy in the absence of coronary

155 nt additional investigation as predictors of left ventricular hypertrophy in these patients.

156 2 and redistribution of LTCC were studied in left ventricular hypertrophy in vivo and in cultured adu

157 contractile dysfunction in pressure-overload left ventricular hypertrophy in vivo.

158 icacy in inhibiting tumor growth in mice and left-ventricular hypertrophy in rats and in the bovine c

159 new non-AF cardiovascular diagnoses, such as left ventricular hypertrophy, in 28 participants (4.6%).

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

161 Predictors of left ventricular hypertrophy included systolic BP, femal

162 Prevalence of left ventricular hypertrophy increased from 7.5% (95% CI

163 The prevalence of hypertension and left ventricular hypertrophy increased with the degree o

164 with a HFHS diet prevent the development of left ventricular hypertrophy, interstitial fibrosis, and

165 We hypothesized that athletic left ventricular hypertrophy is a consequence of increas

166 Left ventricular hypertrophy is absent in the minority o

167 Left ventricular hypertrophy is an initial compensatory

168 Left ventricular hypertrophy is rare in children with TN

169 t are especially prevalent in late life (eg, left ventricular hypertrophy, ischemic heart disease, he

170 arrowing and then examine the development of left ventricular hypertrophy, its subsequent decompensat

171 osclerosis, volume overload, and progressive left ventricular hypertrophy, leading to elevated N-term

172 pEF, characterized by diastolic dysfunction, left ventricular hypertrophy, left atrial dilatation, an

173 n, sleep disordered breathing, inflammation, left ventricular hypertrophy, left atrial enlargement, a

174 Left ventricular hypertrophy, left atrial volume, AEVS,

175 pecific model additionally included smoking, left ventricular hypertrophy, left bundle branch block,

176 minal probrain natriuretic peptide level and left ventricular hypertrophy, left ventricular systolic

177 1 in the DT (FGFR1(DT-cKO) mice) resulted in left ventricular hypertrophy (LVH) and decreased kidney

178 Left ventricular hypertrophy (LVH) and diastolic dysfunc

179 Individuals with left ventricular hypertrophy (LVH) and elevated cardiac

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

181 Left ventricular hypertrophy (LVH) and late gadolinium e

182 this study was to examine the prevalence of left ventricular hypertrophy (LVH) and left ventricular

183 ed patients with baseline moderate or severe left ventricular hypertrophy (LVH) and paired measuremen

184 -based renal sympathetic denervation (RD) on left ventricular hypertrophy (LVH) and systolic and dias

185 ne the association of exercise capacity with left ventricular hypertrophy (LVH) and systolic/diastoli

186 tected in 40% of cases, including idiopathic left ventricular hypertrophy (LVH) and/or fibrosis (n =

187 ences between physiological and pathological left ventricular hypertrophy (LVH) are of intense intere

188 The prevalence of left ventricular hypertrophy (LVH) assessed by echocardi

189 Left ventricular hypertrophy (LVH) associates with incre

190 tress identify asymptomatic individuals with left ventricular hypertrophy (LVH) at higher risk for he

191 by mutations in sarcomere protein genes, and left ventricular hypertrophy (LVH) develops as an adapti

192 ns seem to induce profibrotic changes before left ventricular hypertrophy (LVH) develops.

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

194 Reduction of electrocardiographic left ventricular hypertrophy (LVH) has been associated w

195 A malignant subphenotype of left ventricular hypertrophy (LVH) has been described, i

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

197 Prevalence of concentric left ventricular hypertrophy (LVH) improved from 28% at

198 ic impact of ECG left ventricular strain and left ventricular hypertrophy (LVH) in asymptomatic aorti

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

200 ibitors proved to be effective in regressing left ventricular hypertrophy (LVH) in renal transplant r

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

202 ates in pig cardiac tissue, with and without left ventricular hypertrophy (LVH) induced by aortic ban

203 Left ventricular hypertrophy (LVH) is a major risk facto

204 Left ventricular hypertrophy (LVH) is an important mecha

205 Left ventricular hypertrophy (LVH) is associated with el

206 Left ventricular hypertrophy (LVH) is common in T2DM and

207 Left ventricular hypertrophy (LVH) is usually accompanie

208 BP including coronary artery disease (CAD), left ventricular hypertrophy (LVH) or stroke.

209 Left ventricular hypertrophy (LVH) typically manifests d

210 Left ventricular hypertrophy (LVH) was present in 60 sub

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

212 8 weeks after ascending aortic constriction (left ventricular hypertrophy (LVH)) or sham operation.

213 dy sought to examine the association between left ventricular hypertrophy (LVH), de fi ned by cardiac

214 s was evaluated with respect to diagnosis of left ventricular hypertrophy (LVH), eligibility for dise

215 ts with chronic kidney disease (CKD) reduces left ventricular hypertrophy (LVH), which is a risk fact

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

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

218 55 healthy athletes with mild physiological left ventricular hypertrophy (LVH).

219 in CKD, it may contribute mechanistically to left ventricular hypertrophy (LVH).

220 structural changes before the development of left ventricular hypertrophy (LVH).

221 intracellular lipid disorder that can cause left ventricular hypertrophy (LVH).

222 re impaired in HCM mutation carriers without left ventricular hypertrophy (LVH).

223 nt in arterial compliance might also regress left ventricular hypertrophy (LVH).

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

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

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

227 Left ventricular hypertrophy (LVH; high LV mass [LVM]) i

228 25 patients with essential hypertension and left ventricular hypertrophy (LVH[+]) and 24 normal cont

229 patients (49 years, 43% male, 24 [55%] with left ventricular hypertrophy [LVH]) and 27 healthy contr

230 ts, accelerated coronary atherosclerosis and left ventricular hypertrophy manifest in the fourth deca

231 Persistence of the left ventricular hypertrophy may result from the combine

232 Arterial stiffness and left ventricular hypertrophy may significantly influence

233 resistance, thus leading to hypertension and left ventricular hypertrophy, metabolic syndrome/diabete

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

235 thesize that altered metabolic properties in left ventricular hypertrophy modulate DeltaPsi(m) spatio

236 variety of cardiac disease processes such as left ventricular hypertrophy, myocardial ischemia, and d

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

238 ere stable, treatment-naive patients (mainly left ventricular hypertrophy-negative); advanced disease

239 ge, gender, hypertension, diabetes mellitus, left ventricular hypertrophy, obesity, serum total chole

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

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

242 Left ventricular hypertrophy on ECG was a strong predict

243 In select carriers without left ventricular hypertrophy on echocardiogram, SCD occu

244 event, it was independently associated with left ventricular hypertrophy only in women.

245 Left ventricular hypertrophy or concentric remodeling, L

246 seline muscle contraction was not altered in left ventricular hypertrophy or failing hearts.

247 rofibrotic state preceded the development of left ventricular hypertrophy or fibrosis visible on MRI.

248 Cardiac structural abnormalities, left ventricular hypertrophy, or concentric geometry, we

249 al fibrosis in the absence of myocarditis or left ventricular hypertrophy, or other known pathogenese

250 However, correlation with left ventricular hypertrophy parameters holds true for o

251 ncrease in log FGF-23; P=0.01; odds ratio of left ventricular hypertrophy per 1-SD increase in log FG

252 pe analyses we find association of NRG1 with left ventricular hypertrophy phenotypes, fibrinogen and

253 ACSM3, ERI2, IL18RAP, IL23RAP and NRG1) with left ventricular hypertrophy phenotypes.

254 natriuretic peptide, which is induced during left ventricular hypertrophy, plays an anti-fibrogenic a

255 After 1 year of ERT initiation, left ventricular hypertrophy-positive patients have a de

256 Twenty patients starting ERT (60% left ventricular hypertrophy-positive) were compared wit

257 ere stable, established ERT patients (mainly left ventricular hypertrophy-positive).

258 ), aortic dissection (3, 8%), and idiopathic left ventricular hypertrophy/possible hypertrophic cardi

259 Rather than developing compensatory left ventricular hypertrophy, pressure overload in cardi

260 aving a higher proportion of males, smokers, left ventricular hypertrophy, previous left heart cathet

261 abnormalities included voltage criteria for left ventricular hypertrophy, prolongation of the correc

262 esis, A(3)R KO attenuated 5-week TAC-induced left ventricular hypertrophy (ratio of ventricular mass/

263 oidosis (CA) from other causes of concentric left ventricular hypertrophy remains a clinical challeng

264 s are decreased in pressure overload-induced left ventricular hypertrophy, resulting in action potent

265 >2.1 differentiated CA from other causes of left ventricular hypertrophy (sensitivity, 88%; specific

266 ic BP, hypertension, cardiovascular disease, left ventricular hypertrophy, smoking, alcohol use, educ

267 up to 8 months enabled modeling of polygenic left ventricular hypertrophy starting from patient cells

268 so in carriers of sarcomere mutation without left ventricular hypertrophy, suggesting that contractil

269 rbor silent cTOD (i.e., myocardial ischemia, left ventricular hypertrophy, systolic dysfunction, dias

270 the trigger, not the result, of pathological left ventricular hypertrophy through NF-kappaB-related p

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

272 e-duration product, and Sokolow-Lyon voltage left ventricular hypertrophy treated as time-varying cov

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

274 ties (long PR, complete bundle branch block, left ventricular hypertrophy voltage criteria, long QTc,

275 The OR for left ventricular hypertrophy was 4.8 in men (95% CI: 1.0

276 The risk of adverse outcome associated with left ventricular hypertrophy was additive to the risk as

277 Extreme left ventricular hypertrophy was most frequently associa

278 Left ventricular hypertrophy was observed in LKB1-KO mic

279 Left ventricular hypertrophy was particularly marked (ma

280 val [CI], -15.4 to -0.01), particularly when left ventricular hypertrophy was present (-18.6 g per sq

281 Left ventricular hypertrophy was present in 144 athletes

282 Left ventricular hypertrophy was present in 19 individua

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

284 However, left ventricular hypertrophy was prevented by simvastati

285 Extreme left ventricular hypertrophy was the most common risk fa

286 Left ventricular hypertrophy was the most prevalent (29.

287 To assess the relationship between BP and left ventricular hypertrophy, we prospectively analyzed

288 ntricular ejection fraction, and presence of left ventricular hypertrophy were associated with greate

289 acement for aortic stenosis with evidence of left ventricular hypertrophy were randomly assigned to G

290 Hypertension and left ventricular hypertrophy were the risk factors most

291 els and evidence on the electrocardiogram of left ventricular hypertrophy), which later formed the ba

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

293 ertensive patients with electrocardiographic left ventricular hypertrophy with no history of AF, in s

294 arker for SCD risk based on ECG criteria for left ventricular hypertrophy with repolarization abnorma

295 ECG left ventricular hypertrophy with strain is associated w

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

297 However, ECG markers of left ventricular hypertrophy, with or without repolariza

298 ic response in an aortic-banded rat model of left ventricular hypertrophy, with reduced left ventricu

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

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