ライフサイエンスコーパス: ventricular remodeling

1 diography and their value in preventing left ventricular remodeling.

2 ents with comparable degrees of PH and right ventricular remodeling.

3 l changes in the heart in a process known as ventricular remodeling.

4 sociated with durable repair and may prevent ventricular remodeling.

5 wound healing and scar formation and affects ventricular remodeling.

6 largely prevented fibrosis and limited left ventricular remodeling.

7 option for patients with postinfarction left ventricular remodeling.

8 myocardial infarction (MI) accelerates left ventricular remodeling.

9 nfarct inflammation, and curbed post-MI left ventricular remodeling.

10 d cellular mechanisms governing pathological ventricular remodeling.

11 ent quality of life, and may promote reverse ventricular remodeling.

12 iac pathologies, including post-infarct left ventricular remodeling.

13 by interfering with lung vascular and right ventricular remodeling.

14 into the association between AF and adverse ventricular remodeling.

15 nt functional capacity, quality of life, and ventricular remodeling.

16 athways in promoting cardiac hypertrophy and ventricular remodeling.

17 romotes cardiac dysfunction, cell death, and ventricular remodeling.

18 cs and regional function, and in attenuating ventricular remodeling.

19 rine infarcts and consequently enhances left ventricular remodeling.

20 etic peptide (BNP), and fully prevented left-ventricular remodeling.

21 l of the mitral valve (MV) to compensate for ventricular remodeling.

22 ogenesis in response to ischemia, leading to ventricular remodeling.

23 mice and rats showed signs of more favorable ventricular remodeling.

24 cardiac contractile performance, and halted ventricular remodeling.

25 revented diastolic dysfunction, and improved ventricular remodeling.

26 ocardial infarction (MI) and subsequent left ventricular remodeling.

27 ng tissue, which often leads to adverse left ventricular remodeling.

28 luded improved contractile function and left ventricular remodeling.

29 rdium in the infarct zone, and superior left ventricular remodeling.

30 s been implicated in cardiac hypertrophy and ventricular remodeling.

31 -dependent signaling pathways that influence ventricular remodeling.

32 urgical therapies aimed at achieving reverse ventricular remodeling.

33 c functional recovery and prevention of left ventricular remodeling.

34 ymptoms, exercise tolerance, and reversal of ventricular remodeling.

35 tricular systolic function, and reduced left ventricular remodeling.

36 reduces systolic dysfunction, and attenuates ventricular remodeling.

37 broblasts and myocytes to alter survival and ventricular remodeling.

38 nce imaging (MRI) in studying postinfarction ventricular remodeling.

39 s increased collagen turnover culminating in ventricular remodeling.

40 , improve myocardial function, and attenuate ventricular remodeling.

41 ies support a key role for cytokines in left ventricular remodeling.

42 oblasts is implicated in infarct healing and ventricular remodeling.

43 l ECM early after coronary occlusion lessens ventricular remodeling.

44 e in the development and progression of left ventricular remodeling.

45 fibroblast state that underlies fibrosis and ventricular remodeling.

46 a Bcl-2-mediated reduction in apoptosis and ventricular remodeling.

47 morbidity and mortality associated with left ventricular remodeling.

48 ht be partially explained by a positive left ventricular remodeling.

49 severity, symptom improvement, and positive ventricular remodeling.

50 ould improve cardiac function and ameliorate ventricular remodeling.

51 ial injury and its predictive value for left ventricular remodeling.

52 regurgitation is indicated to avoid adverse ventricular remodeling.

53 xerted a sustained beneficial effect on left ventricular remodeling.

54 ocardium and has been linked to adverse left ventricular remodeling.

55 d the angiogenic defect and ameliorated left ventricular remodeling.

56 tress-induced cell death and adverse cardiac ventricular remodeling.

57 rovoke left ventricular dysfunction and left ventricular remodeling.

58 ocyte contractility and reduction in adverse ventricular remodeling.

59 at regulates post-myocardial infarction left ventricular remodeling.

60 as a potential therapeutic target to prevent ventricular remodeling.

61 c and diastolic function, and decreased left ventricular remodeling.

62 ailure-related urgent care, and adverse left ventricular remodeling.

63 e clinical outcomes and prevent adverse left ventricular remodeling.

64 59.3+/-7.9%, with prevalent concentric left ventricular remodeling (34%) and hypertrophy (43%), and

65 ed cardiac function at baseline and impaired ventricular remodeling 7 days after nonreperfused AMI.

66 model, prior angina remained protective for ventricular remodeling after adjusting for age, gender,

67 physiological mechanisms of inflammation and ventricular remodeling after AMI and the results of clin

68 sis and survival of cardiac myocyte and left ventricular remodeling after AMI is unknown.

69 aks of SDF-1 and CXCR4, has no major role in ventricular remodeling after AMI.

70 clude that NP12 might be useful for limiting ventricular remodeling after an AMI.

71 Myocardial inflammation is critical for ventricular remodeling after ischemia.

72 ysiological hypertrophy and mitigate adverse ventricular remodeling after ischemic injury.

73 ovide a novel means to favorably modify left ventricular remodeling after MI.

74 eutic targets that can influence healing and ventricular remodeling after MI.

75 metalloproteinases (MMPs) contribute to left ventricular remodeling after myocardial infarction (MI).

76 ix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI).

77 lasma RNA from patients with or without left ventricular remodeling after myocardial infarction.

78 an important role in the progress of adverse ventricular remodeling after myocardial infarction.

79 verse cardiovascular events and adverse left ventricular remodeling after myocardial infarction.

80 feasible and may have beneficial effects on ventricular remodeling after myocardial infarction.

81 Inflammation contributes to ventricular remodeling after myocardial ischemia, but it

82 E. p38gamma MAPK contributes to left ventricular remodeling after pathologic stress and disin

83 p3 on cardiomyocyte death, infarct size, and ventricular remodeling after surgical ischemia/reperfusi

84 Blockade Benefits in Clinical Evolution and Ventricular Remodeling After Transcatheter Aortic Valve

85 Blockade Benefits in Clinical Evolution and Ventricular Remodeling After Transcatheter Aortic Valve

86 n was associated with significant atrial and ventricular remodeling, along with systolic dysfunction

87 BP, the incidence of hypertension, and left ventricular remodeling among collegiate ASF athletes.

88 ies production and again observed worse left ventricular remodeling and a lower ejection fraction in

89 ellular matrix expansion is a key element of ventricular remodeling and a potential therapeutic targe

90 ) mice demonstrated significantly attenuated ventricular remodeling and a smaller decrease in ejectio

91 ha specifically in cardiomyocytes attenuates ventricular remodeling and cardiac dysfunction after myo

92 d posited as the central underlying cause of ventricular remodeling and cardiac dysfunction following

93 d their angiogenic ability, attenuating left ventricular remodeling and cardiac fibrosis.

94 tractive therapeutic targets for controlling ventricular remodeling and clinical progression.

95 is limited in preventing the progression of ventricular remodeling and congestive heart failure.

96 zone, reduced scar size, and attenuated left ventricular remodeling and contractile dysfunction at 28

97 tivation that result in distinct pathways of ventricular remodeling and contractile performance.

98 post-infarction progression of negative left ventricular remodeling and decline in cardiac function i

99 dium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy.

100 contributions of cardiomyocyte autophagy to ventricular remodeling and disease pathogenesis are bein

101 The beneficial effects of CPCs on left ventricular remodeling and dysfunction are sustained for

102 kout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with con

103 IK-5001), to prevent or reverse adverse left ventricular remodeling and dysfunction in patients after

104 rtension, and renal insufficiency drive left ventricular remodeling and dysfunction through systemic

105 (LacZ) group; MSC(HO-1) also attenuated left ventricular remodeling and enhanced the functional recov

106 that a GHRH-agonist (GHRH-A; JI-38) reverses ventricular remodeling and enhances functional recovery

107 est negative effect on infarct size and left ventricular remodeling and function, as well as a signif

108 ne or in combination with parameters of left ventricular remodeling and function, yielded an improvem

109 vide evidence for beneficial effects on left ventricular remodeling and functional capacity.

110 Left ventricular remodeling and global and regional function

111 ular biomaterials hold promise to limit left ventricular remodeling and heart failure precipitated by

112 wth is crucial for the management of adverse ventricular remodeling and heart failure.

113 ptotic signaling pathways that contribute to ventricular remodeling and heart failure.

114 yme 5-alpha-reductase, improves pathological ventricular remodeling and heart failure.

115 stem cells (CBSCs) have been shown to reduce ventricular remodeling and improve cardiac function in a

116 ll as new therapies, can successfully affect ventricular remodeling and improve cardiac function.

117 poetin alfa would be associated with reverse ventricular remodeling and improved exercise capacity an

118 one cardiac myocytes resulting in beneficial ventricular remodeling and improved global left ventricu

119 This study also shows that CRT reverses ventricular remodeling and improves myocardial performan

120 Several biological pathways are activated in ventricular remodeling and in overt heart failure (HF).

121 greater MR was associated with adverse left ventricular remodeling and increased likelihood of death

122 Ventricular remodeling and infarct size were compared in

123 ational research into the pathophysiology of ventricular remodeling and is an ideal testing platform

124 valve repair is associated with adverse left ventricular remodeling and late death.

125 n of inflammation in the heart provokes left ventricular remodeling and left ventricular dysfunction.

126 Women demonstrate more concentric left ventricular remodeling and less ventricular dilatation i

127 ct border zone may play an important role in ventricular remodeling and lethal arrhythmia.

128 -angiotensin system (RAS) inhibitors on left ventricular remodeling and major clinical outcomes follo

129 are relevant to the understanding of post-MI ventricular remodeling and may contribute to the develop

130 y and sufficient for key features of adverse ventricular remodeling and may provide a novel therapeut

131 pathways that may contribute to adverse left ventricular remodeling and mitochondrial dysfunction to

132 Parameters of ventricular remodeling and modulation of cardio-renal sy

133 xerted a long-term beneficial effect on left ventricular remodeling and more effectively restored the

134 ry and mitosis were associated with improved ventricular remodeling and myocardial function, reduced

135 nfarcts and to examine the resulting cardiac ventricular remodeling and performance.

136 K-3alpha expression in cardiomyocytes limits ventricular remodeling and preserves cardiac function po

137 nd to be most effective in ameliorating left ventricular remodeling and preserving function.

138 o-fibrotic signaling pathways before adverse ventricular remodeling and progression of HF.

139 ith biventricular pacemakers with respect to ventricular remodeling and reduction in heart failure ho

140 in the risk region, along with improved left ventricular remodeling and regional and global left vent

141 failure (HF) is essential to prevent adverse ventricular remodeling and restore organ functionality i

142 cells overexpressing Akt (Akt-MSCs) inhibits ventricular remodeling and restores cardiac function mea

143 artery systolic pressure but mainly on left ventricular remodeling and septal function.

144 ent of DCM in DMD/BMD patients would lead to ventricular remodeling and that specific dystrophin gene

145 ac myocyte death contributes to pathological ventricular remodeling and the progression of myocardial

146 study was to define CF heterogeneity during ventricular remodeling and the underlying mechanisms tha

147 T1R-targeted imaging to predict the risk for ventricular remodeling and to monitor the efficacy of an

148 urn may trigger pathways leading to aberrant ventricular remodeling and ultimately a dilated cardiomy

149 py did not improve clinical outcomes or left ventricular remodeling and was associated with potential

150 PPCI, and it is associated with adverse left ventricular remodeling and worse clinical outcomes.

151 ve response and inhibiting pathological left ventricular remodeling and, therefore, may be a useful c

152 rincipally caused by global or regional left ventricular remodeling and/or severe left atrial dilatio

153 left ventricular dilation, and adverse left ventricular remodeling, and a significant decrease in LV

154 used to determine cardiac function and left ventricular remodeling, and atrial remodeling was monito

155 Apoptosis, left ventricular remodeling, and cardiac function were tested

156 cardiac fibrosis, congestive heart failure, ventricular remodeling, and diabetic nephropathy.

157 yocytes, which further alters contractility, ventricular remodeling, and disease susceptibility.

158 nalysis revealed maximal attenuation of left ventricular remodeling, and echocardiography showed the

159 include molecules involved in angiogenesis, ventricular remodeling, and fibrotic tissue formation, w

160 s through the temporal evolution of healing, ventricular remodeling, and function after myocardial in

161 erzone neovasculogenesis, attenuates adverse ventricular remodeling, and preserves ventricular functi

162 ortant independent predictor of adverse left ventricular remodeling, and recent evidences support the

163 reduce weight, have salutary effects on left ventricular remodeling, and reduce hospitalization for H

164 ate local myocardial inflammation, attenuate ventricular remodeling, and subsequently improve cardiac

165 ischemia causes cardiomyocyte death, adverse ventricular remodeling, and ventricular dysfunction.

166 at Grx-1 induces angiogenesis and diminishes ventricular remodeling apparently through neovasculariza

167 tive effects of aliskiren and its effects on ventricular remodeling are currently planned or underway

168 Diastolic dysfunction and left ventricular remodeling are most marked in severe and ear

169 also ameliorates cardiac function and limits ventricular remodeling as assessed by fluorodeoxyglucose

170 may be an important mechanism of maladaptive ventricular remodeling as mediated by cardiac fibroblast

171 illary/arteriolar density along with reduced ventricular remodeling, as assessed by echocardiography

172 Left ventricular remodeling, as commonly measured by left ven

173 alization for heart failure, or adverse left ventricular remodeling at 1 year.

174 ith placebo and did not prevent adverse left ventricular remodeling at 1 year.

175 cardial cavity volumes at day 3, followed by ventricular remodeling at day 30, and recovery at day 60

176 lic volume index (LVESVI), a measure of left ventricular remodeling, at 1 year.

177 tion, functional improvements, and favorable ventricular remodeling, at 1 year.

178 1 results in attenuated post-infarction left ventricular remodeling, at the expense of a prolonged in

179 ron deposition, infarct resorption, and left ventricular remodeling between day 7 (acute) and week 8

180 nicity is an established determinant of left ventricular remodeling; black athletes (BAs) exhibit mor

181 ar mechanisms that underlie TTNtv-associated ventricular remodeling but also offer potential targets

182 myocardium plays a significant role in left ventricular remodeling, but not infarct size.

183 omyocytes, MCP-1-/- mice had attenuated left ventricular remodeling, but similar infarct size when co

184 These findings support adverse left ventricular remodeling by prenatal T excess.

185 emodynamic profiles and induces reverse left ventricular remodeling by reducing left ventricular prel

186 ased hypertrophic markers leading to adverse ventricular remodeling characterized by myosin heavy cha

187 arger infarct scars and more pronounced left ventricular remodeling compared with wild-type mice.

188 Hypertension (HTN) causes concentric left ventricular remodeling, defined as an increased relative

189 adequacy of this increase relative to right ventricular remodeling determines TR severity.

190 Study of Biomarkers, Symptom Improvement and Ventricular Remodeling During Entresto Therapy for Heart

191 ular-arterial interactions that promote left ventricular remodeling, dysfunction, and failure.

192 MMP inhibition attenuates left ventricular remodeling even when the dominant collagenas

193 k of functional recovery and adverse LV left ventricular remodeling extending to remote myocardium.

194 ction, development of vulnerable plaque, and ventricular remodeling following acute myocardial infarc

195 trophic response, interstitial fibrosis, and ventricular remodeling following long-term pressure over

196 the role of Grx-1 in neovascularization and ventricular remodeling following MI.

197 to better understand the pathophysiology of ventricular remodeling following myocardial infarction (

198 Whether ventricular remodeling from hypertrophic cardiomyopathy

199 with high-output HF displayed eccentric left ventricular remodeling, greater natriuretic peptide acti

200 80-3006 mL]; P<0.0001), more concentric left ventricular remodeling, greater right ventricular dilata

201 P=0.004) and the likelihood of adverse left ventricular remodeling (>20% change in left ventricular

202 Parameters of left ventricular remodeling have been quantified as risk fact

203 Changes in left ventricular remodeling have not been adequately evaluate

204 ly affect postinfarct myocardial and LV left ventricular remodeling; hemorrhagic infarcts behave wors

205 A clinical score (RAISE) that used left ventricular remodeling (hypertrophy/diastolic dysfunctio

206 FMR occurs when ventricular remodeling impairs valve function.

207 toprolol) attenuates the progression of left ventricular remodeling in a rat model of myocardial infa

208 ers were added if echocardiography showed no ventricular remodeling in angiotensin-converting enzyme

209 Beta-blocker therapy can ameliorate left ventricular remodeling in asymptomatic patients with lef

210 hether beta-blocker therapy ameliorates left ventricular remodeling in asymptomatic patients with lef

211 cardiomyopathy, was the commonest pattern of ventricular remodeling in ATTR.

212 y diagnosis and treatment of DCM may lead to ventricular remodeling in DMD/BMD patients.

213 inked to general inflammation and to adverse ventricular remodeling in heart failure.

214 medical therapy that attenuates adverse left ventricular remodeling in patients with chronic primary

215 athways important in the progression of left ventricular remodeling in patients with CPMR may lead to

216 it(+) cardiac stem cells (CSCs) improve left ventricular remodeling in porcine models and clinical tr

217 functional status, and induces reverse left ventricular remodeling in selected populations with hear

218 ghts into the pathophysiology of MI and left ventricular remodeling in small-animal models.

219 injury, and it is a strong predictor of left ventricular remodeling in ST-segment-elevation myocardia

220 educe mortality, morbidity, and adverse left ventricular remodeling in such patients.

221 burden, infarct resorption, and adverse left ventricular remodeling in the chronic phase of MI in can

222 ng-1 in increasing angiogenesis and reducing ventricular remodeling in the infarcted diabetic myocard

223 y myocardial Bnip3 as a major determinant of ventricular remodeling in the infarcted heart, suggestin

224 ons in the short term and attenuated adverse ventricular remodeling in the long term.

225 specific proapoptotic gene, Bnip3, minimizes ventricular remodeling in the mouse, despite having no e

226 CSC activation are critical determinants of ventricular remodeling in this patient population.

227 Adverse ventricular remodeling including cardiomyocyte hypertrop

228 60.7 + or - 2.2% in vehicle, reduced adverse ventricular remodeling, increased myocardial VEGF produc

229 was to describe the long-term course of left ventricular remodeling induced by cardiac resynchronizat

230 estigate role of ROCK1 in the development of ventricular remodeling induced by transverse aortic band

231 Disease-related left ventricular remodeling is a complex process involving ca

232 Left ventricular remodeling is a major cause of progressive h

233 Left ventricular remodeling is a precursor of LV dysfunction,

234 Arrhythmogenic ventricular remodeling is hallmarked by both reduced gap

235 regurgitation and enhanced reversal of left ventricular remodeling is possible when subvalvular tech

236 Ventricular remodeling is strongly correlated with impro

237 Left ventricular remodeling is the principal cause of progres

238 such as hypertrophy and other types of left ventricular remodeling, ischemia/reperfusion injury, ang

239 important insights into postinfarction left ventricular remodeling, it has not been possible to defi

240 mitral regurgitation results in adverse left ventricular remodeling, its effect on the mitral valve l

241 ter systolic valve performance, similar left ventricular remodeling, more paravalvular regurgitation,

242 as associated with reduction of adverse left ventricular remodeling, noninfarct myocardial fibrosis,

243 1 [vascular cell protein 1]) and C5 for left ventricular remodeling; NUP210 (expressed during myogeni

244 Ventricular remodeling of both geometry and fiber struct

245 IIT was not superior to MCT in changing left ventricular remodeling or aerobic capacity, and its feas

246 n mutation carriers and noncarriers (no left ventricular remodeling or fibrosis, normal left ventricu

247 tion and is an independent predictor of left ventricular remodeling over time.

248 insulin-like growth factor I (IGF-I) on left ventricular remodeling, partly through its antiapoptotic

249 nction, novel strategies are needed to limit ventricular remodeling post-MI.

250 We use left ventricular remodeling postmyocardial infarction as an e

251 mass alone predicted incident HF, concentric ventricular remodeling predicted incident stroke and CHD

252 est the hypothesis that the severity of left ventricular remodeling predicts the response to treatmen

253 fibroblasts (CFs) have a central role in the ventricular remodeling process associated with different

254 ractile parameters were associated with left ventricular remodeling, recapitulation of fetal gene exp

255 modynamic severity of stenosis, adverse left ventricular remodeling, reduced left ventricular longitu

256 material treatment of MI and subsequent left ventricular remodeling remain the same, namely, left ven

257 activation conspire to propagate maladaptive ventricular remodeling responsible for the insidious nat

258 tate, inhibition of maladaptive adverse left ventricular remodeling, reversal of cardiac and peripher

259 Left ventricular remodeling secondary to acute myocardial inf

260 Left ventricular remodeling seems to be an important factor i

261 sympathetic activity, attenuates the adverse ventricular remodeling seen in heart failure, and decrea

262 proving ventricular efficiency and reversing ventricular remodeling should be in the armamentarium of

263 reductions in inflammation, left atrial and ventricular remodeling, sleep apnea, blood pressure, and

264 den cardiac death, and modulation of adverse ventricular remodeling still remain elusive goals.

265 we found only a modest acceleration of left ventricular remodeling, suggesting that, in individuals

266 ility studies are predictive of reverse left-ventricular remodeling, symptom improvement, and patient

267 ta-blockade was associated with adverse left ventricular remodeling, systolic dysfunction, and a redu

268 alve in the setting of advanced adverse left ventricular remodeling that alters the alignment charact

269 nal and inflammatory activation, and adverse ventricular remodeling that leads to heart failure progr

270 ation might partially counteract the adverse ventricular remodeling that occurs after infarction.

271 he development of hypertension and secondary ventricular remodeling that occurs with anti-vascular en

272 12 months of age the T2DN(mtFHH) showed left ventricular remodeling that was verified by histology.

273 logical changes responsible for adverse left ventricular remodeling, the relationship between inflamm

274 of limiting myocardial injury and subsequent ventricular remodeling, the translation of effective the

275 in LVEF; however, trastuzumab-mediated left ventricular remodeling-the primary outcome-was not preve

276 During the early phases of left ventricular remodeling, there was a significant increase

277 to 12-month-old mice to determine linkage to ventricular remodeling (VR), ER, and heart failure (HF).

278 Adverse left ventricular remodeling was defined as an increase of 15%

279 another 6 sheep (tethered plus MI), and left ventricular remodeling was limited by external constrain

280 Negative ventricular remodeling was not observed if CSCs retained

281 of asymptomatic individuals, concentric left ventricular remodeling was related to decreased regional

282 The only predictor of left ventricular remodeling was treatment with sonothrombolys

283 To relate inflammatory activity to left ventricular remodeling, we used a combination of noninva

284 ing and cardiac fibrosis during hypertrophic ventricular remodeling, we used a well-established mouse

285 well as echocardiographic indicators of left ventricular remodeling, were associated with greatly inc

286 g the hemodynamic consequences and extent of ventricular remodeling, which is an important predictor

287 Chronic HDTBR leads to ventricular remodeling, which is not seen with equivalen

288 eline with a cardiac phenotype of concentric ventricular remodeling, which protected them from progre

289 oved cardiac contractility and reversed left ventricular remodeling, which was accompanied by a norma

290 h focusing on mechanical options for reverse ventricular remodeling will be referenced and summarized

291 ending artery occlusion in swine caused left ventricular remodeling with a decrease of ejection fract

292 ontrol group was more likely to exhibit left ventricular remodeling with an odds ratio of 2.79 ([95%

293 MR), mitral leaflet closure is restricted by ventricular remodeling with displacement of the papillar

294 hase; the Reduction of Infarct Expansion and Ventricular Remodeling With Erythropoietin After Large M

295 systemic tunicamycin (TM) developed adverse ventricular remodeling with excessive levels of the ER r

296 ardial infarction and developed pathological ventricular remodeling with increased cardiomyocyte apop

297 109 genes important in volume-overload left ventricular remodeling with levels in normal hearts (n=5

298 t caused a complex, heterogeneous pattern of ventricular remodeling with wide variations in clinical

299 OPCAT demonstrated heterogeneous patterns of ventricular remodeling, with high prevalence of structur

300 The major process to reverse ventricular remodeling would be the enhancement of regen