ライフサイエンスコーパス: ventricular remodeling

1 d cellular mechanisms governing pathological ventricular remodeling.

2 xerted a sustained beneficial effect on left ventricular remodeling.

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

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

5 by interfering with lung vascular and right ventricular remodeling.

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

7 into the association between AF and adverse ventricular remodeling.

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

9 athways in promoting cardiac hypertrophy and ventricular remodeling.

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

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

12 rine infarcts and consequently enhances left ventricular remodeling.

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

14 d the angiogenic defect and ameliorated left ventricular remodeling.

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

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

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

18 cardiac contractile performance, and halted ventricular remodeling.

19 revented diastolic dysfunction, and improved ventricular remodeling.

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

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

22 luded improved contractile function and left ventricular remodeling.

23 s been implicated in cardiac hypertrophy and ventricular remodeling.

24 -dependent signaling pathways that influence ventricular remodeling.

25 urgical therapies aimed at achieving reverse ventricular remodeling.

26 rovoke left ventricular dysfunction and left ventricular remodeling.

27 c functional recovery and prevention of left ventricular remodeling.

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

29 reduces systolic dysfunction, and attenuates ventricular remodeling.

30 broblasts and myocytes to alter survival and ventricular remodeling.

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

32 s increased collagen turnover culminating in ventricular remodeling.

33 , improve myocardial function, and attenuate ventricular remodeling.

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

35 oblasts is implicated in infarct healing and ventricular remodeling.

36 l ECM early after coronary occlusion lessens ventricular remodeling.

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

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

39 morbidity and mortality associated with left ventricular remodeling.

40 may participate in mechanically induced left ventricular remodeling.

41 ve understanding of the role of MMPs in left ventricular remodeling.

42 predisposition to myocardial infarction and ventricular remodeling.

43 infarcted regions, as well as attenuate left ventricular remodeling.

44 ogression of left ventricular dysfunction or ventricular remodeling.

45 nstant of relaxation or any variable of left ventricular remodeling.

46 o partially reverse systolic dysfunction and ventricular remodeling.

47 at regulates post-myocardial infarction left ventricular remodeling.

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

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

50 e clinical outcomes and prevent adverse left ventricular remodeling.

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

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

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

54 sociated with durable repair and may prevent ventricular remodeling.

55 regurgitation is indicated to avoid adverse ventricular remodeling.

56 wound healing and scar formation and affects ventricular remodeling.

57 largely prevented fibrosis and limited left ventricular remodeling.

58 option for patients with postinfarction left ventricular remodeling.

59 myocardial infarction (MI) accelerates left ventricular remodeling.

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

61 59.3+/-7.9%, with prevalent concentric left ventricular remodeling (34%) and hypertrophy (43%), and

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

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

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

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

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

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

68 In concert with a reduction in left ventricular remodeling after anterior infarction, angiot

69 Left ventricular remodeling after infarction is accompanied b

70 ions may be an important determinant of left ventricular remodeling after infarction.

71 Myocardial inflammation is critical for ventricular remodeling after ischemia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 Left ventricular remodeling and cardiac function were improve

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

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

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

91 est new therapeutic targets for limiting the ventricular remodeling and dilatation process characteri

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

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

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

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

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

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

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

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

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

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

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

103 Left ventricular remodeling and global and regional function

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

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

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

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

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

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

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

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

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

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

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

115 Ventricular remodeling and infarct size were compared in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 ethering geometry toward normal, using a new ventricular remodeling approach based on 3D echo finding

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

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

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

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

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

157 Left ventricular remodeling, as commonly measured by left ven

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

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

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

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

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

163 1 results in attenuated post-infarction left ventricular remodeling, at the expense of a prolonged in

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

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

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

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

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

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

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

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

172 lude improved infarct healing, limitation of ventricular remodeling, decreased ventricular arrhythmia

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

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

175 othesized that these effects would attenuate ventricular remodeling early after MI.

176 vorable cardiac effects associated with left ventricular remodeling early after myocardial infarction

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

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

179 At 6 weeks after aortic banding, left ventricular remodeling, extent of hypertrophy, and funct

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

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

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

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

184 Whether ventricular remodeling from hypertrophic cardiomyopathy

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

186 80-3006 mL]; P<0.0001), more concentric left ventricular remodeling, greater right ventricular dilata

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

188 Nonetheless, favorable ventricular remodeling has been reported in asymptomatic

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

190 Changes in left ventricular remodeling have not been adequately evaluate

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

192 FMR occurs when ventricular remodeling impairs valve function.

193 abnormalities associated with postinfarction ventricular remodeling in a new, large animal model.

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

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

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

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

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

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

200 ix metalloproteinases (MMPs) attenuates left ventricular remodeling in experimental MI.

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

202 interaction of ASA and beta-blockers on left ventricular remodeling in patients with heart failure.

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

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

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

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

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

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

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

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

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

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

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

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

215 Adverse ventricular remodeling including cardiomyocyte hypertrop

216 60.7 + or - 2.2% in vehicle, reduced adverse ventricular remodeling, increased myocardial VEGF produc

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

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

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

220 Left ventricular remodeling is a major cause of progressive h

221 Left ventricular remodeling is a precursor of LV dysfunction,

222 Left ventricular remodeling is an important sequela of myocar

223 Postinfarction ventricular remodeling is associated with lengthening an

224 Arrhythmogenic ventricular remodeling is hallmarked by both reduced gap

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

226 Ventricular remodeling is strongly correlated with impro

227 Left ventricular remodeling is the principal cause of progres

228 nitial damage to the myocardium, progressive ventricular remodeling is ultimately a maladaptive proce

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

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

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

232 Postinfarction left ventricular remodeling (LVR) is associated with reductio

233 The underlying mechanisms by which left ventricular remodeling (LVR) leads to congestive heart f

234 n pigs, demonstrating either successful left ventricular remodeling (LVR, n = 8) or congestive heart

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

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

237 Ventricular remodeling of both geometry and fiber struct

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

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

240 scar formation (chi2 = 10.0, P<.01) and left ventricular remodeling (P<.05).

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

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

243 We use left ventricular remodeling postmyocardial infarction as an e

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

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

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

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

248 Ventricular remodeling refers to changes in left ventric

249 Ventricular remodeling refers to changes in ventricular

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

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

252 Left ventricular remodeling secondary to acute myocardial inf

253 Left ventricular remodeling seems to be an important factor i

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

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

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

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

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

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

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

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

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

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

264 12 months of age the T2DN(mtFHH) showed left ventricular remodeling that was verified by histology.

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

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

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

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

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

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

271 ights in proportion to body growth, but left ventricular remodeling was minor, and a decrease in the

272 Negative ventricular remodeling was not observed if CSCs retained

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

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

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

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

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

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

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

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

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

282 pression and normally functioning concentric ventricular remodeling with decreased cardiomyocyte size

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

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

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

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

287 nontransgenic mice exhibited concentric left ventricular remodeling with maintained ejection performa

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

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

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