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

1 myocardium in the infarct zone, and superior left ventricular remodeling.

2 in murine infarcts and consequently enhances left ventricular remodeling.

3 ounding tissue, which often leads to adverse left ventricular remodeling.

4 , included improved contractile function and left ventricular remodeling.

5 t ventricular systolic function, and reduced left ventricular remodeling.

6 ardiac functional recovery and prevention of left ventricular remodeling.

7 studies support a key role for cytokines in left ventricular remodeling.

8 t role in the development and progression of left ventricular remodeling.

9 duce morbidity and mortality associated with left ventricular remodeling.

10 t might be partially explained by a positive left ventricular remodeling.

11 cies may participate in mechanically induced left ventricular remodeling.

12 improve understanding of the role of MMPs in left ventricular remodeling.

13 t noninfarcted regions, as well as attenuate left ventricular remodeling.

14 me constant of relaxation or any variable of left ventricular remodeling.

15 functional recovery, and reduced maladaptive left ventricular remodeling.

16 CI) affects myocardial infarct (MI) size and left ventricular remodeling.

17 tion of myocardial IR injury with subsequent left ventricular remodeling.

18 ion, inhibits cardiac fibrosis, and improves left ventricular remodeling.

19 s, via uncertain mechanisms that may include left ventricular remodeling.

20 et associated with reduced arterial flow and left ventricular remodeling.

21 for years, and is associated with subsequent left ventricular remodeling.

22 determine their associations with long-term left ventricular remodeling.

23 ciated with adverse outcomes and distinctive left ventricular remodeling.

24 lial response to injury, vascular aging, and left ventricular remodeling.

25 s in achieved medication doses or indices of left ventricular remodeling.

26 t (OSU-ERb-012) to inhibit T cells and blunt left ventricular remodeling.

27 ocardial injury and its predictive value for left ventricular remodeling.

28 and exerted a sustained beneficial effect on left ventricular remodeling.

29 ic myocardium and has been linked to adverse left ventricular remodeling.

30 escued the angiogenic defect and ameliorated left ventricular remodeling.

31 to provoke left ventricular dysfunction and left ventricular remodeling.

32 hocardiography and their value in preventing left ventricular remodeling.

33 me that regulates post-myocardial infarction left ventricular remodeling.

34 stolic and diastolic function, and decreased left ventricular remodeling.

35 art failure-related urgent care, and adverse left ventricular remodeling.

36 mprove clinical outcomes and prevent adverse left ventricular remodeling.

37 MAD-3 largely prevented fibrosis and limited left ventricular remodeling.

38 ment option for patients with postinfarction left ventricular remodeling.

39 st-myocardial infarction (MI) and subsequent left ventricular remodeling.

40 after myocardial infarction (MI) accelerates left ventricular remodeling.

41 ted infarct inflammation, and curbed post-MI left ventricular remodeling.

42 cardiac pathologies, including post-infarct left ventricular remodeling.

43 triuretic peptide (BNP), and fully prevented left-ventricular remodeling.

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

45 rent hypertension had a higher proportion of left ventricular remodeling (79.0%) compared with all ot

46 ogenesis and survival of cardiac myocyte and left ventricular remodeling after AMI is unknown.

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

48 Left ventricular remodeling after infarction is accompan

49 d regions may be an important determinant of left ventricular remodeling after infarction.

50 ay provide a novel means to favorably modify left ventricular remodeling after MI.

51 y regulated cellular processes orchestrating left ventricular remodeling after myocardial I/R followi

52 trix metalloproteinases (MMPs) contribute to left ventricular remodeling after myocardial infarction

53 matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction

54 or adverse cardiovascular events and adverse left ventricular remodeling after myocardial infarction.

55 in plasma RNA from patients with or without left ventricular remodeling after myocardial infarction.

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

57 amine BP, the incidence of hypertension, and left ventricular remodeling among collegiate ASF athlete

58 species production and again observed worse left ventricular remodeling and a lower ejection fractio

59 ageable intramyocardial hydrogel delivery on left ventricular remodeling and angiogenesis after MI.

60 omoted their angiogenic ability, attenuating left ventricular remodeling and cardiac fibrosis.

61 Left ventricular remodeling and cardiac function were im

62 rder zone, reduced scar size, and attenuated left ventricular remodeling and contractile dysfunction

63 the post-infarction progression of negative left ventricular remodeling and decline in cardiac funct

64 yocardium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy.

65 The beneficial effects of CPCs on left ventricular remodeling and dysfunction are sustaine

66 old (IK-5001), to prevent or reverse adverse left ventricular remodeling and dysfunction in patients

67 hypertension, and renal insufficiency drive left ventricular remodeling and dysfunction through syst

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

69 articipants with predisposed HFpEF had worse left ventricular remodeling and function and higher syst

70 greatest negative effect on infarct size and left ventricular remodeling and function, as well as a s

71 a alone or in combination with parameters of left ventricular remodeling and function, yielded an imp

72 s provide evidence for beneficial effects on left ventricular remodeling and functional capacity.

73 Left ventricular remodeling and global and regional func

74 acellular biomaterials hold promise to limit left ventricular remodeling and heart failure precipitat

75 tissues for the treatment of postinfarction left ventricular remodeling and heart failure.

76 itation (MR) result in different patterns of left ventricular remodeling and hypertrophy.

77 hydrogel early post-MI resulted in decreased left ventricular remodeling and increased alphavbeta3-in

78 te or greater MR was associated with adverse left ventricular remodeling and increased likelihood of

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

80 vation of inflammation in the heart provokes left ventricular remodeling and left ventricular dysfunc

81 Women demonstrate more concentric left ventricular remodeling and less ventricular dilatat

82 renin-angiotensin system (RAS) inhibitors on left ventricular remodeling and major clinical outcomes

83 ling pathways that may contribute to adverse left ventricular remodeling and mitochondrial dysfunctio

84 PMA exerted a long-term beneficial effect on left ventricular remodeling and more effectively restore

85 myocardial infarction (MI) areas can reduce left ventricular remodeling and potentially increase ang

86 e found to be most effective in ameliorating left ventricular remodeling and preserving function.

87 dium in the risk region, along with improved left ventricular remodeling and regional and global left

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

89 Pathologic left ventricular remodeling and valvular heart disease m

90 therapy did not improve clinical outcomes or left ventricular remodeling and was associated with pote

91 hs-cTnT) and I (hs-cTnI) are associated with left ventricular remodeling and with incident heart fail

92 post-PPCI, and it is associated with adverse left ventricular remodeling and worse clinical outcomes.

93 tective response and inhibiting pathological left ventricular remodeling and, therefore, may be a use

94 is principally caused by global or regional left ventricular remodeling and/or severe left atrial di

95 ithout timely intervention it drives adverse left-ventricular remodeling and heart failure.

96 ophy, left ventricular dilation, and adverse left ventricular remodeling, and a significant decrease

97 y was used to determine cardiac function and left ventricular remodeling, and atrial remodeling was m

98 Apoptosis, left ventricular remodeling, and cardiac function were t

99 ric analysis revealed maximal attenuation of left ventricular remodeling, and echocardiography showed

100 r important independent predictor of adverse left ventricular remodeling, and recent evidences suppor

101 ure, reduce weight, have salutary effects on left ventricular remodeling, and reduce hospitalization

102 We examined left ventricular remodeling, and the cell biological, bi

103 Diastolic dysfunction and left ventricular remodeling are most marked in severe an

104 Left ventricular remodeling, as commonly measured by lef

105 ospitalization for heart failure, or adverse left ventricular remodeling at 1 year.

106 ose with placebo and did not prevent adverse left ventricular remodeling at 1 year.

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

108 MCP-1 results in attenuated post-infarction left ventricular remodeling, at the expense of a prolong

109 MO, iron deposition, infarct resorption, and left ventricular remodeling between day 7 (acute) and we

110 Ethnicity is an established determinant of left ventricular remodeling; black athletes (BAs) exhibi

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

112 cardiomyocytes, MCP-1-/- mice had attenuated left ventricular remodeling, but similar infarct size wh

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

114 ves hemodynamic profiles and induces reverse left ventricular remodeling by reducing left ventricular

115 ped larger infarct scars and more pronounced left ventricular remodeling compared with wild-type mice

116 Hypertension (HTN) causes concentric left ventricular remodeling, defined as an increased rel

117 subclinical cardiovascular disease including left ventricular remodeling, diastolic dysfunction, coro

118 Left ventricular remodeling due to pressure overload is

119 We defined a priori 3 different patterns of left ventricular remodeling during follow-up: (1) an inc

120 ntricular-arterial interactions that promote left ventricular remodeling, dysfunction, and failure.

121 ve favorable cardiac effects associated with left ventricular remodeling early after myocardial infar

122 MMP inhibition attenuates left ventricular remodeling even when the dominant colla

123 h lack of functional recovery and adverse LV left ventricular remodeling extending to remote myocardi

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

125 Left ventricular remodeling following acute myocardial i

126 Left ventricular remodeling following myocardial infarct

127 cardiac magnetic resonance imaging assessed left ventricular remodeling, global longitudinal strain,

128 ects with high-output HF displayed eccentric left ventricular remodeling, greater natriuretic peptide

129 L [2380-3006 mL]; P<0.0001), more concentric left ventricular remodeling, greater right ventricular d

130 .72]; P=0.004) and the likelihood of adverse left ventricular remodeling (>20% change in left ventric

131 Metrics of left ventricular remodeling had novel associations with

132 Parameters of left ventricular remodeling have been quantified as risk

133 Changes in left ventricular remodeling have not been adequately eva

134 icantly affect postinfarct myocardial and LV left ventricular remodeling; hemorrhagic infarcts behave

135 A clinical score (RAISE) that used left ventricular remodeling (hypertrophy/diastolic dysfu

136 of metoprolol) attenuates the progression of left ventricular remodeling in a rat model of myocardial

137 Beta-blocker therapy can ameliorate left ventricular remodeling in asymptomatic patients wit

138 ted whether beta-blocker therapy ameliorates left ventricular remodeling in asymptomatic patients wit

139 nificantly blunted these changes and stopped left ventricular remodeling in both the sexes.

140 matrix metalloproteinases (MMPs) attenuates left ventricular remodeling in experimental MI.

141 elease of apelin improves heart function and left ventricular remodeling in mice with myocardial infa

142 oven medical therapy that attenuates adverse left ventricular remodeling in patients with chronic pri

143 lar pathways important in the progression of left ventricular remodeling in patients with CPMR may le

144 ible interaction of ASA and beta-blockers on left ventricular remodeling in patients with heart failu

145 d c-kit(+) cardiac stem cells (CSCs) improve left ventricular remodeling in porcine models and clinic

146 roves functional status, and induces reverse left ventricular remodeling in selected populations with

147 insights into the pathophysiology of MI and left ventricular remodeling in small-animal models.

148 dial injury, and it is a strong predictor of left ventricular remodeling in ST-segment-elevation myoc

149 ght reduce mortality, morbidity, and adverse left ventricular remodeling in such patients.

150 tory burden, infarct resorption, and adverse left ventricular remodeling in the chronic phase of MI i

151 rt half-life prevents studying its impact on left ventricular remodeling in the long term.

152 sion, regardless of HDP history, had greater left ventricular remodeling, including greater relative

153 ial volume, left ventricular mass index, and left ventricular remodeling index (all P<0.05).

154 atrial volume, left ventricular mass index, left ventricular remodeling index, and left ventricular

155 tudy was to describe the long-term course of left ventricular remodeling induced by cardiac resynchro

156 Disease-related left ventricular remodeling is a complex process involvi

157 Left ventricular remodeling is a major cause of progress

158 Left ventricular remodeling is a precursor of LV dysfunc

159 Left ventricular remodeling is an important sequela of m

160 itral regurgitation and enhanced reversal of left ventricular remodeling is possible when subvalvular

161 Left ventricular remodeling is the principal cause of pr

162 ease, such as hypertrophy and other types of left ventricular remodeling, ischemia/reperfusion injury

163 vided important insights into postinfarction left ventricular remodeling, it has not been possible to

164 onic mitral regurgitation results in adverse left ventricular remodeling, its effect on the mitral va

165 Postinfarction left ventricular remodeling (LVR) is associated with red

166 The underlying mechanisms by which left ventricular remodeling (LVR) leads to congestive he

167 ion in pigs, demonstrating either successful left ventricular remodeling (LVR, n = 8) or congestive h

168 h better systolic valve performance, similar left ventricular remodeling, more paravalvular regurgita

169 olute regression was the most common type of left ventricular remodeling (n=9, 31%), followed by prog

170 ids was associated with reduction of adverse left ventricular remodeling, noninfarct myocardial fibro

171 VCAM1 [vascular cell protein 1]) and C5 for left ventricular remodeling; NUP210 (expressed during my

172 HIIT was not superior to MCT in changing left ventricular remodeling or aerobic capacity, and its

173 etween mutation carriers and noncarriers (no left ventricular remodeling or fibrosis, normal left ven

174 nfarction and is an independent predictor of left ventricular remodeling over time.

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

176 s of insulin-like growth factor I (IGF-I) on left ventricular remodeling, partly through its antiapop

177 e used cardiac magnetic resonance to compare left ventricular remodeling patterns, systemic forward s

178 We use left ventricular remodeling postmyocardial infarction as

179 to test the hypothesis that the severity of left ventricular remodeling predicts the response to tre

180 contractile parameters were associated with left ventricular remodeling, recapitulation of fetal gen

181 n, hemodynamic severity of stenosis, adverse left ventricular remodeling, reduced left ventricular lo

182 r biomaterial treatment of MI and subsequent left ventricular remodeling remain the same, namely, lef

183 age state, inhibition of maladaptive adverse left ventricular remodeling, reversal of cardiac and per

184 Left ventricular remodeling secondary to acute myocardia

185 Left ventricular remodeling seems to be an important fac

186 ization of pro-hypertrophic and pro-fibrotic left ventricular remodeling signaling evidenced on whole

187 ever, we found only a modest acceleration of left ventricular remodeling, suggesting that, in individ

188 viability studies are predictive of reverse left-ventricular remodeling, symptom improvement, and pa

189 ve beta-blockade was associated with adverse left ventricular remodeling, systolic dysfunction, and a

190 ral valve in the setting of advanced adverse left ventricular remodeling that alters the alignment ch

191 t at 12 months of age the T2DN(mtFHH) showed left ventricular remodeling that was verified by histolo

192 e biological changes responsible for adverse left ventricular remodeling, the relationship between in

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

194 During the early phases of left ventricular remodeling, there was a significant inc

195 subjects, we measured cardiac energetics and left ventricular remodeling using noninvasive magnetic r

196 The former is secondary to left ventricular remodeling usually in the setting of he

197 Adverse left ventricular remodeling was defined as an increase o

198 n in another 6 sheep (tethered plus MI), and left ventricular remodeling was limited by external cons

199 ar weights in proportion to body growth, but left ventricular remodeling was minor, and a decrease in

200 tudy of asymptomatic individuals, concentric left ventricular remodeling was related to decreased reg

201 The only predictor of left ventricular remodeling was treatment with sonothrom

202 To relate inflammatory activity to left ventricular remodeling, we used a combination of no

203 , as well as echocardiographic indicators of left ventricular remodeling, were associated with greatl

204 improved cardiac contractility and reversed left ventricular remodeling, which was accompanied by a

205 descending artery occlusion in swine caused left ventricular remodeling with a decrease of ejection

206 the control group was more likely to exhibit left ventricular remodeling with an odds ratio of 2.79 (

207 ls of 109 genes important in volume-overload left ventricular remodeling with levels in normal hearts

208 reas nontransgenic mice exhibited concentric left ventricular remodeling with maintained ejection per