ライフサイエンスコーパス: post-MI

1 ays, and 2.58 [2.21 to 3.00] for AF >30 days post MI).

2 (MI) (plus 1 infused off-protocol 14 months post-MI).

3 etween 3 and 30 days, and 392 [54%] >30 days post-MI).

4 roliferation and subsequent cardiac recovery post MI.

5 MI, whereas depleting B-cells is beneficial post MI.

6 ial activation and myocardial arteriogenesis post MI.

7 ctivator compared with wild-type mice 3 days post MI.

8 tor mice compared with wild-type mice 5 days post MI.

9 s) production, and myocardial arteriogenesis post MI.

10 esonance 2 days (n=286) and 6 months (n=228) post MI.

11 ratios and improved ejection fraction at d5 post-MI.

12 LVEF and ISZ were assessed 4 months post-MI.

13 ibitor improved myocardial insulin signaling post-MI.

14 lar dilation with dysfunction and HF at 4 wk post-MI.

15 ar remodeling and preserves cardiac function post-MI.

16 , Treg cells might influence cardiac healing post-MI.

17 stitutes a novel approach to improve healing post-MI.

18 ling and preserves left ventricular function post-MI.

19 s are needed to limit ventricular remodeling post-MI.

20 ship between scar size and ejection fraction post-MI.

21 t to predict unlabeled MIPIN protein changes post-MI.

22 altered the course of adverse LV remodeling post-MI.

23 ice but increased in wild-type mice at day 7 post-MI.

24 ardiac fibrosis and improve cardiac function post-MI.

25 rtality because of increased cardiac rupture post-MI.

26 icial effects of sEHIs in cardiac remodeling post-MI.

27 patients selected for high risk of SCA early post-MI.

28 k for adverse vascular and fibrogenic events post-MI.

29 o had a WCD prescribed in the first 3 months post-MI.

30 ted particles are injected at 7 or more days post-MI.

31 on admission, 24 hours post-MI, and 4 months post-MI.

32 se highest risk patients may improve outcome post-MI.

33 nce imaging 1 week pre-injection and 4 weeks post-MI.

34 eft ventricular free wall thinning at 4 days post-MI.

35 sed 20-fold at 3 days and 50-fold at 14 days post-MI.

36 mortality by increasing cardiac fibrogenesis post-MI.

37 eta-adrenergic receptor signaling at 4 weeks post-MI.

38 late gadolinium enhancement at days 1 and 21 post-MI.

39 PW1(+) cells differentiated into fibroblasts post-MI.

40 rt rate variability were registered at day 5 post-MI.

41 L in the recovery or rehabilitation stage of post-MI.

42 imary determinant in heart failure pathology post-MI.

43 levels were up-regulated in the circulation post-MI.

44 proinflammatory and favor adverse remodeling post-MI.

45 intrinsic cardiac nervous system is reduced post-MI.

46 tic stimulation of cardiac lymphangiogenesis post-MI.

47 g between day 7 (acute) and week 8 (chronic) post-MI.

48 ry of Ang-(1-9) reduced sudden cardiac death post-MI.

49 t manner and limited precollector remodeling post-MI.

50 Efferent inputs to neurons were maintained post-MI.

51 d proteins is reduced in ERK5(-/-) platelets post-MI.

52 However, the clinical relevance of post-MI (18)F-FDG uptake in the heart has not been eluci

53 increased mortality during the first 10 days post-MI (43% versus 22%; P=0.04), and postmortem examina

54 Nine post-MI (5 placebo versus 4 n-3 PUFA) and 2 sham dogs di

55 y decreased to ventricular vs. atrial pacing post-MI (63% in control vs. 44% in MI to ventricular pac

56 We evaluated the prognostic impact of HF post MI according to preserved/reduced ejection fraction

57 However, the role of 15-epi LXA4 in post-MI acute inflammatory response and resolving phase

58 The extent of post-MI AdipoR1 phosphorylation positively correlated wi

59 c-specific GRK2 knockout virtually abolished post-MI AdipoR1 phosphorylation, whereas virus-mediated

60 support cardiac function in the early phase post MI and identifying the processes that initiate tran

61 g, increased by >60% from baseline at 5 days post-MI and by >100% at 21 days post-MI in the Ad-GFP on

62 sence of high-fat feeding beginning at day 7 post-MI and continuing for 4 weeks.

63 a linear relationship between T (req) 2 days post-MI and global longitudinal strain 6 months later (r

64 I), we found that platelet ERK5 is activated post-MI and that platelet-specific ERK5(-/-) mice have l

65 e a relationship between stem cell treatment post-MI and the modification of proteolytic pathways, ge

66 samples were obtained on admission, 24 hours post-MI, and 4 months post-MI.

67 ersistent MT1-MMP promoter activity occurred post-MI, and increased myocardial MT1-MMP levels resulte

68 MMP-28 expression decreased post-MI, and its cell source shifted from myocytes to ma

69 remodeling may be affected by MPC injection post-MI, and whether these effects are concentration-dep

70 e is known about race and sex differences in post-MI angina and long-term risk of unplanned rehospita

71 We examined race and sex differences in post-MI angina frequency and 1-year unplanned rehospital

72 Better treatment of post-MI angina may improve patient quality of life and q

73 ale patients, given their high prevalence of post-MI angina.

74 a significant difference in their effect in post-MI animal studies.

75 studies reveal that the majority of VTs late post-MI arise from the infarct border zone (IBZ).

76 erstand how the left ventricle (LV) remodels post-MI at both the molecular and cellular levels, we pr

77 use or cardiovascular readmission at 30 days post MI between transferred-in and direct-arrival patien

78 The presented insight into post-MI bone marrow activation identifies a mechanistic

79 The C-1158/59 fragment was identified post-MI, both in human plasma and mouse LV, at levels th

80 MI border zone and proliferating at 72 hours post-MI but had no effect on initial cardiac injury or s

81 imilar in both groups at baseline and 3 days post-MI but increased significantly in the HIF-1alpha si

82 t with p1158/59 reduced LV dilation at day 7 post-MI by preserving LV structure (p < 0.05 vs. control

83 ricryptin p1158/59 facilitates LV remodeling post-MI by regulating scar formation through targeted EC

84 s of PKA phosphorylation at this site averts post MI cardiac pump dysfunction.

85 , there was no difference in infarct size or post-MI cardiac function between the methods.

86 the beneficial effects of FoxO4 deletion on post-MI cardiac function.

87 eta2ARKO BMT mice displayed severely reduced post-MI cardiac infiltration of leukocytes with reciproc

88 myocyte Ca(2+)-handling defects could avert post-MI cardiac pump dysfunction.

89 unctional significance of CCR9 in regulating post-MI cardiac remodeling and its underlying mechanism.

90 Post-MI cardiac remodeling is a multifaceted process tha

91 table thermoresponsive hydrogel to attenuate post-MI cardiac remodeling.

92 Blocking post-MI TRPC activity improved post-MI cardiac structure and function.

93 At 3 months post-MI, cardiac structure and function were evaluated b

94 Available data in animal models of post-MI cardiogenic shock and ischemia/reperfusion injur

95 Mortality rates in post-MI cardiogenic shock approach 50% despite rapid rev

96 Therapeutic hypothermia for post-MI cardiogenic shock has multiple potentially benef

97 y offer advances in treatment and outcome in post-MI cardiogenic shock.

98 sponse as a potential therapeutic target for post-MI cardioprotection.

99 lantation might not be considered during the post-MI care transition.

100 findings suggest the potential to transform post-MI care.

101 In the post-MI cohort, the fully adherent group had a significa

102 for people who quit smoking after MI versus post-MI continuing smokers was 0.54 (95% confidence inte

103 snus quitters had half the mortality risk of post-MI continuing snus users (hazard ratio, 0.51; 95% c

104 in post-MI snus quitters (n=675) relative to post-MI continuing snus users (n=1799) using Cox proport

105 (14.8-23.6) per 1000 person-years at risk in post-MI continuing snus users.

106 2KO mice showed better cardiac function than post-MI control mice, which is explained by an improved

107 aintained in post-MI GRK2KO myocytes than in post-MI control myocytes because of better-maintained L-

108 n inflammation and wound healing proteins on post-MI day 7.

109 Higher risk of post-MI death among women in comparison to men was restr

110 The higher risk of post-MI death among women with MI-CAD was most pronounce

111 not A2BKO, cells significantly reduced both post-MI decline in cardiac function and adverse remodeli

112 d left ventricular function at up to 8 weeks post-MI despite demonstrating significantly more hypertr

113 trols, but echocardiography at 1 and 2 weeks post MI detected no differences in cardiac function.

114 uitment to the remote zone may contribute to post-MI dilation.

115 eptibility in both noninfarcted and low-risk post-MI dogs.

116 rculating S1P levels, nor does it ameliorate post-MI dysfunction, as in wild-type mice.

117 Post-MI edema in patients follows a bimodal pattern that

118 At 3 months post-MI, ejection fraction increased by 12% relative to

119 The goal of our study was to quantify post-MI electrical remodeling by measuring the sum absol

120 ervention in the thrombotic and inflammatory post-MI environment.

121 yocardial edema persisted for several months post-MI, extending from the infarct to noninfarcted myoc

122 Post MI, f/f/Cre mice showed compromised survival, highe

123 Eight weeks post MI, fate mapping and flow cytometry revealed that a

124 (em2Mcwi)), we assessed the role of Sh2b3 in post-MI fibrosis, leukocyte infiltration, angiogenesis,

125 -LXA4 (1 microg/kg/day) was injected 3 hours post-MI for (d)1 or continued daily till d5.

126 from border and remote regions are preserved post-MI, giving rise to a 'neural sensory border zone'.

127 Interestingly, post-MI GRK2KO mice showed better cardiac function than

128 e SR Ca(2+) content was better maintained in post-MI GRK2KO myocytes than in post-MI control myocytes

129 mmed ventricular stimulation (within 1 week) post-MI has been able to identify long-term ventricular

130 A uniform reduction in TIMP-4 post-MI has been observed.

131 sex, and obstructive CAD status and outcomes post-MI has not been established.

132 d was the greatest for AF occurring >30 days post MI (hazard ratio [95% confidence interval] 1.63 [1.

133 neglected, disregarding its contribution to post-MI heart failure (HF) development.

134 farct healing, and attenuated development of post-MI heart failure after coronary ligation as measure

135 and infarct reduce inflammation and diminish post-MI heart failure in ApoE(-/-) mice with atheroscler

136 uggesting that the increased wall tension in post-MI heart failure stimulates local macrophage prolif

137 s and display compromised tissue healing and post-MI heart failure.

138 may present a therapeutic target to prevent post-MI heart failure.

139 issue repair after infarction and to prevent post-MI heart failure.

140 et activation, reduced MI size, and improved post-MI heart function.

141 crease in Krebs cycle activity in the 6-week post-MI heart may represent an early maladaptive phase i

142 roves the efficiency of CBT with MSCs in the post-MI heart.

143 y underlie, in part, arrhythmogenesis in the post-MI heart.

144 ved angiogenesis as well as functionality of post-MI hearts.

145 ing risks, the cumulative incidence rates of post-MI HF among patients with 0 or 1, 2, and 3 diseased

146 In vivo, we show that Meto arrests post-MI HF progression in mice as much as chronic S1P tr

147 xtent of angiographic CAD is an indicator of post-MI HF regardless of HF type and independent of recu

148 Post-MI HF was induced by coronary artery occlusion.

149 diac function and beta-adrenergic reserve in post-MI HF.

150 The LV tensile strength at day 3 post-MI, however, was similar between the 2 genotypes.

151 a phenotype similar to that of HDC(-/-) mice post-MI; however, in contrast to HDC(-/-) mice, the bene

152 ll-specific knockout mice showed significant post-MI improvement of cardiac function and reduction of

153 regulator of cardiac repair and regeneration post MI in neonatal hearts.

154 nctional role of Treg cells in wound healing post-MI in a mouse model of permanent left coronary arte

155 ine-4-yl)urea (TPPU), which was started 1 wk post-MI in a murine model, results in a significant impr

156 tural and functional remodelling of the ICNS post-MI in a porcine model (control (n = 16) vs. healed

157 specific myofilament protein, is proteolyzed post-MI in humans, which results in an N-terminal fragme

158 Pharmacological inhibition of miR-22 post-MI in older mice activated cardiac autophagy, preve

159 ne at 5 days post-MI and by >100% at 21 days post-MI in the Ad-GFP only group.

160 y modulating cardiac fibrosis and remodeling post-MI, in part through the STAT6-dependent signaling p

161 Anti-interleukin-1beta treatment dampens the post-MI increase in hematopoietic stem cell proliferatio

162 /-0.12 and 0.61+/-0.19 for 1, 7, and 99 days post-MI, indicating the potential for adequate delivery

163 Local overexpression of SCF post-MI induces the recruitment of c-kit(+) cells at the

164 myocardial infarction (MI), but its role in post-MI inflammation and fibrosis is completely unknown.

165 rst time that SH2B3 is a crucial mediator of post-MI inflammation and fibrosis.

166 gnificant difference in cardiac function and post-MI inflammation from those of control littermates.

167 as a crucial early danger signal triggering post-MI inflammation.

168 pi-LXA4 will expedite the resolving phase in post-MI inflammation.

169 Post MI, inflammatory response was not altered by ADAM17

170 ventricular function, but as early as 1 week post-MI, KO mice had significantly more left ventricular

171 Cardiac remodeling post-MI leads to progressive impaired cardiac function c

172 , LIF+BMP-2 precommitted mES cells, improved post-MI left ventricular functions, and enhanced capilla

173 attenuated infarct inflammation, and curbed post-MI left ventricular remodeling.

174 Post-MI leukocyte density, residence time in the infarct

175 tional analysis of the MIPIN showed that the post-MI LV exhibited increased representation of protein

176 f metformin, a drug associated with improved post-MI LV function in experimental studies.

177 proapoptotic condition contributing to poor post-MI LV function.

178 golimod mitigated the development of adverse post-MI LV remodeling 1 month after MI.

179 on profiles related to factors that regulate post-MI LV remodeling and repair.

180 ) and would be associated with parameters of post-MI LV remodeling.

181 nt manner, and thereby influenced indices of post-MI LV remodeling.

182 improved systolic LV function, and mitigated post-MI LV remodeling.

183 Seven days post-MI, LV function and parameters of LV remodeling wer

184 To identify novel biomarkers predicting post-MI LVEF and ISZ, we performed metabolic profiling i

185 HDL triglyceride concentrations predict post-MI LVEF and ISZ.

186 Decreased cardiac function post-MI may result, in part, from the ability of hC0C1f

187 Twenty-four hours post-MI measurements of high-density lipoprotein (HDL) t

188 acid-based anti-miR-34a treatment diminished post-MI miR-34a upregulation in adult hearts and signifi

189 1-shortening DLLs enables the measurement of post-MI monocyte and/or macrophage spatiotemporal kineti

190 f endothelial cell adhesion molecules curbed post-MI monocyte recruitment to the remote myocardium an

191 The association between depression and post-MI mortality is complex, possibly being limited to

192 ntil the relationship between depression and post-MI mortality is understood fully, clinical trials a

193 t post MI, the sorafenib-induced increase in post-MI mortality was eliminated, cardiac function was i

194 sonance (CMR) is an independent predictor of post-MI mortality.

195 of 11+/-5 months tended to have higher early post-MI MRGlc.

196 ontent was increased by nearly 2-fold in the post-MI MT1-MMPexp compared with WT.

197 ytic activity was increased by 4-fold in the post-MI MT1-MMPexp group.

198 ), and LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT (41 +/- 2 versu

199 In the post-MI MT1-MMPexp mice, LV myocardial MMP activity, as

200 the causal relationship between calpain and post-MI myocardial remodeling has not been fully underst

201 e the effects of ES cell-based therapies for post-MI myocardial repair and regeneration.

202 had no effect on infarct size, fibrosis, or post-MI neovascularization.

203 trend is consistent with the displacement of post-MI outcomes toward noncardiovascular events, highli

204 We found that post-MI p-cSrc interacts with ZO-1 as Cx43 begins to dec

205 0 mumol/L ADP) that persisted up to 24 hours post-MI (P<0.05).

206 Alternans Testing for Risk Stratification of Post MI Patients; NCT00305240).

207 st discriminatory power to differentiate the post-MI patients (at 1 year) from the controls.

208 Data were analyzed for 4,015 post-MI patients and 12,976 patients with ATH.

209 pport the use of intensive statin therapy in post-MI patients and provide estimates of the expected L

210 ed in 53 age-matched control subjects and 32 post-MI patients from day 1 through 180 after MI.

211 f the linear parameters to differentiate the post-MI patients from the controls.

212 easible, such a strategy would help identify post-MI patients likely to develop heart failure.

213 ic temporal pattern of MMP/TIMPs occurred in post-MI patients that included an early and robust rise

214 Adverse electrical remodeling in post-MI patients was characterized by wide QRS, increase

215 ia could decrease morbidity and mortality in post-MI patients with cardiogenic shock and warrants stu

216 association with 1-year ICD implantation in post-MI patients with low EF.

217 In post-MI patients with preserved ejection fraction and le

218 are important prior to implementation in all post-MI patients.

219 a well-tolerated and effective treatment for post-MI patients.

220 mpact of a polypill strategy on adherence in post-MI patients.

221 evaluating long-term therapies among elderly post-MI patients.

222 Hippo pathway effectors, developed profound post-MI pericardial inflammation and myocardial fibrosis

223 eate the actual causes of death in the early post-MI period and which interventions can be implemente

224 At 4 weeks post-MI, plasma levels of both norepinephrine and epinep

225 ears; 74% male) underwent mitral surgery for post-MI PMR from January 1980 through December 2000.

226 Surgery for post-MI PMR involves a notable operative mortality, but

227 a threshold effect at >80% adherence in the post-MI population; at least a 40% level of long-term ad

228 mber of M2-like macrophages and enhanced the post-MI prognosis of WT mice, corresponding with amplifi

229 e applied in the clinical setting to improve post-MI prognostication and identify appropriate therapi

230 ating regional myocardial strain and work in post-MI rats with and without heart failure.

231 ral-mediated gene delivery in vivo in 2-week post-MI rats, a time point around which circulating aldo

232 ator of exercise-induced cardioprotection in post-MI rats.

233 to our understanding of the role of EPCs in post-MI recovery and on the sex discrepancy in cardiac e

234 ghts the key role of cardiomyocyte ADAM17 in post-MI recovery by regulating VEGFR2 transcription and

235 ole in adaptive immune regulation during the post-MI recovery phase.

236 o, the significance of lymphocytes in humans post MI remains unclear, primarily as a result of method

237 therapeutic concept may be used to attenuate post-MI remodeling and heart failure.

238 2 in failing cardiomyocytes, contributing to post-MI remodeling and HF progression.

239 creases risk of cardiac rupture, accentuates post-MI remodeling and left ventricular dysfunction, and

240 Deletion of GSK-3beta protects against post-MI remodeling and promotes stress-induced cardiomyo

241 However, GSK-3beta does regulate post-MI remodeling because the GSK-3beta knockouts had l

242 Their origin and roles in post-MI remodeling of nonischemic remote myocardium, how

243 ocomposite material can favorably affect the post-MI remodeling process and therefore holds promise a

244 proteolytic pathways that contribute to the post-MI remodeling process has also been examined.

245 st with regard to the natural history of the post-MI remodeling process.

246 owever, the greatest effects with respect to post-MI remodeling were identified at lower MPC concentr

247 Given the complexity of post-MI remodeling, imaging modalities must be equally d

248 ning treatment fields for the attenuation of post-MI remodeling, such as cardiac restraint devices an

249 n this controlled model, moderate MR worsens post-MI remodeling, with reduced contractility.

250 n in adult hearts and significantly improved post-MI remodeling.

251 e as a means to interrupt the progression of post-MI remodeling.

252 cogen synthase kinase-3alpha (GSK-3alpha) in post-MI remodeling.

253 for new therapeutic targets to improve early post-MI remodeling.

254 response to the renin-angiotensin system and post-MI remodeling.

255 es to ameliorate post-myocardial infarction (post-MI) remodeling, as they enhance endogenous cardiac

256 solving mediators as the emerging factor for post-MI reparative mechanisms-translational leukocyte mo

257 The single patient infused 14 months post-MI responded similarly.

258 ished the first knowledge map related to the post-MI response, providing a major step towards enhanci

259 preserved left ventricular systolic function post-MI, restoring cardiac function.

260 tal data, a time window between days 4 and 7 post-MI seems a good compromise solution for standardiza

261 In addition, post-MI sequelae, including left ventricular thrombus an

262 peutic strategy for cardiogenic shock in the post-MI setting.

263 We investigated the risk of mortality in post-MI snus quitters (n=675) relative to post-MI contin

264 , 5.7-16.3) per 1000 person-years at risk in post-MI snus quitters and 18.7 (14.8-23.6) per 1000 pers

265 After adjustment for age and sex, post-MI snus quitters had half the mortality risk of pos

266 hared risk factors (eg, atherosclerosis) and post-MI stroke.

267 ial canonical (TRPC) channels contributes to post-MI structural and functional remodeling.

268 Abrogation of CCR9 improved the post-MI survival rate and left ventricular (LV) dysfunct

269 Overall, 28-day post-MI survival rate was 68% with MI-N and 48% with MI-

270 fore transplantation, which also resulted in post-MI survival rates comparable to those in WT BMT mic

271 Post-MI survival was reduced (67% versus 46%, p < 0.05),

272 FoxO4(-/-) mice had a significantly higher post-MI survival, better cardiac function, and reduced i

273 th control mice, suggesting markedly reduced post-MI sympathetic activation.

274 eater degree of LA dilation at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early an

275 GF2 effects when administered early vs. late post-MI that may be important to consider in the develop

276 vel collagen-derived matricryptins generated post-MI that mediate remodeling of the left ventricle (L

277 Post MI, the diversity of leukocytes, such as neutrophil

278 reated animals received metoprolol treatment post MI, the sorafenib-induced increase in post-MI morta

279 the other hand, when administered at Day 28 post-MI, the effects of IL-4c were diminished, suggestin

280 endogenous cardiac lymphangiogenic response post-MI, the remodeling and dysfunction of collecting du

281 -day and 3-month waiting periods in patients post-MI, the WCD successfully treated SCA in 1.4%, and t

282 her demonstrating its promise as a potential post-MI therapy.

283 ving phase early to discontinue inflammation post-MI, thereby reducing LV dysfunction.

284 Ad-GFP-TIMP4 and hTIMP-4exp groups at these post-MI time points.

285 Targeted delivery of VEGF to post-MI tissue resulted in significant increase in fract

286 y of low doses of proangiogenic compounds to post-MI tissue results in significant improvements in ca

287 To determine whether post-MI transendocardial injection of allogeneic CBSCs r

288 In vivo, early post-MI treatment with p1158/59 reduced LV dilation at d

289 Blocking post-MI TRPC activity improved post-MI cardiac structure

290 immunolocalization for active c-Src (p-cSrc) post-MI using a canine model of coronary occlusion.

291 ressing cells and histamine in heart failure post-MI using HDC-EGFP transgenic mice and HDC-knockout

292 indings are relevant to the understanding of post-MI ventricular remodeling and may contribute to the

293 cacy of autologous BMC delivery 2 to 3 weeks post-MI warrants investigation.

294 Myocardial hemorrhage 2 days post MI was associated with clinical characteristics ind

295 rdiovascular medication adherence at 6 weeks post MI, we stratified patients into self-reported high

296 between exercise and improved heart function post MI, we subjected MI-rats, induced by left coronary

297 tricular function evident as early as 1 week post-MI, we examined infarct size following a 48-hour co

298 changes in cardiac function and vasculature post-MI were quantified in a rat MI model.

299 ng revealed that LV volumes at days 7 and 28 post-MI were significantly lower in the EcSOD group comp

300 gration into the infarcted myocardium 5 days post MI, which was inhibited by ACK2.