ライフサイエンスコーパス: post-MI

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

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

3 roliferation and subsequent cardiac recovery post MI.

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

5 ial activation and myocardial arteriogenesis post MI.

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

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

8 s) production, and myocardial arteriogenesis post MI.

9 -lowering therapy, and LDL-C achieved 1-year post MI.

10 oprotein cholesterol (LDL-C) achieved 1-year post MI.

11 on (MI) with oral administration immediately post-MI.

12 aluate sphingolipid metabolism and signaling post-MI.

13 mortality by increasing cardiac fibrogenesis post-MI.

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

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

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

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

18 cular ejection fraction measured at 4 months post-MI.

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

20 proinflammatory and favor adverse remodeling post-MI.

21 intrinsic cardiac nervous system is reduced post-MI.

22 tic stimulation of cardiac lymphangiogenesis post-MI.

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

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

25 t manner and limited precollector remodeling post-MI.

26 Efferent inputs to neurons were maintained post-MI.

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

28 ibitor improved myocardial insulin signaling post-MI.

29 ted pro-inflammatory or reparative responses post-MI.

30 with KE-2 did not influence cardiac fibrosis post-MI.

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

32 smaller scar size than control mice 28 days post-MI.

33 and A3 received oral atorvastatin within 2 h post-MI.

34 ar remodeling and preserves cardiac function post-MI.

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

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

37 ling and preserves left ventricular function post-MI.

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

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

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

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

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

43 ardiac fibrosis and improve cardiac function post-MI.

44 rtality because of increased cardiac rupture post-MI.

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

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

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

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

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

50 sed the expression of Mmp14 (MT1-MMP) 7 days post-MI.

51 rs (SRCs) attenuates pathological remodeling post-MI.

52 presented with left ventricular dysfunction post-MI.

53 ystemically delivering miR-19a/19b into mice post-MI.

54 ring therapy in young FH and non-FH patients post-MI.

55 asuring Gal-3 levels for risk stratification post-MI.

56 re new independent markers of LV dysfunction post-MI.

57 arity to cells recovered from control hearts post-MI.

58 an independent predictor of mortality and HF post-MI.

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

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

61 imary determinant in heart failure pathology post-MI.

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

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

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

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

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

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

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

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

70 attributed the improvement in heart function post-MI after AC modRNA delivery to decreased ceramide l

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

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

73 r 10 mg/kg, IV) was administered immediately post-MI and compared to free AZM (F-AZM).

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

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

76 cular ejection fraction measured at 4 months post-MI and identified proteins potentially coregulated

77 T to cardiac fibrosis and adverse remodeling post-MI and identify Mphi MT1-MMP as a key regulator of

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

79 c magnetic resonance analysis (days 3 and 42 post-MI) and molecular/histological studies were perform

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

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

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

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

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

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

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

87 We studied the mechanisms triggering these post-MI arrhythmias in vivo and their relation to region

88 ri-infarct region as source and substrate of post-MI arrhythmias.

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

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

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

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

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

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

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

96 nal KO (MAC-Mmp14 KO) resulted in attenuated post-MI cardiac dysfunction, reduced fibrosis, and prese

97 genes and the direct role of these cells in post-MI cardiac fibrosis.

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

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

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

101 Post-MI cardiac remodeling is a multifaceted process tha

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

103 e pericardial cavity accelerated maladaptive post-MI cardiac remodeling.

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

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

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

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

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

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

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

111 A) was a dominant cardiac antigen triggering post-MI CD4+ T cell activation in mice.

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

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

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

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

116 (14.8-23.6) per 1000 person-years at risk in post-MI continuing snus users.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 promising radiotracer for in vivo imaging of post-MI fibroblast activation.

132 Post-MI fibrosis progression is characterized by a decre

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

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

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

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

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

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

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

140 hil accumulation, which resulted in impaired post-MI healing compared with WT.

141 c delivery of small molecules to improve the post-MI healing process.

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

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

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

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

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

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

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

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

150 Cardiomyocytes from post-MI hearts exhibited increasing T-system disarray as

151 ated cardiac overexpression of circFndc3b in post-MI hearts reduces cardiomyocyte apoptosis, enhances

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

153 es a cardioprotective role of eosinophils in post-MI hearts.

154 which is significantly down-regulated in the post-MI hearts.

155 dentified 36 plasma proteins associated with post-MI HF (data set 2), whereas single-cell transcripto

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

157 nderstanding plasma proteins associated with post-MI HF and their gene expression may identify new ca

158 ioritized protein candidates associated with post-MI HF for further mechanistic and clinical validati

159 er correlations among patients who developed post-MI HF in comparison with event-free controls (data

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

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

162 entified proteins potentially coregulated in post-MI HF using weighted gene co-expression network ana

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

164 sets included well-established biomarkers of post-MI HF: N-terminal B-type natriuretic peptide and tr

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

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

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

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

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

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

171 s to measure 1305 plasma proteins at 1 month post-MI in a New Zealand cohort (CDCS [Coronary Disease

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

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

174 ve cardiac recovery and reduce heart failure post-MI in humans.

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

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

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

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

179 /-0.12 and 0.61+/-0.19 for 1, 7, and 99 days post-MI, indicating the potential for adequate delivery

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

181 MCB-613, when given within hours post MI, induces lasting protection from adverse remodel

182 urther dissection of the heart-brain axis in post MI inflammation.

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

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

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

186 eir functions in macrophage polarization and post-MI inflammation, remodeling, and healing are not we

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

188 urther dissection of the heart-brain axis in post-MI inflammation.

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

190 Post MI, inflammatory response was not altered by ADAM17

191 At 1 week post-MI, lack of Gal-3 markedly attenuated F4/80+ macrop

192 eneficial effects of cell-based therapy in a post-MI large mammalian model, a finding with potential

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

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

195 left ventricular dysfunction and remodeling post-MI (left ventricular ejection fraction, 41+/-11 in

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

197 emature MI are not recommended for intensive post-MI lipid management.

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

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

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

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

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

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

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

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

206 Post-MI MAC-Mmp14 KO hearts contained fewer cells underg

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

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

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

210 1-shortening DLLs enables the measurement of post-MI monocyte and/or macrophage spatiotemporal kineti

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

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

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

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

215 function, reduced MI scar size, and enhanced post-MI neovascularization in MI mouse model.

216 poptosis, reduced MI scar size, and promoted post-MI neovascularization, whereas IL-10 knockout EPC-d

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

218 sal of Cardiac Remodelling]) of 223 patients post-MI, of which 33 patients were hospitalized for HF (

219 rategies are needed to reduce disparities in post-MI outcomes.

220 0 mumol/L ADP) that persisted up to 24 hours post-MI (P<0.05).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 The initial post-MI pro-inflammatory response followed by reparative

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

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

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

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

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

241 al analysis, beta-blocker use beyond 3 years post-MI, regardless of the dose achieved, was not associ

242 owing effects on mortality: unrevascularized post-MI relative risk (RR) 0.68 (95% CI, 0.45-1.03); P=0

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

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

245 2 in failing cardiomyocytes, contributing to post-MI remodeling and HF progression.

246 ction/myocardial infarction (MI) in mice and post-MI remodeling in rats.

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

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

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

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

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

252 duction of I/R injury in the early phases of post-MI remodeling.

253 ibitor decreases post-myocardial infarction (post-MI) remodeling and leads to improvement in cardiac

254 Other properties of post-MI remodelling are present in both peri-infarct and

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

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

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

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

259 ental and clinical trials, including time of post-MI scan, acquisition protocols, and, more important

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

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

262 Echocardiography performed 4 weeks post-MI showed that P1 MI and sham mice (n = 22, each) h

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

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

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

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

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

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

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

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

277 At 4 weeks post-MI, the natural evolution of fibrosis in Gal-3 knoc

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

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

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

281 ent and necessary to induce cardioprotection post-MI, thereby highlighting the therapeutic potential

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

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

284 ) with confirmed HF were randomized one-week post-MI to treatment with vehicle (water), sacubitril/va

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

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

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

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

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

290 ugh all developmental pathways contribute to post-MI vessel growth in the neonate, none are active du

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

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

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

294 EF at the time of MI and within 180 days post-MI were determined from all available medical recor

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

296 s in a porcine model of cardiac cell therapy post-MI, whereby dual RB1 and CDKN2a inactivation in adu

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

298 lized for HF in comparison with 250 patients post-MI who remained event free over a median follow-up

299 isease Cohort Study]) including 181 patients post-MI who were subsequently hospitalized for HF in com

300 ardiac dysfunction, cell death, and fibrosis post-MI, with concurrent acute increase of heart and chr