ライフサイエンスコーパス: myocardial infarct

1 were the predominant source of IL-10 in the myocardial infarct.

2 d by Marlex mesh placed over the anticipated myocardial infarct.

3 d in myocytes in the viable border zone of a myocardial infarct.

4 liability and accuracy in the measurement of myocardial infarcts.

5 is the main cause of coronary thrombosis and myocardial infarcts.

6 rates of arrhythmias in patients with healed myocardial infarcts.

7 nutes in persistently occluded or reperfused myocardial infarcts.

8 T were performed in six patients with healed myocardial infarcts.

9 lly provide new contractile tissue to repair myocardial infarcts.

10 Otherwise, myocarditis would commonly follow myocardial infarcts.

11 the beneficial effects of hMSCs in mice with myocardial infarcts.

12 ey after intravenous infusion into mice with myocardial infarcts.

13 fibrosis and vascular maturation in healing myocardial infarcts.

14 ed growth factor (PDGF) signaling in healing myocardial infarcts.

15 ng leptin levels by 38%, resulted in smaller myocardial infarcts (27% reduction), and improved recove

16 ed circulating leptin levels by 41%, smaller myocardial infarcts (29% reduction), and greater recover

17 imary prevention trials include the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Cana

18 ested a prospective hypothesis that European Myocardial Infarct Amiodarone Trial (EMIAT) patients wit

19 The European Myocardial Infarct Amiodarone Trial (EMIAT) was a random

20 ntrast-enhanced MR imaging for assessment of myocardial infarct and (b). cine MR imaging for assessme

21 eling during pathological conditions such as myocardial infarct and hypertension.

22 ugh its receptor ST2 protects the heart from myocardial infarct and hypertrophy in animal models but,

23 many devastating clinical conditions such as myocardial infarct and stroke.

24 (18)F-FDG PET/MR scans of a canine model of myocardial infarct and was demonstrated in a human subje

25 ed cardiomyocytes to partially remuscularize myocardial infarcts and attenuate heart failure encourag

26 r CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mec

27 wth factor (TGF-beta), is induced in healing myocardial infarcts and plays a role in suppressing the

28 occlusive proximal coronary artery disease, myocardial infarcts, and early mortality.

29 The mechanical properties of healing myocardial infarcts are an important determinant of LV f

30 Myocardial infarcts are routinely detected by nuclear im

31 SPECT and CMR detect transmural myocardial infarcts at similar rates.

32 to CA-125; the patient died as a result of a myocardial infarct before evidence of clinical progressi

33 served in the central necrotic zone of acute myocardial infarcts, but not in myocardium remote from t

34 Attempts to repair myocardial infarcts by transplanting cardiomyocytes or s

35 ith MRI, the complexity and heterogeneity of myocardial infarcts can be demonstrated.

36 determine whether the epicardial extent of a myocardial infarct could be defined during sinus rhythm.

37 To treat cardiac injuries created by myocardial infarcts, current approaches seek to add cell

38 We report that, in the presence of an acute myocardial infarct, cytokine-mediated translocation of B

39 ension was associated with increased risk of myocardial infarct death (HR, 2.15 [95% CI, 1.35-3.41]),

40 ial infarcts (HR, 1.75 [95% CI, 1.40-2.19]), myocardial infarct death (HR, 3.00 [95% CI, 1.98-4.55]),

41 eral of the agents to slow conduction in the myocardial infarcted dog hearts.

42 Human CDCs injected into the border zone of myocardial infarcts engrafted and migrated into the infa

43 In depolarized myocardial infarct epicardial border zones, the cardiac

44 In depolarized myocardial infarct epicardial border zones, the cardiac

45 properties of collagen structure in healing myocardial infarcts have been characterized previously,

46 Myocardial infarcts heal by scar formation because there

47 Myocardial infarcts heal by scarring because myocardium

48 o examine whether MCP-1 critically regulates myocardial infarct healing, we studied the effects of MC

49 ogenesis, tumor progression, metastasis, and myocardial infarct healing.

50 eceptor blockers and aldosterone in the post-myocardial infarct heart failure patient.

51 In the present study, we quantify myocardial infarct heterogeneity by contrast-enhanced MR

52 eart disease (HR, 1.44 [95% CI, 1.24-1.68]), myocardial infarcts (HR, 1.75 [95% CI, 1.40-2.19]), myoc

53 us, redo, diabetes, ejection fraction, prior myocardial infarct, hyperlipidemia, or creatinine level.

54 were injected into the border zone of acute myocardial infarcts in immunodeficient mice.

55 f FASTSPECT imaging for measurement of acute myocardial infarcts in rat hearts.

56 e search terms "smoking ban" and "heart" or "myocardial infarct." Investigators supplied additional d

57 es (MMP) and MMP inhibitors (TIMPs) within a myocardial infarct (MI) contributes to left ventricular

58 In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCI

59 y may reduce ischemia-reperfusion injury and myocardial infarct (MI) size.

60 of major adverse cardiovascular events than myocardial infarct (MI) size.

61 s in approximately 12-week sham-operated and myocardial infarcted (MI) rats.

62 3 developed type 2 diabetes, and 15 suffered myocardial infarcts (MIs).

63 transplants exhibit long-term survival in a myocardial infarct model and contribute to long-term imp

64 farct size and improved function in a murine myocardial infarct model compared with WT-MSCs.

65 he potential to allow visualization of acute myocardial infarcts, MVO zones, and patchy microinfarcts

66 ys; the diagnoses in the other patients were myocardial infarct (n = 2), septicemia (n = 2), adult re

67 d resolved more slowly than those of typical myocardial infarct necrosis in nonimmunosuppressed patie

68 poxic episodes such as those associated with myocardial infarcts, obstructive sleep apneas, apneas of

69 Three had a recent myocardial infarct of an age less than the duration of u

70 id not affect exocytosis and inflammation in myocardial infarcts of eNOS knockout mice.

71 or MINOCA revealed the presence of a typical myocardial infarct on cardiac magnetic resonance imaging

72 were considered equivocal for assessment of myocardial infarct on the basis of fixed perfusion defec

73 major perioperative morbidity--specifically, myocardial infarct, perioperative hemorrhage, or portal

74 n three patients with no clinical history of myocardial infarct prior to imaging.

75 uced by approximately 30%, and the volume of myocardial infarcts produced by occlusion of the left an

76 In the myocardial infarct, R2* value increased from 41.0+/-12.0

77 Myocardial infarcted rats and aorto-caval fistulated rat

78 To determine the role of FGF2 in myocardial infarct repair, we studied the evolution of l

79 etal muscle-derived myoendothelial cells for myocardial infarct repair.

80 ajor adverse cardiac event (MACE), such as a myocardial infarct, revascularization, cardiac death, or

81 -43%) in cardiomyocytes in vitro and reduced myocardial infarct size (-63%) after ischemia/reperfusio

82 ischemia, demonstrated significantly reduced myocardial infarct size (22.8+/-3.1%, mean+/-SEM) as com

83 ients demonstrated a 38% reduction in median myocardial infarct size (25th and 75th percentile) compa

84 rfusion and produced a profound reduction in myocardial infarct size (expressed as a percent of the a

85 Myocardial infarct size (IS) was determined by tetrazoli

86 IS, 28.5 +/- 4%) displayed a 54% decrease in myocardial infarct size (P < .001).

87 oning) proved highly efficacious in reducing myocardial infarct size (relative reduction, 86%, 39%, a

88 o ischemia-reperfusion significantly reduced myocardial infarct size after 20 min ischemia and 30 min

89 We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injur

90 tl1 to mice resulted in a 66.0% reduction in myocardial infarct size after ischemia/reperfusion injur

91 Myocardial infarct size and apoptosis, production of per

92 veloped pressure and aortic flow and reduced myocardial infarct size and apoptotic cell death with lo

93 eatment with ACE inhibitors or ARBs on acute myocardial infarct size and arrhythmias are unknown.

94 pretreatment with captopril and losartan on myocardial infarct size and arrhythmias in a rat model o

95 tischemic ventricular dysfunction, increased myocardial infarct size and cardiomyocyte apoptosis comp

96 was to quantitate the relation between final myocardial infarct size and duration of symptoms before

97 Likewise, CTRP9-KO mice showed increased myocardial infarct size and elevated expression of infla

98 in 2 days, an effect associated with reduced myocardial infarct size and improved heart function.

99 bitor tyrphostin AG490 showed a reduction in myocardial infarct size and in number of cardiomyocytes

100 ppressed efferocytosis preceded increases in myocardial infarct size and led to delayed inflammation

101 emonstrate for the first time in humans that myocardial infarct size and left ventricular function af

102 Unexpectedly, myocardial infarct size and neutrophil infiltration/acti

103 compare the effects of early and late PC on myocardial infarct size and postischemic dysfunction in

104 neutrophil adhesion protein CD18 could limit myocardial infarct size and preserve left ventricular fu

105 ion, the most effective therapy for reducing myocardial infarct size and preserving left ventricular

106 ations into the effects of chronic uremia on myocardial infarct size and the protective effects of is

107 elays within this early time period on final myocardial infarct size are unknown.

108 The primary end point was myocardial infarct size as assessed by cardiac enzymes,

109 Primary endpoint was myocardial infarct size as assessed by cardiac magnetic

110 ardial injury and was associated with larger myocardial infarct size assessed at 6 months.

111 ocardial infarction, cardiac arrhythmia, and myocardial infarct size assessed by cardiac magnetic res

112 irus expressing miR-21 (Ad-miR-21) decreased myocardial infarct size by 29% at 24 h and decreased the

113 tosis by 48%, lipid peroxidation by 39%, and myocardial infarct size by 45%, and improved left ventri

114 myocardial ischemia/reperfusion, attenuated myocardial infarct size by 47%, and preserved left ventr

115 Simvastatin treatment attenuated myocardial infarct size by 58% in wild-type but not eNOS

116 In phase II, IB-MECA reduced myocardial infarct size by 61%; infarct size (tetrazoliu

117 e past 3 years that have attempted to reduce myocardial infarct size by administration of adjunctive

118 Limitation of myocardial infarct size by an earlier brief complete occ

119 led ischemic postconditioning (IPoC), reduce myocardial infarct size by approximately 40% in animal m

120 antibody given before reperfusion can limit myocardial infarct size by nearly 50% and preserve globa

121 Reduction of myocardial infarct size by remote ischemic preconditioni

122 We have shown that myocardial infarct size can be reduced by topical coolin

123 as to investigate the effects of DMI-4983 on myocardial infarct size caused by regional ischemia and

124 CPA; 100 microgram/kg) significantly reduced myocardial infarct size compared with control animals, a

125 striction without muscle stimulation reduced myocardial infarct size considerably.

126 Myocardial infarct size following 60 minutes coronary ar

127 decreased vascular inflammation and reduced myocardial infarct size following ischemia and reperfusi

128 histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even wh

129 adolescent period and male gender increased myocardial infarct size in a young rat model of ischemia

130 Inhibition of leukocyte adhesion can reduce myocardial infarct size in animals.

131 itional studies, rosuvastatin did not affect myocardial infarct size in eNOS-deficient mice compared

132 h mitochondrial division inhibitor-1 reduced myocardial infarct size in mice subject to coronary arte

133 nhibition of PYK2 activation by Na2S reduced myocardial infarct size in mice.

134 best compounds (11f) is also shown to reduce myocardial infarct size in rat.

135 14643) also cause a substantial reduction of myocardial infarct size in the rat.

136 2 and PGA1) cause a substantial reduction of myocardial infarct size in the rat.

137 e accurate means of noninvasively estimating myocardial infarct size in this canine model than two-di

138 endothelial cell adhesion molecules decrease myocardial infarct size in vivo.

139 increases plasma IL-10 levels and decreases myocardial infarct size in wild-type mice but not in lit

140 Myocardial infarct size is a major determinant of left v

141 Myocardial infarct size is a major determinant of progno

142 nversion time (TI) and their interactions on myocardial infarct size measurements to establish the fo

143 Our study assesses the effect on myocardial infarct size of preconditioning at a distance

144 months, the oxygen group had an increase in myocardial infarct size on cardiac magnetic resonance (n

145 oes not substantially or consistently reduce myocardial infarct size or neutrophil accumulation in do

146 erapy resulted in a significant reduction in myocardial infarct size per area at risk compared with s

147 ngioplasty, it has become possible to reduce myocardial infarct size through early reperfusion.

148 Myocardial infarct size was also reduced in FGF2 Tg hear

149 Myocardial infarct size was determined by triphenyltetra

150 Myocardial infarct size was increased in uremic animals,

151 Myocardial infarct size was increased, and coronary flow

152 Myocardial infarct size was measured through triphenylte

153 No difference of myocardial infarct size was observed between groups.

154 myocardial ischemia and 72 h of reperfusion, myocardial infarct size was reduced by 42% in the transg

155 Myocardial infarct size was reduced significantly, from

156 trin2 KO mice were subjected to in vivo I/R, myocardial infarct size was significantly greater in Ses

157 iac function was significantly improved, and myocardial infarct size was significantly reduced after

158 Myocardial infarct size was significantly smaller in gro

159 Myocardial infarct size was similar between study groups

160 owed that adjunctive therapy further reduced myocardial infarct size when coupled with reperfusion.

161 ontinued interest in the concept of limiting myocardial infarct size with adjunctive agents administe

162 n of the VEGFR2/VE-cadherin complex, reduced myocardial infarct size, and the extent of no-reflow in

163 Acute myocardial infarct size, extent of microvascular obstruc

164 r-to-balloon time, leading to a reduction in myocardial infarct size, hospital length of stay, and to

165 eficient (APN-KO) mice resulted in increased myocardial infarct size, myocardial apoptosis and tumor

166 ltrasound targeted hs-MB destruction limited myocardial infarct size, preserved left ventricular func

167 one reductase gene (GSNOR(-/-)) have reduced myocardial infarct size, preserved ventricular systolic

168 the result of which is a marked reduction in myocardial infarct size, severity of stunning, or incide

169 terventions have been investigated to reduce myocardial infarct size.

170 R injury in humans, and reduces experimental myocardial infarct size.

171 episodes of VT and VF, as well as decreased myocardial infarct size.

172 peptide resulted in significant reduction of myocardial infarct size.

173 e as an adjunct to thrombolysis would reduce myocardial infarct size.

174 are predictors of ST-segment resolution and myocardial infarct size.

175 may attenuate reperfusion injury and reduce myocardial infarct size.

176 ioning may be useful means by which to limit myocardial infarct size.

177 tion, reactive oxygen species formation, and myocardial infarct size.

178 to increase plasma IL-10 levels and decrease myocardial infarct size.

179 rates that a probiotic supplement can reduce myocardial infarct size.

180 cNAc levels in vivo was sufficient to reduce myocardial infarct size.

181 de sustained ischemia lead to a reduction in myocardial infarct size.

182 Both myocardial infarct size/area at risk and O2(-) productio

183 Unexpectedly, however, the myocardial infarct size/area at risk was greater, despit

184 Myocardial infarct size/area at risk was reduced by 51.2

185 itric oxide synthase (iNOS) markedly reduces myocardial infarct size; this effect is associated with

186 hrombolytic therapy and who had thallium-201 myocardial infarct-size measurements performed several w

187 wth factor (phVEGF165) in the border zone of myocardial infarct tissue in rat hearts were investigate

188 (99m)Tc-Glucarate marks acute myocardial infarct very early after occlusion and appear

189 One animal with a myocardial infarct was analyzed separately.

190 Myocardial infarct was induced by balloon occlusion of t

191 ogical conditions, extensive regeneration of myocardial infarcts was reported recently after direct s

192 Canine myocardial infarcts were created by coronary ligation.

193 Myocardial infarcts were created in Yorkshire pigs (n=6)

194 Fischer rats with one-week-old myocardial infarcts were injected with collagen or salin

195 ceptor (IGF-1R) in the stressed cells, large myocardial infarcts were produced in Fischer 344 rats at

196 iffusing capacity, and one patient died of a myocardial infarct while improving on therapy.

197 sustained VTs from six patients with healed myocardial infarcts who were undergoing arrhythmia surge

198 Noninvasive imaging of myocardial infarcts with 99mTc glucarate is possible wit