ライフサイエンスコーパス: myocardial dysfunction

1 ed bodyweight loss, behavioral sickness, and myocardial dysfunction.

2 a-induced and reactive oxygen species-driven myocardial dysfunction.

3 and increased severity of postresuscitation myocardial dysfunction.

4 PL) on plasma lipoproteins may contribute to myocardial dysfunction.

5 nflammation and atherosclerosis in incipient myocardial dysfunction.

6 s and endothelial cells that leads to severe myocardial dysfunction.

7 sordered Na+ and Ca2+ homeostasis leading to myocardial dysfunction.

8 linked to inflammation and sepsis-associated myocardial dysfunction.

9 OSA) is associated with oxidative stress and myocardial dysfunction.

10 rrhythmias and intensifies postresuscitation myocardial dysfunction.

11 l transition from compensatory remodeling to myocardial dysfunction.

12 ic agent for management of postresuscitation myocardial dysfunction.

13 rate imaging permit recognition of regional myocardial dysfunction.

14 d 17% had a cardiac cause other than primary myocardial dysfunction.

15 CIH leads to oxidative stress and LV myocardial dysfunction.

16 elaxation is a cardinal feature of senescent myocardial dysfunction.

17 aureus sepsis is associated with significant myocardial dysfunction.

18 iod and may play a role in postresuscitation myocardial dysfunction.

19 increases the severity of postresuscitation myocardial dysfunction.

20 athophysiology of cardiovascular disease and myocardial dysfunction.

21 recurrent VF, and lessened postresuscitation myocardial dysfunction.

22 roves risk prediction in patients with acute myocardial dysfunction.

23 vered and thereby minimize postresuscitation myocardial dysfunction.

24 d increase the severity of postresuscitation myocardial dysfunction.

25 jective, quantitative assessment of regional myocardial dysfunction.

26 failure is thought to exacerbate underlying myocardial dysfunction.

27 -1beta and thereby prevents ischemia-induced myocardial dysfunction.

28 noninsulin-dependent diabetes mellitus, and myocardial dysfunction.

29 d increase the severity of postresuscitation myocardial dysfunction.

30 urate identification and grading of regional myocardial dysfunction.

31 hypertrophy and contributes to postischemic myocardial dysfunction.

32 rdiomyocyte structure and function can cause myocardial dysfunction.

33 se interact to accelerate the progression of myocardial dysfunction.

34 ibition could not reverse, endotoxin-induced myocardial dysfunction.

35 may be useful to treat inflammatory-induced myocardial dysfunction.

36 matory T cells that appears to contribute to myocardial dysfunction.

37 ificantly less severity of postresuscitation myocardial dysfunction.

38 s rates and (2) persistent post-countershock myocardial dysfunction.

39 ptor densities can potentially contribute to myocardial dysfunction.

40 characterization of various types of altered myocardial dysfunction.

41 e not associated with less postresuscitation myocardial dysfunction.

42 arization of ischemic myocardium accentuates myocardial dysfunction.

43 ression and other conditions of inflammatory myocardial dysfunction.

44 mia and consequently accentuate postischemic myocardial dysfunction.

45 ne MRI for identifying regions of reversible myocardial dysfunction.

46 ha, an autocrine contributor to postischemic myocardial dysfunction.

47 n, or calsequestrin participate in senescent myocardial dysfunction.

48 lity, localized neutrophil accumulation, and myocardial dysfunction.

49 for peroxynitrite in inflammation-associated myocardial dysfunction.

50 iomyopathy and may contribute to progressive myocardial dysfunction.

51 ar (LV) mechanics and can detect subclinical myocardial dysfunction.

52 (HD) induces left ventricular (LV) transient myocardial dysfunction.

53 valvular heart disease who have significant myocardial dysfunction.

54 e to coronary artery aneurysms formation and myocardial dysfunction.

55 ing ventricular output and promoting further myocardial dysfunction.

56 ve stroke prevention via therapies for early myocardial dysfunction.

57 of MWI may be a more sensitive indicator of myocardial dysfunction.

58 this fails, metabolic inflexibility leads to myocardial dysfunction.

59 imaging surrogates for diffuse fibrosis and myocardial dysfunction.

60 er insights into the primary pathogenesis of myocardial dysfunction.

61 ergic drugs for supporting endotoxin-induced myocardial dysfunction.

62 c features, pathogenesis, family history, or myocardial dysfunction.

63 ids with cardiac lipotoxicity and subsequent myocardial dysfunction.

64 pathways in the heart that may contribute to myocardial dysfunction.

65 d graft-derived vasculature, and ameliorated myocardial dysfunction.

66 s as possible contributors to HIV-associated myocardial dysfunction.

67 degree of neurologic injury, and severity of myocardial dysfunction.

68 etween endothelial dysfunction and intrinsic myocardial dysfunction.

69 esponse to CVB3 infection and contributes to myocardial dysfunction.

70 AFLD) and appears to also be associated with myocardial dysfunction.

71 ent proinflammatory mediator that may induce myocardial dysfunction.

72 DA5 mice were protected against EMCV-induced myocardial dysfunction.

73 cting the heart from direct viral injury and myocardial dysfunction.

74 tibility of certain T2DM patients to develop myocardial dysfunction.

75 ments in functional recovery and ameliorated myocardial dysfunction.

76 -grade arteriovenous block in the absence of myocardial dysfunction (2D) if not already tried; 5) in

77 cardiac depression, exaggerated postischemic myocardial dysfunction, abnormalities in mitochondrial r

78 f could, at least in obesity, pose a risk of myocardial dysfunction above and beyond known cardiovasc

79 ns unclear if HSP70 can also protect against myocardial dysfunction after brief ischemia.

80 Previous studies demonstrated myocardial dysfunction after electrical shock and indica

81 Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complemen

82 n4 reduces adverse myocardial remodeling and myocardial dysfunction after MI.

83 cess of defibrillation and postresuscitation myocardial dysfunction after prolonged ventricular fibri

84 Although myocardial dysfunction after resuscitation from ventricu

85 y, can reliably predict recovery of regional myocardial dysfunction after revascularization in these

86 with oxidative stress and mitochondrial and myocardial dysfunction, although interaction among which

87 In addition to primary myocardial dysfunction, anatomical and pathophysiologica

88 g-term AAS use appears to be associated with myocardial dysfunction and accelerated coronary atherosc

89 analyze the association between severity of myocardial dysfunction and adverse outcome as defined by

90 myocardial infarction results in progressive myocardial dysfunction and adversely affects prognosis.

91 conditions include thrombotic complications, myocardial dysfunction and arrhythmia, acute coronary sy

92 FAO disorders often present in infancy with myocardial dysfunction and arrhythmias after exposure to

93 a (TNF-alpha) is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischem

94 -dependent protein kinase II (CaMKII) favors myocardial dysfunction and cell membrane electrical inst

95 s a taurine transporter whose involvement in myocardial dysfunction and DCM is supported by numerous

96 3 overexpression (NOS3TG) are protected from myocardial dysfunction and death associated with endotox

97 increases the severity of postresuscitation myocardial dysfunction and decreases the duration of sur

98 Severe myocardial dysfunction and dysrhythmias may accompany re

99 novel insights into potential mechanisms of myocardial dysfunction and early mortality in obesity.

100 rplay between eCyPA (extracellular CyPA) and myocardial dysfunction and evaluate the therapeutic pote

101 esis of HF, elucidating distinct patterns of myocardial dysfunction and events that are associated wi

102 pressure or volume over-load hypertrophy to myocardial dysfunction and failure.

103 by the risk of life-threatening arrhythmias, myocardial dysfunction and fibrofatty replacement of myo

104 Lethality correlated with severe myocardial dysfunction and fulminant heart failure.

105 AF is uncommon and occurs in the setting of myocardial dysfunction and graft rejection.

106 y recognized phenomenon of postresuscitation myocardial dysfunction and hamper efforts to reestablish

107 sed systemic inflammation has been linked to myocardial dysfunction and heart failure in patients wit

108 ility regions and novel biomarkers linked to myocardial dysfunction and heart failure, we performed t

109 chemotherapeutic drugs can themselves cause myocardial dysfunction and heart failure.

110 cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved survival.

111 ence can occur and contribute to age-related myocardial dysfunction and in the wider setting to agein

112 s whether CCI is associated with subclinical myocardial dysfunction and incident HF.

113 minimized the severity of postresuscitation myocardial dysfunction and increased the duration of pos

114 TNF contributes to postischemic myocardial dysfunction and induces proinflammatory signa

115 nd local inflammatory cytokine production to myocardial dysfunction and injury occurring during ische

116 Sepsis can be complicated by severe myocardial dysfunction and is associated with increased

117 We hypothesized that MIF-induced myocardial dysfunction and mitochondrial respiration def

118 ment sensitivity to Ca(2+), thereby reducing myocardial dysfunction and mortality in murine models of

119 die prematurely during swimming and display myocardial dysfunction and necrosis.

120 n in the rescue mode, normalized LPS-induced myocardial dysfunction and partially restored abnormal c

121 tionship between cardiomyocyte infection and myocardial dysfunction and pathology has not been establ

122 elate with the severity of postresuscitation myocardial dysfunction and postresuscitation survival.

123 oncentrations are increased in patients with myocardial dysfunction and predict poor outcome.

124 sonance imaging (CMR) can predict reversible myocardial dysfunction and remodeling in heart failure p

125 equently associated with pathological atrial myocardial dysfunction and remodeling, a triad that has

126 n patients with more extensive CAD and worse myocardial dysfunction and remodeling.

127 f interleukin 6 strongly predicted degree of myocardial dysfunction and severity of disease in childr

128 id U-74389G would minimize postresuscitation myocardial dysfunction and thereby improve neurologicall

129 g CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby improve postresuscita

130 cations contribute to the pathophysiology of myocardial dysfunction and thus may provide a target for

131 Interstitial fibrosis can lead to myocardial dysfunction and ultimately heart failure.

132 eveloped shock (with biochemical evidence of myocardial dysfunction) and required inotropic support a

133 longitudinal strain, CMR-derived measures of myocardial dysfunction, and cardiac biomarkers are worth

134 eculation of the left ventricle, progressive myocardial dysfunction, and early mortality.

135 iated with impaired insulin/IGF1R signaling, myocardial dysfunction, and fibrosis.

136 ation, whether patients with AD present with myocardial dysfunction, and if the 2 conditions bear a c

137 ld hypothermia, attenuated postresuscitation myocardial dysfunction, and improved neurologic outcome

138 c resuscitation, minimized postresuscitation myocardial dysfunction, and increased the duration of po

139 characterized the biology of the associated myocardial dysfunction, and tested novel therapeutic str

140 ntial cardiac donors show various degrees of myocardial dysfunction, and the most severely affected h

141 atrol on cecal ligation and puncture-induced myocardial dysfunction are associated with increased per

142 Hemodynamic instability and myocardial dysfunction are major factors preventing the

143 ms underlying repetitive stunning-associated myocardial dysfunction are not clear.

144 astolic characteristics of postresuscitation myocardial dysfunction are not well defined.

145 ssion of HSP70 protects against postischemic myocardial dysfunction as shown by better preserved myoc

146 r added to vasopressor in the presence of a) myocardial dysfunction as suggested by elevated cardiac

147 urrent ventricular fibrillation or transient myocardial dysfunction as with epinephrine alone.

148 All exhibited severe myocardial dysfunction at extracorporeal membrane oxygen

149 technique enables motion-based detection of myocardial dysfunction at noncontrast cardiac MRI, facil

150 Myocardial NOS3 prevented postcardiac arrest myocardial dysfunction, attenuated end-organ damage, and

151 sensitive enough in depicting early signs of myocardial dysfunction before irreversible myocardial da

152 Strain echocardiography reveals myocardial dysfunction before significant changes in eje

153 ssue Doppler and could detect early regional myocardial dysfunction before the onset of congestive he

154 gnized to cause cardiomyocyte (CM) death and myocardial dysfunction, but the role of cell-matrix inte

155 dden cardiac arrest is limited by postarrest myocardial dysfunction, but understanding of this phenom

156 hypothesized that detailed investigation of myocardial dysfunction by echocardiography can provide i

157 evidence that refutes the notion that acute myocardial dysfunction by high-dose TAT-HKII peptide adm

158 counteracted cecal ligation puncture-induced myocardial dysfunction by improving left ventricular pre

159 ts of repetitive shocks on postresuscitation myocardial dysfunction by using an isolated rat heart mo

160 if the molecular signals responsible for the myocardial dysfunction can be identified and blocked.

161 Reversible myocardial dysfunction can be identified by contrast-enh

162 rst time that impairment of angiogenesis and myocardial dysfunction can be regulated by Ad.Trx1 gene

163 As these patients reach adulthood, myocardial dysfunction can occur, leading to cardiac tra

164 ures progressive adverse cardiac remodeling, myocardial dysfunction, capillary rarefaction, and inter

165 All patients had severe myocardial dysfunction (cardiac index 3 L/min per m(2) o

166 Improved postresuscitation myocardial dysfunction (cardiac index, dP/dt40, -dP/dt)

167 Remarkably, CBD attenuated myocardial dysfunction, cardiac fibrosis, oxidative/nitr

168 rogressively, particularly with the onset of myocardial dysfunction (caspase-3 7.92 +/- 1.19 vs. 1.00

169 energy phosphate metabolism may underlie the myocardial dysfunction caused by hypobaric hypoxia.

170 Myocardial dysfunction caused by sepsis, usually termed

171 sudden death (5 of 7 families), progressive myocardial dysfunction causing death or heart transplant

172 t (or myocarditis) is the proximate cause of myocardial dysfunction, causing injury that can range fr

173 treatment for fatal arrhythmia, it produces myocardial dysfunction closely related to the intensity

174 ar voltage mapping can identify irreversible myocardial dysfunction consistent with fibrosis, even in

175 As myocardial dysfunction contributes to poor outcome in cr

176 Myocardial dysfunction contributes to the high mortality

177 as well as support and even reverse existing myocardial dysfunction, deferring the need for heart tra

178 FA pretreatment blunts myocardial dysfunction during ischemia and ameliorates p

179 chemic period may be the main determinant of myocardial dysfunction during reperfusion.

180 c hypertrophy, interstitial fibrosis, severe myocardial dysfunction, 'fetal' gene induction, apoptosi

181 Myocardial dysfunction has been demonstrated in MFS pati

182 Indeed, postresuscitation myocardial dysfunction has been implicated as a potentia

183 urrent levels to minimize post-resuscitation myocardial dysfunction has been largely unexplored.

184 Postresuscitation myocardial dysfunction has been recognized as a leading

185 Postresuscitation myocardial dysfunction has been recognized as a leading

186 Postresuscitation myocardial dysfunction has more recently emerged as a po

187 Treatment of such postresuscitation myocardial dysfunction has not been examined previously.

188 Treatment of progressive myocardial dysfunction has relied on conventional eviden

189 Significantly higher rates of myocardial dysfunction have been noted in individuals wi

190 prolonged primary MR leads to LV remodeling, myocardial dysfunction, heart failure, and death.

191 ischemic encephalopathy (HIE) are at risk of myocardial dysfunction; however, echocardiography studie

192 lood and organ nitrite depletion, reversible myocardial dysfunction, impaired alveolar gas exchange,

193 The post cardiac arrest syndrome subsumes myocardial dysfunction, impaired microcirculation, syste

194 en subclinical atherosclerosis and incipient myocardial dysfunction in a population free of clinical

195 retention was an independent determinant of myocardial dysfunction in cardiac amyloidosis.

196 onsible for the vicious cycle of progressive myocardial dysfunction in chronic heart failure.

197 atients, are postulated to contribute to the myocardial dysfunction in diabetes.

198 Myocardial dysfunction in endotoxemia correlates mainly

199 yperglycemia-induced JunD downregulation and myocardial dysfunction in experimental and human diabete

200 r the short- and long-term, without signs of myocardial dysfunction in healthy humans, except in very

201 have been implicated in the pathogenesis of myocardial dysfunction in ischemia-reperfusion injury, s

202 death may have a role in the pathogenesis of myocardial dysfunction in meningococcal septicemia.

203 uated cardioprotective strategies to prevent myocardial dysfunction in patients who are receiving car

204 useful in the identification of subclinical myocardial dysfunction in patients with DM.

205 ortant target for novel therapies to reverse myocardial dysfunction in patients with meningococcal se

206 e responsiveness is associated with advanced myocardial dysfunction in patients with RA.

207 curately identify early coronary disease and myocardial dysfunction in persons with end-stage liver d

208 ng of either TNF-alpha or IL-1beta may limit myocardial dysfunction in sepsis.

209 The aim of our study was to explore myocardial dysfunction in severe sepsis.

210 The present study demonstrates myocardial dysfunction in severe sepsis.

211 oronary artery stenosis can lead to regional myocardial dysfunction in the absence of myocardial infa

212 lower and minimized early postresuscitation myocardial dysfunction in the rectilinear biphasic, dual

213 Postresuscitation myocardial dysfunction in this animal model was characte

214 volved in the mechanism of postresuscitation myocardial dysfunction in this setting.

215 tigate the role of NOS2 in endotoxin-induced myocardial dysfunction in vivo, we studied wild-type and

216 investigated the role of CD14 in LPS-induced myocardial dysfunction in vivo.

217 ced reactive oxygen species accumulation and myocardial dysfunction in wild-type mice.

218 peptido-agonist conferred protection against myocardial dysfunction in wild-type, but not Fpr2/3(-/-)

219 Hyper-aldosteronism is associated with myocardial dysfunction including induction of cardiac fi

220 As our knowledge and understanding of myocardial dysfunction increases, particularly in the ne

221 sion (autoradiography and binding assay) and myocardial dysfunction, indicated by increases in corona

222 ors of myocardial damage, including regional myocardial dysfunction, infarct distribution, infarct si

223 stigated the effects of cannabidiol (CBD) on myocardial dysfunction, inflammation, oxidative/nitrativ

224 , we explored the role of CB(1) receptors in myocardial dysfunction, inflammation, oxidative/nitrativ

225 -induced nitroxidative stress, inflammation, myocardial dysfunction, injury, and adverse remodeling.

226 Myocardial dysfunction is a characteristic component of

227 Myocardial dysfunction is a common and important problem

228 Myocardial dysfunction is a frequent complication in pat

229 Myocardial dysfunction is a major consequence of septic

230 of severe LV pressure overload hypertrophy, myocardial dysfunction is associated with increased micr

231 Myocardial dysfunction is commonly associated with accum

232 Complete recovery from myocardial dysfunction is expected after dual coronary r

233 These results indicate that myocardial dysfunction is largely caused by the removal

234 Whether myocardial dysfunction is mediated directly by nitric ox

235 ardial infarction (MI) exacerbates long-term myocardial dysfunction is not known.

236 ata indicate that lipopolysaccharide-induced myocardial dysfunction is not solely caused by elevated

237 Postresuscitation myocardial dysfunction is one of the leading causes of e

238 mental doses of high-dose insulin therapy if myocardial dysfunction is present (2D), IV lipid-emulsio

239 The severity of postresuscitation myocardial dysfunction is related, at least in part, to

240 tion (ECMO) is used in the setting of severe myocardial dysfunction, left ventricular end-diastolic a

241 onversely, rather than being a root cause of myocardial dysfunction, left ventricular noncompaction m

242 rioration, requiring mechanical ventilation; myocardial dysfunction may accompany respiratory decompe

243 Anthracycline-induced cardiotoxicity and myocardial dysfunction may be associated with apoptosis.

244 ion per se, a better understanding of septic myocardial dysfunction may be usefully extended to other

245 atients treated with VA-ECMO had more severe myocardial dysfunction (mean cardiac index 1.5 L/min per

246 for both) and correlated with the degree of myocardial dysfunction measured by strain parameters.

247 sion Cardiac MRI feature tracking identifies myocardial dysfunction not only in participants with ove

248 To avoid irreversible myocardial dysfunction, novel biomarkers are advocated t

249 Myocardial dysfunction occurred early after return of sp

250 inflammatory mediators either contribute to myocardial dysfunction or are elaborated systemically by

251 uccessful resuscitation achieved, reversible myocardial dysfunction, or "stunning," may occur.

252 /- 1.4, p < .005) and less postresuscitation myocardial dysfunction (p < .05).

253 imaging to elucidate the pathophysiology of myocardial dysfunction, prognosticate long-term clinical

254 ost studies, patients exhibited shock due to myocardial dysfunction rather than distributive/vasopleg

255 in adenosine-AR signaling were secondary to myocardial dysfunction rather than to TNF overexpression

256 tion of functional recovery in patients with myocardial dysfunction referred for revascularization.

257 ng disordered cell membrane excitability and myocardial dysfunction remain uncertain.

258 ar mechanisms responsible for sepsis-induced myocardial dysfunction remain undefined.

259 ide (NO) in lipopolysaccharide (LPS)-induced myocardial dysfunction remains controversial as some inv

260 e contributes to both systolic and diastolic myocardial dysfunction, respectively.

261 Estrogen protects against endothelial and myocardial dysfunction resulting from brief ischemia/rep

262 In the face of pre-existing myocardial dysfunction resulting from preoperative press

263 f subclinical left ventricular (LV) regional myocardial dysfunction (RMD) measured by magnetic resona

264 establishing energy depletion as a cause of myocardial dysfunction, should be relevant to the acquir

265 Despite the absence of myocardial dysfunction, steady-state NCX1 transcript and

266 st-cardiac arrest syndrome are brain injury, myocardial dysfunction, systemic ischemia/reperfusion re

267 al defibrillation had less postresuscitation myocardial dysfunction than rectilinear biphasic and dua

268 Myocardial dysfunction that can ultimately lead to strok

269 s a complex clinical syndrome resulting from myocardial dysfunction that impairs the cardiovascular s

270 ve important implications for explaining the myocardial dysfunction that is associated with increased

271 ovides evidence of dyssynchrony and regional myocardial dysfunction that occurs early with compensato

272 trast, banded animals treated with T4 had no myocardial dysfunction; these hearts had increased contr

273 R-92a in mice attenuated the infarct-related myocardial dysfunction to a larger extent than cardiomyo

274 s in understanding of the molecular basis of myocardial dysfunction, together with the development of

275 nces in understanding the molecular basis of myocardial dysfunction, together with the evolution of i

276 s in understanding of the molecular basis of myocardial dysfunction, together with the evolution of i

277 s in understanding of the molecular basis of myocardial dysfunction, together with the evolution of i

278 in the myocardium and serum from donors with myocardial dysfunction (unused donors) and compared them

279 eveloped rodent models of in vivo postarrest myocardial dysfunction using extracorporeal membrane oxy

280 broad, encompassing coronary artery disease, myocardial dysfunction, valvular abnormalities, and peri

281 ative settings: agents for the management of myocardial dysfunction, vasomotor dysfunction, pulmonary

282 Endotoxin-induced myocardial dysfunction was associated with increased ven

283 rated that the severity of postresuscitation myocardial dysfunction was closely related to the magnit

284 Regional myocardial dysfunction was defined as the presence of im

285 perimental observation that the magnitude of myocardial dysfunction was in part related to the energy

286 tion left ventricular systolic and diastolic myocardial dysfunction was reversible after 72 hrs in th

287 To investigate determinants of incipient myocardial dysfunction, we examined the association betw

288 ne levels in 13 patients with stress-related myocardial dysfunction were compared with those in 7 pat

289 Maximum survival and minimum myocardial dysfunction were observed with the low-capaci

290 scitation, and severity of postresuscitation myocardial dysfunction were observed.

291 b may attenuate or prevent postresuscitation myocardial dysfunction when administered immediately aft

292 inotropic drug for supporting sepsis-induced myocardial dysfunction when cardiac output index remains

293 involves a downward spiral: Ischemia causes myocardial dysfunction, which, in turn, worsens ischemia

294 dyssynchrony may mediate the association of myocardial dysfunction with age and LV hypertrophy.

295 SC) is a syndrome characterized by transient myocardial dysfunction with unknown etiology.

296 zebrafish (Danio rerio) embryos resulted in myocardial dysfunctions with disintegration of the sarco

297 Brief ischemic periods lead to myocardial dysfunction without myocardial infarction.