ライフサイエンスコーパス: cardiac dysfunction

1 hypertrophy of cardiac myocytes and overall cardiac dysfunction.

2 nse to doxorubicin-induced mitochondrial and cardiac dysfunction.

3 erized as having subclinical or unrecognized cardiac dysfunction.

4 penings followed by mitochondrial damage and cardiac dysfunction.

5 the life span will determine progression of cardiac dysfunction.

6 also improved FA metabolism and ameliorated cardiac dysfunction.

7 ting CVB3-induced myocarditis and preventing cardiac dysfunction.

8 nary hypertension, and reduced the degree of cardiac dysfunction.

9 enovirus infection may contribute to ongoing cardiac dysfunction.

10 ene (Edn1) expression is sufficient to cause cardiac dysfunction.

11 could be a potential therapy for DOX-induced cardiac dysfunction.

12 e targets in the setting of sepsis to reduce cardiac dysfunction.

13 nd provide possible mechanistic insight into cardiac dysfunction.

14 where increased NCX1 activity contributes to cardiac dysfunction.

15 ificantly reduced heart mass and ameliorated cardiac dysfunction.

16 rnitine, which correlated with the degree of cardiac dysfunction.

17 loped hypertension, cardiac hypertrophy, and cardiac dysfunction.

18 , are unusually vulnerable to stress-induced cardiac dysfunction.

19 disease severity, including hypothermia and cardiac dysfunction.

20 wever, it is not clear how diabetes promotes cardiac dysfunction.

21 om 10-day-old mice before the development of cardiac dysfunction.

22 er disease (NAFLD) may increase the risk for cardiac dysfunction.

23 abolished CpG-ODN attenuation of CLP-induced cardiac dysfunction.

24 -positive) breast cancer is dose-independent cardiac dysfunction.

25 hepsin K protects against obesity-associated cardiac dysfunction.

26 respiratory insufficiency but typically not cardiac dysfunction.

27 e.Endoplasmic reticulum (ER) stress promotes cardiac dysfunction.

28 14 of 15) had abnormal cardiac dimensions or cardiac dysfunction.

29 dred fifty (62%) presented with or developed cardiac dysfunction.

30 died uniformly before weaning due to severe cardiac dysfunction.

31 TLR9 ligand, on polymicrobial sepsis-induced cardiac dysfunction.

32 C-PPARgamma) were protected from LPS-induced cardiac dysfunction.

33 ized for cardiac iron overload without overt cardiac dysfunction.

34 16 patients stopped trastuzumab because of cardiac dysfunction.

35 g the underpinnings of inflammation-mediated cardiac dysfunction.

36 ol-ODN or iCpG-ODN did not alter CLP-induced cardiac dysfunction.

37 ergy deprivation accounts for sepsis-related cardiac dysfunction.

38 ntramyocardial TAG levels, lipotoxicity, and cardiac dysfunction.

39 n as a result of both direct lung injury and cardiac dysfunction.

40 al Wnt signaling, for roles in aging-related cardiac dysfunction.

41 ea, which can mask the clinical diagnosis of cardiac dysfunction.

42 aling pathway may provide targets to address cardiac dysfunction.

43 maladaptive and potentially associated with cardiac dysfunction.

44 lopment of beta-AR overstimulation-dependent cardiac dysfunction.

45 ng postinfarction cardiac ECM remodeling and cardiac dysfunction.

46 scle degeneration and weakness contribute to cardiac dysfunction.

47 Treatment was well tolerated with minimal cardiac dysfunction.

48 and in some cases reversed remodeling of the cardiac dysfunction.

49 ith multi-organ failure, high mortality, and cardiac dysfunction.

50 s to changes in cardiac energetics and early cardiac dysfunction.

51 diated reduction in fatty acid oxidation and cardiac dysfunction.

52 ophy without lipid accumulation or immediate cardiac dysfunction.

53 for the treatment of asthma, hypertension or cardiac dysfunction.

54 SOCS3 cKO hearts before the manifestation of cardiac dysfunction.

55 e may potentially be involved in T1D induced cardiac dysfunction.

56 d to halt or even reverse the progression of cardiac dysfunction.

57 ast activation, pathological remodeling, and cardiac dysfunction.

58 ntial target in treating diabetes-associated cardiac dysfunction.

59 has been suggested as a causative factor in cardiac dysfunction.

60 s tonically active in CHF and contributes to cardiac dysfunction.

61 tion of MAPKs and Akt during sepsis: role in cardiac dysfunction.

62 bitor in CLP mice reduced the development of cardiac dysfunction.

63 rment associated with persistent subclinical cardiac dysfunction.

64 y contribute to the occurrence of later life cardiac dysfunction.

65 may be a major worldwide cause of vertebrate cardiac dysfunction.

66 erapeutic target to prevent diabetes-induced cardiac dysfunction.

67 ls, increased triglyceride accumulation, and cardiac dysfunction.

68 molecular analysis to determine the basis of cardiac dysfunction.

69 e subjected to pressure overload ameliorates cardiac dysfunction.

70 ased fibroadipogenesis in the heart and mild cardiac dysfunction.

71 an abnormal endothelial phenotype as well as cardiac dysfunction.

72 els correlate with collagen crosslinking and cardiac dysfunction.

73 sity, diminished vascular patency and severe cardiac dysfunction.

74 studied the role of ACE2 in obesity-mediated cardiac dysfunction.

75 CM) homeostasis is compromised, resulting in cardiac dysfunction.

76 everses pathological cardiac hypertrophy and cardiac dysfunction.

77 ator of doxorubicin- and trastuzumab-induced cardiac dysfunction.

78 Cardiac dysfunction after acute myocardial infarction is

79 betaAR polymorphisms may be associated with cardiac dysfunction after brain death, but these relatio

80 nhibited cardiac hypertrophy and ameliorated cardiac dysfunction after chronic infusion of ISO in mic

81 yR-S2808 is irrelevant to the development of cardiac dysfunction after MI, at least in the mice used

82 ocytes attenuates ventricular remodeling and cardiac dysfunction after myocardial infarction by limit

83 ction of autologous platelet gel ameliorated cardiac dysfunction after myocardial infarction.

84 r initiation and progression, is linked with cardiac dysfunction, allows for the improper physiologic

85 idity and mortality primarily resulting from cardiac dysfunction, although T. cruzi infection results

86 1 mRNA and protein expression while inducing cardiac dysfunction and action potential prolongation.

87 ical remodeling in the heart associated with cardiac dysfunction and adverse outcomes likely mediated

88 -1 degradation and, consequently, diminished cardiac dysfunction and adverse structural remodeling.

89 EF and if chemoreflex activation exacerbates cardiac dysfunction and autonomic imbalance.

90 These early phenotypes of diastolic cardiac dysfunction and blunted lusitropic response of c

91 ented transverse aortic constriction-induced cardiac dysfunction and cardiac fibrosis and blocked car

92 Population-based estimates of cardiac dysfunction and clinical heart failure (HF) rema

93 at 6-7 weeks of age when the models display cardiac dysfunction and conduction abnormalities.

94 iotoxicity (ACT) manifesting as asymptomatic cardiac dysfunction and congestive heart failure in up t

95 echanisms of Volume Overload-Aim 1 [SCCOR in Cardiac Dysfunction and Disease]; NCT01052428).

96 ythmias occurred early and in the absence of cardiac dysfunction and excess cardiac fibroadipocytes,

97 MRI techniques to identify early markers of cardiac dysfunction and follow disease progression in th

98 Lastly, and most importantly, cardiac dysfunction and heart failure are potentially co

99 Diabetes mellitus causes cardiac dysfunction and heart failure that is associated

100 nd imaging aspects of cancer therapy-related cardiac dysfunction and heart failure.

101 nd imaging aspects of cancer therapy-related cardiac dysfunction and heart failure.

102 Klotho-deficient mice exhibited cardiac dysfunction and hypertrophy before 12 weeks of a

103 c mice (Tg) limited infarct size, attenuated cardiac dysfunction and improved cardiomyocyte survival

104 In vivo, Hrd1 knockdown exacerbated cardiac dysfunction and increased apoptosis and cardiac

105 Cardiac steatosis and fibrosis may underlie cardiac dysfunction and increased cardiovascular morbidi

106 tions of catecholamines accompanied by acute cardiac dysfunction and increased strong expressions of

107 stimulation, DKO mice are protected against cardiac dysfunction and interstitial fibrosis.

108 controls, CKD mice exhibited exacerbation of cardiac dysfunction and lung inflammation, greater incre

109 Dusp4 causes cardiac dysfunction and may contribute to the developmen

110 , DOX treatment resulted in markedly greater cardiac dysfunction and mortality in CM-BRCA2(-/-) mice

111 n of PPARgamma in LPS-treated mice prevented cardiac dysfunction and mortality, despite development o

112 F1 knockout (KO) mice were protected against cardiac dysfunction and pathological development induced

113 Myocardial scarring leads to cardiac dysfunction and poor prognosis.

114 dentified functional markers of EV71-related cardiac dysfunction and potential treatment options.

115 ections to prevent the abrupt progression to cardiac dysfunction and pulmonary edema by using an anim

116 ainstem encephalitis progressing abruptly to cardiac dysfunction and pulmonary edema causes rapid dea

117 cessive release of catecholamines to prevent cardiac dysfunction and pulmonary edema for increasing s

118 nistered to C57BL/6 mice (wild type) induced cardiac dysfunction and reduced fatty acid oxidation and

119 dysinhibition, upheld(101) hearts exhibited cardiac dysfunction and remodeling comparable to that ob

120 in which a complex interrelationship between cardiac dysfunction and renal dysfunction exists.

121 dema, and interstitial fibrosis and prevents cardiac dysfunction and SCD.

122 the silencing of Sox102F resulted in severe cardiac dysfunction and structural defects with disrupte

123 portunities for a more timely recognition of cardiac dysfunction and subsequent optimization of the h

124 ate that glucotoxicity by itself can trigger cardiac dysfunction and that a glucose-lowering agent ca

125 1) receptors attenuated the diabetes-induced cardiac dysfunction and the above-mentioned pathological

126 y of renal transplantation in the setting of cardiac dysfunction and the effect of renal transplantat

127 actice, 46% of patients developed persistent cardiac dysfunction and their medium-term survival was p

128 Our prior studies suggest biventricular cardiac dysfunction and vascular impairment in baboons w

129 /)(-) and Npr2(+/)(-);Ldlr-/- mice developed cardiac dysfunction and ventricular fibrosis.

130 pproaches that alter serum S1P may attenuate cardiac dysfunction and whether S1P signaling might serv

131 r modulated targets showed the enrichment of cardiac dysfunctions and HF categories.

132 iated with fatal neonatal disease, liver and cardiac dysfunction, and anemia.

133 T) and PG(TR) mice exhibited fibro-adiposis, cardiac dysfunction, and premature death.

134 RK2 by RKIP induced cardiomyocyte apoptosis, cardiac dysfunction, and signs of heart failure.

135 athogenic Escherichia coli strain can induce cardiac dysfunction, and to elucidate any mechanisms inv

136 flammation, hemostasis, thrombin generation, cardiac dysfunction, and vascular stiffness and identifi

137 ivation of SGK1 in mice increased mortality, cardiac dysfunction, and ventricular arrhythmias.

138 reduced cardiomyocyte autophagy, exacerbated cardiac dysfunctions, and increased mortality in diabeti

139 not confer protection against CLP-triggered cardiac dysfunction, apoptosis and inflammatory response

140 d concomitant pulmonary vascular disease and cardiac dysfunction are associated with poor prognosis.

141 proximal to the receptor in contributing to cardiac dysfunction are not known.

142 ent of cardiac myocytes by fibro-adipocytes, cardiac dysfunction, arrhythmias, and sudden death.

143 We identified systolic cardiac dysfunction as a major determinant of outcome.

144 however, lack of Epac1 prevented subsequent cardiac dysfunction as a result of decreased cardiac myo

145 CpG-ODN prevented CLP-induced cardiac dysfunction, as evidenced by maintenance of the

146 iated reduction of mitochondria, and treated cardiac dysfunction, as well as it improved survival, de

147 we hypothesized that rapamycin would prevent cardiac dysfunction associated with type 2 diabetes (T2D

148 l, restored plasma NOx and protected against cardiac dysfunction at adulthood.

149 ion, neonatal dexamethasone therapy promotes cardiac dysfunction at adulthood.

150 ned according to self-report, and those with cardiac dysfunction but without clinical HF were charact

151 Cell death is rare in sepsis-induced cardiac dysfunction, but cardiomyocyte injury occurs.

152 crotubule network likely promote MIF-induced cardiac dysfunction by 1) altering with mitochondrial tu

153 rvivors with normal 3D LVEFs had evidence of cardiac dysfunction by global longitudinal strain (28%),

154 tential roles in inflammation, fibrosis, and cardiac dysfunction: C-reactive protein (CRP); NT-pro-B-

155 nitor cell (CPC) function, and that neonatal cardiac dysfunction can be rescued by in utero injection

156 erse aortic constriction induced significant cardiac dysfunction, cardiac fibrosis, and cardiac fibro

157 s cardiac fatty acid oxidation, and promotes cardiac dysfunction; cardiac defects can be prevented wi

158 cassettes to hearts of mice with established cardiac dysfunction caused by aortic-banding.

159 Mice overexpressing ANGPTL2 in heart show cardiac dysfunction caused by both inactivation of AKT a

160 However, cardiac dysfunction caused by DOX limits its clinical us

161 Thus, preexisting CKD aggravates the cardiac dysfunction caused by sepsis or endotoxemia in m

162 Cardiac dysfunction (CD) is a recognized risk associated

163 intense inflammatory response that promotes cardiac dysfunction, cell death, and ventricular remodel

164 logue protected against vascular, renal, and cardiac dysfunction, characterized by reduced hypertroph

165 to be central to cancer therapeutics-related cardiac dysfunction (CTRCD).

166 ncreased risk of cancer therapeutics-related cardiac dysfunction (CTRCD).

167 STZ-induced diabetic mice exhibited distinct cardiac dysfunction, dampened intracellular calcium hand

168 ion, intramyocardial bleeding, and increased cardiac dysfunction, despite equal infarct sizes.

169 anthracycline exposure demonstrate signs of cardiac dysfunction detectable by CMR, with the RV also

170 Cardiac dysfunction determines prognosis in amyloid ligh

171 Cardiac dysfunction develops during sepsis in humans and

172 reperfusion (IR) is the most common cause of cardiac dysfunction due to local cell death and a tempor

173 bility transition pore (mPTP) is involved in cardiac dysfunction during chronic beta-adrenergic recep

174 of p38, revealing a fundamental mechanism of cardiac dysfunction during insulin resistance and type 2

175 ost-pathogen interactions that contribute to cardiac dysfunction during invasive pneumococcal disease

176 ed mechanisms responsible for development of cardiac dysfunction during sepsis.

177 The aim of this study was to examine cardiac dysfunction during the first 2 weeks after isola

178 The molecular underpinnings of cardiac dysfunction during the inflammatory surge of ear

179 y 4 weeks post-I/R, wild-type mice showed no cardiac dysfunction, elevated TIMP4 levels (to baseline)

180 itudinal strain (GLS) can detect subclinical cardiac dysfunction even when LVEF is normal.

181 This study examined the role of TLR3 in cardiac dysfunction following cecal ligation and punctur

182 yocytes and the mechanism by which it causes cardiac dysfunction have not been described.

183 After adjustment for cardiac dysfunction, higher serum creatinine, lower FEV1

184 line metabolites have a primary role in this cardiac dysfunction; however, information on the molecul

185 erval [CI], 1.05-5.35; P = .04) and systolic cardiac dysfunction (HR = 3.54; 95% CI, 1.60-8.10; P < .

186 SFN significantly prevented diabetes-induced cardiac dysfunction, hypertrophy and fibrosis.

187 acorporeal membrane oxygenation was used for cardiac dysfunction in 3,005 patients (66.5%), cardiopul

188 ociations were found between betaAR SNPs and cardiac dysfunction in 364 donors managed from 2007-2008

189 inhibitor-1 (I-1c) has been shown to reverse cardiac dysfunction in a model of ischemic HF.

190 study sought to determine the prevalence of cardiac dysfunction in adult survivors of childhood mali

191 consensus on the diagnosis and treatment of cardiac dysfunction in beta-thalassemia major (TM).

192 otential contribution of the CSAR control of cardiac dysfunction in both normal and chronic heart fai

193 hatase 1B (PTP1B) is associated with reduced cardiac dysfunction in CHF.

194 otoxicity, and advancements in therapies for cardiac dysfunction in children after anthracycline trea

195 Cardiac dysfunction in CKD is characterized by aberrant

196 hibition of IkappaB kinase (IKK) reduces the cardiac dysfunction in CKD sepsis.

197 in and target the spectral manifestations of cardiac dysfunction in critical illness.

198 andidate mechanism behind the development of cardiac dysfunction in diabetes.

199 tered ZIP7 and ZnT7 activity, contributes to cardiac dysfunction in diabetes.

200 asome inhibition is also sufficient to cause cardiac dysfunction in healthy pigs, and patients using

201 tion of SPARC gene expression may ameliorate cardiac dysfunction in humans.

202 e the discussion regarding the potential for cardiac dysfunction in individuals in whom the risk is s

203 Mst1 promoted cardiac dysfunction in mice subjected to myocardial infa

204 d infarct size and prevented postreperfusion cardiac dysfunction in mice with myocardial I/R injury.

205 of MMP-13 prevented isoproterenol-dependent cardiac dysfunction in mice.

206 timicrobial peptide Pep2.5 may attenuate the cardiac dysfunction in murine polymicrobial sepsis throu

207 cells as integrators of perivascular CF and cardiac dysfunction in nonischemic HF.

208 ation of lipid intermediates, contributes to cardiac dysfunction in obesity and diabetes mellitus.

209 Cardiac dysfunction in patients with liver cirrhosis is

210 g is postulated as a major driving force for cardiac dysfunction in patients with type 2 diabetes; ho

211 gh rate of myocardial fibrosis and increased cardiac dysfunction in people living with HIV.

212 he TLR3 activity may be useful in preventing cardiac dysfunction in sepsis.

213 t TLR3 plays a deleterious role in mediating cardiac dysfunction in sepsis.

214 examine the causes, mechanisms and impact of cardiac dysfunction in silico.

215 d here suggest an accelerated development of cardiac dysfunction in SIRT5KO mice in response to TAC,

216 mmendations for prevention and monitoring of cardiac dysfunction in survivors of adult-onset cancers.

217 ow that chronic rapamycin treatment prevents cardiac dysfunction in T2D mice, possibly through attenu

218 esulted in severe dilated cardiomyopathy and cardiac dysfunction in the absence of stress.

219 sponsible for the impaired FA metabolism and cardiac dysfunction in the failing heart.

220 Cardiac dysfunction in the setting of isolated traumatic

221 ces likely contributes to the development of cardiac dysfunction in this setting.

222 utophagy is an adaptive response that limits cardiac dysfunction in type 1 diabetes, presumably throu

223 myocytes in vitro, which are associated with cardiac dysfunction in vivo.

224 ted the hypertrophic response and attenuated cardiac dysfunction in vivo.

225 5-minute reperfusion) resulted in comparable cardiac dysfunction in wild-type and TIMP4(-/-) mice.

226 mic delivery of CTRP9 attenuated LPS-induced cardiac dysfunction in WT mice but not in muscle-specifi

227 ression, such as ventricular enlargement and cardiac dysfunction, in ARVD/C are relatively scarce.

228 CpG-ODN prevents CLP-induced cardiac dysfunction, in part through activation of PI3K/

229 derate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricu

230 ited a significant attenuation of HF-related cardiac dysfunction, including LV end-diastolic pressure

231 TSD patients, which raises the likelihood of cardiac dysfunction induced by long-term stress exposure

232 rat model of "systemic inflammation-induced cardiac dysfunction" induced by intraperitoneal lipopoly

233 1 (CB(1)) receptors have been implicated in cardiac dysfunction, inflammation, and cell death associ

234 Cardiac dysfunction influences candidate selection for k

235 evidence suggests that echinocandin-related cardiac dysfunction is a mitochondrial drug-induced dise

236 Cardiac dysfunction is a prominent cause of mortality in

237 Purpose Cardiac dysfunction is a serious adverse effect of certa

238 potential of DPPIV inhibition in preventing cardiac dysfunction is also investigated.

239 Diabetic cardiac dysfunction is associated with decreased rates o

240 ediated betaAR desensitization that precedes cardiac dysfunction is associated with selective upregul

241 Reversible stress-induced cardiac dysfunction is frequently seen as a complication

242 Cardiac dysfunction is often associated with a shift in

243 Among Hispanics/Latinos, most cardiac dysfunction is subclinical or unrecognized, with

244 The prevailing view is that MFS-associated cardiac dysfunction is the result of aortic and/or valvu

245 eart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI.

246 Cardiac dysfunction may account for some of the unexplai

247 ctin for adjuvant therapies in iron-overload cardiac dysfunction may be an option in the future.

248 st that strategies to upregulate BAG3 during cardiac dysfunction may be beneficial.

249 In women with CHD, cardiac dysfunction may compromise uteroplacental flow a

250 opose that angiogenic imbalance and residual cardiac dysfunction may exist even after recovery from P

251 Early detection of cardiac dysfunction may identify a high-risk subset of s

252 osis (T2* 6-20 milliseconds) and no signs of cardiac dysfunction (mean age, 19.8 years).

253 ted with fatal infantile disease, liver, and cardiac dysfunction, neuropathy, and anemia.

254 omozygous Celf1 knock-out neonates exhibited cardiac dysfunction not observed in older homozygous ani

255 non-invasive method for characterizing early cardiac dysfunction, not detectable by conventional echo

256 g of SCN5A may contribute to a subset of the cardiac dysfunctions observed in myotonic dystrophy.

257 loss of both CM Tln1 and Tln2 and found that cardiac dysfunction occurred by 4 wk with 100% mortality

258 Cardiac dysfunction occurred in 29 (6.0%) patients (12 [

259 No major cardiac dysfunctions occurred.

260 compensatory responses are not sustainable, cardiac dysfunction occurs, leading to cardiomyopathy.

261 associated with subclinical or unrecognized cardiac dysfunction (odds ratio: 0.1; 95% confidence int

262 perspective develops cancer therapy-related cardiac dysfunction or a high-risk cardiovascular patien

263 lethal cardiac arrhythmias in the absence of cardiac dysfunction or fibroadiposis, palmoplantar kerat

264 Preceding cardiac dysfunction or ventricular arrhythmias are assoc

265 = .02]); interleukin-6 levels (p = .04); and cardiac dysfunction (p = .05).

266 chocardiography in these mouse models showed cardiac dysfunction paralleling betaAR desensitization i

267 monitoring of tissue iron sequestration and cardiac dysfunction- parameters essential for the precli

268 al PTP1B deficiency, is sufficient to reduce cardiac dysfunction post myocardial infarction.

269 The severity of cardiac dysfunction predicts mortality in patients with

270 Compared with those with clinical cardiac dysfunction, prevalent coronary heart disease wa

271 ts for future studies focused on the complex cardiac dysfunction processes through more efficient har

272 Diabetes is a cause of cardiac dysfunction, reduced myocardial perfusion, and u

273 oved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling.

274 ial-specific antioxidant before the onset of cardiac dysfunction rescues the metabolic defects.

275 modulate FA transfer to the heart and remedy cardiac dysfunction resulting from altered energy substr

276 96.1% of the cardiac dysfunction seen was subclinical or unrecognized

277 Hence, cardiac dysfunction should be targeted as a potentially

278 in risk factors; 7) post-ASO arrhythmias and cardiac dysfunction should raise suspicion of coronary i

279 could not prevent betaAR desensitization or cardiac dysfunction showing that GRK2 recruitment to the

280 Sepsis induced cardiac dysfunction (SIC) is a severe complication to se

281 nfiltration, fibrous tissue replacement, and cardiac dysfunction similar to those of ARVC patients.

282 Reversal of MF improves key measures of cardiac dysfunction, so reversal of MF represents a like

283 However, how elevated CELF1 level leads to cardiac dysfunction, such as conduction defect, DCM, and

284 ion are less prone to fibrotic remodeling or cardiac dysfunction than hearts with a lipolytic defect

285 ata suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activat

286 ytes (CMs), resulting in redox imbalance and cardiac dysfunction that can be functionally measured an

287 ic environment is accompanied by subclinical cardiac dysfunction, the extent of which correlates with

288 otherapy are at risk for trastuzumab-related cardiac dysfunction (TRCD).

289 ptin activates mechanisms that contribute to cardiac dysfunction under physiological conditions.

290 creased infarct size and modestly attenuated cardiac dysfunction up to 3 months after coronary ligati

291 Cardiac dysfunction was defined as left ventricular ejec

292 Polymicrobial sepsis-induced cardiac dysfunction was produced by cecal ligation punct

293 The presence of cardiac dysfunction was strongly associated with mortali

294 ic steroids causes cardiac myocyte death and cardiac dysfunction, we examined heart function in Na/K-

295 ys that are potentially involved in T1D with cardiac dysfunction, we sought to identify differentiall

296 Heart failure, cardiac death, and cardiac dysfunction were infrequent in both treatment gr

297 ntials were prolonged, but no arrhythmias or cardiac dysfunction were noted.

298 h cardiac-specific Klf4 deficiency developed cardiac dysfunction with aging or in response to pressur

299 Previously undiagnosed cardiac dysfunction with preserved ejection fraction was

300 Cardiac dysfunction with sepsis is associated with both