ライフサイエンスコーパス: heart failure

1 diorenal Rescue Study in Acute Decompensated Heart Failure).

2 cular Remodeling During Entresto Therapy for Heart Failure).

3 and protein expression in these two forms of heart failure.

4 es and therapies have emerged for dystrophic heart failure.

5 er inflammation is a cause or consequence of heart failure.

6 creasing PDE4B in the heart is beneficial in heart failure.

7 standing of biological mechanisms underlying heart failure.

8 es but up to 55% among patients with CKD and heart failure.

9 tive targets for developing therapeutics for heart failure.

10 ving the heart's workload after the onset of heart failure.

11 nfluence long-term outcomes in patients with heart failure.

12 heart attack, stroke, or hospitalization for heart failure.

13 ocess that contributes to the development of heart failure.

14 re improves quality of life in patients with heart failure.

15 nd the resulting ischaemic heart disease and heart failure.

16 ry rate], 5%) pointed to pathways altered in heart failure.

17 it-list mortality and hospitalization due to heart failure.

18 t and design for caregivers of patients with heart failure.

19 e most debilitating in terms of prognosis is heart failure.

20 preclinical mouse models of hypertrophy and heart failure.

21 oved healing after infarction and attenuated heart failure.

22 ction and dysfunction of heart and kidney in heart failure.

23 caspase-activatable provector in a model of heart failure.

24 this pathway as a potential target in human heart failure.

25 f muscular dystrophy patients with end-stage heart failure.

26 miR-21 inhibition in a large animal model of heart failure.

27 etween rest fragmentation index and incident heart failure.

28 , during beta-adrenergic stimulation, and in heart failure.

29 echocardiographically) and clinical signs of heart failure.

30 ains to be established for models of chronic heart failure.

31 to an epidemic of diabetes mellitus-induced heart failure.

32 tments for HFpEF, which accounts for ~50% of heart failure.

33 d functional changes in the heart leading to heart failure.

34 ach to ameliorate metabolic dysregulation in heart failure.

35 inical trials for cardiovascular disease and heart failure.

36 fects of SDOH in an underserved patient with heart failure.

37 namely arrhythmogenesis and progression into heart failure.

38 ated pulmonary vascular resistance and right heart failure.

39 r, this has never been investigated in human heart failure.

40 bally, with survivors at risk for subsequent heart failure.

41 pressure regulation and reducing the risk of heart failure.

42 adian pattern of occurrence in patients with heart failure.

43 improve self-care behaviour in patients with heart failure.

44 ociated with acute myocardial infarction and heart failure.

45 iated with excess morbidity and mortality in heart failure.

46 -dose intravascular cocaine results in acute heart failure.

47 ment of KEs as a treatment for patients with heart failure.

48 lar and renal outcomes with empagliflozin in heart failure.

49 e (C index, 0.696 [95% CI, 0.692-0.700]) and heart failure (0.621 [95% CI, 0.617-0.625]).

50 using C(2)HEST to 1.92 using CHARGE-AF), and heart failure (1.91 using CHA(2)DS(2)-VASc to 2.58 using

51 al fibrillation, 1.75 (95% CI 1.56-1.97) for heart failure, 1.76 (95% CI 1.51-2.05) for acute myocard

52 fraction after MI (7% versus 12%), previous heart failure (10% versus 19%), atrial fibrillation (6%

53 se; odds ratio, 2.70; 95% CI, 2.08 to 3.51), heart failure (15.3%, vs. 5.6% among those without heart

54 flammatory cardiac disease (3.75%), ischemic heart failure (2%), or healthy blood donors (0.3%).

55 p < 0.001), and showed higher rates of acute heart failure (45% vs. 38.3%; p = 0.005).

56 vs. 81.7 years), with a lower prevalence of heart failure (55.9% vs. 65.8%) but more likely a lower-

57 Acute decompensated heart failure (ADHF) is a highly morbid condition among

58 atients hospitalized for acute decompensated heart failure (ADHF) was well-tolerated and led to impro

59 h lower incidence of hospital admissions for heart failure (adjusted rate ratio compared with non-inv

60 ntation, and the end points of mortality and heart failure admissions in the CASTLE-AF study (Cathete

61 ipartum cardiomyopathy is a form of systolic heart failure affecting young women toward the end of pr

62 In patients with heart failure and a reduced ejection fraction, empaglifl

63 and typical cardiovascular diagnoses such as heart failure and acute myocardial infarction, need freq

64 unctional consequences and associations with heart failure and arrhythmias.

65 in quality of life among men and women with heart failure and assessed for differential effects of t

66 rithm for meta-analytic methodology for both heart failure and cardiac arrhythmias because the confid

67 ernative to dantrolene for therapies against heart failure and cardiac arrhythmias.

68 as a composite of total hospitalisations for heart failure and cardiovascular death up to 52 weeks af

69 Exercise intolerance, associated with heart failure and death in general populations, is not w

70 t adverse remodeling is the leading cause of heart failure and death in the USA, there is an urgent u

71 pulmonary vasculature that results in right heart failure and death, are usually assessed with invas

72 Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options,

73 t disease patients with symptomatic systolic heart failure and electrical dyssynchrony, CRT was assoc

74 ion between NSAID use and increased risks of heart failure and elevated blood pressure, subsequent st

75 ning the molecular mechanisms of age-related heart failure and highlight exercise as a valuable exper

76 ally, it discusses the changes that occur in heart failure and how these may result in heart failure

77 ozin reduced the risk of death and worsening heart failure and improved symptoms across the broad spe

78 management of volume status in patients with heart failure and may represent a mechanism contributing

79 Rehospitalization for heart failure and pacemaker implantation were more frequ

80 o our hospital with decompensated congestive heart failure and pericardial effusion diagnosed on echo

81 (MD) patients and often results in advanced heart failure and premature death.

82 provide an additional approach for treating heart failure and reduce the risk for sudden cardiac dea

83 on and cardiovascular death in patients with heart failure and reduced ejection fraction (HFrEF).

84 known about how these 2 peptides compare in heart failure and reduced ejection fraction, especially

85 amic genomic regulatory landscape underlying heart failure and serves as an important resource for un

86 vents (death, myocardial infarction, stroke, heart failure) and COVID-19 cardiorespiratory ordinal se

87 n Strategy Evaluation in Acute Decompensated Heart Failure), and CARRESS-HF (Cardiorenal Rescue Study

88 hospitalizations-1 chest pain, 2 dyspnea, 1 heart failure, and 1 syncope) over 368+/-156 days follow

89 w RGS2 protein levels, such as hypertension, heart failure, and anxiety.

90 ular diseases (e.g., coronary heart disease, heart failure, and atrial fibrillation).

91 mes (myocardial infarction, ischemic stroke, heart failure, and cardiovascular mortality).

92 and a priori baseline covariates (e.g., age, heart failure, and facility-level characteristics), we a

93 large vessel atheroma, atrial fibrillation, heart failure, and heart valve disease.

94 aptive immune systems in the pathogenesis of heart failure, and highlights the results of phase III c

95 Cardiac arrhythmias, heart failure, and nonfatal coronary syndromes are also

96 cardiovascular death, rehospitalization for heart failure, and pacemaker implantation after a TAVR p

97 ardial infarction, cerebrovascular accident, heart failure, and peripheral arterial disease), kidney

98 ctural disruptions that increase the risk of heart failure are only starting to be discovered.

99 o become a therapeutic target for preventing heart failure-associated ventricular arrhythmia.

100 of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure

101 relatives of index patients with unexplained heart failure at a tertiary referral center.

102 therapeutic promise in improving outcomes in heart failure, atrial fibrillation, and, in preclinical

103 ial disclosed DAPA's benefits in symptomatic heart failure, but the underlying mechanism remains larg

104 remise that mitochondrial Kac contributes to heart failure by disrupting oxidative metabolism.

105 , during beta-adrenergic stimulation, and in heart failure by mechanisms converging at the alpha(1C)

106 elephone follow-up after hospitalization for heart failure can increase 7-day follow-up and reduce in

107 patients 18 to 85 years of age admitted for heart failure, cardiogenic shock, or LVAD implantation f

108 nsidering antecedent cardiac conditions (ie, heart failure/cardiomyopathy, hypertension, myocardial i

109 atherosclerotic events, hospitalization for heart failure, cardiovascular and total mortality, and p

110 hest radiography in patients with congestive heart failure (CHF).

111 isorders with iron deficiency, which include heart failure, chronic kidney disease, inflammatory bowe

112 s study examined the rates and predictors of heart failure clinical trial publication and how they ha

113 The rates of heart failure clinical trial publication or reporting of

114 udy assessed cross-sectional analysis of all heart failure clinical trials registered on ClinicalTria

115 8+/-13 years; 22% black) enrolled in 3 acute heart failure clinical trials: ROSE-AHF (Renal Optimizat

116 Among patients with heart failure, combined beta-blocker and renin-angiotens

117 als, investigating optimal dietary sodium in heart failure comes with challenges, including need for

118 a 57% increased risk of developing incident heart failure compared to a subject at the 10th percenti

119 Acute heart failure confers a worse prognosis, and although lu

120 f death for cardiovascular deaths related to heart failure (CV-HF) and comparison to cancer deaths ha

121 licly available data sets of human and mouse heart failure, demonstrated that EPRS acted as an integr

122 Whether men and women with heart failure derive similar benefit from palliative car

123 alve surgery can mitigate the progression to heart failure, disability, and death.

124 regressed out confounding factors including heart failure disease status and used the G-SCI (Genotyp

125 Optimization Strategies Evaluation in Acute Heart Failure), DOSE-AHF (Diuretic Optimization Strategy

126 provides a tool for further investigation of heart failure drug therapies.

127 pro BNP in Patients Stabilized From an Acute Heart Failure Episode), the in-hospital initiation of sa

128 phy and diastolic dysfunction, which lead to heart failure, especially heart failure with preserved e

129 uctural remodeling ( EF >5% and ESV 10%) and heart failure event/cardiovascular death.

130 etic status and its implications on incident heart failure events and all-cause mortality.

131 t of SGLT2 inhibition on fatal and non-fatal heart failure events and renal outcomes in all randomly

132 e range, 14.8-33.4) months, 52 deaths and 24 heart failure events occurred.

133 number of inpatient and outpatient worsening heart failure events, with benefits seen early after ini

134 invasive Remote Monitoring for Prediction of Heart Failure Exacerbation) examined the performance of

135 prognosis remains poor as many patients with heart failure experience symptoms that negatively impact

136 01), with a significant increase in reported heart failure from 1.64% (95% CI 0.82-2.65) to 11.72% (3

137 re enrolled during hospitalisation for acute heart failure from 358 centres in 44 countries on six co

138 often have a genetic cause, and the field of heart failure genetics is progressing rapidly.

139 bundance of Proteobacteria in the congestive heart failure group (p = 0.014), particularly due to an

140 Heart failure has previously been linked to sleep disord

141 We hypothesised that dogs with congestive heart failure have quantifiable dysbiosis compared to he

142 ased risk of ESKD, with the highest risk for heart failure (hazard ratio, 11.40; 95% confidence inter

143 replacement, and, in the setting of advanced heart failure, heart transplant and left ventricular ass

144 lity care to a large cohort of patients with heart failure, heart transplantation, and left ventricul

145 , 95% CI, 1.28-2.09, P value = 8.07 x 10-5), heart failure (HF) (OR = 1.61, 95% CI, 1.32-1.95, P valu

146 ts with New York Heart Association Class III heart failure (HF) and a prior HF hospitalization (HFH)

147 (SGLT2i) improves outcomes in patients with heart failure (HF) and reduced ejection fraction (HFrEF)

148 compensated hypertrophy (CH) until signs of heart failure (HF) are apparent using a trans-aortic pre

149 Although care of patients with heart failure (HF) has improved in the past decade, impo

150 Patients with heart failure (HF) have multiple coexisting comorbiditie

151 rimarily global neurohormonal dysregulation, heart failure (HF) is a growing pandemic with increasing

152 Heart failure (HF) is a leading cause of hospitalization

153 Heart failure (HF) is a major cardiovascular disease wor

154 Heart failure (HF) is a major source of morbidity and mo

155 As a leading cause of death and morbidity, heart failure (HF) is responsible for a large portion of

156 se (ACHD) die after the age of 40 years, and heart failure (HF) is the most common cause of death.

157 Patients with heart failure (HF) often have multiple chronic condition

158 nctional Mitral Regurgitation), treatment of heart failure (HF) patients with moderate-severe or seve

159 a major determinant of clinical outcomes in heart failure (HF) patients.

160 nown about the association of GlycA with the heart failure (HF) subtypes: heart failure with preserve

161 h has been implicated in the pathogenesis of heart failure (HF) with preserved ejection fraction (HFp

162 Heart failure (HF) with reduced contractile function is

163 farction (MI), ischemic heart disease (IHD), heart failure (HF), atrial fibrillation (AF), stroke, pe

164 sed with T2D, we predicted five-year risk of heart failure (HF), myocardial infarction (MI), stroke (

165 Heart failure (HF), the leading cause of death in develo

166 about PA and GOCD in patients with advanced heart failure (HF).

167 (T2DM) is associated with a higher risk for heart failure (HF).

168 directed radiation are at increased risk for heart failure (HF).

169 217 total heart failure hospitalisations occurred in the ferric ca

170 revascularization, stroke, all-cause death, heart failure hospitalization after 2 years.

171 Subsequent heart failure hospitalization and all-cause death were a

172 otransporter 2 inhibitors reduce the risk of heart failure hospitalization and cardiovascular death i

173 cotransporter-2 (SGLT-2) inhibitors reduced heart failure hospitalization and end-stage renal diseas

174 herapies and presented an increased risk for heart failure hospitalization that warrants further stud

175 mary outcome (cardiovascular death and total heart failure hospitalization), its components, myocardi

176 recurrent MI or coronary revascularization), heart failure hospitalization, and all-cause mortality (

177 unstable angina with revascularization, and heart failure hospitalization.

178 strain for a combined end point (events) of heart failure hospitalizations and cardiovascular death.

179 Empagliflozin reduced the total number of heart failure hospitalizations that required intensive c

180 Secondary outcomes included trend of heart failure hospitalizations.

181 years, the mean CHA(2)DS(2)-VASc (congestive heart failure, hypertension, 65 years of age and older,

182 ffective in both prevention and treatment of heart failure in 2 preclinical animal models.

183 a combination of coronary heart disease and heart failure in addition to T2D had the largest effect

184 hic recordings at baseline predicts incident heart failure in community-based elderly individuals.

185 Mitochondrial dysfunction contributes to heart failure in diabetes.

186 y immunoadsorption has been shown to improve heart failure in small studies.

187 75 years and older with a diagnosis of acute heart failure in the ED from December 2018 to September

188 ardiomyopathies, which are a common cause of heart failure in young people, have increased during the

189 tions between brain structure and markers of heart failure including ejection fraction and NT-proBNP.

190 apies to target macrophage metabolism during heart failure, including antidiabetic therapies, anti-in

191 Heart failure, induced via myocardial infarction, causes

192 evated intracardiac pressure attributable to heart failure induces electrical and structural remodeli

193 Heart failure is a clinical syndrome that affects >6.5 m

194 tions, during sympathetic activation, and in heart failure is a major determinant of cardiac physiolo

195 Heart failure is a major public health problem affecting

196 Heart failure is a prominent complication of type 2 diab

197 s, particularly for the nonfamilial forms of heart failure, is still poorly understood.

198 nnel and acquired conditions associated with heart failure, ischemia, and atrial fibrillation, enhanc

199 d Taiwan showed a significant improvement in heart failure knowledge at six months' follow-up (SMD 0.

200 , we demonstrated that in humans with stable heart failure, left ventricular contractility could be a

201 e similar between groups by age (mean, ~79), heart failure, lung disease, and influenza and pneumococ

202 ns in the OptiLink HF trial (Optimization of Heart Failure Management Using OptiVol(TM) Fluid Status

203 etic efficiency in black patients with acute heart failure may be related to racial differences in ac

204 l injection of an antimiR to miR-370-3p into heart failure mice silences miR-370-3p and restores HCN4

205 ion-, and myocardial infarction (MI)-induced heart failure mouse models.

206 Ten trials were of heart failure (n = 4068 patients), 11 of mixed disease (

207 failure (15.3%, vs. 5.6% among those without heart failure; odds ratio, 2.48; 95% CI, 1.62 to 3.79),

208 combined risk of death, hospitalization for heart failure or an emergent/urgent heart failure visit

209 ent of type 2 diabetes mellitus, considering heart failure or kidney outcomes within the primary outc

210 were older, presented with acute congestive heart failure or non-ST-segment-elevation myocardial inf

211 Patients with congestive heart failure or reduced left ventricular ejection fract

212 evious 6 months or who had severe congestive heart failure or severe renal impairment were excluded.

213 y cause significant morbidity and death from heart failure or ventricular arrhythmias.

214 1.3, 3.4 per doubling; P = .004), history of heart failure (OR 1.3; 95% CI: 1.1, 1.6, P = .01), and c

215 netically predicted alcohol consumption with heart failure (OR, 1.00 [95% CI, 0.68-1.47]; P=0.996), v

216 e of incident myocardial infarction, stroke, heart failure, or CVD death) separately in white and bla

217 anism contributing to the superior long-term heart failure outcomes observed with these agents.

218 e number of patients with MI develop chronic heart failure over time.

219 ed inhibitory strategies have been tested in heart failure patients as well as healthy volunteers to

220 spitalizations (1998-2017), 108 638 incident heart failure patients were identified.

221 nt of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitat

222 nt of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitat

223 nt of the MitraClip Percutaneous Therapy for Heart Failure Patients with Functional Mitral Regurgitat

224 Heart failure patients with reduced ejection fraction (H

225 i-diabetic agents and statins on outcomes in heart failure patients without atherosclerotic diseases,

226 for the identification of Stage A (at risk) heart failure patients.

227 theter Ablation for Atrial Fibrillation With Heart Failure) population.

228 arget to improve cardiac recovery and reduce heart failure post-MI in humans.

229 ies of febrile pediatric patients with acute heart failure potentially associated with SARS-CoV-2 inf

230 ntly presented chronic lung disease, chronic heart failure, prior endocarditis, and degenerative valv

231 During the pandemic, the heart failure program at New York-Presbyterian Hospital

232 The diabetic, hypertensive heart failure rat (mRen27/tetO-shIR) were treated with e

233 in a constellation of signs and symptoms of heart failure referred to as congestion.

234 e <30 mL/min per 1.73 m(2)) from the Swedish Heart Failure Registry between 2001 and 2016.

235 iomarkers and the risk of all-cause death or heart failure-related hospital admission (DHFA) was asse

236 orrected P=0.002), and rehospitalization for heart failure (relative risk, 0.84; corrected P<0.0001).

237 of developing the outcomes of mortality and heart failure remained similar across years, although th

238 Acute decompensated heart failure remains the most common cause of hospitali

239 munodeficiency virus (HIV) imparts increased heart failure risk to women.

240 ed for Meta-Analysis Global Group in Chronic Heart Failure score, genotype, level of BB exposure, and

241 pies targeting inflammatory processes in the heart failure setting, such as anti-inflammatory and imm

242 he Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart

243 ege of Cardiology/American Heart Association/Heart Failure Society of America for the identification

244 Failure Society of America and the Japanese Heart Failure Society.

245 patients with diabetes and recent worsening heart failure, sotagliflozin therapy, initiated before o

246 site of (1) death; (2) rehospitalization for heart failure symptoms and valve prosthesis complication

247 s LV diastolic dysfunction typically precede heart failure symptoms, we anticipate that the results o

248 e performed at early stages of the patient's heart failure symptoms.

249 gher risk of mortality and developing severe heart failure symptoms.

250 been reported in some patients with advanced heart failure (termed responders [R]) following left ven

251 ve higher rates of hospitalization for acute heart failure than other race/ethnic groups.

252 s and hospitalizations and urgent visits for heart failure than placebo.

253 Among patients with high-risk heart failure, the incidence of death from cardiovascula

254 For heart failure, the pooled proportion, based on 38 studie

255 induces pathological cardiac hypertrophy and heart failure through persistent activation of mTOR.

256 admitted to our hospital with decompensated heart failure to be evaluated for a heart transplant.

257 61 other patients (52%) developed refractory heart failure to disabling New York Heart Association fu

258 flozin and Prevention of Adverse Outcomes in Heart Failure) trial disclosed DAPA's benefits in sympto

259 e BeAT-HF (Baroreflex Activation Therapy for Heart Failure) trial was a multicenter, prospective, ran

260 SAVR, TAVR, and disease symptoms (congestive heart failure, unstable angina, non-ST-elevation myocard

261 k scores and 5-year incident AF, stroke, and heart failure using Cox proportional hazards modeling, 5

262 tion for heart failure or an emergent/urgent heart failure visit requiring intravenous treatment (415

263 rdiovascular death or hospital admission for heart failure was 0.38 (95% CI 0.30-0.47).

264 cardiovascular causes or hospitalization for heart failure was lower among those who received vericig

265 cardial infarction, or rehospitalization for heart failure was not different between the 2 groups (od

266 Heart failure was recorded via a clinical interview duri

267 ysis of the PAL-HF trial (Palliative Care in Heart Failure), we analyzed differences in quality of li

268 scular death or first hospital admission for heart failure; we also assessed these endpoints individu

269 who were recently hospitalized for worsening heart failure were randomly assigned to receive sotaglif

270 ataxia, muscle weakness, type 2 diabetes and heart failure, which are caused by impaired mitochondria

271 CICR is disrupted in cardiac hypertrophy and heart failure, which is associated with loss of T-tubule

272 ight be able to identify those patients with heart failure who have a cardio-inflammatory phenotype a

273 CAT (Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist) trial part

274 sult in significant metabolic perturbations, heart failure with both preserved and reduced ejection f

275 Chronotropic incompetence is common in heart failure with preserved ejection fraction (HFpEF) a

276 GlycA with the heart failure (HF) subtypes: heart failure with preserved ejection fraction (HFpEF) o

277 ays an important role in the pathogenesis of heart failure with preserved ejection fraction (HFpEF).

278 duces cardiac inflammation in a rat model of heart failure with preserved ejection fraction (HFpEF).

279 age are at high risk for the development of heart failure with preserved ejection fraction (HFpEF).

280 es correlated with NAFLD among patients with heart failure with preserved ejection fraction (HFpEF).

281 ion, which lead to heart failure, especially heart failure with preserved ejection fraction.

282 in heart failure and how these may result in heart failure with preserved versus reduced ejection fra

283 potentially distinct contribution to ESKD of heart failure with preserved versus reduced ejection fra

284 in understanding how to manage patients with heart failure with recovered ejection fraction (HFrecEF)

285 A state of heart failure with reduced ejection fraction (HF-rEF) wa

286 nhibitors) reduce mortality in patients with heart failure with reduced ejection fraction (HFrEF) bey

287 Patients with heart failure with reduced ejection fraction (HFrEF; hea

288 use a cohort of Medicare beneficiaries with heart failure with reduced ejection fraction and existin

289 Patients with heart failure with reduced ejection fraction and left bu

290 ion Fraction) trial randomized patients with heart failure with reduced ejection fraction from a dive

291 ion for atrial fibrillation in patients with heart failure with reduced ejection fraction may improve

292 t are effective but expensive, patients with heart failure with reduced ejection fraction provide an

293 (A Study of Vericiguat in Participants With Heart Failure With Reduced Ejection Fraction) trial on t

294 r Intensification of Medications for Chronic Heart Failure with Reduced Ejection Fraction) trial rand

295 ing whether OM improves symptoms and HRQL in heart failure with reduced ejection fraction.

296 with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction.

297 The rats develop heart failure with reduced ejection fraction.

298 ending to patients without diabetes who have heart failure with reduced ejection fraction.

299 ilure with reduced ejection fraction (HFrEF; heart failure with reduced left ventricular ejection fra

300 enal outcomes, including hospitalization for heart failure, with this benefit extending to patients w