ライフサイエンスコーパス: chronic heart failure

1 ert a prognostic benefit in the treatment of chronic heart failure.

2 implies therapeutic efficacy in settings of chronic heart failure.

3 val in multicenter hospital outpatients with chronic heart failure.

4 l renal hemodynamic effects in patients with chronic heart failure.

5 ne A1-receptor agonists for the treatment of chronic heart failure.

6 ) and in hearts from patients with end-stage chronic heart failure.

7 probe for signs of efficacy in patients with chronic heart failure.

8 risk of all-cause mortality in patients with chronic heart failure.

9 h higher mortality in patients with acquired chronic heart failure.

10 ent optimal medical therapy in patients with chronic heart failure.

11 oblast regeneration is further enhanced with chronic heart failure.

12 ctivity in healthy animals and humans and in chronic heart failure.

13 atment strategies for patients with advanced chronic heart failure.

14 n independent predictor of adverse events in chronic heart failure.

15 measures of renal function in patients with chronic heart failure.

16 appears promising in patients suffering from chronic heart failure.

17 (VO(2)) is well established in patients with chronic heart failure.

18 biological processes as a prognostic tool in chronic heart failure.

19 icity throughout life and in the presence of chronic heart failure.

20 natriuretic peptide to monitor patients with chronic heart failure.

21 tenuated catabolic muscle wasting induced by chronic heart failure.

22 eached the top tier of medical therapies for chronic heart failure.

23 cle of progressive myocardial dysfunction in chronic heart failure.

24 questrin transgenic mice, a genetic model of chronic heart failure.

25 ral AT2R may be beneficial in the setting of chronic heart failure.

26 th disease severity and clinical outcomes in chronic heart failure.

27 contribute to development and progression of chronic heart failure.

28 n extensively investigated in both acute and chronic heart failure.

29 myocardium in the setting of acute injury or chronic heart failure.

30 ate cell for cardiac repair in patients with chronic heart failure.

31 gnosis of anemia in ambulatory patients with chronic heart failure.

32 mprove cardiac performance of postinfarction chronic heart failure.

33 during hospitalization for decompensation of chronic heart failure.

34 or device explantation in most patients with chronic heart failure.

35 yocardial recovery in patients with advanced chronic heart failure.

36 patients with acute myocardial infarction or chronic heart failure.

37 hyperadrenergic state is a seminal aspect of chronic heart failure.

38 f AG10 in ATTR-CM patients with symptomatic, chronic heart failure.

39 of diagnosis and prognosis in patients with chronic heart failure.

40 and dilutional hyponatremia associated with chronic heart failure.

41 gic, device-based treatment of patients with chronic heart failure.

42 ng hemoglobin levels can improve outcomes in chronic heart failure.

43 n women, approaching values seen with severe chronic heart failure.

44 een shown to improve endothelial function in chronic heart failure.

45 uggests a pathogenic role for T cells during chronic heart failure.

46 and remains to be established for models of chronic heart failure.

47 nd CT-proET-1 were elevated in patients with chronic heart failure.

48 olving diabetic or nondiabetic patients with chronic heart failure.

49 tors of all-cause mortality in patients with chronic heart failure.

50 l metabolic impairment is a major feature in chronic heart failure.

51 emoglobin, left ventricular dysfunction, and chronic heart failure.

52 ng enzyme inhibitor therapy in patients with chronic heart failure.

53 lower serum chloride in patients with stable chronic heart failure.

54 th increased mortality risk in patients with chronic heart failure.

55 n in healthy volunteers and in patients with chronic heart failure.

56 tion remain primary issues for patients with chronic heart failure.

57 abnormalities are prevalent in patients with chronic heart failure.

58 ropic support or metabolic derangements from chronic heart failure.

59 Cpc-PH is rare in chronic heart failure.

60 ], and MAGGIC [Meta-Analysis Global Group in Chronic Heart Failure]).

61 subnetworks in different pathologies such as chronic heart failure (21 genes), breast cancer (16 gene

62 Leading causes of death were chronic heart failure (42%), pneumonia (10%), sudden-car

63 h New York Heart Association class II to III chronic heart failure, 6 patients undergoing diagnostic

64 METHOD AND RESULTS: Ten patients with chronic heart failure (9 males; age 65+/-12; ejection fr

65 We reviewed 1,318 consecutive patients with chronic heart failure admitted for ADHF to the Cleveland

66 g in the nonischemic myocardium in mice with chronic heart failure after coronary ligation.

67 Moreover, chronic heart failure after myocardial infarction and pe

68 With chronic heart failure already an epidemic in the USA, it

69 In 25 patients with chronic heart failure and 25 control subjects, we examin

70 l mitral regurgitation (MR) in patients with chronic heart failure and a reduced ejection fraction.

71 Chronic heart failure and cardiac arrhythmias have high

72 identify the pathophysiological link between chronic heart failure and catabolic bone remodeling.

73 Emerging evidence on patients with chronic heart failure and chronic kidney disease has ide

74 is a predictor of death among patients with chronic heart failure and cirrhosis.

75 features of volume overload in patients with chronic heart failure and help guide individualized, app

76 The prevention of worsening chronic heart failure and hospitalisations for acute dec

77 via ganglionic blockade and were enhanced in chronic heart failure and in hypoxia.

78 ymptoms and quality of life in patients with chronic heart failure and iron deficiency.

79 recruited patients with stable, symptomatic chronic heart failure and left ventricular ejection frac

80 w devices and transcatheter interventions in chronic heart failure and of new drugs for acute heart f

81 CZ696 Compared to Valsartan in Patients With Chronic Heart Failure and Preserved Left-ventricular Eje

82 prevent cardiac arrhythmias in patients with chronic heart failure and reduced left ventricular eject

83 VNS) is an emerging therapy for treatment of chronic heart failure and remains a standard of therapy

84 uld have a beneficial effect in iron-induced chronic heart failure and to elucidate its regulation in

85 ensated heart failure modifies the course of chronic heart failure and worsens outcomes via a combina

86 ng the MAGGIC (Meta-Analysis Global Group in Chronic Heart Failure) and EMPHASIS-HF (Eplerenone in Mi

87 C risk scores (Meta-Analysis Global Group in Chronic Heart Failure) and lower Kansas City Cardiomyopa

88 d interleukin-6, play a pathogenetic role in chronic heart failure, and anti-inflammatory immune ther

89 ting that type 2 diabetes mellitus, obesity, chronic heart failure, and chronic kidney failure are ch

90 uences in diseases such as cancer, diabetes, chronic heart failure, and in aging.

91 s used after acute myocardial infarction, in chronic heart failure, and in stable angina pectoris.

92 after PEG include sex, hypoalbuminemia, age, chronic heart failure, and subtotal gastrectomy.

93 main determinant of long-term mortality and chronic heart failure, and thus, the possibility of limi

94 Among patients with chronic heart failure, angiotensin-converting-enzyme (AC

95 ntricular ejection fraction in patients with chronic heart failure (ANOVA; P<0.001 for all).

96 inical follow-up in ambulatory patients with chronic heart failure are highly associated with an incr

97 ts in acute cardiac diseases, its effects on chronic heart failure are less clear.

98 diovascular events but data in patients with chronic heart failure are scarce.

99 ynamic effects of serelaxin in patients with chronic heart failure are unknown.

100 AY 1021189), currently in phase 3 trials for chronic heart failure, are now reported.

101 lar tissue were collected from patients with chronic heart failure at LVAD implant and explant (n = 1

102 gnostic impact of anemia in outpatients with chronic heart failure attending specialized heart failur

103 n cardiomyocytes derived from a rat model of chronic heart failure, beta2ARs were redistributed from

104 of death and hospitalization in persons with chronic heart failure between 1996 and 2002 within a lar

105 able to improve cardiac function in ischemic chronic heart failure but has a risk of arrhythmia occur

106 gy surplus (ie, type 2 diabetes mellitus and chronic heart failure), but SGLT2 inhibitors activate SI

107 iated with reduced survival in patients with chronic heart failure, but may be improved with cardiac

108 function after myocardial infarction and in chronic heart failure, but the extent of benefit and of

109 ined role in the diagnosis and management of chronic heart failure, but their role in patients with l

110 catecholamine requirements in patients with chronic heart failure by improving cardiac efficiency; h

111 emodynamic support in patients with advanced chronic heart failure can result in significant improvem

112 ncy anaemia--notably chronic kidney disease, chronic heart failure, cancer, and inflammatory bowel di

113 for treatment of various comorbidities, eg, chronic heart failure, cardiac arrhythmias and chronic r

114 trial of exercise training in patients with chronic heart failure caused by left ventricular systoli

115 with type 2 diabetes (T2DM) and pre-existing chronic heart failure (CHF) (New York Heart Association

116 nction is associated with the progression of chronic heart failure (CHF) and a poor prognosis.

117 ventrolateral medulla (RVLM) of rabbits with chronic heart failure (CHF) and in the RVLM of normal ra

118 emic and nonanemic patients with symptomatic chronic heart failure (CHF) and iron deficiency.

119 Muscle wasting occurs in both chronic heart failure (CHF) and normal aging and contrib

120 circulating CD34(+) cells from patients with chronic heart failure (CHF) and the role for their cardi

121 cificity of skeletal muscle abnormalities in chronic heart failure (CHF) has not been defined.

122 Chronic heart failure (CHF) impairs nitric oxide (NO)-me

123 Chronic heart failure (CHF) induces endothelial dysfunct

124 Chronic heart failure (CHF) is a leading cause of mortal

125 Chronic heart failure (CHF) is a major public health pro

126 Chronic heart failure (CHF) is a recognized health probl

127 Chronic heart failure (CHF) is associated with a 4-fold

128 rison of 2 common forms of multidisciplinary chronic heart failure (CHF) management.

129 erload left ventricular hypertrophy (LVH) to chronic heart failure (CHF) may involve a relative defic

130 g heat stress is substantially attenuated in chronic heart failure (CHF) patients.

131 rm exercise training program is not known in chronic heart failure (CHF) patients.

132 Chronic heart failure (CHF) results in blunting of arter

133 nce and excessive sympatho-excitation in the chronic heart failure (CHF) state.

134 ol of cardiac dysfunction in both normal and chronic heart failure (CHF) states remains unknown.

135 HFpEF rats displayed [mean +/- SD; chronic heart failure (CHF) vs. Sham, respectively] a ma

136 Development of CKD secondary to chronic heart failure (CHF), known as cardiorenal syndro

137 are also frequent symptoms in patients with chronic heart failure (CHF).

138 patients with acute myocardial infarction or chronic heart failure (CHF).

139 spective molecular pathways in patients with chronic heart failure (CHF).

140 mechanism involved in the pathophysiology of chronic heart failure (CHF).

141 on and inflammatory markers in patients with chronic heart failure (CHF).

142 is potentiated in clinical and experimental chronic heart failure (CHF).

143 l role in the sympathoexcitation observed in chronic heart failure (CHF).

144 responsiveness during exercise as well as in chronic heart failure (CHF).

145 in cardiac function, and the development of chronic heart failure (CHF).

146 he symptoms and reflex abnormalities seen in chronic heart failure (CHF).

147 d strength in elderly people especially with chronic heart failure (CHF).

148 mia incidence and contribute to mortality in chronic heart failure (CHF).

149 o the exaggerated global sympathetic tone in chronic heart failure (CHF).

150 is a major contributor to the progression of chronic heart failure (CHF).

151 c incompetence (CI), is commonly observed in chronic heart failure (CHF).

152 with New York Heart Association Class II-III chronic heart failure, comparing 300 mg allopurinol, 600

153 ar mortality, myocardial infarction, stroke, chronic heart failure, composite vascular outcomes, comp

154 Chronic heart failure continues to impose a substantial

155 RATIONALE: In patients with chronic heart failure, daytime oscillatory breathing at

156 a large Italian population of patients with chronic heart failure enrolled in a multicenter clinical

157 We examined 6975 patients with chronic heart failure enrolled in the Gruppo Italiano pe

158 tricular (LV) remodelling and development of chronic heart failure exacerbated, as measured by 3D-ech

159 (Exercise Training for Chronic Heart Failure [ExTraMATCH II]: protocol for an i

160 with dilated cardiomyopathy and symptomatic chronic heart failure from ages 6 months to 18 years; IS

161 e of antithrombotic therapy in patients with chronic heart failure has long been debated.

162 ow (BM) cell injection for treating ischemic chronic heart failure has not been established.

163 Participant flow through RCTs in chronic heart failure has not been uniformly reported, a

164 Patients with chronic heart failure have impaired long-term survival,

165 ing heart rate and outcomes in patients with chronic heart failure (HF) according to baseline left ve

166 disease and poor prognosis of patients with chronic heart failure (HF) and aortic stenosis.

167 Chronic heart failure (HF) and erectile dysfunction (ED)

168 Patients with chronic heart failure (HF) are at increased risk of both

169 e resultant healthcare costs associated with chronic heart failure (HF) are increasing and arguably r

170 Approximately half of all patients with chronic heart failure (HF) have a decreased ejection fra

171 Worsening chronic heart failure (HF) is a major public health prob

172 Chronic heart failure (HF) is associated with altered si

173 Chronic heart failure (HF) is characterized by sympathet

174 miologically representative outpatients with chronic heart failure (HF) is lacking.

175 Classification of chronic heart failure (HF) is on the basis of criteria t

176 The role of mononuclear phagocytes in chronic heart failure (HF) is unknown.

177 physiological role in cardiac remodeling and chronic heart failure (HF) is unknown.

178 ated differences in etiology and outcomes in chronic heart failure (HF) patients from 5 randomized tr

179 a-blockers reduce morbidity and mortality in chronic heart failure (HF) patients with reduced ejectio

180 Patients with chronic heart failure (HF) secondary to left ventricular

181 he aim of this study was to evaluate whether chronic heart failure (HF) therapy guided by concentrati

182 oxin on outcomes in ambulatory patients with chronic heart failure (HF) with reduced ejection fractio

183 cal, and social functioning of patients with chronic heart failure (HF), a reality that can lead to p

184 Iron repletion augments exercise capacity in chronic heart failure (HF), but there is a lack of mecha

185 ic and diastolic properties in patients with chronic heart failure (HF), compare these changes in pat

186 levels may improve outcomes in patients with chronic heart failure (HF), especially in younger patien

187 as been extensively studied in patients with chronic heart failure (HF), with only limited success.

188 about its prognostic value in patients with chronic heart failure (HF).

189 ociated with worse outcomes in patients with chronic heart failure (HF).

190 their associations with clinical outcomes in chronic heart failure (HF).

191 tions like stable coronary artery disease or chronic heart failure (HF).

192 rcise (CPX) tests in stable outpatients with chronic heart failure (HF).

193 kinase 1 (sFlt-1) as clinical biomarkers in chronic heart failure (HF).

194 lular, and molecular remodeling in dogs with chronic heart failure (HF).

195 rtant component of the treatment regimen for chronic heart failure (HF).

196 he diagnosis and treatment of both acute and chronic heart failure (HF).

197 n demonstrated in subgroups of patients with chronic heart failure (HF).

198 nd the mechanisms behind the pathogenesis of chronic heart failure (HF).

199 used to determine prognosis in patients with chronic heart failure (HF).

200 ventricular dysfunction (ALVD, n = 130), and chronic heart failure (HF, n = 52).

201 power of BNP concentrations in children with chronic heart failure, however, are not known.

202 ced inflammatory and oxidative pathology and chronic heart failure in chagasic rats.

203 and Drug Administration for the treatment of chronic heart failure in more than a decade: the aldoste

204 atients) and 11 studies on the management of chronic heart failure in primary care or outpatient sett

205 ures for patients hospitalized with acute or chronic heart failure in the ARIC (Atherosclerosis Risk

206 poxia, ischemia and ischemia-reperfusion, in chronic heart failure in transgenic mice and in myocytes

207 Chronic heart failure is a common complication in patien

208 Chronic heart failure is a worldwide cause of mortality

209 Chronic heart failure is accompanied by anorexia and inc

210 ysiological process that ultimately leads to chronic heart failure is cardiac remodelling in response

211 ptions, the clinical course of patients with chronic heart failure is notoriously difficult to predic

212 -CHF (Biology Study to Tailored Treatment in Chronic Heart Failure) is a multicenter, multinational,

213 ilure study randomized 469 participants with chronic heart failure (left ventricular ejection fractio

214 rt Association (NYHA) functional class II-IV chronic heart failure, left ventricular (LV) systolic dy

215 h New York Heart Association Class II to III chronic heart failure, left ventricular ejection fractio

216 In patients with chronic heart failure-like myocarditis (n = 40; mean age

217 ing parameters for the diagnosis of acute or chronic heart failure-like myocarditis and might be supe

218 (SHFM) and the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) risk calculator.

219 Dyssynchronous chronic heart failure may attenuate suction, because reg

220 d feasible and safe with signs of benefit in chronic heart failure, meriting definitive clinical eval

221 Using a rat postinfarction chronic heart failure model, we compared skeletal myobla

222 atherosclerotic events (e.g., patients with chronic heart failure, most treated with an ACE inhibito

223 intensive care unit (n = 68) and with stable chronic heart failure (n = 57).

224 Patients with chronic heart failure (n = 9) and controls (n = 6) were

225 agement of Persistent Atrial Fibrillation in Chronic Heart Failure; NCT00878384).

226 the use of angiotensin receptor blockers for chronic heart failure, nesiritide for acute heart failur

227 rolled trial, we assigned 5050 patients with chronic heart failure (New York Heart Association class

228 In outpatients with chronic heart failure, no conclusive association between

229 t to reverse the devastating consequences of chronic heart failure of ischemic and nonischemic origin

230 Chronic heart failure often results in catabolic muscle

231 gate in rats the impact of MI and subsequent chronic heart failure on the cardiac lymphatic network.

232 In patients with chronic heart failure, ongoing myocardial injury partial

233 es, including the inclusion of patients with chronic heart failure or mild acute heart failure, use o

234 MPO in patients with acute decompensation of chronic heart failure over a one week course.

235 , a large number of patients with MI develop chronic heart failure over time.

236 on Morbidity and Mortality of Patients With Chronic Heart Failure [PARADIGM-HF]; NCT01035255).

237 Ambulatory chronic heart failure patients (n = 988) with normal sin

238 to serial measurements, we evaluated stable chronic heart failure patients every 3 months for 2 year

239 All 2,679 symptomatic chronic heart failure patients from the North American C

240 In ambulatory chronic heart failure patients, a score derived from mul

241 entially novel laboratory markers of risk in chronic heart failure patients.

242 were independent predictors of mortality in chronic heart failure patients.

243 lated cardiomyopathy (DCM), a major cause of chronic heart failure, presumably through altering cardi

244 e frequently presented chronic lung disease, chronic heart failure, prior endocarditis, and degenerat

245 reatment discontinuation in large studies in chronic heart failure published since 1990.

246 zing Intracardiac Pressures in Patients with Chronic Heart Failure (REDUCEhf) study allowed assessmen

247 indicate that restoring carotid body KLF2 in chronic heart failure reduces sympathetic nerve activity

248 Despite this, chronic heart failure remains a major cause of illness a

249 Chronic heart failure remains a major cause of mortality

250 ith clinical characteristics consistent with chronic heart failure requiring implantation of a contin

251 The chronic heart failure-rescuing properties of myocardial

252 lammatory process occurring in patients with chronic heart failure, review different therapeutic tech

253 to the MAGGIC (Meta-Analysis Global Group in Chronic Heart Failure Risk Score) risk score.

254 peptides, and Meta-Analysis Global Group in Chronic Heart Failure risk score.

255 Treatment for Depression in Individuals With Chronic Heart Failure [SADHART-CHF]; NCT00078286).

256 , time-updated Meta-Analysis Global Group in Chronic Heart Failure score, and time-updated New York H

257 , adjusted for Meta-Analysis Global Group in Chronic Heart Failure score, genotype, level of BB expos

258 ay important roles in the pathophysiology of chronic heart failure secondary to chronic left ventricu

259 In patients with chronic heart failure, serelaxin increased renal plasma

260 Among patients with postinfarction chronic heart failure, shock wave-facilitated intracoron

261 yndromes are commonly defined as a change in chronic heart failure signs and symptoms requiring urgen

262 RECENT FINDINGS: In chronic heart failure, studies suggest that a strategy o

263 line Against Depression and Heart Disease in Chronic Heart Failure study randomized 469 participants

264 VINDICATE (VitamIN D treatIng patients with Chronic heArT failurE) study was undertaken to establish

265 Compared with chronic heart failure subjects, plasma ADMA was signific

266 diseases, eg, myocardial infarction (MI) and chronic heart failure, suggesting that cardiac lymphatic

267 lts and a major cause of morbidity caused by chronic heart failure symptoms.

268 irst time in a large cohort of patients with chronic heart failure that moderate wine consumption is

269 Our results suggest low use of EMB in chronic heart failure that responds to usual care.

270 therapeutic options for initial surgery and chronic heart failure that results from failed palliatio

271 In patients with chronic heart failure, the addition of aliskiren to enal

272 In acute decompensation of chronic heart failure, the change in the inflammatory cy

273 stems Biology Study to Tailored Treatment in Chronic Heart Failure]), the relationship between PENK a

274 n highly successful in reducing mortality in chronic heart failure, this has not been matched by simi

275 In a large contemporary population with chronic heart failure, this model offers good ability to

276 ha protects muscle from catabolic wasting in chronic heart failure through enhanced nitric oxide anti

277 ntrolled trial conducted among patients with chronic heart failure treated at Goethe University Frank

278 a suggest that HMGB1 may be valuable for the chronic heart failure treatment.

279 line Against Depression and Heart Disease in Chronic Heart Failure) trial was a randomized, double-bl

280 Chronic heart failure was induced by coronary ligation i

281 he complexity of the immune system's role in chronic heart failure, which has led to an oversimplifie

282 ive, part of the management of patients with chronic heart failure who are receiving appropriate medi

283 s, sST2 measurement identifies patients with chronic heart failure who may particularly benefit from

284 ay be appropriate in patients with worsening chronic heart failure who remain symptomatic.

285 ousand sixteen patients with stable systolic chronic heart failure who were using either carvedilol o

286 domized controlled clinical trials (RCTs) in chronic heart failure with >400 participants and utilizi

287 ndocardial pacing (BIVendo) in patients with chronic heart failure with an emphasis on the underlying

288 of OM on symptoms and HRQL in patients with chronic heart failure with reduced ejection fraction and

289 In patients with chronic heart failure with reduced ejection fraction and

290 Chronic heart failure with reduced ejection fraction imp

291 New York Heart Association (NYHA) class III chronic heart failure with reduced ejection fraction wer

292 Tool for Intensification of Medications for Chronic Heart Failure with Reduced Ejection Fraction) tr

293 Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Reduced Ejection Fraction), e

294 Empagliflozin Outcome Trial in Patients With Chronic Heart Failure With Reduced Ejection Fraction), e

295 wever, progress has been consistent only for chronic heart failure with reduced ejection fraction.

296 al of 2 new drugs, both for the treatment of chronic heart failure with reduced ejection fraction: iv

297 del for risk stratification in patients with chronic heart failure with systolic dysfunction, using p

298 stic information in ambulatory patients with chronic heart failure with systolic dysfunction.

299 lar structure are significantly disrupted in chronic heart failure, with important functional sequela

300 e dimethylaminohydrolase-1 were increased in chronic heart failure without elevated sPAP (<50 mm Hg),