ライフサイエンスコーパス: chronic heart failure

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

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

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

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

5 oblast regeneration is further enhanced with chronic heart failure.

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

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

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

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

10 appears promising in patients suffering from chronic heart failure.

11 olving diabetic or nondiabetic patients with chronic heart failure.

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

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

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

15 natriuretic peptide to monitor patients with chronic heart failure.

16 tenuated catabolic muscle wasting induced by chronic heart failure.

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

18 cle of progressive myocardial dysfunction in chronic heart failure.

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

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

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

22 contribute to development and progression of chronic heart failure.

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

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

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

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

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

28 mprove cardiac performance of postinfarction chronic heart failure.

29 during hospitalization for decompensation of chronic heart failure.

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

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

32 patients with acute myocardial infarction or chronic heart failure.

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

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

35 and dilutional hyponatremia associated with chronic heart failure.

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

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

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

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

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

41 and non-ischemic etiologies) and symptomatic chronic heart failure.

42 d improve clinical outcomes in patients with chronic heart failure.

43 t is activated in samples from patients with chronic heart failure.

44 tion therapy (CRT) in selected patients with chronic heart failure.

45 e regulation may have the opposite effect in chronic heart failure.

46 ations in understanding beta1AR signaling in chronic heart failure.

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

48 s actually contribute to the pathogenesis of chronic heart failure.

49 the rate of death or hospitalization due to chronic heart failure.

50 h acutely after myocardial infarction and in chronic heart failure.

51 ts the response to treatment and outcomes in chronic heart failure.

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

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

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

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

56 abnormalities are prevalent in patients with chronic heart failure.

57 ropic support or metabolic derangements from chronic heart failure.

58 Cpc-PH is rare in chronic heart failure.

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

60 implies therapeutic efficacy in settings of chronic heart failure.

61 val in multicenter hospital outpatients with chronic heart failure.

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

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

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

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

66 quency of the C34T mutation in patients with chronic heart failure (14.8%) was not different from tha

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

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

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

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

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

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

73 Moreover, chronic heart failure after myocardial infarction and pe

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

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

76 th New York Heart Association class II to IV chronic heart failure and a left ventricular ejection fr

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

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

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

80 or blockers (ARBs) in treating patients with chronic heart failure and high-risk acute myocardial inf

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

82 rt failure hospitalizations in patients with chronic heart failure and in patients with high-risk acu

83 hospitalization among patients with advanced chronic heart failure and intraventricular conduction de

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

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

86 the prevention of skeletal muscle wasting in chronic heart failure and potentially other chronic dise

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 The mortality of chronic heart failure (CHF) doubles either when CHF pati

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

124 Patients with chronic heart failure (CHF) have a resting restrictive v

125 verse effects of depression in patients with chronic heart failure (CHF) have been well studied, the

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

127 Chronic heart failure (CHF) induces endothelial dysfunct

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

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

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

131 Chronic heart failure (CHF) is an important cause of hos

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

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

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

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

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

137 carotid body (CB) chemoreceptor activity in chronic heart failure (CHF) rabbits.

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

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

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

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

142 tant determinant of outcome in subjects with chronic heart failure (CHF), but baseline or serial chan

143 found to relate to outcome in patients with chronic heart failure (CHF), but in an opposite directio

144 ion is known to be impaired in subjects with chronic heart failure (CHF), but the association between

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

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

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

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

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

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

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

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

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

154 ther aspirin should be used in patients with chronic heart failure (CHF).

155 n geriatric populations and in patients with chronic heart failure (CHF).

156 flow and cardiovascular reflex regulation in chronic heart failure (CHF).

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

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

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

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

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

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

163 two groups of dogs with pacing-induced overt chronic heart failure (CHF; 240 bpm for 10 d): Group 1 (

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

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

166 Chronic heart failure continues to impose a substantial

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

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

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

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

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

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

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

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

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

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

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

178 the mode of death in patients with advanced chronic heart failure (HF) and intraventricular conducti

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

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

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

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

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

184 Treatment of chronic heart failure (HF) is based on interference with

185 Chronic heart failure (HF) is characterized by sympathet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Chronic heart failure imposes a significant health burde

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

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

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

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

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

217 Chronic heart failure is a worldwide cause of mortality

218 Chronic heart failure is accompanied by anorexia and inc

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

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

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

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

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

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

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

226 Dyssynchronous chronic heart failure may attenuate suction, because reg

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

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

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

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

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

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

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

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

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

236 Chronic heart failure often results in catabolic muscle

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

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

239 f Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study randomized 949

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

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

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

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

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

245 3DE represents a novel technique to identify chronic heart failure patients who may otherwise not be

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

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

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

249 iotensin-converting enzyme plus aldactone in chronic heart failure patients.

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

251 gene, which is known to improve survival in chronic heart failure, protects against cardiac dysfunct

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

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

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

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

256 Chronic heart failure remains a major cause of mortality

257 ion of Mechanical Assistance in Treatment of Chronic Heart Failure (REMATCH) trial enrolled patients

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

259 The chronic heart failure-rescuing properties of myocardial

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

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

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

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

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

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

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

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

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

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

270 legedly asymptomatic patients) on a par with chronic heart failure subjects.

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

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

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

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

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

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

277 have demonstrated benefits in patients with chronic heart failure, the benefit attributable to patie

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

279 In chronic heart failure, the lung endothelial permeability

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

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

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

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

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

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

286 Chronic heart failure was induced by coronary ligation i

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

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

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

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

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

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

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

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

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

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),