ライフサイエンスコーパス: decompensate

1 ding the high-risk situation where a patient decompensates.

2 ongestive heart failure (primary diagnosis), decompensated advanced liver disease, cancer with or wit

3 tients with underlying mitochondrial disease decompensate after seemingly trivial viral infections.

4 Six esotropic patients decompensated after a mean of 6 years; 5 of these patien

5 fMLP-induced RB of PMN from patients with decompensated alcoholic cirrhosis was strongly impaired

6 siologic K(+) intake (5% K(+)), AS(-/-) mice decompensated and became hyperkalemic.

7 ical response, the patient remained severely decompensated and re-transplantation was performed after

8 Two eyes decompensated and required a regraft, whereas the remain

9 eption of cirrhosis as either compensated or decompensated and the recent, more complex models of cir

10 Cheyne-Stokes breathing are associated with decompensated and/or incident heart failure.

11 Erbin(-/-) mice rapidly develop decompensated cardiac hypertrophy, and following severe

12 gard to horizontal deviations, patients with decompensated childhood strabismus with a combination of

13 ng directly from acute liver failure or from decompensated chronic liver disease is an increasing pro

14 in the prevalence of cirrhosis (1.7%-2.2%), decompensated cirrhosis (1.1%-1.2%), and HCC (0.03%-0.13

15 in the prevalence of cirrhosis (3.5%-13.2%), decompensated cirrhosis (1.9%-5.8%), and HCC (0.07%-1.6%

16 produced the largest absolute reductions in decompensated cirrhosis (16%) and hepatocellular carcino

17 is hypothesis and included 522 patients with decompensated cirrhosis (237 with ACLF) and 40 healthy s

18 f patients with HIV who had cirrhosis (66%), decompensated cirrhosis (62%), and HCC (80%).

19 ected with HCV genotypes 1 through 6 who had decompensated cirrhosis (classified as Child-Pugh-Turcot

20 therapy, recently approved for patients with decompensated cirrhosis (DC) secondary to hepatitis C vi

21 hronic HCV only, 9% with cirrhosis, 12% with decompensated cirrhosis (DCC), 2% with liver cancer, 2%

22 ients with hepatocellular carcinoma (HCC) or decompensated cirrhosis (DCC).

23 ge IV disease (HR, 1.40; 95% CI, 1.24-1.58), decompensated cirrhosis (HR, 1.49; 95% CI, 1.30-1.70), a

24 CI], 2.62-4.49; P < .001, log-rank test) and decompensated cirrhosis (RR = 4.11; 95% CI, 2.95-5.70; P

25 [CI]=1.11-2.11; log-rank test; P<0.001) and decompensated cirrhosis (RR=2.01; 95% CI=1.07-3.79; log-

26 re grouped into HBV-related (subdivided into decompensated cirrhosis [DCC] and hepatocellular carcino

27 cs of systemic inflammation in patients with decompensated cirrhosis and ACLF, with special emphasis

28 Characteristics of decompensated cirrhosis and acute-on-chronic liver failu

29 Primary HCV infection resulted in decompensated cirrhosis and death within 2-8 years in 4

30 the only effective therapy for patients with decompensated cirrhosis and fulminant liver failure.

31 V, the number of individuals with cirrhosis, decompensated cirrhosis and HCC will continue to increas

32 f patients developing HCV-related cirrhosis, decompensated cirrhosis and HCC will increase substantia

33 s of end-stage liver disease (ESLD), such as decompensated cirrhosis and liver cancer.

34 st cost-effective strategy for patients with decompensated cirrhosis and MELD score greater than 13.

35 controlled trials of adults (>18 years) with decompensated cirrhosis and type 1 hepatorenal syndrome

36 18 years or older with any HCV genotype and decompensated cirrhosis at screening.

37 advanced liver disease, including those with decompensated cirrhosis before and after liver transplan

38 advanced liver disease, including those with decompensated cirrhosis before or after liver transplant

39 bservational cohort study of inpatients with decompensated cirrhosis between 2010 and 2013.

40 tes incubated with plasma from patients with decompensated cirrhosis carrying the protective SNP geno

41 The prevalence of patients with decompensated cirrhosis doubled, from 5% in 1996 to 11%

42 rcaserin in a morbidly obese individual with decompensated cirrhosis evaluated for LT listing.

43 ecrease the 15-year cumulative incidences of decompensated cirrhosis from 12.2% to 4.5%, hepatocellul

44 ificantly larger proportion of patients with decompensated cirrhosis given a combination of G-CSF and

45 nt-reported outcomes (PROs) in patients with decompensated cirrhosis given a fixed-dose combination o

46 Patients with decompensated cirrhosis have significantly reduced survi

47 cellular carcinoma, and 203,000 will develop decompensated cirrhosis in the next 35 years.

48 Management of obesity and decompensated cirrhosis in those requiring liver transpl

49 Decompensated cirrhosis is characterized by disturbed sy

50 irus (HCV) ages, the number of patients with decompensated cirrhosis is expected to increase.

51 e risk of infection in patients with acutely decompensated cirrhosis or ESLD.

52 ction of any genotype and either compensated/decompensated cirrhosis or posttransplantation recurrenc

53 that the optimal MELD threshold below which decompensated cirrhosis patients should receive HCV trea

54 One patient who had decompensated cirrhosis prior to treatment initiation di

55 Patients with decompensated cirrhosis receiving DAAs present lower res

56 prospective study, consecutive patients with decompensated cirrhosis seen at the Institute of Liver a

57 267 patients with HCV-related decompensated cirrhosis were included.

58 ASTRAL-4) in which patients with HCV-related decompensated cirrhosis were randomly assigned to an all

59 th fibrosing cholestatic hepatitis (FCH) and decompensated cirrhosis who had a life expectancy of 1 y

60 Os was observed in patients with HCV-related decompensated cirrhosis who were given sofosbuvir and ve

61 ve was to identify LT-eligible patients with decompensated cirrhosis who would benefit (and not benef

62 ere is a concern that the cured patient with decompensated cirrhosis will find themselves in "MELD pu

63 Incidence of decompensated cirrhosis will increase 168% to 105,430 ca

64 after their primary HCV infection developed decompensated cirrhosis within 17 months to 6 years afte

65 and the number progressing from infection to decompensated cirrhosis would decline by 65%.

66 32% had a diagnosis of cirrhosis (9.9% with decompensated cirrhosis), 36% had a Fibrosis-4 index sco

67 ort screening leads to 84,000 fewer cases of decompensated cirrhosis, 46,000 fewer cases of hepatocel

68 Among the full cohort with compensated or decompensated cirrhosis, 61% (504 of 830) died during th

69 could prevent approximately 124,200 cases of decompensated cirrhosis, 78,800 cases of hepatocellular

70 ver function in patients with compensated or decompensated cirrhosis, and delay or obviate the need f

71 lculated the annual prevalence of cirrhosis, decompensated cirrhosis, and HCC in a national sample of

72 time trends in the prevalence of cirrhosis, decompensated cirrhosis, and hepatocellular carcinoma (H

73 ency is common among patients with HCV, with decompensated cirrhosis, and in the posttransplant setti

74 treatment of CHB in pregnancy, coinfection, decompensated cirrhosis, and posttransplant is safe and

75 ents with cirrhosis, particularly those with decompensated cirrhosis, are at increased risk of bacter

76 f HCV incidence, prevalence, compensated and decompensated cirrhosis, hepatocellular carcinoma, liver

77 H-fibrosis, NASH-compensated cirrhosis, NASH-decompensated cirrhosis, hepatocellular carcinoma, liver

78 advanced liver disease, including those with decompensated cirrhosis, in routine practice (all curren

79 including patients with HIV/HCV coinfection, decompensated cirrhosis, liver and kidney transplants, a

80 eatening liver disease (acute liver failure, decompensated cirrhosis, or severe hepatitis flare) and

81 nsideration are patients with compensated or decompensated cirrhosis, organ transplantation, acute he

82 0.61; 95% CI, 0.47-0.79) among patients with decompensated cirrhosis, the median survival benefit was

83 ended in specific patient groups: those with decompensated cirrhosis, those coinfected with human imm

84 ) correlates with mortality in patients with decompensated cirrhosis, who are almost invariably sarco

85 should be used with caution in patients with decompensated cirrhosis.

86 response in patients with HCV infection and decompensated cirrhosis.

87 on, including transplantation for those with decompensated cirrhosis.

88 rgery with excellent outcomes for those with decompensated cirrhosis.

89 ould be considered in patients admitted with decompensated cirrhosis.

90 e systemic immune responses in patients with decompensated cirrhosis.

91 te exacerbation of the SI already present in decompensated cirrhosis.

92 ot been extensively studied in patients with decompensated cirrhosis.

93 tibiotic prophylaxis improved survival among decompensated cohort following PUB.

94 re-transplantation for recipients who remain decompensated despite virological response and is likely

95 and predischarge BNP levels in patients with decompensated diastolic heart failure have been prognost

96 n range from 1% in early cirrhosis to 57% in decompensated disease.

97 ollected prospectively from 39 patients with decompensated end-stage systolic heart failure (92% male

98 y artery occlusion pressure in patients with decompensated end-stage systolic heart failure was recen

99 y artery occlusion pressure in patients with decompensated end-stage systolic heart failure.

100 y artery occlusion pressure in patients with decompensated end-stage systolic heart failure.

101 uiring antibiotics (20% vs. 1%), and hepatic decompensating events (20% vs. 3%; all P < 0.01).

102 patocytes derived from cirrhotic livers with decompensated function failed to maintain metabolic or s

103 ry and sustain cardiac output in the face of decompensating function.

104 interferon-alpha and ribavirin who developed decompensated graft cirrhosis 6 years after a first live

105 Acute decompensated heart failure (ADHF) can be complicated by

106 M) code criteria, do not differentiate acute decompensated heart failure (ADHF) from chronic stable H

107 Estimates of the numbers and rates of acute decompensated heart failure (ADHF) hospitalization are c

108 Acute decompensated heart failure (ADHF) requiring hospitaliza

109 Background: Acute decompensated heart failure (ADHF) requiring hospitaliza

110 Acute decompensated heart failure (ADHF) was a frequent common

111 ure), 7,141 patients hospitalized with acute decompensated heart failure (ADHF) were randomized to re

112 d volume overload are the hallmarks of acute decompensated heart failure (ADHF), and loop diuretics h

113 ently poses a therapeutic challenge in acute decompensated heart failure (ADHF).

114 h acute cardiac illness, most commonly acute decompensated heart failure (ADHF).

115 with improvement in renal function in acute decompensated heart failure (ADHF).

116 emoglobin in patients hospitalized for acute decompensated heart failure (AHF).

117 e a context for Acute Study of Nesiritide in Decompensated Heart Failure (ASCEND-HF) trial, we design

118 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND-HF), we assessed fac

119 E-AHF) and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trials during h

120 ic Optimization Strategy Evaluation in Acute Decompensated Heart Failure (DOSE-AHF) and Cardiorenal R

121 Currently, therapeutic options for decompensated heart failure (HF) are limited.

122 ltrafiltration (SCUF) in patients with acute decompensated heart failure (HF) refractory to intensive

123 xtracorporeal membrane oxygenation for acute decompensated heart failure (i.e., cardiogenic shock com

124 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure [ASCEND-HF]; NCT00475852).

125 ined tachyarrhythmia (atrial/ventricular) or decompensated heart failure admission/transplantation/de

126 admission to discharge in consecutive acute decompensated heart failure admissions (n=656).

127 al function during hospitalization for acute decompensated heart failure and associated outcomes.

128 HF) trials during hospitalization with acute decompensated heart failure and clinical congestion.

129 is a primary therapeutic objective in acute decompensated heart failure and commonly monitored with

130 tal of 40 consecutive patients with advanced decompensated heart failure and CRT implanted >3 months,

131 tal practice patterns of NIPPV use for acute decompensated heart failure and their relationship with

132 d arginine metabolism in patients with acute decompensated heart failure and to explore possible mech

133 s admitted to a single institution for acute decompensated heart failure and treated with UF: HFLEF (

134 fylline for Patients Hospitalized with Acute Decompensated Heart Failure and Volume Overload to Asses

135 fylline for Patients Hospitalized with Acute Decompensated Heart Failure and Volume Overload to Asses

136 fylline for Patients Hospitalized With Acute Decompensated Heart Failure and Volume Overload to Asses

137 fylline for Patients Hospitalized With Acute Decompensated Heart Failure and Volume Overload to Asses

138 nificantly associated with increased risk of decompensated heart failure and/or development of clinic

139 of hypotension while hospitalized with acute decompensated heart failure are not well understood.

140 e transition from compensated hypertrophy to decompensated heart failure as a result of reduced phosp

141 , and unplanned clinic visits to treat acute decompensated heart failure based on the blinded adjudic

142 in the management of low output syndrome and decompensated heart failure but their effect on mortalit

143 ty of ultrafiltration in patients with acute decompensated heart failure complicated by persistent co

144 When conventional therapy for acute decompensated heart failure fails, mechanical fluid remo

145 e, hemoconcentration during the treatment of decompensated heart failure has been associated with red

146 tion of chronic oral medication during acute decompensated heart failure hospitalization may not be a

147 xtracorporeal membrane oxygenation for acute decompensated heart failure in our ICU (67% of them had

148 prevents the transition from compensated to decompensated heart failure in part via upregulation of

149 technology for inpatient management of acute decompensated heart failure in patients with volume over

150 mass spectrometry in subjects with advanced decompensated heart failure in the intensive care unit (

151 We examined hospitalizations for acute decompensated heart failure in this database from 2005 t

152 association between air pollution and acute decompensated heart failure including hospitalisation an

153 Acute decompensated heart failure is a medical emergency and r

154 Hypotension while hospitalized for acute decompensated heart failure is an independent risk facto

155 SBP reduction) during the treatment of acute decompensated heart failure is strongly and independentl

156 Acute decompensated heart failure modifies the course of chron

157 The Acute Decompensated Heart Failure National Registry (ADHERE) a

158 h heart failure without CRT-D from the Acute Decompensated Heart Failure National Registry (ADHERE) h

159 Patients from ADHERE (Acute Decompensated Heart Failure National Registry) who were

160 re National Registry-United States and Acute Decompensated Heart Failure National Registry-Internatio

161 re National Registry-United States and Acute Decompensated Heart Failure National Registry-Internatio

162 amined 196 770 AHF admissions from the Acute Decompensated Heart Failure National Registry-United Sta

163 Among both Acute Decompensated Heart Failure National Registry-United Sta

164 ped from 3 clinical databases (ADHERE [Acute Decompensated Heart Failure National Registry], EFFECT s

165 Treatment of decompensated heart failure often includes administratio

166 Clinical manifestations ranged from decompensated heart failure or sudden death in those pre

167 l arrhythmias in this population can lead to decompensated heart failure or thromboembolism and thera

168 gen/creatinine ratio (BUN/Cr) could identify decompensated heart failure patients likely to experienc

169 was then prospectively validated in 50 acute decompensated heart failure patients using meticulously

170 is population with outcomes similar to acute decompensated heart failure patients with low left ventr

171 an treatment inhibits MPO release by PMNs in decompensated heart failure patients.

172 Therapy During Hospital Admission for Acute Decompensated Heart Failure Reduce Mortality and Readmis

173 1.13 [0.92 to 1.37], p = 0.002) in advanced decompensated heart failure subjects.

174 d trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide admini

175 oral neurohormonal antagonists during acute decompensated heart failure treatment negatively influen

176 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure trial.

177 ventilation (NIPPV) for patients with acute decompensated heart failure was introduced almost 20 yea

178 ents hospitalized for the treatment of acute decompensated heart failure will experience significant

179 ients >/=55 years of age admitted with acute decompensated heart failure with preserved ejection frac

180 mong hospitals in the use of NIPPV for acute decompensated heart failure without evidence for differe

181 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure) trial randomized 7,141 hosp

182 Pressure Measurements in Patients With Acute Decompensated Heart Failure) was a single-center prospec

183 of Clinical Effectiveness of Nesiritide and Decompensated Heart Failure), 7,141 patients hospitalize

184 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure).

185 xtracorporeal membrane oxygenation for acute decompensated heart failure, 1-year survival was 42%, bu

186 In patients with acute decompensated heart failure, a positive cardiac troponin

187 s, the hypertrophic response can evolve into decompensated heart failure, although the mechanism(s) u

188 infarction, nonfatal stroke, nonfatal acute decompensated heart failure, and death from cardiovascul

189 patients (acute myocardial infarction, acute decompensated heart failure, biventricular failure, and

190 component of therapy for patients with acute decompensated heart failure, but there are few prospecti

191 should be considered for patients with acute decompensated heart failure, but timing of implantation

192 outcome of hospitalization for management of decompensated heart failure, initiation of mechanical ci

193 arginine metabolism was observed in advanced decompensated heart failure, particularly with pulmonary

194 In patients being treated for acute decompensated heart failure, poor natriuretic response c

195 least 40 years and hospitalization for acute decompensated heart failure, severe systemic infection w

196 r arrhythmias in this population can lead to decompensated heart failure, syncope, and sudden cardiac

197 Among patients with acute decompensated heart failure, there were no significant d

198 al involving patients hospitalized for acute decompensated heart failure, worsened renal function, an

199 assigned a total of 188 patients with acute decompensated heart failure, worsened renal function, an

200 reserved ejection fraction, as well as acute decompensated heart failure.

201 halting the progression from compensated to decompensated heart failure.

202 presenting with cardiogenic shock, and acute decompensated heart failure.

203 frequent cause for hospitalization in acute decompensated heart failure.

204 heart failure sometimes present acutely with decompensated heart failure.

205 ide on renal function in patients with acute decompensated heart failure.

206 nostic factors in patients hospitalized with decompensated heart failure.

207 affect renal function in patients with acute decompensated heart failure.

208 f 487 patients aged >/=75 years admitted for decompensated heart failure.

209 l and a key measure of treatment efficacy in decompensated heart failure.

210 ients hospitalized with a diagnosis of acute decompensated heart failure.

211 gestion, and outcomes in patients with acute decompensated heart failure.

212 tes acute respiratory distress syndrome from decompensated heart failure.

213 g sustained decongestion during treatment of decompensated heart failure.

214 dia (VT) in hospitalized patients with acute decompensated heart failure.

215 dent cohort of 75 subjects treated for acute decompensated heart failure.

216 apy for the treatment of patients with acute decompensated heart failure.

217 ening renal function during the treatment of decompensated heart failure.

218 e, was approved for the treatment of acutely decompensated heart failure.

219 idate drug in clinical trials to treat acute decompensated heart failure.

220 ated patients sometimes present acutely with decompensated heart failure.

221 rapy (CRT) in patients admitted for advanced decompensated heart failure.

222 iming of diuretics among patients with acute decompensated heart failure.

223 cting PCWP in patients admitted for advanced decompensated heart failure.

224 ents (80.5%) who were hospitalized for acute decompensated heart failure.

225 164 individuals (99% men) hospitalized with decompensated heart failure.

226 xtracorporeal membrane oxygenation for acute decompensated heart failure.

227 ean 7.3 years for development of incident or decompensated heart failure.

228 chaemia-reperfusion, cardiac hypertrophy and decompensated heart failure.

229 ortality in patients hospitalized with acute decompensated heart failure: 4 HF-specific mortality pre

230 iveness of Nesiritide in Patients With Acute Decompensated Heart Failure; NCT00475852).

231 he myocardium; in fact, cell therapy for the decompensated heart has to be based on the acquisition o

232 In decompensated hearts, oleate may serve as a beneficial e

233 nt stabilization, and approximately 10% will decompensate hemodynamically and suffer high mortality,

234 is most likely to occur in the presence of a decompensated heterophoria.

235 ometry, for investigating suspected cases of decompensating heterophoria; it is, however, rarely used

236 rom 63 consecutive adult patients with acute decompensated HF admitted to the Heart Failure Intensive

237 mic NaNO2 infusion that may be beneficial in decompensated HF and warrants further evaluation with lo

238 The chance-corrected agreement between acute decompensated HF by physician reviewer panel and the aut

239 n=7534 weighted) events classified as acute decompensated HF by the automated algorithm, and 1748 (6

240 As a group, patients who did not have acute decompensated HF events had no significant changes in eP

241 ophysiology of chronic compensated and acute decompensated HF in both SHF and DHF.

242 Decompensated HF is the main cause of cardiovascular hos

243 r experience, SCUF after admission for acute decompensated HF refractory to standard medical therapy

244 fulness of early SCUF in patients with acute decompensated HF to improve fluid overload and hemodynam

245 the impact of in-hospital guidance for acute decompensated HF treatment by a predefined NT-proBNP tar

246 ptide)-guided therapy in patients with acute decompensated HF using a relative NT-proBNP target has n

247 proBNP-guided therapy of patients with acute decompensated HF using a relative NT-proBNP target would

248 Patients with acute decompensated HF with NT-proBNP levels >1700 ng/L were e

249 ance of troponin elevation in the setting of decompensated HF with preserved ejection fraction (HFpEF

250 for worsening chronic HF (including acutely decompensated HF).

251 heart will progress into a state of chronic decompensated HF, and the hyperactive ANS will continue

252 c attack (TIA), myocardial infarction, acute decompensated HF, or cardiovascular death.

253 events: cardiovascular death, admission for decompensated HF, or clinical HF decompensation requirin

254 e cohorts of patients with chronic and acute decompensated HF, repeated measurements of galectin-3 le

255 In SHF and DHF patients who developed acute decompensated HF, these events were associated with a si

256 al at discharge among patients admitted with decompensated HF.

257 transition from chronic compensated to acute decompensated HF.

258 ws comparative assessment of compensated and decompensated (HF) forms of cardiac hypertrophy because

259 registry participants who were admitted for decompensated HFpEF (ejection fraction >/=50%) from Janu

260 oponin elevation among patients with acutely decompensated HFpEF is associated with worse in-hospital

261 ement of troponin levels among patients with decompensated HFpEF may be useful for risk stratificatio

262 l and long-term outcomes among patients with decompensated HFpEF.

263 nt mechanism contributing to mitotoxicity in decompensating hypertrophy.

264 Using multicenter study data in hospitalized decompensated infected cirrhosis patients, I-ACLF define

265 motes systemic inflammation and lethality in decompensated innate immune responses.

266 The recipient was a 51-year-old man with decompensated liver cirrhosis and hepatocellular carcino

267 early stratify patients with compensated and decompensated liver cirrhosis in two groups with complet

268 dictor of mortality in patients with acutely decompensated liver cirrhosis, though determining CysC a

269 al hemorrhage can be the dominant symptom of decompensated liver cirrhosis, varices and ulcerations i

270 ransplantation may be required in those with decompensated liver disease or HCC, but experience is li

271 offers life-saving therapy for patients with decompensated liver disease or T2 hepatocellular carcino

272 ons, presence of varices, and the absence of decompensated liver disease were associated with a highe

273 liver-related death, liver transplantation, decompensated liver disease, and HCC.

274 infection in reducing the risk of cirrhosis, decompensated liver disease, and hepatocellular carcinom

275 ikelihood of SVR; age, sex, body mass index, decompensated liver disease, diabetes, genotype 1 subtyp

276 titis B virus or HIV infection), evidence of decompensated liver disease, or a history of hepatocellu

277 e of cirrhosis, hepatocellular carcinoma, or decompensated liver disease.

278 BV contributed to the decreased incidence of decompensated liver disease.

279 ed complications (e.g., fulminant hepatitis, decompensated liver, and hepatocellular carcinoma) were

280 erse effects, and 1.8 (1.6-2.4) months in 60 decompensated patients (P < 0.001).

281 lysis, survival was significantly reduced in decompensated patients (p = 0.034).

282 Decompensated patients had a mortality of 25% after 37 a

283 ation with low procedure mortality, bridging decompensated patients to permanent LVAD or heart transp

284 Decompensated patients were also studied for characteris

285 important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.

286 d SMV with or without RBV in compensated and decompensated patients with cirrhosis with HCV GT1 infec

287 uld be a useful pharmacological treatment in decompensated patients with cirrhosis.

288 An elevated admission BUN/Cr identifies decompensated patients with heart failure likely to expe

289 A small percentage of patients decompensated, requiring secondary surgery to restore th

290 ypertrophy (n=8), and patients with PAH with decompensated RV failure (n=14).

291 th compensated RV hypertrophy, patients with decompensated RV failure had decreased miR-126 expressio

292 el resulted to a short microRNA signature of decompensated RV failure, which included the myocardium-

293 ultured endothelial cells from patients with decompensated RV failure.

294 sues from rats with normal, compensated, and decompensated RV hypertrophy, carefully defined based on

295 motes the transition from a compensated to a decompensated RV in PAH.

296 eeded is strategies to prevent transition to decompensated stages.

297 ccurred at 2 weeks in patients with recently decompensated systolic HF treated with anakinra, whereas

298 sment after in-hospital therapy for advanced decompensated systolic HF, allowing clinicians to focus

299 exercise capacity in patients with recently decompensated systolic HF.

300 However, they decompensate with stress.