ライフサイエンスコーパス: decompensate

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

2 d CLD, compensated advanced CLD (CACLD), and decompensated advanced CLD (DACLD).

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

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

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

6 sing tide of alcohol relapse, admissions for decompensated ALD, and an increase in newly diagnosed pa

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

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

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

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

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

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

13 ), acute-on chronic liver failure (AoCLF) or decompensated chronic liver disease (decomp.

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

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

16 PMs from ascites samples of 66 patients with decompensated cirrhosis (19 with SBP) and analyzed them

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

18 es of a separate cohort of 111 patients with decompensated cirrhosis (67 with SBP) and quantified the

19 l in a large cohort of patients with acutely decompensated cirrhosis (AD, n = 52) or acute-on-chronic

20 Independent predictors of mortality were decompensated cirrhosis (adjusted hazard ratio [AHR] 23.

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

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

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

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

25 phageal variceal hemorrhage in patients with decompensated cirrhosis (first section); we reviewed the

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

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

28 as been reported on the real-world clinical (decompensated cirrhosis [DCC] and hepatocellular carcino

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

30 pective cohort of hospitalized patients with decompensated cirrhosis and acute kidney injury.

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

32 bundant, activated, and highly functional in decompensated cirrhosis and are further enriched in SBP.

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

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

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

36 sis progression, and mortality attributed to decompensated cirrhosis and hepatocellular carcinoma and

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

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

39 o-controlled, phase 2 trial in patients with decompensated cirrhosis and moderate-to-severe liver fai

40 e that typically precedes the development of decompensated cirrhosis and the accompanying uncertainti

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

42 Conclusion: One third of patients with decompensated cirrhosis are readmitted within 30 days of

43 12.7%) died during follow-up, 33 of whom had decompensated cirrhosis at recruitment.

44 18 years or older with any HCV genotype and decompensated cirrhosis at screening.

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

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

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

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

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

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

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

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

53 Acute kidney injury in decompensated cirrhosis has limited therapeutic options,

54 Patients with decompensated cirrhosis have significantly reduced survi

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

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

57 Decompensated cirrhosis is associated with high morbidit

58 Decompensated cirrhosis is characterized by disturbed sy

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

60 sease distinguishes acute liver failure from decompensated cirrhosis or acute-on-chronic liver failur

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

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

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

64 re to predict 30-day hospital readmission in decompensated cirrhosis patients using the US nationwide

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

66 Patients with decompensated cirrhosis receiving DAAs present lower res

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

68 This validated model enabled patients with decompensated cirrhosis to be stratified into groups wit

69 in 40 mg/day plus rifaximin in patients with decompensated cirrhosis was associated with a significan

70 Decompensated cirrhosis was defined as current or past e

71 267 patients with HCV-related decompensated cirrhosis were included.

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

73 Eighty patients with decompensated cirrhosis were recruited (40 each with and

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

75 Adult patients with confirmed diagnosis of decompensated cirrhosis who were admitted to the ICU bet

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

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

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

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

80 levant outcomes in a cohort of patients with decompensated cirrhosis with acute kidney injury.

81 gulation, and fibrinolysis) in patients with decompensated cirrhosis with and without AKI.

82 , and systemic inflammation in patients with decompensated cirrhosis with and without bacterial infec

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

84 32% had a diagnosis of cirrhosis (9.9% with decompensated cirrhosis), 36% had a Fibrosis-4 index sco

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

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

87 In patients with decompensated cirrhosis, AKI is associated with both hyp

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

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

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

91 stance abuse, sexually transmitted diseases, decompensated cirrhosis, cirrhosis, and hepatitis C viru

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

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

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

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

96 Decompensated cirrhosis, low body mass index and older a

97 0.61; 95% CI, 0.47-0.79) among patients with decompensated cirrhosis, the median survival benefit was

98 he prominence of vascular destabilization in decompensated cirrhosis, we evaluated Angiopoietin-2 to

99 hemodynamic derangements than patients with decompensated cirrhosis, we investigated whether PICD co

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

101 s fluid were collected from 35 patients with decompensated cirrhosis, with or without spontaneous bac

102 e systemic immune responses in patients with decompensated cirrhosis.

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

104 ot been extensively studied in patients with decompensated cirrhosis.

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

106 ity of improved survival among patients with decompensated cirrhosis.

107 response in patients with HCV infection and decompensated cirrhosis.

108 on, including transplantation for those with decompensated cirrhosis.

109 rgery with excellent outcomes for those with decompensated cirrhosis.

110 ontrol bacterial infections in patients with decompensated cirrhosis.

111 rdiocirculatory dysfunction in patients with decompensated cirrhosis.

112 combination with rifaximin, in patients with decompensated cirrhosis.

113 ve cases of AKI in patients hospitalized for decompensated cirrhosis.

114 albumin therapy on outcomes of patients with decompensated cirrhosis.

115 igating the role of statins in patients with decompensated cirrhosis.

116 rding the safety of statins in patients with decompensated cirrhosis.

117 t be of therapeutic benefit in patients with decompensated cirrhosis.

118 osis, and finally, (4) patients with CLD and decompensated cirrhosis.

119 More specifically, in decompensated-cirrhosis patients, "high-risk" grafts did

120 tibiotic prophylaxis improved survival among decompensated cohort following PUB.

121 -old woman was admitted to our hospital with decompensated congestive heart failure and pericardial e

122 Transition to decompensated CPMR is associated with calcium dysregulat

123 Decompensated CPMR was associated with downregulation of

124 ied the study population into compensated or decompensated CPMR.

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

126 ten undetected until irreversible late-stage decompensated disease manifests.

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

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

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

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

131 ngle decompensation; grade 5 = more than one decompensating event; and grade 6 = death.

132 single decompensation; grade 5=more than one decompensating event; and grade 6=death.

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

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

135 57-year-old liver transplant recipient with decompensated graft cirrhosis due to chronic hepatitis E

136 4 patients with CS, the majority were due to decompensated heart failure (50%) or myocardial infarcti

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

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

139 Acute decompensated heart failure (ADHF) is a highly morbid co

140 Acute decompensated heart failure (ADHF) requiring hospitaliza

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

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

143 valsartan in patients hospitalized for acute decompensated heart failure (ADHF) was well-tolerated an

144 vo heart failure (HF)) or worsening (acutely decompensated heart failure (ADHF)) of symptoms and sign

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

146 receptor-like 1, identifies risk in acutely decompensated heart failure (ADHF).

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

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

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

150 rtan (S/V) in stabilized patients with acute decompensated heart failure (HF) and reduced ejection fr

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

152 fraction, yet is often not primarily due to decompensated heart failure (HF).

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

154 Acute decompensated heart failure accounts for more than 1 mil

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

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

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

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

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

160 In acutely decompensated heart failure and heart failure with prese

161 n for hospitalization in patients with acute decompensated heart failure and is an important target f

162 Failure) that randomized patients with acute decompensated heart failure and preexisting WRF to inten

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

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

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

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

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

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

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

170 ity outcomes for patients admitted for acute decompensated heart failure are poor and have not signif

171 tors when initiated soon after an episode of decompensated heart failure are unknown.

172 ion fraction who were hospitalized for acute decompensated heart failure at 129 sites in the United S

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

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

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

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

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

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

179 mong patients who are hospitalized for acute decompensated heart failure is unknown.

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

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

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

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

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

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

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

187 Treatment of decompensated heart failure often includes administratio

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

189 ip between intensive volume removal in acute decompensated heart failure patients with preexisting wo

190 Conclusions In acute decompensated heart failure patients with preexisting WR

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

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

193 Acute decompensated heart failure remains the most common caus

194 f age, she was admitted to our hospital with decompensated heart failure to be evaluated for a heart

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

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

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

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

199 -HF trial (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) that randomized patients wi

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

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

202 ic Optimization Strategy Evaluation in Acute Decompensated Heart Failure), and CARRESS-HF (Cardiorena

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

204 ARRESS-HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure).

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

206 There were 17 CV events (12%, 6 CV deaths, 6 decompensated heart failure, and 5 arrhythmias; median t

207 ular events were a composite of arrhythmias, decompensated heart failure, and CV death.

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

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

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

211 an overview of the pathophysiology of acute decompensated heart failure, current management strategi

212 f the pathophysiologic derangements in acute decompensated heart failure, denoted by the acronym DRI(

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

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

215 ion fraction who were hospitalized for acute decompensated heart failure, the initiation of sacubitri

216 xtracorporeal membrane oxygenation for acute decompensated heart failure.

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

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

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

220 halting the progression from compensated to decompensated heart failure.

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

222 frequent cause for hospitalization in acute decompensated heart failure.

223 heart failure sometimes present acutely with decompensated heart failure.

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

225 nostic factors in patients hospitalized with decompensated heart failure.

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

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

228 improve the outcomes of patients with acute decompensated heart failure.

229 lity may benefit patients admitted for acute decompensated heart failure.

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

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

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

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

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

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

236 ighted hospitalizations) classified as acute decompensated HF had available ejection fraction data (5

237 18.6 months, comparable to that after first decompensated HF hospitalization, even after age-sex adj

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

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

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

241 Acute decompensated HF was classified by standardized physicia

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

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

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

245 ted with high mortality rates, comparable to decompensated HF, and a major burden of rehospitalizatio

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

247 recorded and categorized as primarily due to decompensated HF, other cardiovascular disease, infectio

248 Among patients admitted for acute decompensated HF, S/V was safe and well tolerated, led t

249 al at discharge among patients admitted with decompensated HF.

250 ulatory patients and 50% patients with acute decompensated HF.

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

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

253 ities among hospitalized patients with acute decompensated HFpEF and HFrEF has increased over time, a

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

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

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

257 persistent upregulation of the HBP triggers decompensated hypertrophy through activation of mTOR whi

258 nt mechanism contributing to mitotoxicity in decompensating hypertrophy.

259 Myxedema coma is a life-threatening form of decompensated hypothyroidism that must be treated with a

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

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

262 une-intervention strategies in patients with decompensated liver cirrhosis and SBP.

263 Acute anaemia in decompensated liver cirrhosis is commonly caused due to

264 Early readmission in patients with decompensated liver cirrhosis leads to an enormous burde

265 orthotopic liver transplantation because of decompensated liver cirrhosis was admitted with acute an

266 partment present in ascites of patients with decompensated liver cirrhosis, and focus especially on M

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

268 A history of decompensated liver disease (hazard ratio, 1.57; 95% con

269 nd highly effective in HCV-HIV patients with decompensated liver disease and post-LT, with post-LT su

270 Thirteen participants died, 10 with decompensated liver disease pre-LT and three post-LT.

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

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

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

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

275 e participants required subsequent LT, 7 for decompensated liver disease.

276 tween patients with compensated (n=6) versus decompensated (n=6) CPMR.

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

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

279 Decompensated patients often pose a complex challenge wh

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

281 Decompensated patients were also studied for characteris

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

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

284 In decompensated patients, treatments aim at lowering the r

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

286 ctly leads to right ventricular hypertrophy, decompensated right-sided heart failure, and death.

287 s also studied in the RVfib of patients with decompensated RV failure (n=11) versus control (n=7).

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

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

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

291 ultured endothelial cells from patients with decompensated RV failure.

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

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

294 At the decompensated stage of hypertrophy, isolated hearts were

295 h defines the transition from compensated to decompensated stage.

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

297 exercise capacity in patients with recently decompensated systolic HF.

298 lial cells density (ECD) drops, the HCEC may decompensate to keep cornea dehydration which leads to c

299 in experimental pressure overload (6-fold in decompensated versus sham mice).

300 le spectrum of disease (compensated, acutely decompensated without ACLF, and ACLF).