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1 ongestive heart failure (primary diagnosis), decompensated advanced liver disease, cancer with or wit
5 ical response, the patient remained severely decompensated and re-transplantation was performed after
7 eption of cirrhosis as either compensated or decompensated and the recent, more complex models of cir
10 gard to horizontal deviations, patients with decompensated childhood strabismus with a combination of
11 ng directly from acute liver failure or from decompensated chronic liver disease is an increasing pro
12 in the prevalence of cirrhosis (1.7%-2.2%), decompensated cirrhosis (1.1%-1.2%), and HCC (0.03%-0.13
13 in the prevalence of cirrhosis (3.5%-13.2%), decompensated cirrhosis (1.9%-5.8%), and HCC (0.07%-1.6%
14 produced the largest absolute reductions in decompensated cirrhosis (16%) and hepatocellular carcino
15 is hypothesis and included 522 patients with decompensated cirrhosis (237 with ACLF) and 40 healthy s
17 ected with HCV genotypes 1 through 6 who had decompensated cirrhosis (classified as Child-Pugh-Turcot
18 therapy, recently approved for patients with decompensated cirrhosis (DC) secondary to hepatitis C vi
19 hronic HCV only, 9% with cirrhosis, 12% with decompensated cirrhosis (DCC), 2% with liver cancer, 2%
21 ge IV disease (HR, 1.40; 95% CI, 1.24-1.58), decompensated cirrhosis (HR, 1.49; 95% CI, 1.30-1.70), a
22 CI], 2.62-4.49; P < .001, log-rank test) and decompensated cirrhosis (RR = 4.11; 95% CI, 2.95-5.70; P
23 [CI]=1.11-2.11; log-rank test; P<0.001) and decompensated cirrhosis (RR=2.01; 95% CI=1.07-3.79; log-
24 re grouped into HBV-related (subdivided into decompensated cirrhosis [DCC] and hepatocellular carcino
25 cs of systemic inflammation in patients with decompensated cirrhosis and ACLF, with special emphasis
28 the only effective therapy for patients with decompensated cirrhosis and fulminant liver failure.
29 V, the number of individuals with cirrhosis, decompensated cirrhosis and HCC will continue to increas
30 f patients developing HCV-related cirrhosis, decompensated cirrhosis and HCC will increase substantia
32 st cost-effective strategy for patients with decompensated cirrhosis and MELD score greater than 13.
33 controlled trials of adults (>18 years) with decompensated cirrhosis and type 1 hepatorenal syndrome
34 nd decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developi
36 advanced liver disease, including those with decompensated cirrhosis before and after liver transplan
37 advanced liver disease, including those with decompensated cirrhosis before or after liver transplant
39 tes incubated with plasma from patients with decompensated cirrhosis carrying the protective SNP geno
42 ecrease the 15-year cumulative incidences of decompensated cirrhosis from 12.2% to 4.5%, hepatocellul
43 ificantly larger proportion of patients with decompensated cirrhosis given a combination of G-CSF and
44 nt-reported outcomes (PROs) in patients with decompensated cirrhosis given a fixed-dose combination o
51 ction of any genotype and either compensated/decompensated cirrhosis or posttransplantation recurrenc
52 that the optimal MELD threshold below which decompensated cirrhosis patients should receive HCV trea
55 prospective study, consecutive patients with decompensated cirrhosis seen at the Institute of Liver a
57 ASTRAL-4) in which patients with HCV-related decompensated cirrhosis were randomly assigned to an all
58 th fibrosing cholestatic hepatitis (FCH) and decompensated cirrhosis who had a life expectancy of 1 y
59 Os was observed in patients with HCV-related decompensated cirrhosis who were given sofosbuvir and ve
60 ve was to identify LT-eligible patients with decompensated cirrhosis who would benefit (and not benef
61 ere is a concern that the cured patient with decompensated cirrhosis will find themselves in "MELD pu
63 after their primary HCV infection developed decompensated cirrhosis within 17 months to 6 years afte
65 32% had a diagnosis of cirrhosis (9.9% with decompensated cirrhosis), 36% had a Fibrosis-4 index sco
66 ort screening leads to 84,000 fewer cases of decompensated cirrhosis, 46,000 fewer cases of hepatocel
67 Among the full cohort with compensated or decompensated cirrhosis, 61% (504 of 830) died during th
68 could prevent approximately 124,200 cases of decompensated cirrhosis, 78,800 cases of hepatocellular
69 ver function in patients with compensated or decompensated cirrhosis, and delay or obviate the need f
70 lculated the annual prevalence of cirrhosis, decompensated cirrhosis, and HCC in a national sample of
71 time trends in the prevalence of cirrhosis, decompensated cirrhosis, and hepatocellular carcinoma (H
72 ency is common among patients with HCV, with decompensated cirrhosis, and in the posttransplant setti
73 treatment of CHB in pregnancy, coinfection, decompensated cirrhosis, and posttransplant is safe and
74 ents with cirrhosis, particularly those with decompensated cirrhosis, are at increased risk of bacter
75 f HCV incidence, prevalence, compensated and decompensated cirrhosis, hepatocellular carcinoma, liver
76 H-fibrosis, NASH-compensated cirrhosis, NASH-decompensated cirrhosis, hepatocellular carcinoma, liver
77 advanced liver disease, including those with decompensated cirrhosis, in routine practice (all curren
78 including patients with HIV/HCV coinfection, decompensated cirrhosis, liver and kidney transplants, a
79 eatening liver disease (acute liver failure, decompensated cirrhosis, or severe hepatitis flare) and
80 nsideration are patients with compensated or decompensated cirrhosis, organ transplantation, acute he
81 0.61; 95% CI, 0.47-0.79) among patients with decompensated cirrhosis, the median survival benefit was
82 ended in specific patient groups: those with decompensated cirrhosis, those coinfected with human imm
83 ) correlates with mortality in patients with decompensated cirrhosis, who are almost invariably sarco
93 re-transplantation for recipients who remain decompensated despite virological response and is likely
94 and predischarge BNP levels in patients with decompensated diastolic heart failure have been prognost
96 ollected prospectively from 39 patients with decompensated end-stage systolic heart failure (92% male
97 y artery occlusion pressure in patients with decompensated end-stage systolic heart failure was recen
100 patocytes derived from cirrhotic livers with decompensated function failed to maintain metabolic or s
101 interferon-alpha and ribavirin who developed decompensated graft cirrhosis 6 years after a first live
103 M) code criteria, do not differentiate acute decompensated heart failure (ADHF) from chronic stable H
104 Estimates of the numbers and rates of acute decompensated heart failure (ADHF) hospitalization are c
108 ure), 7,141 patients hospitalized with acute decompensated heart failure (ADHF) were randomized to re
109 d volume overload are the hallmarks of acute decompensated heart failure (ADHF), and loop diuretics h
114 e a context for Acute Study of Nesiritide in Decompensated Heart Failure (ASCEND-HF) trial, we design
115 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND-HF), we assessed fac
116 E-AHF) and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trials during h
117 ic Optimization Strategy Evaluation in Acute Decompensated Heart Failure (DOSE-AHF) and Cardiorenal R
118 ospective consecutive patients with advanced decompensated heart failure (ejection fraction < or =30%
120 ltrafiltration (SCUF) in patients with acute decompensated heart failure (HF) refractory to intensive
121 xtracorporeal membrane oxygenation for acute decompensated heart failure (i.e., cardiogenic shock com
122 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure [ASCEND-HF]; NCT00475852).
123 ined tachyarrhythmia (atrial/ventricular) or decompensated heart failure admission/transplantation/de
125 al function during hospitalization for acute decompensated heart failure and associated outcomes.
126 HF) trials during hospitalization with acute decompensated heart failure and clinical congestion.
127 is a primary therapeutic objective in acute decompensated heart failure and commonly monitored with
128 tal of 40 consecutive patients with advanced decompensated heart failure and CRT implanted >3 months,
129 tal practice patterns of NIPPV use for acute decompensated heart failure and their relationship with
130 d arginine metabolism in patients with acute decompensated heart failure and to explore possible mech
131 s admitted to a single institution for acute decompensated heart failure and treated with UF: HFLEF (
132 fylline for Patients Hospitalized with Acute Decompensated Heart Failure and Volume Overload to Asses
133 fylline for Patients Hospitalized with Acute Decompensated Heart Failure and Volume Overload to Asses
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 nificantly associated with increased risk of decompensated heart failure and/or development of clinic
137 of hypotension while hospitalized with acute decompensated heart failure are not well understood.
138 e transition from compensated hypertrophy to decompensated heart failure as a result of reduced phosp
139 , and unplanned clinic visits to treat acute decompensated heart failure based on the blinded adjudic
140 in the management of low output syndrome and decompensated heart failure but their effect on mortalit
141 ty of ultrafiltration in patients with acute decompensated heart failure complicated by persistent co
143 e, hemoconcentration during the treatment of decompensated heart failure has been associated with red
144 anagement strategy for patients with acutely decompensated heart failure has been limited to the use
145 tion of chronic oral medication during acute decompensated heart failure hospitalization may not be a
146 xtracorporeal membrane oxygenation for acute decompensated heart failure in our ICU (67% of them had
147 prevents the transition from compensated to decompensated heart failure in part via upregulation of
148 technology for inpatient management of acute decompensated heart failure in patients with volume over
149 mass spectrometry in subjects with advanced decompensated heart failure in the intensive care unit (
151 association between air pollution and acute decompensated heart failure including hospitalisation an
153 Hypotension while hospitalized for acute decompensated heart failure is an independent risk facto
154 SBP reduction) during the treatment of acute decompensated heart failure is strongly and independentl
157 h heart failure without CRT-D from the Acute Decompensated Heart Failure National Registry (ADHERE) h
159 re National Registry-United States and Acute Decompensated Heart Failure National Registry-Internatio
160 re National Registry-United States and Acute Decompensated Heart Failure National Registry-Internatio
161 amined 196 770 AHF admissions from the Acute Decompensated Heart Failure National Registry-United Sta
163 ped from 3 clinical databases (ADHERE [Acute Decompensated Heart Failure National Registry], EFFECT s
166 l arrhythmias in this population can lead to decompensated heart failure or thromboembolism and thera
167 gen/creatinine ratio (BUN/Cr) could identify decompensated heart failure patients likely to experienc
168 was then prospectively validated in 50 acute decompensated heart failure patients using meticulously
169 is population with outcomes similar to acute decompensated heart failure patients with low left ventr
171 with greater iBNP levels (Registry for Acute Decompensated Heart Failure Patients; NCT00366639).
172 Therapy During Hospital Admission for Acute Decompensated Heart Failure Reduce Mortality and Readmis
174 d trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide admini
175 rt study of 218 patients admitted with acute decompensated heart failure to the Nashville VA Medical
176 oral neurohormonal antagonists during acute decompensated heart failure treatment negatively influen
178 ventilation (NIPPV) for patients with acute decompensated heart failure was introduced almost 20 yea
179 ents hospitalized for the treatment of acute decompensated heart failure will experience significant
180 ients >/=55 years of age admitted with acute decompensated heart failure with preserved ejection frac
181 mong hospitals in the use of NIPPV for acute decompensated heart failure without evidence for differe
182 y of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure) trial randomized 7,141 hosp
183 Pressure Measurements in Patients With Acute Decompensated Heart Failure) was a single-center prospec
184 of Clinical Effectiveness of Nesiritide and Decompensated Heart Failure), 7,141 patients hospitalize
186 xtracorporeal membrane oxygenation for acute decompensated heart failure, 1-year survival was 42%, bu
188 s, the hypertrophic response can evolve into decompensated heart failure, although the mechanism(s) u
189 infarction, nonfatal stroke, nonfatal acute decompensated heart failure, and death from cardiovascul
190 patients (acute myocardial infarction, acute decompensated heart failure, biventricular failure, and
191 component of therapy for patients with acute decompensated heart failure, but there are few prospecti
192 should be considered for patients with acute decompensated heart failure, but timing of implantation
193 outcome of hospitalization for management of decompensated heart failure, initiation of mechanical ci
194 arginine metabolism was observed in advanced decompensated heart failure, particularly with pulmonary
196 least 40 years and hospitalization for acute decompensated heart failure, severe systemic infection w
197 r arrhythmias in this population can lead to decompensated heart failure, syncope, and sudden cardiac
199 al involving patients hospitalized for acute decompensated heart failure, worsened renal function, an
200 assigned a total of 188 patients with acute decompensated heart failure, worsened renal function, an
230 ortality in patients hospitalized with acute decompensated heart failure: 4 HF-specific mortality pre
232 he myocardium; in fact, cell therapy for the decompensated heart has to be based on the acquisition o
235 rom 63 consecutive adult patients with acute decompensated HF admitted to the Heart Failure Intensive
236 mic NaNO2 infusion that may be beneficial in decompensated HF and warrants further evaluation with lo
237 The chance-corrected agreement between acute decompensated HF by physician reviewer panel and the aut
238 n=7534 weighted) events classified as acute decompensated HF by the automated algorithm, and 1748 (6
239 As a group, patients who did not have acute decompensated HF events had no significant changes in eP
242 locker therapy in patients hospitalized with decompensated HF is associated with lower post-discharge
244 r experience, SCUF after admission for acute decompensated HF refractory to standard medical therapy
245 fulness of early SCUF in patients with acute decompensated HF to improve fluid overload and hemodynam
246 the impact of in-hospital guidance for acute decompensated HF treatment by a predefined NT-proBNP tar
247 ptide)-guided therapy in patients with acute decompensated HF using a relative NT-proBNP target has n
248 proBNP-guided therapy of patients with acute decompensated HF using a relative NT-proBNP target would
250 ance of troponin elevation in the setting of decompensated HF with preserved ejection fraction (HFpEF
252 heart will progress into a state of chronic decompensated HF, and the hyperactive ANS will continue
255 events: cardiovascular death, admission for decompensated HF, or clinical HF decompensation requirin
256 e cohorts of patients with chronic and acute decompensated HF, repeated measurements of galectin-3 le
257 In SHF and DHF patients who developed acute decompensated HF, these events were associated with a si
260 ws comparative assessment of compensated and decompensated (HF) forms of cardiac hypertrophy because
261 registry participants who were admitted for decompensated HFpEF (ejection fraction >/=50%) from Janu
262 oponin elevation among patients with acutely decompensated HFpEF is associated with worse in-hospital
263 ement of troponin levels among patients with decompensated HFpEF may be useful for risk stratificatio
265 Using multicenter study data in hospitalized decompensated infected cirrhosis patients, I-ACLF define
267 The recipient was a 51-year-old man with decompensated liver cirrhosis and hepatocellular carcino
268 early stratify patients with compensated and decompensated liver cirrhosis in two groups with complet
269 dictor of mortality in patients with acutely decompensated liver cirrhosis, though determining CysC a
270 al hemorrhage can be the dominant symptom of decompensated liver cirrhosis, varices and ulcerations i
271 ransplantation may be required in those with decompensated liver disease or HCC, but experience is li
272 offers life-saving therapy for patients with decompensated liver disease or T2 hepatocellular carcino
273 ons, presence of varices, and the absence of decompensated liver disease were associated with a highe
275 infection in reducing the risk of cirrhosis, decompensated liver disease, and hepatocellular carcinom
276 ikelihood of SVR; age, sex, body mass index, decompensated liver disease, diabetes, genotype 1 subtyp
277 titis B virus or HIV infection), evidence of decompensated liver disease, or a history of hepatocellu
280 ed complications (e.g., fulminant hepatitis, decompensated liver, and hepatocellular carcinoma) were
284 ation with low procedure mortality, bridging decompensated patients to permanent LVAD or heart transp
287 d SMV with or without RBV in compensated and decompensated patients with cirrhosis with HCV GT1 infec
289 An elevated admission BUN/Cr identifies decompensated patients with heart failure likely to expe
292 th compensated RV hypertrophy, patients with decompensated RV failure had decreased miR-126 expressio
293 el resulted to a short microRNA signature of decompensated RV failure, which included the myocardium-
295 sues from rats with normal, compensated, and decompensated RV hypertrophy, carefully defined based on
298 ccurred at 2 weeks in patients with recently decompensated systolic HF treated with anakinra, whereas
299 sment after in-hospital therapy for advanced decompensated systolic HF, allowing clinicians to focus
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