ライフサイエンスコーパス: pulmonary congestion

1 ng and cardiomyocyte apoptosis and minimized pulmonary congestion.

2 intrathoracic impedance, which is related to pulmonary congestion.

3 uated TAC induced myocardial hypertrophy and pulmonary congestion.

4 when combined with near-threshold levels of pulmonary congestion.

5 en delivered during near-threshold levels of pulmonary congestion.

6 ted RAR responses to substance P and to mild pulmonary congestion.

7 le reversing cardiac remodeling and reducing pulmonary congestion.

8 hambers, which is associated with detectable pulmonary congestion.

9 preload and afterload, which in turn lead to pulmonary congestion.

10 th MI complicated by systolic dysfunction or pulmonary congestion.

11 hypoperfusion = 14 (3%), Group B = isolated pulmonary congestion = 32 (6%), Group C = isolated hypop

12 +/- 2.3vs 8.0 +/- 2.3 points, p = 0.59) and pulmonary congestion (82.5 vs 89.1%, p = 0.19), respecti

13 hmias, heart block, asystole, development of pulmonary congestion, acute mitral regurgitation and car

14 ), and clinical indices of disease severity (pulmonary congestion, aerobic capacity, and cardiovascul

15 We sought to evaluate the frequency of pulmonary congestion and associated clinical and hemodyn

16 cated by left ventricular dysfunction and/or pulmonary congestion and at least 1 risk-enhancing facto

17 ricular (LV) afterload in VA-ECLS can worsen pulmonary congestion and compromise myocardial recovery.

18 ic constriction, S2814A mice did not exhibit pulmonary congestion and had reduced levels of atrial na

19 implantation, possibly because of decreased pulmonary congestion and improved renal perfusion.

20 Changes in pulmonary congestion and volume assessment score were si

21 rcise, as well as worse cardiac dysfunction, pulmonary congestion, and biomarkers of cardiovascular r

22 ardiac hypertrophy, ventricular dysfunction, pulmonary congestion, and cardiac fibrosis after chronic

23 s with development of biventricular failure, pulmonary congestion, and death.

24 al signs, symptoms, radiographic evidence of pulmonary congestion, and echocardiographic evidence of

25 he increase in RAR activity produced by mild pulmonary congestion, and evokes an augmented response f

26 Lung ultrasound detects pulmonary congestion as B-lines at rest, and more freque

27 Such fluid retention can ultimately lead to pulmonary congestion, ascites or peripheral edema.

28 n, reduced exercise tolerance, and increased pulmonary congestion associated with cardiac lipid overl

29 Absence of pulmonary congestion at initial clinical evaluation does

30 had 141 adjudicated HF hospitalizations with pulmonary congestion at least 60 days after implantation

31 Detection of exercise-induced pulmonary congestion by lung ultrasound is an independen

32 ities in ventilatory control and efficiency, pulmonary congestion, capillary stress failure, and even

33 diography; however, whether exercise-induced pulmonary congestion carries prognostic implications is

34 KO mice showed reduced cardiac hypertrophy, pulmonary congestion, concentric LV wall thickness, LV d

35 Absence of pulmonary congestion detected by LUS implied a negative

36 zed that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from pre-clin

37 Virus infection is followed by intense pulmonary congestion due to an extensive influx of macro

38 Transient pulmonary congestion during exercise is emerging as an i

39 ften accompanied by RWMA, abnormal LVCR, and pulmonary congestion during stress, and shows independen

40 ant proportion of patients with shock had no pulmonary congestion (Group C = 28%, 95% CI, 24% to 31%)

41 ary, lung ultrasound can detect asymptomatic pulmonary congestion in hemodialysis patients, and the r

42 ngs support an energetic basis for transient pulmonary congestion in HFpEF.

43 ry proton density mapping revealed transient pulmonary congestion in patients with HFpEF (+4.4% [0.5,

44 Including the degree of pulmonary congestion in the model significantly improved

45 The prevalence of pulmonary congestion in the setting of CS is uncertain.

46 Pulmonary congestion increased at 30-day (OR: 3.86; 95%

47 Pulmonary congestion increased the 90-day odds of HF rea

48 here was further lung damage due to elevated pulmonary congestion, inflammatory cell infiltration, ir

49 Pulmonary congestion is highly prevalent and often asymp

50 s recommended as a first-line test to assess pulmonary congestion, it has never been tested in this s

51 ased carotid pressures, cardiac hypertrophy, pulmonary congestion, loss of baroreflex sensitivity (al

52 Secondary endpoints included a change in pulmonary congestion (lung ultrasound), loop diuretic ef

53 were divided into four groups: Group A = no pulmonary congestion/no hypoperfusion = 14 (3%), Group B

54 Moreover, absence of pulmonary congestion on LUS provided an excellent negati

55 atrial fibrillation, renal dysfunction, and pulmonary congestion on presentation (all P<0.001).

56 ce P augments the stimulatory effect of mild pulmonary congestion on RAR activity, most probably by e

57 (2) clinical pulmonary edema, (3) radiologic pulmonary congestion or edema, or (4) left ventricular s

58 ed by left ventricular systolic dysfunction, pulmonary congestion, or both and >=1 of 8 risk-augmenti

59 reduced left ventricular ejection fraction, pulmonary congestion, or both to receive either sacubitr

60 ed by left ventricular systolic dysfunction, pulmonary congestion, or both.

61 B-lines identify the pulmonary congestion phenotype at rest, and more frequen

62 n a neural network to identify cardiomegaly, pulmonary congestion, pleural effusion, pulmonary opacit

63 luding pneumonia, bronchospasm, atelectasis, pulmonary congestion, respiratory failure, pleural effus

64 th left ventricular systolic dysfunction and pulmonary congestion, sacubitril/valsartan-compared with

65 While CXR assessment for "pulmonary congestion" supports suspected-HF evaluation i

66 action (HFpEF) typically develop dyspnea and pulmonary congestion upon exercise.

67 m of atrial natriuretic peptide, may improve pulmonary congestion via vasodilation and enhanced diure

68 The development of exercise-induced pulmonary congestion was associated with lower phosphocr

69 Mild pulmonary congestion was produced by inflating a balloon

70 Near-threshold levels of pulmonary congestion were produced by increasing left at

71 ed serious adverse events: not transplanted- pulmonary congestion with epilepticus (likely not relate