ライフサイエンスコーパス: LVEDP

1 LVEDP was elevated after L-NMMA and hemoglobin but reduc

2 LVEDP>18 and IMR>32 combined was associated with major a

3 lly established thresholds for IMR (>32) and LVEDP (>18 mm Hg) were predefined.

4 relationship between increases in [ADP] and LVEDP was found (r2=.66, P=.001).

5 erfusion caused a marked increase in CPP and LVEDP and a decrease in dLVP, indicating severe cardiac

6 ) prevented the reduction in +dP/dt, Ecs and LVEDP.

7 IMR and LVEDP in combination have incremental value for risk str

8 The clinical significance of IMR and LVEDP in combination is unknown.

9 IMR and LVEDP were both measured in 131 patients (mean age 59 10

10 IMR and LVEDP were prospectively measured in a prespecified subs

11 ing (201)Tl LHR was calculated manually, and LVEDP was obtained at catheterization.

12 iac output (340+/-20/880+/-40.3 mL/min), and LVEDP (11.3+/-2.2/0.3+/-2.9 mm Hg).

13 P) to systolic blood pressure (SBP): [(DBP - LVEDP)/SBP] x 100.

14 alysis of PFR, TPFR, and 1/3FR for detecting LVEDPs of >or=18 mm Hg showed areas under the curve of 0

15 cificity, and predictive power for detecting LVEDPs of >or=18 mm Hg.

16 lidocaine, blood pressure, HR, LVSP, dp/dt, LVEDP and ESPVR decreased in CHF rats whereas lidocaine

17 c volumes and further increased the elevated LVEDP, neither of which was seen in sham rats.

18 ertension, or arterial stiffening exacerbate LVEDP, allowing EF to remain normal even at high filling

19 The area under the curve for LVEDP during reperfusion was smaller in CP plus Ran vers

20 Area under the curve for LVEDP during the entire ischemic period was also smaller

21 s, it mitigated wall strain rise for a given LVEDP.

22 w LVEDP ( 18), 18 (14%) had low IMR and high LVEDP, 31 (24%) had high IMR and low LVEDP, while 29 (22

23 LVEDP, while 29 (22%) had high IMR and high LVEDP.

24 maintained <40 micromol/L, and no change in LVEDP was observed.

25 The increase in LVEDP was closely related to the increase in free [MgADP

26 l stiffness, or hypertension, could increase LVEDP into the HF range without reducing EF.

27 While elevated LV stiffness increased LVEDP and LV wall stress, it mitigated wall strain rise

28 ring demand ischemia when DCS had increased (LVEDP pretachycardia versus posttachycardia, 15+/-1 vers

29 ree patients (40%) had low IMR ( 32) and low LVEDP ( 18), 18 (14%) had low IMR and high LVEDP, 31 (24

30 nd high LVEDP, 31 (24%) had high IMR and low LVEDP, while 29 (22%) had high IMR and high LVEDP.

31 improved cardiac functions including LVESP, LVEDP, dp/dtmax, and - dp/dtmax.

32 veloped left ventricular pressure (dLVP=LVSP-LVEDP), ischemia-reperfusion caused a marked increase in

33 29 (interquartile range, 17-55), the median LVEDP was 17 mm Hg (interquartile range, 12-21), and the

34 The percent increase (from baseline) of LVEDP measured at the end of 30-minute reperfusion was s

35 eveloped cardiorenal model, sensitivities of LVEDP to potential contributing mechanisms of HFpEF, inc

36 d 2) for the secondary analysis mPAWP and/or LVEDP >11 mm Hg, representing the upper limit of normal.

37 FP: 1) for the primary analysis mPAWP and/or LVEDP >15 mm Hg, as recommended by the current pulmonary

38 vated left ventricle end diastolic pressure (LVEDP > 20mmHg).

39 in left ventricular end diastolic pressure (LVEDP) and 38% increase in the time constant of pressure

40 sed left ventricular end-diastolic pressure (LVEDP) and left ventricular end-diastolic volume (preloa

41 and left ventricular end-diastolic pressure (LVEDP) are acute, prognostic biomarkers in patients unde

42 of left ventricular end-diastolic pressure (LVEDP) by > or =20 mm Hg (ie, cardiac contracture).

43 of left ventricular end-diastolic pressure (LVEDP) in LVH during 2DG perfusion, and this increase wa

44 little effect on LV end-diastolic pressure (LVEDP) or the end-diastolic P-V relationship (EDPVR) in

45 and left ventricular end-diastolic pressure (LVEDP) to systolic blood pressure (SBP): [(DBP - LVEDP)/

46 LV end-diastolic pressure (LVEDP) was unchanged following PAB deflation.

47 and left ventricular end-diastolic pressure (LVEDP) were utilized for assessment of LVFP.

48 P), left ventricular end-diastolic pressure (LVEDP), and developed left ventricular pressure (dLVP=LV

49 d cardiac output, LV end-diastolic pressure (LVEDP), and peak LV pressure (LVPmax).

50 ced left ventricular end-diastolic pressure (LVEDP), but not left ventricular end-diastolic volume, c

51 g cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at LV pressure of 40 mm Hg

52 ted left ventricular end-diastolic pressure (LVEDP), which adds prognostic value in CAD.

53 HF (left ventricular end diastolic pressure (LVEDP): 6 +/- 1 versus 14 +/- 1 mmHg, respectively, P <

54 mic left ventricular end-diastolic pressure [LVEDP] increased 10 mm Hg, P<0.001, n=38).

55 ilat did not inhibit contractility or reduce LVEDP during dobutamine infusion.

56 Ran added to CP reduced LVEDP at the end of ischemia from 41+/-5 mm Hg in CP alo

57 , n=6) reduced DCS to pretachycardia values (LVEDP post-QSR, 15+/-1 mm Hg, P<0.001), ie, elicited a r

58 s was 50.6% (95% CI, 2.7-98.2; P=0.033) when LVEDP>18 was added to IMR>32.

59 d coronary flow reserve were associated with LVEDP/IMR group, as was hospitalization for heart failur

60 volume (r = 0.56, P = 0.031) correlated with LVEDP.

61 ftware showed a significant correlation with LVEDP.

62 PFR, and 1/3FR correlated significantly with LVEDP (r= -0.53, 0.45, and -0.45, respectively; P=0.0000