ライフサイエンスコーパス: atrial contraction

1 cardiac phases: midsystole, middiastole, and atrial contraction.

2 consistent with its positive impact on left atrial contraction.

3 ufficient to compensate for an impairment of atrial contraction.

4 eak velocity of pulmonary venous flow during atrial contraction.

5 cle when the foramen ovale was closed during atrial contraction.

6 ocated on atrial axial tubules that regulate atrial contraction.

7 k A wave velocity minus velocity at onset of atrial contraction]).

8 stole, and the shortest were obtained during atrial contraction (40% variation per cardiac cycle).

9 The mean depth was greater during atrial contraction (6.3 mm +/- 2.1) than in midsystole (

10 points of the waveform: point 1, peak of the atrial contraction (a wave); point 2, the left atrial pr

11 e Mlc2a gene resulted in severely diminished atrial contraction and consequent embryonic lethality at

12 ide important insight into the regulation of atrial contraction and describe potential therapeutic ta

13 ons and flow, and myh6 morphants, which lack atrial contraction and exhibit reduced flow.

14 , right ventricular pacing without preceding atrial contraction, and dual-chamber pacing at AV delays

15 les--in particular, reverse flow velocity at atrial contraction; and 5) increasing LA pressure result

16 s to understand how the processes regulating atrial contraction are remodelled during ageing and prov

17 ection within the venous waveform signifying atrial contraction] at or below baseline; DV no A).

18 ary veins and transmitral flow duration with atrial contraction correlated with LV filling pressure i

19 of E (initial peak velocity), A (velocity at atrial contraction), deceleration time (time from E velo

20 filling rates of the early filling phase and atrial contraction [E/A ratio]).

21 ract, and LV free wall, as well as premature atrial contractions, from the left atrial appendage at a

22 The difference between flow duration with atrial contraction in the pulmonary veins and transmitra

23 ak pulmonary venous reverse flow velocity at atrial contraction increased significantly, without bein

24 naling complex that may enhance the speed of atrial contraction independently of phospholamban regula

25 ned analysis of both flow velocity curves at atrial contraction is a reliable, feasible predictor of

26 These data suggest that organized atrial contraction is needed to maintain normal endocard

27 ection fraction (P=0.03), lower LA strain at atrial contraction (LASac; P<0.001), higher LAV (P<0.003

28 ) weak-atriumm58 mutant (wea) with inhibited atrial contraction leading to a highly undeveloped ventr

29 During atrial contraction, MVG was similarly low (P<0.01) in bo

30 e lengths, left atrial dimensions, premature atrial contraction (PAC) frequency, and atrial vulnerabi

31 al isolation was able to eliminate premature atrial contractions (PACs) and AF in six of 21 patients

32 nt SVT is initiated by spontaneous premature atrial contractions (PACs) and is terminated by spontane

33 Premature atrial contractions (PACs) are independent predictors of

34 Premature atrial contractions (PACs) play a critical role in AF pa

35 ed as the presence of either >/=30 premature atrial contractions (PACs)/hour daily or any runs of >/=

36 P < .001) and LA left atrium strain rate at atrial contraction peak ( SRA LA strain rate at atrial c

37 at atrial contraction peak LA strain rate at atrial contraction peak (beta coefficient -0.0028, P = .

38 0.0019, P = .016) and SRA LA strain rate at atrial contraction peak (beta coefficient = -0.0022, P =

39 ial contraction peak ( SRA LA strain rate at atrial contraction peak ) (-1.50 +/- 0.62 vs -1.78 +/- 0

40 0.0016, P = .027), and SRA LA strain rate at atrial contraction peak LA strain rate at atrial contrac

41 ), early diastolic (SRe), and late diastolic atrial contraction phases (SRa) were analyzed by dedicat

42 ed a linear relation with LA pressure before atrial contraction (r = 0.80, p < 0.005), confirming the

43 eaks 1 and 2) reflected rapid LV filling and atrial contraction, respectively.

44 ial peak atrial longitudinal strain and peak atrial contraction strain showed a similar, although non

45 bal peak atrial longitudinal strain and peak atrial contraction strain significantly decreased after

46 ing time indicated augmented contribution of atrial contraction toward LV filling (P<.05).

47 Peak left atrial contraction velocities (measured from the transmi

48 ximum LA volumes (VOLmax) and volumes before atrial contraction (VOLbac) were measured; LAPEF was cal

49 e time-velocity integral of each flow during atrial contraction was measured.

50 manometer catheter, and LA dP/dt(max) during atrial contraction was obtained.