ライフサイエンスコーパス: subendocardium

1 ents, 163 (84%) were infarcts limited to the subendocardium.

2 ther than decrease neovascularization in the subendocardium.

3 iastolic perfusion time, particularly in the subendocardium.

4 se cases hyperenhancement was limited to the subendocardium.

5 urrent (INa) density in subepicardium versus subendocardium.

6 N2BA being present in larger amounts in the subendocardium.

7 0.05), with hypoperfusion most severe in the subendocardium.

8 tramural microcirculation, especially at the subendocardium.

9 is region and much more modestly in the deep subendocardium.

10 reatest reduction in the subendocardium (LAD subendocardium 0.28+/-0.02 versus 0.42+/-0.04 mL x g(-1)

11 07; midwall, 0.21+/-0.12 versus 0.10+/-0.11; subendocardium, -0.19+/-0.23 versus -0.11+/-0.16; P<0.05

12 n comparison with the normal remote regions (subendocardium: 0.80 +/- 0.06 versus 1.07 +/- 0.06 mL.mi

13 D/normal), which averaged 2.5 +/- 0.2 in the subendocardium, 1.9 +/- 0.2 in the midmyocardium, and 1.

14 /-1.9 vs. -1.8+/-1.0% for Err, p < 0.05) and subendocardium (-2.0+/-1.4 vs. 2.8+/-0.8%, 2.4+/-1.7 vs.

15 nificant increases in collagen volume in the subendocardium (5.2 +/- 1.4% versus 1.2 +/- 0.3%, P < .0

16 ubepicardium (20% depth), midwall (50%), and subendocardium (80%) in both regions were computed.

17 Among the six dogs that had their subendocardium ablated, reentrant wave fronts were prese

18 nce of reentry was not different between the subendocardium-ablated group versus the nonablated group

19 The subendocardium and mid-wall of the left ventricle (LV) p

20 Electric activation started at the apical subendocardium and showed significant delay in reaching

21 or MR imaging SI expressed as ratios between subendocardium and subepicardium (P = .40 and P = .46, r

22 ion of the dephosphorylated Cx43 in both the subendocardium and subepicardium layers.

23 ercent circumferential shortening within the subendocardium and subepicardium of infarcted and noninf

24 Preserved cell networks were observed in the subendocardium and subepicardium of the infarct.

25 re measured separately from left ventricular subendocardium and subepicardium, right ventricle, and p

26 rol region) were acquired selectively in the subendocardium and subepicardium.

27 ridamole 0.56 mg/kg) MBF and CVR in both the subendocardium and subepicardium.

28 l segment shortening was measured within the subendocardium and subepicardum of each region of HYPER

29 ubmitted to the highest wall stress, ie, the subendocardium, and (2) the proteasome system is require

30 myocardial perfusion in the subepicardium or subendocardium, and did not change expression of the ind

31 raphically subdivided into subepicardium and subendocardium, and microvessels (<500 microm in diamete

32 were found specifically in left ventricular subendocardium but not in left ventricular subepicardium

33 sions that unlike RFA are not limited to the subendocardium, but also eliminate viable myocardium sep

34 ous ventricular arrhythmias initiated in the subendocardium by a focal mechanism and conducted with a

35 ant mechanism, and 15 (42%) initiated in the subendocardium by a focal mechanism.

36 ell-coupled myocardium, EAD formation in the subendocardium can be the source of focal arrhythmias or

37 a lower Vmax in subepicardium compared with subendocardium cardiomyocytes, which was paralleled by a

38 Percent circumferential shortening in the subendocardium decreased by -13 +/- 5% in the control gr

39 bepicardium (EPI), mid myocardium (MID), and subendocardium (ENDO), respectively.

40 and exhibited a 2-component slow rise at the subendocardium in 3 failing hearts.

41 reaction, was higher in subepicardium versus subendocardium in both left and right ventricles, with l

42 inus action potential duration was longer at subendocardium in failing compared with nonfailing heart

43 CVR was more severely impaired in the subendocardium in patients with LVH attributable to seve

44 est action potentials were found in the deep subendocardium in wedge preparations isolated from the a

45 brosis and amyloid infiltration at the base, subendocardium, inferior wall, and septum more than the

46 weeks after MI, but the response within the subendocardium is not predictive.

47 ch layer, with the greatest reduction in the subendocardium (LAD subendocardium 0.28+/-0.02 versus 0.

48 ever, were greater in EXP versus CTRL in the subendocardium (lateral: -0.08+/-0.05 versus 0.02+/-0.14

49 circumflex regions (P<0.05) measured in the subendocardium, mid-wall, and subepicardium.

50 ells derived from the basal left ventricular subendocardium, midmyocardium, and subepicardium.

51 Twenty-one (58%) initiated in the subendocardium, midmyocardium, or epicardium by a macror

52 In the subendocardium of HC pigs, the intramyocardial density o

53 ted to the atrioventricular junction and the subendocardium of the ventricular septum.

54 e idiopathic cardiomyopathy can arise in the subendocardium or subepicardium by a focal mechanism.

55 ation of survival genes was more profound in subendocardium over subepicardium, reflecting that this

56 ificantly reduced (P < 0.05) in the ischemic subendocardium (PET = 1.12 +/- 0.45; microspheres = 1.09

57 +/- 0.5; P = 0.39) in comparison with remote subendocardium (PET = 1.7 +/- 0.62; microspheres = 1.64

58 s in discrete subsets of myocytes within the subendocardium rather than uniformly throughout the hear

59 , and 506+/-35 ms for the subepi-, mid-, and subendocardium, respectively, while reducing transmural

60 lcium transient relaxation was slower at the subendocardium than at the subepicardium in both groups.

61 ion in stress MBF was more pronounced in the subendocardium than subepicardium.

62 reticulum Ca(2+)-ATPase 2a was lower at the subendocardium than the subepicardium in both nonfailing

63 covered gelatinous fibers in the ventricular subendocardium that he thought were muscular.

64 This effect of PFA extended from the subendocardium through collagen and fat to the epicardia

65 s gradually from a right-handed helix in the subendocardium to a left-handed helix in the subepicardi

66 rs, which are oriented longitudinally in the subendocardium, transversely in the midmyocardium, and o

67 oseptum (versus anterolateral wall), and the subendocardium (versus subepicardium); P<0.05 for all.

68 culum Ca(2+)-ATPase 2a protein expression at subendocardium was lower in hearts with ischemic cardiom

69 The response of vessels to ADP from the subendocardium was significantly reduced in all groups c

70 oped hyperproliferative vascular foci in the subendocardium, which lacked microvascular organization

71 ding in LVH is reduced preferentially in the subendocardium with consequent attenuation of the action

72 have reduced perfusion, particularly in the subendocardium with greater reductions with LVH, storage

73 A is less uniform and largely limited to the subendocardium with minimal effect on viable myocardium