ライフサイエンスコーパス: myocardial necrosis

1 ay cause arterial thrombosis with consequent myocardial necrosis.

2 e platelet aggregation in the ventricles and myocardial necrosis.

3 present in 69 patients, and 41 of 69 showed myocardial necrosis.

4 ocardial staining to define area at risk and myocardial necrosis.

5 haracterized by microvascular thrombosis and myocardial necrosis.

6 between the extent of myocardium at risk and myocardial necrosis.

7 did not sensitize mice to radiation-induced myocardial necrosis.

8 differentiation of myocardial stunning from myocardial necrosis.

9 tal with acute coronary syndrome may signify myocardial necrosis.

10 gory of CABG and considered as high risk for myocardial necrosis.

11 ts anti-inflammatory activity or by reducing myocardial necrosis.

12 to the hospital who had no evidence of acute myocardial necrosis.

13 olinium enhancement identified the extent of myocardial necrosis.

14 ate postischemic ventricular arrhythmias and myocardial necrosis.

15 r reperfusion and increased infarct size and myocardial necrosis.

16 ar smooth muscle relaxant prevented onset of myocardial necrosis.

17 ltration occurs, occasionally accompanied by myocardial necrosis.

18 chloride (TTC) staining was used to identify myocardial necrosis.

19 chnique alone for identifying the absence of myocardial necrosis.

20 roke (3), or elevated troponin I, reflecting myocardial necrosis (25).

21 Moreover, inhibition of p38 MAPK attenuated myocardial necrosis after a prolonged reperfusion.

22 y was to assess the role of serum markers of myocardial necrosis after cardiac surgery.

23 o contribute to both cardiac dysfunction and myocardial necrosis after reperfusion of an ischemic hea

24 have reported elevated levels of markers of myocardial necrosis among critically ill patients, the a

25 nt modifications of tPA and TM, resulting in myocardial necrosis and depressed cardiac function.

26 rtum females by 6 months of age, when severe myocardial necrosis and fibrosis and extensive dystrophi

27 renal dysfunction, neurohumoral activation, myocardial necrosis and fibrosis biomarkers, and the sev

28 Likewise, myocardial necrosis and hepatic glycogen depletion with

29 less than 4.0 hours was critical in reducing myocardial necrosis and improving heart function and 30-

30 MR can predict subsequent risk of developing myocardial necrosis and may guide adjunctive prevention

31 ice and found that this results in extensive myocardial necrosis and systolic dysfunction.

32 latory perfusion as the basis to distinguish myocardial necrosis and viability in the post-infarct st

33 Location of septal reduction, extent of myocardial necrosis, and conduction system abnormalities

34 inant of reactive oxygen species generation, myocardial necrosis, and left ventricular function follo

35 reconditioning response would result in less myocardial necrosis as assessed by postprocedure creatin

36 atelet-driven inflammation by LIBS-MPIOs and myocardial necrosis by late gadolinium enhancement.

37 Myocardial necrosis can occur during percutaneous corona

38 duces superior platelet inhibition and lower myocardial necrosis compared with high-dose (600 mg) or

39 dels to significantly diminish the extent of myocardial necrosis consequent to coronary occlusion.

40 In patients without evidence of myocardial necrosis (defined as those who were negative

41 ts showed extensive endothelial cell damage, myocardial necrosis, fibrin deposition, and other signs

42 Myocardial necrosis/fibroplasia, fluid requirements, car

43 lar endothelial NO production and attenuates myocardial necrosis following ischemia and reperfusion i

44 rcellular adhesion molecule-1 also minimizes myocardial necrosis following ischemia and reperfusion.

45 requency energy is used to create a targeted myocardial necrosis for the treatment of various arrhyth

46 ase) lowering the threshold of detection for myocardial necrosis from 0.20 to 0.05 ng/mL with a sensi

47 vel at or above the decision limit for acute myocardial necrosis (> or = 0.03 ng/mL).

48 at risk for cardiac events in the absence of myocardial necrosis, highlighting its potential usefulne

49 In the absence of myocardial necrosis, I/R resulted in persistent fibrosis

50 vation prevents vascular renarrowing per se, myocardial necrosis impairs the clinical manifestation o

51 ch together may account for the expansion of myocardial necrosis in the setting of acute IR.

52 eads again to vascular dysfunction and acute myocardial necrosis, indicating that predilection for ca

53 ray of other myocardial processes that cause myocardial necrosis, infiltration, or fibrosis.

54 Because myocardial necrosis is associated with myocardial thinni

55 tal LV function and the transmural extent of myocardial necrosis is complex.

56 Myocardial necrosis is not a prerequisite for LV remodel

57 ologic basis for differential enhancement of myocardial necrosis is the greater distribution volume o

58 n of inflammatory activity and the extent of myocardial necrosis itself are of great clinical and pro

59 contractile dysfunction without significant myocardial necrosis (left ventricular pressure-volume cu

60 r computed tomography (MDCT) for quantifying myocardial necrosis, microvascular obstruction, and chro

61 cute coronary syndromes may be a response to myocardial necrosis or may reflect the inflammatory proc

62 anges in functional stenosis severity, acute myocardial necrosis, or fibrotic scar.

63 hemia-reperfusion also experienced increased myocardial necrosis (P<0.01 versus control diet), which

64 Inflammation and myocardial necrosis play important roles in ischemia/rep

65 10 min before R significantly inhibited the myocardial necrosis seen 4.5 h post-R compared with that

66 rades circulating catecholamines and reduces myocardial necrosis, suggesting that it may protect agai

67 (common in high-voltage electrical injury), myocardial necrosis, the level of central nervous system

68 te gadolinium enhancement was used to depict myocardial necrosis; these imaging experiments were also

69 Myocardial necrosis triggers an inflammatory reaction th

70 Histological and biochemical evidence of myocardial necrosis was absent in group 2.

71 Myocardial necrosis was assessed by measurements of card

72 h radionuclide ventriculography (n = 8), and myocardial necrosis was looked for with trichlorotetrazo

73 Myocardial necrosis was reduced by approximately 40% wit

74 he difference between myocardium at risk and myocardial necrosis, was associated with regional and gl

75 function, extent of myocardium at risk, and myocardial necrosis were quantified by cardiac magnetic

76 o-enzyme A (CoA) reductase inhibitor, limits myocardial necrosis when administered as an adjunct to r

77 f attenuated periprocedural inflammation and myocardial necrosis with a strategy of GP IIb/IIIa inhib

78 trategy (MMS) testing for several markers of myocardial necrosis with different time-to-positivity pr

79 Histopathology revealed myocardial necrosis with dystrophic calcification.

80 ials should ensure systematic evaluation for myocardial necrosis, with attention paid to multivariabl

81 lity and (2) the occurrence of perioperative myocardial necrosis would affect late regional wall moti