ライフサイエンスコーパス: postinfarction

1 fraction do not change after the first week postinfarction.

2 h infarct size, and is detected even 3 weeks postinfarction.

3 Patient subgroups with severe postinfarction angina or a strongly positive exercise to

4 Unstable angina or postinfarction angina was present in 83% of patients bef

5 udy in which 4,098 patients with unstable or postinfarction angina were randomized to receive either

6 rest angina within 48 h of presentation; C = postinfarction angina; and c = angina refractory to maxi

7 ging was then confirmed in a canine model of postinfarction angiogenesis.

8 f long-term SCS on ventricular function in a postinfarction canine heart failure model.

9 1-MMP as a key MMP responsible for effecting postinfarction cardiac ECM remodeling and cardiac dysfun

10 monstrate a specific causal role for GRK2 in postinfarction cardiac remodeling and heart failure and

11 Postinfarction cardiac repair is regulated through timel

12 m 24 patients (mean age 69 +/- 9 years) with postinfarction cardiomyopathy (ejection fraction 33 +/-

13 Substrate mapping in patients with postinfarction cardiomyopathy and VT may involve lowerin

14 ith acute infarcts, 20 hearts with end-stage postinfarction cardiomyopathy, and 12 control hearts.

15 voltage on an electroanatomic voltage map in postinfarction cardiomyopathy.

16 cDNA rescued heart failure in a rat model of postinfarction cardiomyopathy.

17 Using a rat postinfarction chronic heart failure model, we compared

18 Among patients with postinfarction chronic heart failure, shock wave-facilit

19 subsequently improve cardiac performance of postinfarction chronic heart failure.

20 apy was capable of improving function of the postinfarction chronically failing heart, there was late

21 tion modulated the local inflammation in the postinfarction chronically failing myocardium, particula

22 mic (but not nonarrhythmic) death in a large postinfarction cohort.

23 obstruction remained a prognostic marker of postinfarction complications (chi2 = 5.17, P<.05).

24 rse functional recovery and a higher risk of postinfarction complications.

25 At postinfarction day 2, eight sheep were randomized to the

26 ther with myocardial regeneration attenuated postinfarction dilated myopathy, reduced infarct size an

27 multivariable regression analysis of 1-week postinfarction end-systolic volume index, regional left

28 a promising option in patients with chronic postinfarction heart failure (ischemic cardiomyopathy [I

29 proves in vivo cardiac function in rats with postinfarction heart failure (MI).

30 uclear cells (BMCs) in patients with chronic postinfarction heart failure may be attributed to impair

31 ventricular myocytes from rats with chronic postinfarction heart failure.

32 systolic [Ca2+]i in myocytes from rats with postinfarction heart failure.

33 erve is depressed in myocytes from rats with postinfarction heart failure.

34 n left ventricular (LV) diastolic filling in postinfarction heart failure.

35 administration can alter the progression of postinfarction heart failure.

36 rotegerin were confirmed in a mouse model of postinfarction heart failure.

37 ponse may hold promise for the prevention of postinfarction heart failure.

38 fects of HGF gene transfer in a rat model of postinfarction heart failure.

39 rphic ventricular tachycardia (SMVT), in the postinfarction heart, generally considered secondary to

40 ul to identify arrhythmogenic regions in the postinfarction heart.

41 HODS AND CgA processing was characterized in postinfarction HF mice and in patients with acute HF, an

42 acquired previously at 1, 2, 3, and 6 weeks postinfarction in a rat ligation model.

43 identification of patients with uncontrolled postinfarction inflammation and defective cardiac repair

44 kine receptor 5 (CCR5) prevents uncontrolled postinfarction inflammation and protects from adverse re

45 Here, we investigated the role of CD73 in postinfarction inflammation, cardiac repair, and remodel

46 of immune pathways, impaired suppression of postinfarction inflammation, perturbed spatial containme

47 CCR5-mediated Treg recruitment may restrain postinfarction inflammation, preventing excessive matrix

48 tions may play an active role in restraining postinfarction inflammation.

49 IL-1 is critically involved in the postinfarction inflammatory reaction and mediates advers

50 signaling is important for resolution of the postinfarction inflammatory reaction and regulates fibro

51 In summary, the postinfarction inflammatory response and resultant repai

52 entuation, prolongation, or expansion of the postinfarction inflammatory response results in worse re

53 infarcts and plays a role in suppressing the postinfarction inflammatory response, inhibiting local a

54 F-beta, suggesting an enhanced and prolonged postinfarction inflammatory response.

55 Using a swine model of postinfarction left ventricle (LV) remodeling, we invest

56 er ligation, nontransgenic HF mice exhibited postinfarction left ventricular (LV) remodeling and dysf

57 terogeneity and bioenergetic consequences of postinfarction left ventricular (LV) remodeling and the

58 Postinfarction left ventricular remodeling (LVR) is asso

59 r mass have provided important insights into postinfarction left ventricular remodeling, it has not b

60 exciting treatment option for patients with postinfarction left ventricular remodeling.

61 Mean aortic pressure improved from postinfarction levels but did not return to normal.

62 +AT(1) blockade shows promise in attenuating postinfarction LV remodeling but was not clearly superio

63 y of myocardial bioenergetics in hearts with postinfarction LV remodeling can be alleviated by the hE

64 Altered LV architecture and function during postinfarction LV remodeling provide an important substr

65 ly, in vivo treatment with CORM-3 alleviated postinfarction LV remodeling, p53 expression, and apopto

66 Heart failure development in postinfarction mice was associated with progressive t-tu

67 Postinfarction MO occurs because prolonged ischemia prod

68 ir combination in a well-characterized ovine postinfarction model.

69 Postinfarction mortality was not significantly different

70 n fraction and may be associated with higher postinfarction mortality.

71 cell therapy may be an attractive source for postinfarction myocardial repair and regeneration.

72 aging of fibrosis in a mouse model of healed postinfarction myocardial scarring.

73 rrhythmic death and other-cause mortality in postinfarction patients in the Cardiac Arrhythmic Suppre

74 Although the overall mortality in postinfarction patients presenting with hemodynamically

75 We studied 13 consecutive postinfarction patients undergoing MDCT before ablation.

76 in reduced clinical events in revascularized postinfarction patients with average cholesterol levels.

77 antial reduction in mortality with an ICD in postinfarction patients with depressed ejection fraction

78 d indications for prophylactic use of ICD in postinfarction patients with ejection fraction of 30% or

79 In postinfarction patients with severe left ventricular dys

80 Postinfarction patients with severe left ventricular dys

81 sk for recurrent coronary events in diabetic postinfarction patients, but not in nondiabetic postinfa

82 In postinfarction patients, elevated IgG aCL and low IgM aC

83 tinfarction patients, but not in nondiabetic postinfarction patients, supportive of an important role

84 recurrent coronary event risk among diabetic postinfarction patients, we investigated a function-alte

85 with the risk of recurrent cardiac events in postinfarction patients.

86 ndependently to recurrent coronary events in postinfarction patients.

87 tions and ambient particle concentrations in postinfarction patients.

88 state of knowledge regarding ICD therapy in postinfarction patients.

89 ary and secondary prevention of mortality in postinfarction patients.

90 a potent and independent risk stratifier in postinfarction patients.

91 se that neurohumoral activation early in the postinfarction period triggers a series of specific infl

92 been established, particularly in the early postinfarction period when regional myocardial perfusion

93 ry normalized S100A1 protein expression in a postinfarction rat heart failure model and reversed cont

94 e the electrophysiological properties of the postinfarction reentrant VT circuit.

95 In postinfarction reentrant VT, conduction velocities are s

96 ronary artery ligation prevented maladaptive postinfarction remodeling and preserved betaAR responsiv

97 for Gal-1 in normal cardiac homeostasis and postinfarction remodeling by preventing cardiac inflamma

98 TSP-1-/- animals had more extensive postinfarction remodeling than wild-type mice, although

99 itochondrial membrane proteins occurs during postinfarction remodeling, and 2) successful myocardial

100 Postinfarction remodeling, including increased intranoda

101 involve contiguous normal myocardium during postinfarction remodeling.

102 urgitation is a consequence, not a cause, of postinfarction remodeling; infarct expansion is the more

103 We hypothesized that IL-1 may regulate postinfarction repair and remodeling through cell-specif

104 growth factor signaling critically regulates postinfarction repair.

105 ks after starting ginseng treatment (8 weeks postinfarction) revealed nearly complete reversibility o

106 not explained by imbalances in predictors of postinfarction risk or therapy other than aspirin (Cox h

107 This study evaluates a novel method for postinfarction risk stratification based on frequency-do

108 201Tl imaging has been widely used for postinfarction risk stratification.

109 tic fibers in myocardial infarction (MI) and postinfarction scar remodeling.

110 otential for noninvasive characterization of postinfarction scar remodeling.

111 Fifty minutes after EP-3533 injection, the postinfarction scar tissue samples, as compared with the

112 image enhancement kinetic properties of the postinfarction scar, normal myocardium, and blood were c

113 for gadopentetate dimeglumine in regions of postinfarction scarring (mean, 194.8 minutes +/-116.8 [s

114 ogenic Factors and Recurrent Coronary Events postinfarction study.

115 ce exhibited significantly (P<0.05) improved postinfarction survival (94% versus 57%) and less LV dil

116 Compared with WT HF, 4-week postinfarction survival was significantly improved in bo

117 indicator of the extent of viable myocardium postinfarction than contractile reserve, especially in t

118 cardial infarction, and the role of standard postinfarction therapies in affected patients.

119 L-arginine, when added to standard postinfarction therapies, does not improve vascular stif

120 12 patients at 11+/-3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV t

121 Recent rest pain and refractory or postinfarction UA, or both, are strongly associated with

122 he infarcted pig model leads to reduction of postinfarction VAs and myocardial sympathetic effectors.

123 d bioenergetic abnormalities associated with postinfarction ventricular remodeling in a new, large an

124 Postinfarction ventricular remodeling is associated with

125 magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling.

126 Postinfarction ventricular septal defect carries a grim

127 Factors associated with death after postinfarction ventricular septal defect closure include

128 Postinfarction ventricular septal defect closure was att

129 Percutaneous closure of postinfarction ventricular septal defect is a reasonably

130 Catheter ablation of postinfarction ventricular tachycardia (VT) may be limit

131 n patients undergoing mapping procedures for postinfarction ventricular tachycardia (VT).

132 itical for the generation and maintenance of postinfarction ventricular tachycardia.

133 aged by MDCT and arrhythmogenic substrate in postinfarction ventricular tachycardia.

134 nonischemic cardiomyopathy, but the use for postinfarction ventricular tachycardias (VT) is less cle

135 Such heating might cure postinfarction VT more successfully and safely than pres

136 lation is potentially useful in >/=6% of the postinfarction VT population, but the number could be su

137 s has not been investigated in patients with postinfarction VT.

138 In patients with postinfarction VT; however, this procedure has been used

139 NRMI and CCP data set, mortality at 90 days postinfarction was similar among patients initially admi

140 ncy lesions in normal endocardial tissue and postinfarction zone can be visualized and quantified wit