ライフサイエンスコーパス: myocardial damage

1 Cardiac troponin-T is a sensitive marker of myocardial damage.

2 d as a strategy for cardiac repair following myocardial damage.

3 h acute coronary syndromes, independently of myocardial damage.

4 nhancement, they are associated with greater myocardial damage.

5 7 weeks, presumably because of irreversible myocardial damage.

6 s a stoichiometric relation to the extent of myocardial damage.

7 been routinely used in children at risk for myocardial damage.

8 vel is the cause or consequence of increased myocardial damage.

9 target for the treatment of ischemia-induced myocardial damage.

10 pHLIP-based binding does not require severe myocardial damage.

11 ion of the MVO zone, perfusion deficits, and myocardial damage.

12 Cardiac troponin (cTn) is a biomarker of myocardial damage.

13 ufficient for the regeneration and repair of myocardial damage.

14 available on its relationship to subclinical myocardial damage.

15 patients is not explained by more pronounced myocardial damage.

16 ients, which is not related to the extent of myocardial damage.

17 eutic applications in patients with ischemic myocardial damage.

18 the nascent biological repair response after myocardial damage.

19 ning of the infarct-related artery may limit myocardial damage.

20 patients, indicating previously unrecognized myocardial damage.

21 (ALDH2) on chronic alcohol ingestion-induced myocardial damage.

22 onance (DE-CMR) can detect minute amounts of myocardial damage.

23 red to be a sensitive marker of ischemia and myocardial damage.

24 s as safe as on-pump surgery and caused less myocardial damage.

25 w therapeutic target in the setting of acute myocardial damage.

26 e are hypoenhanced and correspond to greater myocardial damage acutely.

27 sed load or genetic cardiomyopathies, reduce myocardial damage after acute and chronic myocardial inf

28 es of LV function may not accurately reflect myocardial damage after acute myocardial infarction (MI)

29 cathelicidin, has shown efficacy in limiting myocardial damage after experimental ischemia in rodent

30 y contributing to cellular Ca2+ overload and myocardial damage after ischemia and reperfusion.

31 Inclacumab appears to reduce myocardial damage after PCI in patients with non-ST-segm

32 tus on admission was associated with greater myocardial damage and an increased risk for major advers

33 acute liver failure, to detect unrecognized myocardial damage and as a marker of unfavorable outcome

34 The reduction in myocardial damage and cellular infiltration was not sign

35 ure, low DBP was associated with subclinical myocardial damage and CHD events.

36 might have the intrinsic capacity to repair myocardial damage and completely recover cardiac functio

37 department, including patients with minimal myocardial damage and higher risk for short-term death a

38 OX-2 prolongs allograft survival and reduces myocardial damage and inflammation during acute cardiac

39 LV) function is sensitive in detecting early myocardial damage and may have prognostic implications i

40 ial infarction (AMI) is common and increases myocardial damage and mortality.

41 d cTnT in children relate to the severity of myocardial damage and predict subsequent subclinical and

42 ses of anthracycline often lead to permanent myocardial damage and reduced functional reserve.

43 treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardia

44 n to evaluate the prognostic significance of myocardial damage and reperfusion injury is lacking.

45 CMR can directly visualize myocardial damage and reperfusion injury, thereby provid

46 is likely critical for the prevention of the myocardial damage and subsequent remodeling observed in

47 sion may determine the eventual magnitude of myocardial damage and thus, patient prognosis after infa

48 rsus intravenous abciximab administration on myocardial damage and/or reperfusion injury.

49 ed isolated AS patients, and those with CAD, myocardial damage, and advanced comorbidities had the wo

50 ased inflammation, enhanced serum markers of myocardial damage, and an increased infiltration of infl

51 deterioration in cardiac activity, ischemic myocardial damage, and contractile dysfunction.

52 l disease, left ventricular function, recent myocardial damage, and female sex) factors.

53 Gross findings at autopsy revealed severe myocardial damage, and histopathological analysis reveal

54 cardiac function and hemodynamics, decrease myocardial damage, and reduce end-organ injury from prol

55 ted expression of pro-hypertrophic miR-208a, myocardial damage, and suppression of cardio-reparative

56 nized that reperfusion per se contributes to myocardial damage, and there is a great interest in iden

57 the left ventricular free wall, with little myocardial damage, and to differentiate into multinuclea

58 s mellitus to the development of subclinical myocardial damage are unclear.

59 reases in hs-cTnT, suggestive of progressive myocardial damage, are independently associated with inc

60 sociated with the development of subclinical myocardial damage, as assessed by hs-cTnT, and those per

61 iabetes mellitus status and hyperglycemia on myocardial damage assessed by cardiovascular magnetic re

62 unction is associated with reduction both in myocardial damage, assessed by creatine phosphokinase re

63 a have been reported about the occurrence of myocardial damage associated with transcatheter aortic v

64 ears to promote atherosclerosis and ischemic myocardial damage, but the results of epidemiological st

65 mpaired RV contractility is due to intrinsic myocardial damage by infundibular distortion, it is chro

66 s or older with Duchenne muscular dystrophy, myocardial damage by late gadolinium enhancement cardiac

67 tivation participates in neutrophil-mediated myocardial damage by regulating the expression of P-sele

68 Furthermore, ameliorating myocardial damage by targeting TRAF3IP2 appears to be mo

69 roponin T (hs-cTnT), a marker of subclinical myocardial damage, can identify individuals at risk for

70 erruptions of precordial compression and the myocardial damage caused by delivery of repetitive and i

71 re, using different rodent models of diffuse myocardial damage causing acute heart failure, we show t

72 ction over the life of the animal results in myocardial damage characterized by cellular degeneration

73 n result in underestimation of the extent of myocardial damage compared with microscopy in animals su

74 valence of cardiac sarcoidosis or associated myocardial damage, defined by the presence of late gadol

75 direct perfusion through the laser channels, myocardial damage, denervation of ischemic myocardium an

76 Myocardial damage detected by DE-CMR appears to be assoc

77 uld be exploited to quantify the severity of myocardial damage due to complement activation.

78 Myocardial damage due to reperfusion of ischemic tissue

79 to evaluate inclacumab for the reduction of myocardial damage during a percutaneous coronary interve

80 conducted to determine whether the amount of myocardial damage during acute coronary syndromes (ACS)

81 creased T lymphocyte activation, and reduced myocardial damage during acute myocarditis in mice.

82 harmacological or genetic approaches reduces myocardial damage during hypoxia/reoxygenation in the pr

83 may represent therapeutic targets to reduce myocardial damage during ischemia, particularly in obese

84 be a useful, noninvasive means of minimizing myocardial damage during surgery, transplantation, or he

85 rct size measured by staining techniques and myocardial damage evaluated histologically were also sig

86 ntibody against PDGF receptor-alpha enhanced myocardial damage evidenced by serum cardiac troponin T

87 in an autocrine/paracrine manner to modulate myocardial damage from ER stresses, including ischemia.

88 In secondary MR, myocardial damage from infarction or cardiomyopathy prod

89 rs during and contributes to the severity of myocardial damage from ischemic heart disease.

90 ur data suggest that the stress of extensive myocardial damage from longstanding hypertrophy may caus

91 ac myocytes plays a primary role in limiting myocardial damage from spreading to neighboring cardiac

92 The author proposes that initial myocardial damage from various mechanisms may lead to an

93 had the best outcome, those with CAD without myocardial damage had intermediate outcome equivalent to

94 After ischemic myocardial damage in a rat model, transient regional AT1

95 Cardiac troponin-T sensitively reflects myocardial damage in children.

96 ession can be a protective factor to prevent myocardial damage in human Chagas disease.

97 erative atrial fibrillation or perioperative myocardial damage in patients undergoing elective cardia

98 This study assessed myocardial damage in patients with chronic isolated mitr

99 g the relationship between hyperglycemia and myocardial damage in STEMI are scarce.

100 protection by reducing inflammation-mediated myocardial damage including apoptosis after I/R injury i

101 yocardial ischemia can result in significant myocardial damage, including myocyte death, fibrosis, an

102 curacy a variety of prognostic indicators of myocardial damage, including regional myocardial dysfunc

103 In addition, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and a

104 acement fibrosis are the prevailing forms of myocardial damage induced by CAN.

105 As epicardial cell reactivation after a myocardial damage is linked with WT1 expression, the pre

106 on reperfused by primary PCI, CMR markers of myocardial damage (IS and especially MO) provide indepen

107 Although myocardial damage/loss remains an insurmountable problem

108 and the duration of survival, a low level of myocardial damage may ultimately be of more consequence

109 Thus, CXCR2 on blood cells is important in myocardial damage, most likely because of CXCR2-mediated

110 rly diagnostics and AVR+CABG before ischemic myocardial damage occurs.

111 These data on myocardial damage of transplanted hearts are consistent

112 Patients with myocardial damage on DE-CMR had a 9-fold higher rate of

113 All patients with myocardial damage on DE-CMR had coronary disease exclude

114 so independently associated with progressive myocardial damage on the basis of estimated annual chang

115 MicroRNA levels were not associated with myocardial damage or activation of inflammation.

116 atients with Duchenne muscular dystrophy and myocardial damage precedes decline in left ventricular s

117 ker that is closely related to the degree of myocardial damage, provides prognostic information, and

118 percutaneous coronary intervention minimizes myocardial damage, reduces infarct size, and decreases m

119 ed conduction system disease and endocardial/myocardial damage resulting in cardiomyopathy.

120 Myocardial damage results in tissue remodeling that, if

121 Myocardial damage scores were worse in the normothermic

122 y provide better protection against ischemic myocardial damage than alpha-stat technique.

123 i-cTn antibodies that participate in ongoing myocardial damage that eventually results in heart failu

124 Complement activation mediates myocardial damage that occurs during ischemia and reperf

125 In patients who exhibited significant myocardial damage, the delivery of >/=50 million MultiSt

126 uld reduce cardiac complications by lowering myocardial damage, thereby reducing future deaths from c

127 myocardial ischemia and reperfusion, causes myocardial damage through multiple processes.

128 examine the incidence and degree of ischemic myocardial damage using cardiac magnetic resonance imagi

129 mine the independent association of DBP with myocardial damage (using high-sensitivity cardiac tropon

130 The reduction in myocardial damage was accompanied by reductions in LV si

131 The increase in myocardial damage was smaller in pigs with double insult

132 thologic events occurring relatively late in myocardial damage, we have identified a potential means

133 or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of

134 ave shown the ability to engraft in areas of myocardial damage, which suggests their use in cell tran