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1 and global circumferential strain as well as myocardial damage.
2 red to be a sensitive marker of ischemia and myocardial damage.
3 s as safe as on-pump surgery and caused less myocardial damage.
4 w therapeutic target in the setting of acute myocardial damage.
5  Cardiac troponin-T is a sensitive marker of myocardial damage.
6 d as a strategy for cardiac repair following myocardial damage.
7 h acute coronary syndromes, independently of myocardial damage.
8 nhancement, they are associated with greater myocardial damage.
9  7 weeks, presumably because of irreversible myocardial damage.
10 s a stoichiometric relation to the extent of myocardial damage.
11  been routinely used in children at risk for myocardial damage.
12 of DCD HTX and correlated with the degree of myocardial damage.
13 ased cardiomyocyte apoptosis, and aggravated myocardial damage.
14 from follow-up CMR to established markers of myocardial damage.
15 target for the treatment of ischemia-induced myocardial damage.
16 eutic applications in patients with ischemic myocardial damage.
17 ning of the infarct-related artery may limit myocardial damage.
18 .01) strains but not ventricular function or myocardial damage.
19 vel is the cause or consequence of increased myocardial damage.
20  pHLIP-based binding does not require severe myocardial damage.
21 ion of the MVO zone, perfusion deficits, and myocardial damage.
22     Cardiac troponin (cTn) is a biomarker of myocardial damage.
23 ufficient for the regeneration and repair of myocardial damage.
24 available on its relationship to subclinical myocardial damage.
25 patients is not explained by more pronounced myocardial damage.
26 ients, which is not related to the extent of myocardial damage.
27 the nascent biological repair response after myocardial damage.
28 patients, indicating previously unrecognized myocardial damage.
29 (ALDH2) on chronic alcohol ingestion-induced myocardial damage.
30 onance (DE-CMR) can detect minute amounts of myocardial damage.
31 ion to genetic predisposition to progressive myocardial damage, a heritable susceptibility to viral i
32 e are hypoenhanced and correspond to greater myocardial damage acutely.
33 sed load or genetic cardiomyopathies, reduce myocardial damage after acute and chronic myocardial inf
34 es of LV function may not accurately reflect myocardial damage after acute myocardial infarction (MI)
35 cathelicidin, has shown efficacy in limiting myocardial damage after experimental ischemia in rodent
36 on of troponin I and HFABP indicate an early myocardial damage after femur fracture in pigs.
37 y contributing to cellular Ca2+ overload and myocardial damage after ischemia and reperfusion.
38                 Inclacumab appears to reduce myocardial damage after PCI in patients with non-ST-segm
39 ist ticagrelor completely reversed increased myocardial damage and adverse cardiac remodeling observe
40 tus on admission was associated with greater myocardial damage and an increased risk for major advers
41  acute liver failure, to detect unrecognized myocardial damage and as a marker of unfavorable outcome
42                             The reduction in myocardial damage and cellular infiltration was not sign
43 ure, low DBP was associated with subclinical myocardial damage and CHD events.
44  might have the intrinsic capacity to repair myocardial damage and completely recover cardiac functio
45 re protected from persistent immune-mediated myocardial damage and decline of cardiac function, likel
46  department, including patients with minimal myocardial damage and higher risk for short-term death a
47 OX-2 prolongs allograft survival and reduces myocardial damage and inflammation during acute cardiac
48 LV) function is sensitive in detecting early myocardial damage and may have prognostic implications i
49 ute inflammation is related to the extent of myocardial damage and may increase infarct size.
50 ial infarction (AMI) is common and increases myocardial damage and mortality.
51 d cTnT in children relate to the severity of myocardial damage and predict subsequent subclinical and
52 ses of anthracycline often lead to permanent myocardial damage and reduced functional reserve.
53  treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardia
54 n to evaluate the prognostic significance of myocardial damage and reperfusion injury is lacking.
55                   CMR can directly visualize myocardial damage and reperfusion injury, thereby provid
56            Hearts exposed to LOX showed more myocardial damage and showed poorer contractile performa
57 is likely critical for the prevention of the myocardial damage and subsequent remodeling observed in
58 sion may determine the eventual magnitude of myocardial damage and thus, patient prognosis after infa
59 rsus intravenous abciximab administration on myocardial damage and/or reperfusion injury.
60 ed isolated AS patients, and those with CAD, myocardial damage, and advanced comorbidities had the wo
61 ased inflammation, enhanced serum markers of myocardial damage, and an increased infiltration of infl
62  deterioration in cardiac activity, ischemic myocardial damage, and contractile dysfunction.
63 l disease, left ventricular function, recent myocardial damage, and female sex) factors.
64    Gross findings at autopsy revealed severe myocardial damage, and histopathological analysis reveal
65  cardiac function and hemodynamics, decrease myocardial damage, and reduce end-organ injury from prol
66 ted expression of pro-hypertrophic miR-208a, myocardial damage, and suppression of cardio-reparative
67 nized that reperfusion per se contributes to myocardial damage, and there is a great interest in iden
68  the left ventricular free wall, with little myocardial damage, and to differentiate into multinuclea
69 s mellitus to the development of subclinical myocardial damage are unclear.
70 reases in hs-cTnT, suggestive of progressive myocardial damage, are independently associated with inc
71 tion of cancer survivorship with subclinical myocardial damage, as assessed by elevated high-sensitiv
72 tion of cancer survivorship with subclinical myocardial damage, as assessed by elevated high-sensitiv
73 sociated with the development of subclinical myocardial damage, as assessed by hs-cTnT, and those per
74 iabetes mellitus status and hyperglycemia on myocardial damage assessed by cardiovascular magnetic re
75 unction is associated with reduction both in myocardial damage, assessed by creatine phosphokinase re
76       However, the mechanism and the type of myocardial damage associated with severe acute respirato
77 a have been reported about the occurrence of myocardial damage associated with transcatheter aortic v
78 ears to promote atherosclerosis and ischemic myocardial damage, but the results of epidemiological st
79 mpaired RV contractility is due to intrinsic myocardial damage by infundibular distortion, it is chro
80 s or older with Duchenne muscular dystrophy, myocardial damage by late gadolinium enhancement cardiac
81 tivation participates in neutrophil-mediated myocardial damage by regulating the expression of P-sele
82                    Furthermore, ameliorating myocardial damage by targeting TRAF3IP2 appears to be mo
83 roponin T (hs-cTnT), a marker of subclinical myocardial damage, can identify individuals at risk for
84 erruptions of precordial compression and the myocardial damage caused by delivery of repetitive and i
85  understanding of the presence and extent of myocardial damage caused by the coronavirus infection.
86 re, using different rodent models of diffuse myocardial damage causing acute heart failure, we show t
87 ction over the life of the animal results in myocardial damage characterized by cellular degeneration
88 n result in underestimation of the extent of myocardial damage compared with microscopy in animals su
89 valence of cardiac sarcoidosis or associated myocardial damage, defined by the presence of late gadol
90 direct perfusion through the laser channels, myocardial damage, denervation of ischemic myocardium an
91                                              Myocardial damage detected by DE-CMR appears to be assoc
92                                              Myocardial damage due to acute ST-segment elevation myoc
93 uld be exploited to quantify the severity of myocardial damage due to complement activation.
94 expression of hypoxia-sensitive proteins and myocardial damage due to ischemia alone.
95                                              Myocardial damage due to reperfusion of ischemic tissue
96  to evaluate inclacumab for the reduction of myocardial damage during a percutaneous coronary interve
97 conducted to determine whether the amount of myocardial damage during acute coronary syndromes (ACS)
98 creased T lymphocyte activation, and reduced myocardial damage during acute myocarditis in mice.
99 harmacological or genetic approaches reduces myocardial damage during hypoxia/reoxygenation in the pr
100  may represent therapeutic targets to reduce myocardial damage during ischemia, particularly in obese
101 be a useful, noninvasive means of minimizing myocardial damage during surgery, transplantation, or he
102 rct size measured by staining techniques and myocardial damage evaluated histologically were also sig
103 ntibody against PDGF receptor-alpha enhanced myocardial damage evidenced by serum cardiac troponin T
104 in an autocrine/paracrine manner to modulate myocardial damage from ER stresses, including ischemia.
105                             In secondary MR, myocardial damage from infarction or cardiomyopathy prod
106 rs during and contributes to the severity of myocardial damage from ischemic heart disease.
107 ur data suggest that the stress of extensive myocardial damage from longstanding hypertrophy may caus
108 ac myocytes plays a primary role in limiting myocardial damage from spreading to neighboring cardiac
109             The author proposes that initial myocardial damage from various mechanisms may lead to an
110 had the best outcome, those with CAD without myocardial damage had intermediate outcome equivalent to
111 f myocardial dysfunction before irreversible myocardial damage has occurred.
112 ory response is essential for minimizing the myocardial damage, healing, and scar formation.
113 VD risk factors in Africans: (a) subclinical myocardial damage (high-sensitivity troponin T (hs-cTnT)
114 re subclinical CVD risk involved subclinical-myocardial damage, hypercoagulability and increased infl
115 ied metabolite of alcohol, can contribute to myocardial damage impairing actin-myosin interaction and
116                               After ischemic myocardial damage in a rat model, transient regional AT1
117 on, yet the mechanistic effect of VA-ECMO on myocardial damage in acute myocardial infarction remains
118      Cardiac troponin-T sensitively reflects myocardial damage in children.
119 o assess the presence, nature, and extent of myocardial damage in hospitalized patients with troponin
120 ession can be a protective factor to prevent myocardial damage in human Chagas disease.
121 ent novel therapeutic approaches to decrease myocardial damage in I/R injury.
122 ADs may play an important role in preventing myocardial damage in OSAHS rabbit model.
123 erative atrial fibrillation or perioperative myocardial damage in patients undergoing elective cardia
124                          This study assessed myocardial damage in patients with chronic isolated mitr
125              Inflammation is a key factor of myocardial damage in reperfused ST-segment-elevation myo
126 g the relationship between hyperglycemia and myocardial damage in STEMI are scarce.
127             The excess burden of subclinical myocardial damage in this population might not be fully
128 we report a novel mechanism of Nrf2-mediated myocardial damage in type 1 diabetes (T1D).
129 protection by reducing inflammation-mediated myocardial damage including apoptosis after I/R injury i
130 yocardial ischemia can result in significant myocardial damage, including myocyte death, fibrosis, an
131 ngs of focal or diffuse myocardial edema and myocardial damage, including presence of late gadolinium
132 curacy a variety of prognostic indicators of myocardial damage, including regional myocardial dysfunc
133   In addition, cancer therapy can also cause myocardial damage, induce endothelial dysfunction, and a
134 acement fibrosis are the prevailing forms of myocardial damage induced by CAN.
135      As epicardial cell reactivation after a myocardial damage is linked with WT1 expression, the pre
136 on reperfused by primary PCI, CMR markers of myocardial damage (IS and especially MO) provide indepen
137                                     Although myocardial damage/loss remains an insurmountable problem
138 and the duration of survival, a low level of myocardial damage may ultimately be of more consequence
139   Thus, CXCR2 on blood cells is important in myocardial damage, most likely because of CXCR2-mediated
140  subclinical CVD risk related to subclinical myocardial damage, neurohormonal dysregulation, inflamma
141 rly diagnostics and AVR+CABG before ischemic myocardial damage occurs.
142                                These data on myocardial damage of transplanted hearts are consistent
143                                Patients with myocardial damage on DE-CMR had a 9-fold higher rate of
144                            All patients with myocardial damage on DE-CMR had coronary disease exclude
145 so independently associated with progressive myocardial damage on the basis of estimated annual chang
146     MicroRNA levels were not associated with myocardial damage or activation of inflammation.
147 atients with Duchenne muscular dystrophy and myocardial damage precedes decline in left ventricular s
148 ker that is closely related to the degree of myocardial damage, provides prognostic information, and
149 percutaneous coronary intervention minimizes myocardial damage, reduces infarct size, and decreases m
150 eft ventricular ejection fraction (LVEF) and myocardial damage remains unclear.
151 ed conduction system disease and endocardial/myocardial damage resulting in cardiomyopathy.
152                                              Myocardial damage results in tissue remodeling that, if
153                                              Myocardial damage scores were worse in the normothermic
154 ated with improved cardiac function, reduced myocardial damage, shock, lung injury and improved survi
155 icts different prognosticating components of myocardial damage such as edema, intramyocardial hemorrh
156 y provide better protection against ischemic myocardial damage than alpha-stat technique.
157 i-cTn antibodies that participate in ongoing myocardial damage that eventually results in heart failu
158               Complement activation mediates myocardial damage that occurs during ischemia and reperf
159        In patients who exhibited significant myocardial damage, the delivery of >/=50 million MultiSt
160 uld reduce cardiac complications by lowering myocardial damage, thereby reducing future deaths from c
161 phy and apoptosis and exacerbate ISO-induced myocardial damage through activation of STAT3 signaling
162  myocardial ischemia and reperfusion, causes myocardial damage through multiple processes.
163 nce of IL-21R may provide protection against myocardial damage, thus providing a new potential therap
164 er to myocardial inflammation and from acute myocardial damage to chronic ventricular dysfunction.
165 ted with MK-0159 show strong protection from myocardial damage upon cardiac I/R injury compared to th
166 examine the incidence and degree of ischemic myocardial damage using cardiac magnetic resonance imagi
167 mine the independent association of DBP with myocardial damage (using high-sensitivity cardiac tropon
168                             The reduction in myocardial damage was accompanied by reductions in LV si
169                              The increase in myocardial damage was smaller in pigs with double insult
170                                              Myocardial damage was studied by measuring troponin rele
171 thologic events occurring relatively late in myocardial damage, we have identified a potential means
172 d electrocardiographic evidence of permanent myocardial damage, were 2.7% and 3.0%, respectively, in
173 or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of
174 ave shown the ability to engraft in areas of myocardial damage, which suggests their use in cell tran

 
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