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1 ore and after TAVR for the assessment of new myocardial injury.
2 tients with type 2 myocardial infarction and myocardial injury.
3 sensitive and specific for the diagnosis of myocardial injury.
4 onset cardiotoxicity and areas of reversible myocardial injury.
5 the absence of clinical and cTnI evidence of myocardial injury.
6 p in knowledge of the repair mechanism after myocardial injury.
7 ) in individuals with no clinically manifest myocardial injury.
8 d not reduce the incidence of periprocedural myocardial injury.
9 nerative potency of transplanted sMSCs after myocardial injury.
10 eans of restoring cardiac function following myocardial injury.
11 onary reperfusion during an acute MI reduces myocardial injury.
12 rdiac troponin T was measured as a marker of myocardial injury.
13 process that increases adjacent to areas of myocardial injury.
14 f their high sensitivity and specificity for myocardial injury.
15 ia, hypothermia, cardioplegia, and traumatic myocardial injury.
16 lian myocardial homeostasis as well as after myocardial injury.
17 ation and role in cardiac regeneration after myocardial injury.
18 re frequently associated with prior or acute myocardial injury.
19 IK) reduces ischemia-related arrhythmias and myocardial injury.
20 rs, and used serum troponin T as an index of myocardial injury.
21 per prosthesis insertion are associated with myocardial injury.
22 g, including 15 (18%) with unsuspected acute myocardial injury.
23 e the area at risk in patients with ischemic myocardial injury.
24 ally identifies clinically unsuspected acute myocardial injury.
25 reflecting the occurrence of periprocedural myocardial injury.
26 -derived cells mediates cardiac repair after myocardial injury.
27 ty for biomarker and pathway discovery after myocardial injury.
28 ory activation occurs in nearly all forms of myocardial injury.
29 ute to arrhythmogenesis around the region of myocardial injury.
30 etaA and Fstl3 were upregulated in models of myocardial injury.
31 cted to function in pathways consistent with myocardial injury.
32 rtunity to establish metabolic signatures of myocardial injury.
33 hanisms to explain reduced vascular leak and myocardial injury.
34 iabetes, hypertension, atherothrombosis, and myocardial injury.
35 persisted regardless of statin use or recent myocardial injury.
36 rticipate in the response to the ISO-induced myocardial injury.
37 tissues and play a crucial role in repairing myocardial injury.
38 n location has been suggested to precipitate myocardial injury.
39 ocus on recent developments in biomarkers of myocardial injury.
40 apidly from the cardiomyocyte in response to myocardial injury.
41 treatment for repairing cardiac tissue after myocardial injury.
42 ventricular images at rest, suggesting prior myocardial injury.
43 ulation or have functional roles relevant to myocardial injury.
44 consequences of NOS1 deficiency in states of myocardial injury.
45 s, aortic valve calcification, and repair of myocardial injury.
46 r relative changes over time, indicate acute myocardial injury.
47 as been associated with a neurogenic form of myocardial injury.
48 the observed estrogen-mediated reduction in myocardial injury.
49 hancement MRI for assessment of irreversible myocardial injury.
50 s, aortic valve calcification, and repair of myocardial injury.
51 are confined to patients with ongoing minute myocardial injury.
52 hic cardiomyopathy, a human model of planned myocardial injury.
53 e and limit deleterious remodeling following myocardial injury.
54 er range of human proteins in the context of myocardial injury.
55 f sympathetic function, thereby resulting in myocardial injury.
56 diagnosis of acute myocardial infarction or myocardial injury.
57 ential to restore contractile function after myocardial injury.
58 pt to the increased mechanical demands after myocardial injury.
59 yocardium may represent a novel biosignal of myocardial injury.
60 or cardiac troponin T (cTnT), a biomarker of myocardial injury.
61 diated via mechanisms other than subclinical myocardial injury.
62 th skeletal muscle damage, rather than acute myocardial injury.
63 significantly improve recovery from ischemic myocardial injury.
64 and significance in the context of ischemic myocardial injury.
65 ted a protective effect of histamine against myocardial injury.
66 proach to promote cardiac regeneration after myocardial injury.
67 ce to chronic beta-adrenergic stress-induced myocardial injury.
68 lation could promote revascularization after myocardial injury.
69 nary blood flow and oxygen supply, and limit myocardial injury.
70 t were increased within 1 hour after planned myocardial injury, 29 were also elevated in patients wit
71 with type 2 myocardial infarction (62.5%) or myocardial injury (72.4%) compared with type 1 myocardia
73 22 (15%) of 145 patients who did not sustain myocardial injury (adjusted hazard ratio, 2.1; 95% confi
75 critical modifiers of anthracycline-related myocardial injury after HCT and creating targeted popula
77 etween these 9p21 variants and perioperative myocardial injury after isolated primary coronary artery
79 ioning (RIPost) will reduce the incidence of myocardial injury after PCI, and whether ischemic condit
81 fore, the different timing and mechanisms of myocardial injury among palliation strategies do not aff
82 emia on admission is associated with greater myocardial injury and an increased risk of major adverse
83 that Nlrp3 inflammasome activation preceded myocardial injury and apoptosis, corroborating a pathoge
85 gmented ischemic AMPK activation and reduced myocardial injury and cardiac contractile dysfunction af
86 identify patients at risk for postoperative myocardial injury and death, measuring cardiac troponin
91 uggests that immune mechanisms contribute to myocardial injury and fibrosis, leading to left ventricu
92 ctile apparatus, are sensitive indicators of myocardial injury and have become central to the diagnos
94 as to determine if biomarkers of subclinical myocardial injury and hemodynamic stress identify asympt
95 erived stem cells (BMC) to specific areas of myocardial injury and immunophenotypic conversion of BMC
98 Index (RDI), is associated with subclinical myocardial injury and increased myocardial wall stress.
99 lly elevated serum cardiac troponin reflects myocardial injury and is associated with increased morta
100 to differentiate reversible and irreversible myocardial injury and its predictive value for left vent
101 le to EMCV infection and develop significant myocardial injury and left ventricular dysfunction.
102 yme B activity can visualize T cell-mediated myocardial injury and monitor the response to an anti-in
103 o cell application, hs-TnT levels to measure myocardial injury and NT-proBNP levels as marker of left
104 ne groups, with reduced levels of markers of myocardial injury and oxidative stress in doxycycline-tr
105 for damage control and tissue remodeling on myocardial injury and principal mediators of pathologica
107 of absolute radiotracer uptake in a model of myocardial injury and should permit quantitative serial
108 Elevation of hsTnT identifies patients with myocardial injury and significant structural heart disea
110 acute coronary syndromes can still result in myocardial injury and subsequent myocardial infarction (
111 t we believe is a novel target for CaMKII in myocardial injury and suggest that CaMKII is broadly imp
112 etabolic profiling in the early detection of myocardial injury and suggest that similar approaches ma
113 ongitudinal association between increases in myocardial injury and the biology of collagen synthesis
114 ction but without hypoxia may increase early myocardial injury and was associated with larger myocard
115 adaptive response to haemodynamic stress or myocardial injury, and allows the heart to meet an incre
117 g differentiates reversible and irreversible myocardial injury, and it is a strong predictor of left
118 d to define the time course of inflammation, myocardial injury, and prothrombotic markers after radio
121 us studies suggesting a possible increase in myocardial injury as a result of coronary vasoconstricti
122 ned with hypothermia suggested a less severe myocardial injury as demonstrated by the significantly r
123 TAVR population demonstrated some degree of myocardial injury as determined by a rise in CK-MB level
124 diography or computed tomography, as well as myocardial injury as indicated by a positive test for ca
126 ative reversible (stunning) and irreversible myocardial injury, as assessed by cardiovascular MRI (CM
127 ermine the predictive value of postoperative myocardial injury, as measured by troponin elevation, on
128 known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategi
129 sequelae of CO poisoning are frequent, with myocardial injury assessed by biomarkers or ECG in 37% o
130 or the secondary end points of perioperative myocardial injury (assessed on the basis of the area und
131 sing CcO activity modulators for controlling myocardial injury associated with ischemia and oxidative
132 poplastic left heart syndrome pose a risk of myocardial injury at different times and through differe
133 inflammatory response during wound healing, myocardial injury, atherosclerosis and autoimmune disord
134 suggesting that hyperglycemia contributes to myocardial injury beyond its effects on development of c
136 or the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abunda
137 pproach for restoring cardiac function after myocardial injury, but the technique thus far has been s
139 s genetic manipulation reduced virus-induced myocardial injury by 40 to 60% and dramatically improved
140 ative stress triggered by inflammation after myocardial injury by expressing potent antioxidant defen
141 early inflammatory repair response to acute myocardial injury by facilitating cardiac leukocyte infi
142 l adipose tissue formation in the context of myocardial injury by redirecting the fate of Wt1(+) line
145 ansient and benign electrographic changes to myocardial injury, cardiomyopathy, and even cardiac deat
146 trate and nitrite supplementation alleviates myocardial injury caused by ischemia-reperfusion and car
147 Phosphodiesterase 5 (PDE5) inhibitors limit myocardial injury caused by stresses, including doxorubi
148 ins were validated in an independent planned myocardial injury cohort (n=15; P<1.33E-04, 1-way repeat
150 eleased from the liver and adipose tissue in myocardial injury, contributing to myocardial protection
153 d segmental myocardial strain and markers of myocardial injury could improve the accuracy of late gad
155 pression and minimizing electrically induced myocardial injury due to repetitive high-current shocks.
156 2 and Nox4 in mediating oxidative stress and myocardial injury during I/R using loss-of-function mous
157 fect of GSK-3beta activation/inhibition upon myocardial injury during prolonged ischemia and I/R.
158 nger isoform-1 (NHE-1) inhibition attenuates myocardial injury during resuscitation from ventricular
159 p < .05).CONCLUSIONS: Zoniporide ameliorated myocardial injury during resuscitation from ventricular
160 usion has the capability of further reducing myocardial injury during ST-segment-elevation myocardial
162 imaging technique allowing the assessment of myocardial injury early after ST-segment-elevation myoca
163 t hearts before, during and after controlled myocardial injury ensured enrichment for candidate bioma
164 vels revealed the presence of ongoing minute myocardial injury even in patients with stable ICM.
165 ndently associated with the risk of ischemic myocardial injury following elective PCI with clopidogre
166 reported that TLR4(-/-) mice show decreased myocardial injury following I/R; however, the protective
168 enuation of both neutrophil accumulation and myocardial injury following myocardial ischemia and repe
170 uripotent stem cells as cellular therapy for myocardial injury has yet to be examined in a large-anim
171 atients with type 2 myocardial infarction or myocardial injury have a similar crude rate of major adv
172 n those with type 2 myocardial infarction or myocardial injury (hazard ratio, 1.71; 95% confidence in
173 inical risk factors have evidence of ongoing myocardial injury, hemodynamic stress, or systemic infla
174 increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac tropo
176 oved cardiac performance in animal models of myocardial injury; however, the benefits observed in cli
177 yocardial infarction and homed to regions of myocardial injury; however, the myocardium contained onl
178 re the relation between thyroid function and myocardial injuries in idiopathic dilated cardiomyopathy
179 sis was type 1 or 2 myocardial infarction or myocardial injury in 1171 (55.2%), 429 (20.2%), and 522
180 8 MAP kinase inhibitor treatment after acute myocardial injury in 8- to 10-week-old rats increases ca
181 ificantly changed in the blood after planned myocardial injury in a derivation cohort (n=20; P<1.05E-
183 r studies; however, comprehensive studies of myocardial injury in acute respiratory distress syndrome
184 We hypothesized that TAT-NSF700 would limit myocardial injury in an in vivo murine model of myocardi
186 before ischemia or at reperfusion decreased myocardial injury in both nondiabetic and diabetic mice.
188 -inducible factor (HIF)-1alpha protects from myocardial injury in diabetic mice by increasing myocard
189 inhibitor LCZ696 may reduce this measure of myocardial injury in heart failure with preserved ejecti
190 complement activation may be responsible for myocardial injury in high-risk female patients during ca
191 Here we show that voluntary exercise reduces myocardial injury in mice following a 4-week training pe
193 servation of cardiac function and attenuates myocardial injury in newborn piglets after asphyxia-reox
194 hyperglycemia has a stronger relationship to myocardial injury in nondiabetic compared with diabetic
195 gly been viewed as an important mechanism of myocardial injury in noninfectious models of cardiac dis
197 sideration as a robust technique to identify myocardial injury in patients with acute myocarditis or
198 However, advanced age, comorbidities, and myocardial injury in patients with heart failure constra
199 protects against endothelial dysfunction and myocardial injury in percutaneous coronary interventions
200 iation between hyperglycemia and subclinical myocardial injury in persons without clinically evident
201 and 2D strain were able to identify residual myocardial injury in post-PPCM women with apparent recov
202 Preventing downregulation of Nampt inhibits myocardial injury in response to myocardial ischemia and
203 lood supply is the primary goal for reducing myocardial injury in subjects with ischemic heart diseas
204 ent depression may be greatest in those with myocardial injury in the first month after the cardiac e
208 ein changes that are novel in the context of myocardial injury, including Dickkopf-related protein 4,
209 f inflammation, neurohumoral activation, and myocardial injury increased the risk for death but poorl
210 derivation and validation cohorts of planned myocardial injury, individuals with spontaneous myocardi
214 l hospitalization and left ventricular mass, myocardial injury is an independent predictor for 30-day
219 COPD) have elevated cardiovascular risk, and myocardial injury is common during severe exacerbations.
221 evidence showed that, in most AIS patients, myocardial injury is not caused by coronary ischemia.
222 e density and diversity and the magnitude of myocardial injury is responsible for the resolving and n
223 en ischemic and various nonischemic forms of myocardial injury, it may be helpful in cases of diagnos
225 ting, where assessment for low-level chronic myocardial injury may enhance risk stratification for he
226 evels of hs-TnT, suggesting that subclinical myocardial injury may play a role in the association bet
228 oponin I, a sensitive and specific marker of myocardial injury, may be elevated in patients with seps
229 vation myocardial infarction and significant myocardial injury (median peak troponin I, 138 ng/dL [li
230 ved subpopulations were examined in a murine myocardial injury model: (1) unselected AMCs, (2) ckit(+
231 RIPC reduces the incidence of postoperative myocardial injury, myocardial infarction, and renal impa
233 -enhancement MRI in identifying irreversible myocardial injury, no study has yet assessed its role as
236 n accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease.
238 culating cardiac troponin (cTn) in detecting myocardial injury (often subclinical) in those with HF.
241 o 17%] increase in the combined end point of myocardial injury or hospitalization for ischemic heart
243 LV) structure and geometry that evolve after myocardial injury or overload usually involve chamber di
244 eployment was not associated with additional myocardial injury or re-elevation of cardiac biomarkers.
245 I was 13% and was independently predicted by myocardial injury (OR, 8.54; 95% CI, 2.17-33.52), prepro
246 is revealed the protective effect of RIPC on myocardial injury (OR: 0.22, 95% CI: 0.07 to 0.67; P=0.0
247 patients with chronic heart failure, ongoing myocardial injury partially results from activation of t
249 e correlations were found between markers of myocardial injury (plasma troponin I, myocardial lactate
252 or pharmacological levels of H2S attenuates myocardial injury, protects blood vessels, limits inflam
255 a into postcardiac arrest care, cerebral and myocardial injuries represent the limiting factors for s
256 raft rejection, as demonstrated by increased myocardial injury, serum cardiac troponin, cellular infi
257 analysis of neonatal and adult responses to myocardial injury should enable identification of the ke
259 In nondiabetic patients, the risk of severe myocardial injury started to rise once admission glucose
260 composite of death and major morbidity (ie, myocardial injury, stroke, renal failure, or respiratory
261 t be too inefficient to repair the extensive myocardial injury that is typical of human disease.
262 reduce cardiac-wall stress and, potentially, myocardial injury, thereby favorably affecting patients'
263 onor, sodium sulfide (Na2S), would attenuate myocardial injury through upregulation of protective mic
264 ed to investigate whether ticagrelor reduces myocardial injury to a greater extent than clopidogrel a
265 t stem cells may be able to home to sites of myocardial injury to assist in tissue regeneration.
266 collagen metabolism, hemodynamic stress, and myocardial injury to evaluate subjects with hypertrophic
268 ar events that underlie the progression from myocardial injury to myocardial infarction (MI) and, ult
269 timate the association between postoperative myocardial injury (troponin I level >0.06 mug/L) and all
270 art is increased may predispose to apoptotic myocardial injury under conditions of physiological stre
272 The novel effect of reducing acute ischemic myocardial injury via increased Akt activity and NO prod
283 over the effects of GSK-3beta inhibition on myocardial injury was reversed by inhibition of autophag
285 e kinases have been shown to protect against myocardial injury, we hypothesized that GLP-1 could dire
289 n those with type 2 myocardial infarction or myocardial injury were because of noncardiovascular caus
290 mia-induced myocardial PKCalpha cleavage and myocardial injury were greatly increased by cardiac-spec
293 nt with these reciprocal effects on post-I/R myocardial injury when levels of GRK2 activity were alte
294 into the infarcted heart leads to increased myocardial injury whereas injection of MSC overexpressin
295 specific transgenic mice were protected from myocardial injury, whereas Thbs4(-/-) mice were sensitiz
296 riptional activation occurred after discrete myocardial injury, which was associated with the develop
297 A) during ischemia/reperfusion (I/R) induced myocardial injury with emphasis on the underlying mechan
298 DE-MRI) can accurately identify irreversible myocardial injury with high spatial and contrast resolut
299 Holter electrocardiographic monitoring, and myocardial injury within 120 hours after surgery, as ass
300 agamma-GRK2 inhibition and/or ablation after myocardial injury would attenuate pathological myofibrob
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