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1 iliated fibroblasts are enriched in areas of myocardial injury.
2 5 times more additional women than men with myocardial injury.
3 hat an MI is just one of many types of acute myocardial injury.
4 , including 5 subtypes of MI and nonischemic myocardial injury.
5 reduction in mRNA biomarkers associated with myocardial injury.
6 opment of sex-specific therapies that reduce myocardial injury.
7 r 7 days after infection could not attenuate myocardial injury.
8 yte recruitment and fate specification after myocardial injury.
9 ted during early (within first 4 h) ischemic myocardial injury.
10 categorized as acute or chronic nonischemic myocardial injury.
11 ty for biomarker and pathway discovery after myocardial injury.
12 significantly improve recovery from ischemic myocardial injury.
13 tients with type 2 myocardial infarction and myocardial injury.
14 ) in individuals with no clinically manifest myocardial injury.
15 eans of restoring cardiac function following myocardial injury.
16 ia, hypothermia, cardioplegia, and traumatic myocardial injury.
17 ory activation occurs in nearly all forms of myocardial injury.
18 cted to function in pathways consistent with myocardial injury.
19 n location has been suggested to precipitate myocardial injury.
20 ulation or have functional roles relevant to myocardial injury.
21 r relative changes over time, indicate acute myocardial injury.
22 r of damaged sarcolemmal membranes following myocardial injury.
23 are confined to patients with ongoing minute myocardial injury.
24 g young adults with type 1 MI, type 2 MI, or myocardial injury.
25 hic cardiomyopathy, a human model of planned myocardial injury.
26 e and limit deleterious remodeling following myocardial injury.
27 er range of human proteins in the context of myocardial injury.
28 f sympathetic function, thereby resulting in myocardial injury.
29 diagnosis of acute myocardial infarction or myocardial injury.
30 ential to restore contractile function after myocardial injury.
31 pt to the increased mechanical demands after myocardial injury.
32 yocardium may represent a novel biosignal of myocardial injury.
33 or cardiac troponin T (cTnT), a biomarker of myocardial injury.
34 diated via mechanisms other than subclinical myocardial injury.
35 th skeletal muscle damage, rather than acute myocardial injury.
36 and significance in the context of ischemic myocardial injury.
37 ted a protective effect of histamine against myocardial injury.
38 proach to promote cardiac regeneration after myocardial injury.
39 ce to chronic beta-adrenergic stress-induced myocardial injury.
40 lation could promote revascularization after myocardial injury.
41 nary blood flow and oxygen supply, and limit myocardial injury.
42 ore and after TAVR for the assessment of new myocardial injury.
43 sensitive and specific for the diagnosis of myocardial injury.
44 onset cardiotoxicity and areas of reversible myocardial injury.
45 the absence of clinical and cTnI evidence of myocardial injury.
46 p in knowledge of the repair mechanism after myocardial injury.
47 resent in nearly two-thirds of patients with myocardial injury.
48 d not reduce the incidence of periprocedural myocardial injury.
49 nerative potency of transplanted sMSCs after myocardial injury.
50 onary reperfusion during an acute MI reduces myocardial injury.
51 nditioning strategies reduced both renal and myocardial injury.
52 rdiac troponin T was measured as a marker of myocardial injury.
53 process that increases adjacent to areas of myocardial injury.
54 f their high sensitivity and specificity for myocardial injury.
55 lian myocardial homeostasis as well as after myocardial injury.
56 ocardial deformation, suggesting subclinical myocardial injury.
57 and the resolution of inflammation following myocardial injury.
58 , intermediary metabolism, and biomarkers of myocardial injury.
59 bo but did not lower the risk of PCI-related myocardial injury.
60 outcome of in-hospital death associated with myocardial injury.
61 tential in clinical application, focusing on myocardial injury.
62 erritin, and fibrinogen were associated with myocardial injury.
63 and vasopressors was associated with smaller myocardial injury.
64 identified ischemia-related and nonischemic myocardial injury.
65 ness, and sepsis, probably cause more of the myocardial injury.
66 e of the ensuing inflammatory response after myocardial injury.
67 icacy and safety in an animal model of acute myocardial injury.
68 images could be acquired in those with acute myocardial injury.
69 h T1 and T2 values in the detection of acute myocardial injury.
70 and have the potential to result in profound myocardial injury.
71 on for patients who experience type 2 MI and myocardial injury.
72 ad type 1 MI, 32% had type 2 MI, and 13% had myocardial injury.
73 (lncRNAs), are proposed novel biomarkers of myocardial injury.
74 nts who have suspected MI or other causes of myocardial injury.
75 phenotype that arises following a variety of myocardial injuries.
76 t were increased within 1 hour after planned myocardial injury, 29 were also elevated in patients wit
77 -up of 10.2 years, mortality was highest for myocardial injury (45.6%), followed by type 2 MI (34.2%)
78 with type 2 myocardial infarction (62.5%) or myocardial injury (72.4%) compared with type 1 myocardia
80 simvastatin treatment reduces biomarkers of myocardial injury after heart transplantation, and-also
81 he role of genetic information in predicting myocardial injury after noncardiac surgery (MINS) remain
83 arterial pressure and the primary outcome of myocardial injury after noncardiac surgery or mortality,
84 ioning (RIPost) will reduce the incidence of myocardial injury after PCI, and whether ischemic condit
86 fore, the different timing and mechanisms of myocardial injury among palliation strategies do not aff
87 the main accepted biomarkers for diagnosing myocardial injury and acute myocardial infarction (AMI).
88 tion increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, parti
89 s, yielding greater clinical sensitivity for myocardial injury and allowing accurate recognition of s
90 that Nlrp3 inflammasome activation preceded myocardial injury and apoptosis, corroborating a pathoge
92 of this study was to describe the degree of myocardial injury and associated outcomes in a large hos
93 gmented ischemic AMPK activation and reduced myocardial injury and cardiac contractile dysfunction af
94 nvestigated the natural history of CMR-based myocardial injury and chamber remodeling over 12 months
96 identify patients at risk for postoperative myocardial injury and death, measuring cardiac troponin
100 as to determine if biomarkers of subclinical myocardial injury and hemodynamic stress identify asympt
102 Index (RDI), is associated with subclinical myocardial injury and increased myocardial wall stress.
104 lly elevated serum cardiac troponin reflects myocardial injury and is associated with increased morta
105 to differentiate reversible and irreversible myocardial injury and its predictive value for left vent
106 le to EMCV infection and develop significant myocardial injury and left ventricular dysfunction.
107 yme B activity can visualize T cell-mediated myocardial injury and monitor the response to an anti-in
108 1 MI, with nearly one-half of patients with myocardial injury and more than one-third of patients wi
109 o cell application, hs-TnT levels to measure myocardial injury and NT-proBNP levels as marker of left
110 ne groups, with reduced levels of markers of myocardial injury and oxidative stress in doxycycline-tr
111 ges in atrial myocardium that correlate with myocardial injury and precede and predict risk of POAF m
113 of absolute radiotracer uptake in a model of myocardial injury and should permit quantitative serial
115 fusion is the most effective way of limiting myocardial injury and subsequent ventricular remodeling,
116 ocardiographic abnormalities associated with myocardial injury and their prognostic impact in patient
118 ction but without hypoxia may increase early myocardial injury and was associated with larger myocard
119 adaptive response to haemodynamic stress or myocardial injury, and allows the heart to meet an incre
121 IL-10 worsened cardiac function, exacerbated myocardial injury, and delayed resolution of inflammatio
122 g differentiates reversible and irreversible myocardial injury, and it is a strong predictor of left
123 ension thresholds that provoke renal injury, myocardial injury, and mortality in critical care patien
124 d to define the time course of inflammation, myocardial injury, and prothrombotic markers after radio
125 rdiomyopathy, coronary spasm, or nonspecific myocardial injury, and the prevalence of COVID-19 diseas
128 Increases in cardiac troponin indicative of myocardial injury are common in patients with coronaviru
130 -19, whereas COVID-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome a
131 us studies suggesting a possible increase in myocardial injury as a result of coronary vasoconstricti
132 ned with hypothermia suggested a less severe myocardial injury as demonstrated by the significantly r
133 TAVR population demonstrated some degree of myocardial injury as determined by a rise in CK-MB level
134 diography or computed tomography, as well as myocardial injury as indicated by a positive test for ca
136 ermine the predictive value of postoperative myocardial injury, as measured by troponin elevation, on
138 known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategi
139 or the secondary end points of perioperative myocardial injury (assessed on the basis of the area und
140 poplastic left heart syndrome pose a risk of myocardial injury at different times and through differe
142 inflammatory response during wound healing, myocardial injury, atherosclerosis and autoimmune disord
143 testing and classification of patients with myocardial injury based on pathogenesis, but the clinica
144 were adjudicated as type 1 MI, type 2 MI, or myocardial injury based on the Fourth Universal Definiti
145 2,072) and 17% (488 of 2,919) of women with myocardial injury before and after implementation, respe
146 infarction, and myocarditis) and secondary (myocardial injury/biomarker elevation and heart failure)
147 or the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abunda
148 pproach for restoring cardiac function after myocardial injury, but the technique thus far has been s
149 tion by 22% (205/916), and acute and chronic myocardial injury by 36% (443/1233) and 43% (389/898), r
150 early inflammatory repair response to acute myocardial injury by facilitating cardiac leukocyte infi
151 l adipose tissue formation in the context of myocardial injury by redirecting the fate of Wt1(+) line
154 ansient and benign electrographic changes to myocardial injury, cardiomyopathy, and even cardiac deat
155 ular deaths were highest in those with acute myocardial injury (cause specific HR 2.65 [95% CI, 2.33-
156 Phosphodiesterase 5 (PDE5) inhibitors limit myocardial injury caused by stresses, including doxorubi
158 essment of ncRNAs and protein biomarkers for myocardial injury, cMyBP-C showed properties as the most
159 ins were validated in an independent planned myocardial injury cohort (n=15; P<1.33E-04, 1-way repeat
160 lated ARDS was associated with lower odds of myocardial injury compared with non-COVID-19-related ARD
161 eleased from the liver and adipose tissue in myocardial injury, contributing to myocardial protection
164 d segmental myocardial strain and markers of myocardial injury could improve the accuracy of late gad
166 went PCI, the primary outcome of PCI-related myocardial injury did not differ between colchicine (n=2
167 ognition of type 2 myocardial infarction and myocardial injury did not lead to changes in investigati
168 performance or mild or moderate disability, myocardial injury, duration of catecholamine support, ma
169 2 and Nox4 in mediating oxidative stress and myocardial injury during I/R using loss-of-function mous
170 usion has the capability of further reducing myocardial injury during ST-segment-elevation myocardial
172 vant clinical factors, even small amounts of myocardial injury (e.g., troponin I >0.03 to 0.09 ng/ml;
173 imaging technique allowing the assessment of myocardial injury early after ST-segment-elevation myoca
174 vels revealed the presence of ongoing minute myocardial injury even in patients with stable ICM.
175 ndently associated with the risk of ischemic myocardial injury following elective PCI with clopidogre
176 ular disease, and >7% of patients experience myocardial injury from the infection (22% of critically
177 only at intermediate and later stages, with myocardial injury (> 6 h) and MI, based on the expressio
178 tients without myocardial injury, those with myocardial injury had more electrocardiographic abnormal
179 uripotent stem cells as cellular therapy for myocardial injury has yet to be examined in a large-anim
180 atients with type 2 myocardial infarction or myocardial injury have a similar crude rate of major adv
181 n those with type 2 myocardial infarction or myocardial injury (hazard ratio, 1.71; 95% confidence in
183 inical risk factors have evidence of ongoing myocardial injury, hemodynamic stress, or systemic infla
185 increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac tropo
186 oved cardiac performance in animal models of myocardial injury; however, the benefits observed in cli
187 yocardial infarction and homed to regions of myocardial injury; however, the myocardium contained onl
188 re the relation between thyroid function and myocardial injuries in idiopathic dilated cardiomyopathy
189 sis was type 1 or 2 myocardial infarction or myocardial injury in 1171 (55.2%), 429 (20.2%), and 522
190 ificantly changed in the blood after planned myocardial injury in a derivation cohort (n=20; P<1.05E-
192 n assays has led to increased recognition of myocardial injury in acute illnesses other than acute co
193 r studies; however, comprehensive studies of myocardial injury in acute respiratory distress syndrome
194 ed them with patients from a cohort study of myocardial injury in ARDS and performed survival analysi
196 he epidemiology and clinical implications of myocardial injury in coronavirus disease 2019 (COVID-19)
199 inhibitor LCZ696 may reduce this measure of myocardial injury in heart failure with preserved ejecti
201 However, advanced age, comorbidities, and myocardial injury in patients with heart failure constra
202 protects against endothelial dysfunction and myocardial injury in percutaneous coronary interventions
203 and 2D strain were able to identify residual myocardial injury in post-PPCM women with apparent recov
204 to determine the prevalence and outcomes of myocardial injury in severe COVID-19 compared with acute
206 lood supply is the primary goal for reducing myocardial injury in subjects with ischemic heart diseas
210 assay with sex-specific thresholds increased myocardial injury in women by 42% and in men by 6%.
211 viously studied heart regeneration following myocardial injury in zebrafish and described each step o
212 ial Infarction provides a taxonomy for acute myocardial injury, including 5 subtypes of MI and nonisc
213 ein changes that are novel in the context of myocardial injury, including Dickkopf-related protein 4,
214 ved macrophages recruited to the heart after myocardial injury, including the mechanisms that regulat
215 f inflammation, neurohumoral activation, and myocardial injury increased the risk for death but poorl
216 derivation and validation cohorts of planned myocardial injury, individuals with spontaneous myocardi
221 COPD) have elevated cardiovascular risk, and myocardial injury is common during severe exacerbations.
225 evidence showed that, in most AIS patients, myocardial injury is not caused by coronary ischemia.
227 e density and diversity and the magnitude of myocardial injury is responsible for the resolving and n
228 nic cardiomyopathy characterized by episodic myocardial injury, left ventricular fibrosis that preced
229 ese proteinases in e.g., heart infection and myocardial injury, liver dysfunction, kidney damage, as
230 ting, where assessment for low-level chronic myocardial injury may enhance risk stratification for he
231 evels of hs-TnT, suggesting that subclinical myocardial injury may play a role in the association bet
233 vation myocardial infarction and significant myocardial injury (median peak troponin I, 138 ng/dL [li
234 d exploring the multifaceted significance of myocardial injury, minimal rejection patterns supported
235 ved subpopulations were examined in a murine myocardial injury model: (1) unselected AMCs, (2) ckit(+
236 sures per day) were strongly associated with myocardial injury, mortality, and renal injury in postop
237 ly available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular infla
238 cardiovascular complications including acute myocardial injury, myocarditis, arrhythmias, and venous
239 n accounts for a substantial fraction of the myocardial injury occurring with ischemic heart disease.
242 eployment was not associated with additional myocardial injury or re-elevation of cardiac biomarkers.
244 e correlations were found between markers of myocardial injury (plasma troponin I, myocardial lactate
247 or pharmacological levels of H2S attenuates myocardial injury, protects blood vessels, limits inflam
254 rs of cardiac fibrosis, cardiac wall stress, myocardial injury, renal function and inflammation, are
255 on biomarkers reflecting myocardial stress, myocardial injury, renal function, and systemic inflamma
256 rowth factor)-beta is critically involved in myocardial injury, repair, and fibrosis, activating both
257 raft rejection, as demonstrated by increased myocardial injury, serum cardiac troponin, cellular infi
258 rity, ranging from fever and inflammation to myocardial injury, shock, and development of coronary ar
259 analysis of neonatal and adult responses to myocardial injury should enable identification of the ke
260 composite of death and major morbidity (ie, myocardial injury, stroke, renal failure, or respiratory
263 reduce cardiac-wall stress and, potentially, myocardial injury, thereby favorably affecting patients'
265 onor, sodium sulfide (Na2S), would attenuate myocardial injury through upregulation of protective mic
266 ed to investigate whether ticagrelor reduces myocardial injury to a greater extent than clopidogrel a
268 timate the association between postoperative myocardial injury (troponin I level >0.06 mug/L) and all
269 tion (T1MI, atherothombotic event), T2MI, or myocardial injury (troponin rise not meeting criteria fo
270 nship between hypotension and a composite of myocardial injury (troponin T >= 0.03 ng/mL without noni
274 positron emission tomography scans, acute LV myocardial injury was associated with myocardial inflamm
284 n those with type 2 myocardial infarction or myocardial injury were because of noncardiovascular caus
288 n why some patients recover without residual myocardial injury whereas others develop dilated cardiom
289 specific transgenic mice were protected from myocardial injury, whereas Thbs4(-/-) mice were sensitiz
290 nts with myocardial ischemia as the cause of myocardial injury, whether attributable to acute atherot
291 A) during ischemia/reperfusion (I/R) induced myocardial injury with emphasis on the underlying mechan
293 um enhancement (90%), even in cases of acute myocardial injury with normal ventricular function (4/5,
294 injury were more affected than those without myocardial injury with respect to all functional paramet
296 e 5.2%, 18.6%, and 31.7% in patients without myocardial injury, with myocardial injury without TTE ab
297 Holter electrocardiographic monitoring, and myocardial injury within 120 hours after surgery, as ass
298 in patients without myocardial injury, with myocardial injury without TTE abnormalities, and with my
300 agamma-GRK2 inhibition and/or ablation after myocardial injury would attenuate pathological myofibrob