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1 sion leads to heart failure and death during acute myocardial ischemia.
2 ecipitously in response to stress, including acute myocardial ischemia.
3 even in the absence of clinically suspected acute myocardial ischemia.
4 nimal underwent 4 episodes of 2.5 minutes of acute myocardial ischemia.
5 efibrillation threshold were not affected by acute myocardial ischemia.
6 ent risk marker in patients who present with acute myocardial ischemia.
7 ies for risk stratification in patients with acute myocardial ischemia.
8 the functional improvement in recovery from acute myocardial ischemia.
9 icular arrhythmias during the early phase of acute myocardial ischemia after ligation of the left ant
10 the vulnerability to fatal arrhythmia during acute myocardial ischemia and provides a plausible mecha
11 and irreversible (infarction) injury during acute myocardial ischemia and reperfusion by a protein k
12 heart rate (HR) variability, HR response to acute myocardial ischemia, and resting catecholamines we
13 ificant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enh
14 of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regio
15 of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regio
16 f cardiac dysfunction and arrhythmias during acute myocardial ischemia, attenuation of norepinephrine
17 t elevation, as seen in Brugada syndrome and acute myocardial ischemia, cannot be fully explained by
18 lectrical uncoupling at gap junctions during acute myocardial ischemia contributes to conduction abno
19 as caused by hypothalamic stimulation during acute myocardial ischemia could be attenuated by afferen
22 ity during acute metabolic stresses, such as acute myocardial ischemia in which both oxidative phosph
23 ort the novel application of metabolomics to acute myocardial ischemia, in which we identified novel
24 nt echocardiographic study before and during acute myocardial ischemia induced by coronary artery occ
27 as to investigate the metabolomic profile of acute myocardial ischemia (MIS) using nuclear magnetic r
28 a handling, ionic imbalances associated with acute myocardial ischemia, neurohumoral changes, and gen
29 s effects of local cardiac AII formed during acute myocardial ischemia or, alternatively, a non-AII-r
30 cerbation of the inflammatory process during acute myocardial ischemia, particularly in the early sta
31 the role of vascular endothelial FasL during acute myocardial ischemia-reperfusion that is closely as
32 ypothesis that ADAMTS13 reduces VWF-mediated acute myocardial ischemia/reperfusion (I/R) injury in mi
34 nificantly increased in rat hearts following acute myocardial ischemia, suggesting it may have import
35 incidence of ventricular arrhythmias during acute myocardial ischemia that can be decreased by affer
36 nds, subendocardial hemorrhage, and signs of acute myocardial ischemia were seen in other animals as
37 diotoxic effects may play important roles in acute myocardial ischemia where Sph1P levels are probabl
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