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1 the functional improvement in recovery from acute myocardial ischemia.
2 ecipitously in response to stress, including acute myocardial ischemia.
3 acy evaluation of anti-arrhythmic therapy in acute myocardial ischemia.
4 even in the absence of clinically suspected acute myocardial ischemia.
5 nimal underwent 4 episodes of 2.5 minutes of acute myocardial ischemia.
6 efibrillation threshold were not affected by acute myocardial ischemia.
7 nary artery disease, but without evidence of acute myocardial ischemia.
8 ent risk marker in patients who present with acute myocardial ischemia.
9 ies for risk stratification in patients with acute myocardial ischemia.
10 sion leads to heart failure and death during acute myocardial ischemia.
11 icular arrhythmias during the early phase of acute myocardial ischemia after ligation of the left ant
12 rovascular dysfunction, can cause chronic or acute myocardial ischemia and may lead to development of
13 the vulnerability to fatal arrhythmia during acute myocardial ischemia and provides a plausible mecha
14 and irreversible (infarction) injury during acute myocardial ischemia and reperfusion by a protein k
15 and structural remodeling from the onset of acute myocardial ischemia and reperfusion to acute and c
16 heart rate (HR) variability, HR response to acute myocardial ischemia, and resting catecholamines we
17 ificant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enh
18 of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regio
19 of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regio
20 f cardiac dysfunction and arrhythmias during acute myocardial ischemia, attenuation of norepinephrine
21 t elevation, as seen in Brugada syndrome and acute myocardial ischemia, cannot be fully explained by
22 lectrical uncoupling at gap junctions during acute myocardial ischemia contributes to conduction abno
23 as caused by hypothalamic stimulation during acute myocardial ischemia could be attenuated by afferen
24 sed methods for the prediction of underlying acute myocardial ischemia in patients with chest pain.
28 ity during acute metabolic stresses, such as acute myocardial ischemia in which both oxidative phosph
29 ort the novel application of metabolomics to acute myocardial ischemia, in which we identified novel
30 nt echocardiographic study before and during acute myocardial ischemia induced by coronary artery occ
34 as to investigate the metabolomic profile of acute myocardial ischemia (MIS) using nuclear magnetic r
35 a handling, ionic imbalances associated with acute myocardial ischemia, neurohumoral changes, and gen
36 s effects of local cardiac AII formed during acute myocardial ischemia or, alternatively, a non-AII-r
37 cerbation of the inflammatory process during acute myocardial ischemia, particularly in the early sta
39 of metabolic alteration in a rat model with acute myocardial ischemia-reperfusion (AMI/R) injury and
40 the role of vascular endothelial FasL during acute myocardial ischemia-reperfusion that is closely as
41 ypothesis that ADAMTS13 reduces VWF-mediated acute myocardial ischemia/reperfusion (I/R) injury in mi
43 nificantly increased in rat hearts following acute myocardial ischemia, suggesting it may have import
44 incidence of ventricular arrhythmias during acute myocardial ischemia that can be decreased by affer
46 nds, subendocardial hemorrhage, and signs of acute myocardial ischemia were seen in other animals as
47 diotoxic effects may play important roles in acute myocardial ischemia where Sph1P levels are probabl