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1 to be more effective in thrombus removal and myocardial reperfusion.
2 ence has accumulated in randomized trials of myocardial reperfusion.
3 uced in wild-type mice at 2 to 6 hours after myocardial reperfusion.
4 s that free radical generation occurs during myocardial reperfusion.
5 ay be considered a reference test for failed myocardial reperfusion.
6 us cannulation of the right atrium and after myocardial reperfusion.
7                                              Myocardial reperfusion after ischemia (I/R), although an
8                                   Suboptimal myocardial reperfusion after PCI in STEMI is common and
9 the rate of distal embolization and impaired myocardial reperfusion after percutaneous coronary inter
10 ht to determine the prognostic importance of myocardial reperfusion after various contemporary interv
11 any as 50% of patients still have suboptimal myocardial reperfusion and experience extensive myocardi
12 in loading dose before elective PCI improves myocardial reperfusion and injury indexes, suggesting a
13  tPA provided additional benefit in terms of myocardial reperfusion, as evidenced by greater resoluti
14 l increases in intracellular Ca(2)(+) during myocardial reperfusion can cause cardiomyocyte death and
15 ation myocardial infarction; however, failed myocardial reperfusion commonly passes undetected in up
16 o tissue injury and repair including stroke, myocardial reperfusion damage, ischemia, cancer, amyloid
17 ow phenomenon." Therefore, GPI might improve myocardial reperfusion, distinct from its effects on epi
18                                         Poor myocardial reperfusion due to distal embolization and mi
19 nary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary
20 n and platelet lysis improves epicardial and myocardial reperfusion in AMI.
21 e ischemic area at risk increased during rat myocardial reperfusion in vivo.
22 tandard clinical measures of the efficacy of myocardial reperfusion, including the ischemic time, ST-
23  for cardioprotective therapies to attenuate myocardial reperfusion injury and decrease infarct size
24 e pathophysiology and clinical expression of myocardial reperfusion injury and discuss the current st
25 ma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play
26 currently under investigation for preventing myocardial reperfusion injury have the potential to impr
27 l and antithrombotic properties that reduces myocardial reperfusion injury in animal models of myocar
28 itric oxide bioavailability, and ameliorated myocardial reperfusion injury in the setting of severe h
29 dings suggest that the blood contribution to myocardial reperfusion injury is amplified in diabetes.
30                                              Myocardial reperfusion injury is associated with the inf
31                                              Myocardial reperfusion injury is mediated in part by acc
32                                              Myocardial reperfusion injury is the result of several c
33 composition were analyzed in mouse models of myocardial reperfusion injury with genetic and pharmacol
34  itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still
35  associated with oxidative stress, including myocardial reperfusion injury, heart transplantation, st
36                                              Myocardial reperfusion injury-triggered by an inevitable
37 trophil-dependent thromboinflammation during myocardial reperfusion injury.
38 elopment for the treatment of hepatitis C or myocardial reperfusion injury.
39 ity resulting in increased cytoprotection in myocardial reperfusion injury.
40 he protective functional phenotype of MIF in myocardial reperfusion injury.
41 uld prevent neutrophil activation and reduce myocardial reperfusion injury.
42 ming may not utilize ADO's potential against myocardial reperfusion injury.
43 ibution of nondiabetic and diabetic blood to myocardial reperfusion injury.
44                                              Myocardial reperfusion is believed to be associated with
45  the poor prognosis is due to lower rates of myocardial reperfusion is unknown.
46  complement activation is a key regulator of myocardial reperfusion ischemic injury.
47 /- 82.6 pmol/mmol by 15 minutes after global myocardial reperfusion (P < .05) and dropped to 181.2 +/
48 Now that we have entered the third decade of myocardial reperfusion therapy, we can expect iterative
49 ly, this was achieved when dosing well after myocardial reperfusion (up to 3 h after), the same time
50 and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy
51 tenting (DS) approach (24-48 hours) improves myocardial reperfusion, versus immediate stenting, in pa