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1 ta4 in a translational large animal model of hibernating myocardium.
2 rapeutic efficacy in a large animal model of hibernating myocardium.
3 nctional recovery after revascularization in hibernating myocardium.
4 nse to dobutamine have been used to identify hibernating myocardium.
5 ventricular arrhythmias, and reperfusion of hibernating myocardium.
6 ustained, the result is necrosis rather than hibernating myocardium.
7 gh-dose dobutamine from inducing ischemia in hibernating myocardium.
8 has been increasingly used for detection of hibernating myocardium.
9 stenosis and to 78+/-17 mL 7 days later with hibernating myocardium.
10 th through myocyte apoptosis in hypoperfused hibernating myocardium.
11 inducing deterioration of wall thickening in hibernating myocardium.
12 by inducing angiogenesis and regeneration in hibernating myocardium.
13 s using a clinically relevant swine model of hibernating myocardium.
14 ncreasing myocardial perfusion in swine with hibernating myocardium.
15 resting myocardial blood flow is reduced in hibernating myocardium.
16 d stability of sympathetic dysinnervation in hibernating myocardium.
17 d for at least 2 mo after the development of hibernating myocardium.
18 ) to improve flow and function in swine with hibernating myocardium.
19 titative CMR perfusion imaging is reduced in hibernating myocardium.
20 beta-receptor adenylyl cyclase signaling in hibernating myocardium.
21 ion is attenuated in patients and swine with hibernating myocardium.
22 mpathetic norepinephrine uptake in pigs with hibernating myocardium.
23 survival of medically treated patients with hibernating myocardium.
24 entricular dysfunction are features of human hibernating myocardium.
25 ative to revascularisation for patients with hibernating myocardium.
26 lic adjustments could facilitate survival of hibernating myocardium.
27 r non-hibernators according to the volume of hibernating myocardium.
28 the excess mortality seen in the setting of hibernating myocardium.
29 the observed depression of function seen in hibernating myocardium.
30 l, molecular, and morphological phenotype of hibernating myocardium.
31 pinephrine uptake-1 mechanism is impaired in hibernating myocardium.
32 injected transendocardially in the areas of hibernating myocardium.
33 he result of a mixture of scarred as well as hibernating myocardium.
34 tural adaptations was evaluated in pigs with hibernating myocardium.
35 ntadecanoic acid (IPPA), to identify viable, hibernating myocardium.
36 EGF(165) GTx may successfully rescue foci of hibernating myocardium.
37 n PET has been used successfully to diagnose hibernating myocardium.
38 cardium having the physiological features of hibernating myocardium.
39 t persistent myocardial stunning can lead to hibernating myocardium, 13 pigs were chronically instrum
44 emodeling in the cardiac interstitium of the hibernating myocardium, an important predictor of recove
45 ibitory cytokines are elevated in regions of hibernating myocardium and account in part for the depre
46 GF-5 may afford a way to restore function in hibernating myocardium and ameliorate heart failure in c
47 renergic receptor densities occur in viable, hibernating myocardium and may account in part for the o
49 f ischemic and dysfunctional myocardium (ie, hibernating myocardium) and infarct size were each indep
52 that can accurately determine the amount of hibernating myocardium as well as the presence and degre
53 identification of candidates with regions of hibernating myocardium, because these patients stand to
54 re is evidence to suggest that patients with hibernating myocardium benefit most from revascularizati
55 measured the expression of survival genes in hibernating myocardium, both in patients surgically trea
56 coplasmic reticulum proteins were present in hibernating myocardium but absent in stunned myocardium
57 hat dobutamine echocardiography can identify hibernating myocardium, but laboratory studies suggest t
59 reas of nonfunctional but viable (stunned or hibernating) myocardium can also contribute to the devel
60 umented with a proximal LAD stenosis develop hibernating myocardium characterized by relative reducti
62 ysiological and molecular characteristics of hibernating myocardium develop rapidly after a critical
65 proved clinically useful for distinguishing hibernating myocardium from irreversibly injured myocard
66 nuclear density to 995+/-100 nuclei/mm(2) in hibernating myocardium from the instrumented group versu
68 acked necrosis, might have been mistaken for hibernating myocardium had only histology been evaluated
69 rsibility of protein changes that develop in hibernating myocardium have an impact on functional reco
72 ion in coronary BF in conscious pigs induced hibernating myocardium, ie, perfusion-contraction matchi
75 ced flow and increased FDG characteristic of hibernating myocardium in similarly instrumented pigs af
78 cyte >10%) and increased glycogen typical of hibernating myocardium in the LAD region (33+/-3% of myo
80 lts indicate that icMSCs improve function in hibernating myocardium independent of coronary flow or r
86 his study was performed to determine whether hibernating myocardium is adaptive or is destined to und
87 lation of oxygen consumption and function in hibernating myocardium is an adaptive response that prev
90 ata indicate that the proteomic phenotype of hibernating myocardium is dynamic and has similarities t
94 0.65+/-0.08 (mean+/-SEM) mL.min(-1).g(-1) in hibernating myocardium of instrumented pigs compared wit
95 F-A improves contractile function of chronic hibernating myocardium of pigs to a level comparable to
96 on tomography identified ischemia, scar, and hibernating myocardium on the survival benefit associate
100 Thus, physiologic and structural features of hibernating myocardium remain constant for at least two
101 ster and more precise method for determining hibernating myocardium remains the holy grail of noninva
102 , can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary
103 in function and oxygen consumption at rest, hibernating myocardium retains the ability to increase m
105 and the presence of ischemia and/or stunned/hibernating myocardium should be assessed for optimal ma
106 designed to study apoptosis in hypoperfused hibernating myocardium subtending severe coronary stenos
107 tricular dysfunction (LVD) may have areas of hibernating myocardium that improve functionally after r
108 this preclinical swine model of ischemic and hibernating myocardium, the combined delivery of circula
109 t in perfusion reserve is well recognized in hibernating myocardium, there is substantial controversy
110 gene expression is regionally upregulated in hibernating myocardium to a level intermediate between t
111 te the serial changes in the response of the hibernating myocardium to dobutamine stimulation after r
113 f contractile reserve and thallium uptake in hibernating myocardium to myocardial structure in humans
114 descending artery (LAD) stenosis to produce hibernating myocardium underwent percutaneous revascular
115 egion (33+/-3% of myocytes from animals with hibernating myocardium versus 15+/-4% of myocytes from s
116 nt in LVEF was associated with the volume of hibernating myocardium (viable myocardium with contracti
117 ascularization in the setting of significant hibernating myocardium was associated with improved surv
120 n the fasting state, FDG uptake in pigs with hibernating myocardium was heterogeneous and was increas
127 n reversible loss of cardiomyocyte function (hibernating myocardium), which is amenable to therapeuti
130 ing artery (LAD) stenosis to produce chronic hibernating myocardium with regional contractile dysfunc
131 tensive defects in HED uptake were found for hibernating myocardium, with regional retention approxim