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1 ard developing a therapeutic agent for acute cardiac ischemia.
2 f failure to hospitalize patients with acute cardiac ischemia.
3 sex, and the absence of typical features of cardiac ischemia.
4 the metabolic and functional consequences of cardiac ischemia.
5 ents annually with symptoms suggesting acute cardiac ischemia.
6 tor for changes in myocardial function after cardiac ischemia.
7 emergency department patients without acute cardiac ischemia.
8 in hospital mortality in patients with acute cardiac ischemia.
9 hage, contraction bands, and signs of global cardiac ischemia.
10 rominent and important pathogenic feature of cardiac ischemia.
11 department with symptoms suggestive of acute cardiac ischemia.
12 hroughout a prolonged 2.5 h period of global cardiac ischemia.
13 nt regulator of the inflammatory response to cardiac ischemia.
14 e normal hearts, but Parkin is protective in cardiac ischemia.
15 ardiac output and result in secondary global cardiac ischemia.
16 nderlying reperfusion injury after prolonged cardiac ischemia.
17 ective in a number of experimental models of cardiac ischemia.
18 nary infusion of BMCs for cell therapy after cardiac ischemia.
19 e role at the intercellular junctions during cardiac ischemia.
20 d sudden death, which occur in patients with cardiac ischemia.
21 ed for patients with recurrent or provocable cardiac ischemia.
22 ior circulation, 4 of arm ischemia, and 2 of cardiac ischemia.
23 es has made them leading candidates to sense cardiac ischemia.
24 thout evidence of active hemorrhage or acute cardiac ischemia.
25 y in African Americans with heart failure or cardiac ischemia.
26 antagonist is cardioprotective during global cardiac ischemia.
27 uation of patients presenting with suspected cardiac ischemia.
28 egeneration and fibrosis suggested sustained cardiac ischemia.
29 in or with symptoms consistent with possible cardiac ischemia.
30 interaction, that of potent protection from cardiac ischemia.
31 nt ventricular tachyarrhythmias during acute cardiac ischemia.
32 ital to triage patients with suspected acute cardiac ischemia.
33 ins of rat hearts either lost or degraded by cardiac ischemia (15- or 60-minute duration) with and wi
35 ercent ultimately met the criteria for acute cardiac ischemia (8 percent had acute myocardial infarct
36 clinical findings suggestive of AMI or acute cardiac ischemia (ACI) but at low risk using a validated
38 f medical conditions, including cerebral and cardiac ischemia, acute kidney injury, and transplantati
39 er understanding into the pathophysiology of cardiac ischemia and infarction, primary diseases of the
41 nt to the emergency department with possible cardiac ischemia and nondiagnostic electrocardiograms (E
42 alterations in fatty acid metabolism during cardiac ischemia and postischemic reperfusion, stimulati
50 g article describes the issues around silent cardiac ischemia and some of the insights obtained in th
51 I) contributes to contractile failure during cardiac ischemia and systolic heart failure, in part due
52 role in diseases such as cancer, stroke, and cardiac ischemia, and participates in a variety of signa
54 tion parallel the altered biology of induced cardiac ischemia but are well tolerated by hibernated ma
55 vity and negative predictive value for acute cardiac ischemia, but use of this method has not been pr
56 ually a transient insult, such as hypoxemia, cardiac ischemia, catecholamine excess, or electrolyte a
57 hypertension, and OSA also may contribute to cardiac ischemia, congestive heart failure, cardiac arrh
58 r electrocardiogram (ECG) findings for acute cardiac ischemia, continuous 12-lead ECG monitoring incr
59 strate that expression of ATF3 is induced by cardiac ischemia coupled with reperfusion (ischemia-repe
67 ong patients presenting to the ED with acute cardiac ischemia, gender does not appear to be an indepe
69 atory studies suggest that in the setting of cardiac ischemia, immediate intravenous glucose-insulin-
70 ptibility of hERG to proteases, we show that cardiac ischemia in a rabbit model was associated with a
71 promote functional recovery in hind-limb and cardiac ischemia in animal models; however, its impact o
74 eceptors are of interest in the treatment of cardiac ischemia, inflammation, and neurodegenerative di
77 acid produced by anaerobic metabolism during cardiac ischemia is among several compounds suggested to
79 ice and Sp1 small interfering RNA in in vivo cardiac ischemia models revealed Sp1-mediated induction
80 5% CI]), AI-only users had a similar risk of cardiac ischemia (myocardial infarction and angina) (adj
81 the impact of beta-blockade on perioperative cardiac ischemia, myocardial infarction, and mortality f
83 phic or cardiac enzyme changes suggestive of cardiac ischemia or injury, and new positive blood cultu
84 k of the most serious cardiovascular events (cardiac ischemia or stroke) was not elevated in AI-only
85 in multiple disorders (hepatitis, brain and cardiac ischemia, pancreatitis, viral infection and infl
87 oronary disease enrolled in the Asymptomatic Cardiac Ischemia Pilot (ACIP) have more episodes of asym
93 nhibitor, and statin agents minimize ongoing cardiac ischemia, prevent thrombus propagation, and redu
98 We hypothesized that riboflavin given during cardiac ischemia-reperfusion (I/R) might reduce subseque
100 singly, MHC-PDK4 mice were not sensitized to cardiac ischemia-reperfusion injury despite a fuel utili
104 xposure induces long-term protection against cardiac ischemia-reperfusion injury, which improves myoc
109 /BB loop mimetic, plays a protective role in cardiac ischemia/reperfusion (I/R) but the molecular mec
110 isms by which TRPM2 channels protect against cardiac ischemia/reperfusion (I/R) injury, we analyzed p
111 uggested to play a crucial role in mediating cardiac ischemia/reperfusion (IR) injury, and the blocka
112 rexpression as well as inhibition of MDM2 on cardiac ischemia/reperfusion injury and hypertrophy.
116 normoxic HIF-1 preservation could attenuate cardiac ischemia/reperfusion injury via a preconditionin
123 expression was significantly increased in a cardiac ischemia/reperfusion model where inflammation an
125 ween three alterations known to occur during cardiac ischemia/reperfusion, mitochondrial Ca(2+) accum
132 egeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac
133 ld-type or mutant ALDH2 who are subjected to cardiac ischemia, such as during coronary bypass surgery
134 n ventricular fibrillation in the setting of cardiac ischemia, sympathetic activation is proarrhythmi
135 ity of acute ischemia predicted by the acute cardiac ischemia time-insensitive predictive instrument
136 cardiac ischemia were enrolled in the Acute Cardiac Ischemia Time-Insensitive Predictive Instrument
137 n linked to tissue damage after neuronal and cardiac ischemias, traumatic spine and brain injuries, a
138 tivation to tissue damage after neuronal and cardiac ischemias, traumatic spine and brain injuries, a
140 t pain or other symptoms suggestive of acute cardiac ischemia were enrolled in the Acute Cardiac Isch
142 ented to the emergency department with acute cardiac ischemia were more likely not to be hospitalized
143 rtant protective mechanism in the setting of cardiac ischemia where arachidonic acid levels are drama
144 ons (e.g. fatty acid oxidation disorders and cardiac ischemia) where long-chain acylcarnitine accumul
145 vation of the sarcolemmal Na/K ATPase during cardiac ischemia, which is masked by an inhibitor of the
146 In particular, hypoxia is associated with cardiac ischemia, which, although initially inducing a p
147 hest pain or other symptoms suggesting acute cardiac ischemia who presented to the emergency departme
148 r patients with symptoms suggestive of acute cardiac ischemia without obvious abnormalities on initia
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