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1 vascular disease), 128294 from stroke (16125 ischemic, 32591 hemorrhagic, and 79578 other), and 67914
3 lar to wild-type aged hearts (i.e., impaired ischemic AMPK activation and higher sensitivity to ische
5 ased Sesn2 levels in aging lead to a blunted ischemic AMPK activation, alterations in substrate metab
7 implicated in the regulation of development, ischemic and dilated cardiomyopathy, and myocardial infa
8 city are nonmodifiable risk factors for both ischemic and hemorrhagic stroke, while hypertension, smo
9 icans experienced higher mortality rates for ischemic and hypertensive heart disease compared with ot
10 relative risk of HF overall and by subtype (ischemic and nonischemic HF) in patients with RA and to
13 atients with an ischemic stroke or transient ischemic attack and insulin resistance, those at higher
15 or operative mortality (<30 days), transient ischemic attack in 1 patient, reoperation for bleeding i
16 PET/CT in 26 patients after recent transient ischemic attack or minor ischemic stroke: 18 patients wi
17 older with a history of stroke or transient ischemic attack to achieve a target systolic blood press
18 y of stroke, systemic embolism, or transient ischemic attack was 39.4%/y versus 30.3%/y without (P=0.
19 acterize death and CVEs (stroke or transient ischemic attack) after HRDM procedures over a 17-year pe
21 abetes mellitus, 30%; prior stroke/transient ischemic attack, 6.5%; arterial disease, 15.9%; all CHAD
24 ction [MI], heart failure, stroke, transient ischemic attack, peripheral arterial complication, and c
25 romboembolic events, MI, stroke or transient ischemic attack, vascular deaths, and major vascular eve
27 IQR]: 0.22 to 1.15; p = 0.008) and transient ischemic attack/stroke (median difference: 0.13; IQR: 0.
28 ere was a similar number of stroke/transient ischemic attack/systemic embolic events (6 versus 10, iE
29 ; P=0.03) and with more strokes or transient ischemic attacks (55 [0.9%] versus 34 [0.5%]; odds ratio
31 recrudescence from mimics, such as transient ischemic attacks, migraine, Todd paralysis, and Uhthoff
33 cient to induce astrocytic activation in the ischemic brain and that astrocytes activated by neuronal
34 that uPA and uPAR expression increase in the ischemic brain during the recovery phase from an acute i
35 rebral artery occlusion, or neonatal hypoxic-ischemic brain injury, Mn preferentially accumulated in
36 at platelets help maintain hemostasis in the ischemic brain, their exact contribution remains ill def
39 urons that promotes synaptic recovery in the ischemic brain.SIGNIFICANCE STATEMENT To date, there is
42 cardioverter defibrillator (ICD) therapy in ischemic cardiomyopathy (ICM) and nonischemic cardiomyop
46 ithout DM, those with DM had higher rates of ischemic cardiomyopathy, LVAD implantation as destinatio
47 modeling in mice with large infarcts, and in ischemic cardiomyopathy, they improve LV function, effec
52 acilitated the discovery of a feature of the ischemic cascade: selective loss of smooth muscle cells
54 nsitivity of spectral analysis to oncosis or ischemic cell death had not previously been studied.
55 ebral embolic protection devices in reducing ischemic central nervous system (CNS) injury during SAVR
56 nd 17 acutely symptomatic patients ([urgent] ischemic cerebrovascular event within the previous 5 day
58 nd mortality; especially if complicated with ischemic colitis, stercoral ulcer formation and subseque
60 ing cells in the LV myocardium in normal and ischemic conditions 7 days after complete ligature of th
62 ied as "target mismatch" if they had a small ischemic core and a large penumbra on their baseline CT
64 baseline computed tomography perfusion (CTP) ischemic core threshold to predict infarction as thrombo
66 the outcomes of patients with large baseline ischemic cores on CTP undergoing ET with the outcomes of
67 ng high-density encapsulation to normoxic or ischemic culture for 12 hours, after which viability and
68 e system to protect liver grafts from lethal ischemic damage before transplantation in a clinically r
70 e extent of ischemia (hazard ratio for small ischemic defects: 2.2, 95% confidence interval [CI], 0.9
71 ectively; hazard ratio for moderate or large ischemic defects: 4.0, 95% CI, 1.5-10.5 and 12.1, 95% CI
72 ND Ninety-nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic
74 onates (>/=36 weeks' gestation) with hypoxic-ischemic encephalopathy at 18 US centers in the Eunice K
78 stinal thrombotic microangiopathy (iTMA) and ischemic enteritis in approximately 50% of infected huma
80 andomization, 478 individuals (4.1%) had 502 ischemic events (306 with myocardial infarction, 113 wit
81 ly associated with increased risks of severe ischemic events (cause-specific hazard, 2.12 [1.14-3.96]
83 ials reduced the 48-hour and 30-day rates of ischemic events during percutaneous coronary interventio
84 ectomy is associated with higher rates of CV ischemic events in older patients and those with a histo
85 T scores undergoing PCI but reduced risk for ischemic events in patients with high scores receiving p
86 f antiplatelet therapy for the prevention of ischemic events in stable patients with symptomatic athe
87 MACE but a higher adjusted risk of recurrent ischemic events primarily because of nonstent-related MI
88 been associated with a high risk of adverse ischemic events, but there is a paucity of contemporary
89 vascular disease and subsequent injury after ischemic events, fundamental knowledge in these areas la
91 -lesion anatomy is associated with increased ischemic events, particularly within the first year afte
92 a considerably higher risk of 2-year adverse ischemic events, with HPR conferring similar risk in SVG
93 in Secondary Prevention of Atherothrombotic Ischemic Events-Thrombolysis in Myocardial Infarction) (
99 at the 90th and 10th percentile was 2.0 for ischemic heart disease (119.1 vs 235.7 deaths per 100000
100 zations, whereas 172 suffered from a chronic ischemic heart disease (CIHD), 126 of whom underwent cha
101 lung cancer (HR = 1.08, 95% CI: 1.02, 1.14), ischemic heart disease (HR = 1.09, 95% CI: 1.02, 1.16),
105 tment in improving survival in patients with ischemic heart disease and reduced ejection fraction.
106 rpose We aimed to predict individual risk of ischemic heart disease and stroke in 5-year survivors of
109 ques in coronary arteries from patients with ischemic heart disease implying a role in human arterial
112 in patients with congestive heart failure or ischemic heart disease than in those without (P = 0.021
113 y, peripheral neuropathy, diabetic foot, and ischemic heart disease were 21.9%, 17.6%, 28.0%, 6.2%, a
114 n patients with hypertrophic cardiomyopathy, ischemic heart disease, diabetes mellitus, and more.
116 s between ingestion of inorganic arsenic and ischemic heart disease, nonmalignant respiratory disease
117 altered abundance in septic cardiomyopathy, ischemic heart disease, or dilated cardiomyopathy, in co
124 larization is an effective means of treating ischemic heart disease; however, current therapeutic rev
125 tained inflammation is a hallmark of chronic ischemic heart failure (HF); however, the pathophysiolog
126 with hs-TnT levels in patients with chronic ischemic heart failure (P=0.0008, n=10, triple measureme
127 transplantation of isolated mitochondria to ischemic heart tissue leads to decreases in cell death,
129 A first-ever HF diagnosis (classified as ischemic HF or nonischemic HF based on the presence of I
133 cental pathologies of inflammatory, hypoxic, ischemic/hypertensive, infectious and thrombotic etiolog
135 all the PCAs resulted in the development of ischemic infarction of the choroid, retinal pigment epit
136 rain during the recovery phase from an acute ischemic injury and that uPA binding to uPAR promotes ne
137 1A, could lead to neuroprotection following ischemic injury in vivo The minimal syntaxin 1A-binding
141 al hemorrhage, hemorrhagic transformation of ischemic injury, and presumed perinatal hemorrhagic stro
146 lurane or sevoflurane administered after the ischemic insult reduced brain infarct percentage and neu
151 after ligation, neutrophil infiltration into ischemic limbs of AMPKalpha2(DeltaMC) mice was lower tha
152 notypic changes are functionally relevant as ischemic macrophages triggered tube-like morphogenesis i
155 ffects of left ventricular (LV) dysfunction, ischemic MR, and left atrial infarction (LAI); and 2) to
157 BAG3(Ile81), but not BAG3(Met81), improved ischemic muscle myopathy and muscle precursor cell diffe
158 production to induce M2-like polarization in ischemic muscle to enhance angiogenesis, arteriogenesis,
160 lated on resident vascular cells from murine ischemic muscles, thus providing a permissive milieu to
162 orphonuclear neutrophils, accumulates within ischemic myocardium and has been linked to adverse left
165 of these were misdiagnosed as glaucoma (two ischemic optic neuropathies and two congenital optic dis
166 dema (CME; n = 3), and nonarteritic anterior ischemic optic neuropathy (n = 1) in the repositioning g
167 hemic syndrome (OIS), non-arteritic anterior ischemic optic neuropathy (NA-AION) and amaurosis fugax
168 have a greater risk of nonarteritic anterior ischemic optic neuropathy (NAION) than nondiabetic patie
169 thienopyridine plus aspirin therapy without ischemic or bleeding events remained on an aspirin regim
174 not associated with a lower risk of primary ischemic outcome at 180 days (odds ratio, 0.96; 95% conf
176 cial actions of ischemic preconditioning and ischemic postconditioning by a mechanism stemming primar
179 erase-5 inhibitors and beneficial actions of ischemic preconditioning and ischemic postconditioning b
180 erved for comparisons involving xanthine and ischemic preconditioning, although the impact of NAC and
181 n of the cGMP-degrading phosphodiesterase-5, ischemic preconditioning, and postconditioning regimens.
186 etal protein paxillin, growth factor-induced ischemic retinopathy in the murine oxygen-induced retino
187 cangrelor alone was associated with similar ischemic risk and lower risk-adjusted bleeding risk comp
191 g to the small heat shock protein (HspB8) in ischemic skeletal muscle cells and enhanced ischemic mus
193 at Cdc25A is activated in neurons undergoing ischemic stress mediated by hypoxia in vitro and global
194 onstrate a cardiac phenotype and response to ischemic stress that is similar to wild-type aged hearts
195 either mutation impacted cardiac response to ischemic stress, isolated hearts were subjected to ische
196 in, driven by a significant 21% reduction in ischemic stroke (3.4% versus 4.1%; HR, 0.79; 95% CI, 0.6
197 60; 95% CI, 0.38-0.95; P=0.030) and 7.6% for ischemic stroke (8.7% versus 16.3%; number needed to tre
199 iated with a significant increase in risk of ischemic stroke (hazard ratio, 1.18; 95% confidence inte
200 y (HR, 0.83; 95% CI, 0.70-0.98; P=0.029) and ischemic stroke (HR, 0.76; 95% CI, 0.63-0.91; P=0.003).
206 ular events including myocardial infarction, ischemic stroke and cardiovascular death, quality-adjust
207 ovascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced
209 rvational study of 94474 patients with acute ischemic stroke and known history of AF admitted from Oc
211 d ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40%]) and 3028
212 ble clinical outcomes in patients with acute ischemic stroke caused by intracranial proximal occlusio
213 e or those who had previously experienced an ischemic stroke displayed a higher risk of stroke if war
214 observed in 2.5% of the patients with acute ischemic stroke due to large vessel occlusion and were m
216 s in this study are as follows: first, acute ischemic stroke hospitalization rates increased signific
217 ociations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stro
218 amen ovale reduces the risk of recurrence of ischemic stroke in patients who have had a cryptogenic i
221 3 years was positively associated with early ischemic stroke in women (HR, 1.10; 95% CI, 1.01-1.20) a
228 To determine whether, among patients with an ischemic stroke or transient ischemic attack and insulin
235 ODUCTION: We aimed to identify whether acute ischemic stroke patients with known complete reperfusion
237 age patient with AF, the threshold of annual ischemic stroke rate where the benefit of anticoagulatio
242 dbrain to label specific neuronal types, and ischemic stroke was induced in the dorsolateral striatum
243 a cryptogenic stroke, the risk of subsequent ischemic stroke was lower among those assigned to PFO cl
245 capable hospitals, 7.5% of all patients with ischemic stroke were treated in the third quarter of 201
247 use of thrombolytic therapy in patients with ischemic stroke who received anticoagulation with NOACs
248 xamine the prevalence of patients with acute ischemic stroke with known history of AF who were not re
249 tion, 113 with stent thrombosis, and 83 with ischemic stroke), and 232 individuals (2.0%) had 235 ble
250 significant association between PPI use and ischemic stroke, after accounting for indications for PP
251 ) with myocardial infarction, 11 (0.9%) with ischemic stroke, and 1 (0.1%) with deep venous thrombosi
252 included a composite of mortality, clinical ischemic stroke, and acute kidney injury within 30 days
255 ing numerous pathologies including migraine, ischemic stroke, aneurysmal subarachnoid hemorrhage, int
256 red a promising neuroprotective treatment of ischemic stroke, but the treatment's various complicatio
258 stics increasing stroke risk include HDP for ischemic stroke, late menopause and gestational hyperten
259 plicated in several neuronal disorders, like ischemic stroke, neuronal inflammation, and pathological
261 t model of upper extremity impairments after ischemic stroke, we examined effects of motor rehabilita
279 For the principal effectiveness end point of ischemic stroke/systemic embolism, no significant differ
280 er recent transient ischemic attack or minor ischemic stroke: 18 patients with culprit carotid stenos
281 vator) is effective in improving outcomes in ischemic stroke; however, there are few data on the use
282 Primary outcomes of inpatient admissions for ischemic strokes and major bleeding were compared across
283 ism accounts for an increasing proportion of ischemic strokes and might multiply several-fold during
285 anch (BRAO) retinal artery occlusion, ocular ischemic syndrome (OIS), non-arteritic anterior ischemic
286 of graft loss per hour increase in the total ischemic time (adjusted hazard ratio, 1.09; 95% confiden
288 on graft outcomes, such that the duration of ischemic time has the greatest impact on graft survival
289 r age, the pathway of donor death, and total ischemic time on graft outcomes, such that the duration
292 y of poor ex vivo perfusion, had longer cold ischemic times, and were transplanted into older recipie
293 relevant endpoints across a spectrum of warm ischemic times, before and during ex vivo heart perfusio
295 estigated the mechanisms of CD34Exo-mediated ischemic tissue repair and therapeutic angiogenesis by s
296 ated molecular pattern (DAMP), released from ischemic tissues and dying cells which, when crystalized
298 DCD grafts in particular are associated with ischemic-type biliary lesions (ITBL) with subsequent imp
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