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1 ris dislodged during the procedure can cause embolic stroke.
2 al fibrillation, ischemic stroke, and cardio-embolic stroke.
3 ) to control atrial fibrillation and prevent embolic stroke.
4  the LAA is believed to decrease the risk of embolic stroke.
5 they require tPA administration following an embolic stroke.
6 tly involved in vascular damage following an embolic stroke.
7 ion during stroke recovery in a rat model of embolic stroke.
8 ceptor antagonist, 7E3 F(ab')2, at 4 h after embolic stroke.
9 d delayed rht-PA treatment in a rat model of embolic stroke.
10 ound to be independent predictors of thrombo-embolic stroke.
11 ases its therapeutic window for treatment of embolic stroke.
12  heart failure, and atrial fibrillation with embolic stroke.
13 pericardiocentesis, and 1 patient with minor embolic stroke.
14 1 in cerebral microvascular remodeling after embolic stroke.
15 lity of life and is associated with risk for embolic stroke.
16 ion is associated with an increased risk for embolic stroke.
17                          There were no major embolic strokes.
18          Carotid stenosis is a key source of embolic strokes.
19 of mitral-valve prolapse among patients with embolic stroke (28 to 40 percent), especially among youn
20 cific WMH lesion pattern among patients with embolic stroke aetiology.
21 is that prevents atrial fibrillation-related embolic stroke and ablation techniques that decrease the
22 diac arrhythmia, is the most common cause of embolic stroke and death associated with heart failure.
23 rdiovascular morbidity and mortality through embolic stroke and heart failure.
24 opment of a three-dimensional simulation for embolic stroke and its application to an in silico clini
25           Male Wistar rats were subjected to embolic stroke and received treatment via a femoral vein
26 es were related to the frequency of probable embolic stroke and to clinical and transthoracic echocar
27           Male Wistar rats were subjected to embolic stroke and treated with the combination of rtPA
28                                           In embolic stroke animals, positron emission tomographic-co
29 hort of consecutive patients presenting with embolic stroke at an academic hospital and tertiary refe
30    Administration of sildenafil to rats with embolic stroke enhances angiogenesis and selectively inc
31 competent 29-year-old male presented with an embolic stroke from an unusual primary cardiac lymphoma.
32 that include a reduction in the incidence of embolic stroke from cardiac, aortic and carotid sites, s
33 lasminogen activator, or both, 4 hours after embolic stroke improves the functional outcome and reduc
34                                    Following embolic stroke in male C57bl/6 mice, thrombolysis using
35            In a clinically relevant model of embolic stroke in rodents, we now show that administrati
36 emorrhage after transient brain ischemia and embolic stroke in rodents.
37 (NILT) improves behavioral outcome following embolic strokes in embolized rabbits and clinical rating
38 is more effective than aspirin in preventing embolic strokes in patients older than 75 years of age,
39 t improving behavioral performance following embolic strokes in rabbits.
40 oof-of-concept for large in silico trials of embolic stroke including 3D information, identifying tha
41 onal cortical blood flow (RCBF) following an embolic stroke is beneficial to neurological outcome.
42                                              Embolic stroke is the most devastating consequence of at
43 ients with non-valvular atrial fibrillation, embolic stroke is thought to be associated with left atr
44  cerebral ischemia using a rabbit small clot embolic stroke model (RSCEM) using clinical rating score
45 used a modification of the rabbit small clot embolic stroke model (RSCEM), a multiple infarct ischemi
46 ical ATP content using the rabbit small clot embolic stroke model (RSCEM), the model originally used
47 infarct ischemia using the rabbit small clot embolic stroke model (RSCEM).
48                        The rabbit large clot embolic stroke model has been used for over 23 years to
49 hemic damage in both size and severity in an embolic stroke model of rat with and without a therapeut
50           Lastly, we show that in the rabbit embolic stroke model, hemorrhages are adjacent to areas
51  a fully blinded and randomized manner in an embolic stroke model, we determined if CEPO would be use
52 s has not been demonstrated using an in vivo embolic stroke model.
53                              In experimental embolic stroke models, MMP inhibitors decreased cerebral
54 7); arrhythmic sudden death (SD) (n=17); and embolic stroke (n=2).
55 ation in the chronic stage of a rat model of embolic stroke (n=6), and (ii) whether this process can
56 elated mortality events (0.64%/y), including embolic stroke (n=6), progressive heart failure or trans
57 tid crush injury (mural thrombosis model) or embolic stroke (occlusive thrombosis model) followed by
58  50% of patients 60 years or younger with an embolic stroke of undetermined source (cryptogenic strok
59 nance imaging (MRI) has revealed fibrosis in embolic stroke of undetermined source (ESUS) patients co
60                                              Embolic stroke of undetermined source (ESUS) refers to a
61      To address this problem, the concept of embolic stroke of undetermined source (ESUS) was develop
62                                     The term embolic stroke of undetermined source (ESUS) was introdu
63  One in six ischaemic stroke patients has an embolic stroke of undetermined source (ESUS), defined as
64 young adults, and most meet criteria for the embolic stroke of undetermined source (ESUS).
65 e, for the treatment of patients with recent embolic stroke of undetermined source and indirect evide
66 isease, leading to the recent formulation of embolic stroke of undetermined source as a distinct targ
67                A proportion of patients with embolic stroke of undetermined source have silent atrial
68 , recent clinical trials have indicated that embolic stroke of undetermined source may often stem fro
69 t on imaging) to predict the likelihood that embolic stroke of undetermined source was caused by a PF
70                                    The term 'embolic stroke of undetermined source' (ESUS) is used to
71 of Systemic Embolism in Patients With Recent Embolic Stroke of Undetermined Source) and the RE-SPECT
72 Versus Acetylsalicylic Acid in Patients With Embolic Stroke of Undetermined Source) provides an oppor
73 Secondary Stroke Prevention in Patients With Embolic Stroke of Undetermined Source).
74 ial cardiomyopathy may explain many cases of embolic stroke of undetermined source, and oral anticoag
75 ested for stroke prevention in patients with embolic stroke of undetermined source, including specifi
76                    Cryptogenic stroke, named embolic stroke of undetermined source, refers to patient
77 etes, are independent predictors of AF after embolic stroke of undetermined source.
78  provide a net benefit in conditions such as embolic stroke of undetermined source.
79 vention of recurrent stroke in patients with embolic stroke of undetermined source.
80 he prevention of thrombosis in patients with embolic stroke of unknown source, heart failure, coronar
81 ing recurrent stroke in patients with recent embolic strokes of undetermined source (ESUS) and left v
82                 Accordingly, we propose that embolic strokes of undetermined source are a therapeutic
83 l anticoagulants for secondary prevention of embolic strokes of undetermined source are warranted.
84 enosis (OR, 7.52; CI, 6.22-9.09; P < 0.001), embolic stroke (OR, 4.43; CI, 3.05-6.42; P < 0.001), hyp
85 cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial p
86 with in-hospital death, nonfatal recurrence, embolic stroke, or delayed normalization of ejection fra
87  8 or more emboli per hour was predictive of embolic stroke (P = 0.0076).
88 ion burden as assessed on the Fazekas scale, embolic stroke pattern, infarct distribution and pertine
89                                    Following embolic stroke, pharmacological thrombolysis limited inf
90 gnificant impact on clot trajectory and thus embolic stroke propensity through the left common caroti
91 o HT data measured histologically at 48 h in embolic stroke rats, the enhanced areas by Gd-DTPA at 24
92 s document provides the current views on (1) embolic/stroke risk, (2) ischemic/thrombotic cardiac ris
93 y cause of death in HCM virtually limited to embolic stroke, supporting a low threshold for initiatin
94 iated with a substantially increased risk of embolic stroke/TIA.
95                  In conclusion, following an embolic stroke, TNFalpha administration increased the in
96 se middle cerebral occlusion (MCAO) model of embolic stroke to study neuronal degeneration following
97  with Gd-DTPA to detect HT in a rat model of embolic stroke treated with rtPA and a glycoprotein IIb/
98                             The incidence of embolic stroke was higher in AFIB (n = 8) vs. no AFIB (n
99                                              Embolic stroke was induced in 8 male Wistar rats and mag
100                            Acute ischemic or embolic stroke was seen in 7 patients (16%) with an over
101 imvastatin-induced neuroprotection following embolic strokes, we used pharmacological intervention wi
102 of sildenafil, male Wistar rats subjected to embolic stroke were treated with sildenafil (n=11) or sa
103 ch curvature is an important risk factor for embolic stroke which should be tested in future clinical
104 major complication of carotid angioplasty is embolic stroke, which may occur after balloon inflation
105 in a nonhuman primate model (n = 2) of acute embolic stroke without or with thrombolytic therapy.

 
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