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Stroke embolic

Del Zoppo GJ, Poeck K, Pessin MS, Wolpert SM, Eurlan AJ, Ferhert A, Alberts MJ, Zivin JA, Wechsler L, Busse O. Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke. Ann Neurol. 1992 32 78-86. [Pg.55]

Dijkhuizen RM, Asahi M, Wu O, Rosen BR, Lo EH. Delayed rt-PA treatment in a rat embolic stroke model Diagnosis and prognosis of ischemic injury and hemorrhagic transformation with magnetic resonance imaging. J Cereb Blood Flow Metab. 2001 21 964-971. [Pg.55]

Zivin JA, Lyden PD, DeGirolami U, Kochhar A, Mazzarella V, Hemenway CC, Johnston P. Tissue plasminogen activator. Reduction of neurologic damage after experimental embolic stroke. Arch Neurol. 1988 45 387-391. [Pg.56]

Lapchak PA, Araujo DM, Pakola S, Song D, Wei J, Zivin JA. Microplasmin a novel thrombolytic that improves behavioral outcome after embolic strokes in rabbits. Stroke 2002 33 2279-2284. [Pg.94]

Mahon BR, Nesbit GM, Barnwell SL, Clark W, Marotta TR, Weill A, Teal PA, Qureshi Al. North American clinical experience with the EKOS MicroLysUS infusion catheter for the treatment of embolic stroke. Am J Neuroradiol 2003 24 534-538. [Pg.96]

Meden P, Overgaard K, Sereghy T, Boysen G. Enhancing the efficacy of thrombolysis by ampa receptor blockade with nbqx in a rat embolic stroke model. J Neurol Sci 1993 119 209-216. [Pg.118]

Zivin JA, Mazzarella V. Tissue plasminogen activator plus glutamate antagonist improves outcome after embolic stroke. Arch Neurol 1991 48 1235-1238. [Pg.118]

Andersen M, Overgaard K, Meden P, Boysen G, Choi SC. Effects of citicoline combined with thrombol3ftic therapy in a rat embolic stroke model. Stroke 1999 30 1464-1471. [Pg.119]

The Heparin in Acute Embolic Stroke Trial (HAEST) was a multicenter, randomized trial of the effect of LMWH (dalteparin 100 lU/kg sc twice daily) or aspirin (160 mg once daily) for the acute treatment of 449 patients with ischemic stroke and atrial fibrillation (AF). The primary outcome was the rate of recurrent stroke within 14 days. No difference in rates of early recurrence (8.5% dalteparin treated vs. 7.5% aspirin treated) or good 3-month functional outcome was found. The frequency of early slCH was 2.7% on dalteparin versus 1.8% on aspirin. [Pg.141]

Sasaki O, Shigekazu T, Koike T, Koizumi T, Tanaka R. Fibrinolytic therapy for acute embolic stroke intravenous, intracarotid, and intra-arterial local approaches. Neurosurgery 1995 36 246-253. [Pg.158]

Cerebral Embolism Study Group. Immediate anticoagulation of embolic stroke a randomized trial. Cerebral Embolism Study Group. Stroke 1983 14 668-676. [Pg.160]

II. Suspected embolic stroke with patent large arteries... [Pg.201]

Cardioembolism Cardioembolism accounts for approximately 30% of all stroke and 25-30% of strokes in the young (age <45 years)." AF accounts for a large proportion of these strokes (15-25%). Symptoms may be suggestive, but they are not diagnostic. Repetitive, stereotyped, transient ischemic attacks (TIAs) are unusual in embolic stroke. The classic presentation for cardioembolism is the sudden onset of maximal symptoms. The size of the embolic material determines, in part, the course of the embolic material. Small emboli can cause retinal ischemic or lacunar symptoms. Posterior cerebral artery territory infarcts, in particular, are often due to cardiac embolism. This predilection is not completely consistent across the various cardiac structural abnormalities that predispose to stroke, and may be due to patterns of blood flow associated with specific cardiac pathologies. [Pg.203]

Dutka, A.J., Kochanek, P.M. and Hallenbeck, J.M. (1989). Influence of granulocytopenia on canine cerebral ischemia induced by air embolism. Stroke 20, 390-395. [Pg.81]

Alteplase (rt-PA) +++ 50-60% ++/++ Bolus followed by infusions over 90 minutes weight-based dosing 2,750 Pulmonary embolism, stroke, clearance of an occluded arteriovenous catheter... [Pg.97]

AF or atrial flutter may be manifested by the entire range of symptoms associated with other supraventricular tachycardias, but syncope is not a common presenting symptom. An additional complication of AF is arterial embolization resulting from atrial stasis and poorly adherent mural thrombi, which accounts for the most devastating complication embolic stroke. Patients with AF and concurrent mitral stenosis or severe systolic HF are at particularly high risk for cerebral embolism. [Pg.75]

Ischemic strokes account for 88% of all strokes and are due either to local thrombus formation or to emboli that occlude a cerebral artery. Cerebral atherosclerosis is a causative factor in most cases of ischemic stroke, although 30% are of unknown etiology. Emboli can arise either from intra- or extracranial arteries. Twenty percent of embolic strokes arise from the heart. [Pg.169]

V.a.1.4. Risks of HRT. HRT slightly increases the risk of DVT, pulmonary embolism, stroke, breast cancer (combined HRT), endometrial cancer (oestrogen-only HRT) and ovarian cancer (oestrogen-only HRT). Current estimates indicate... [Pg.769]

Suzuki M., Sasamata M., and Miyata K. (2003). Neuroprotective effects of YM872 coadministered with t-PA in a rat embolic stroke model. Brain Res. 959 169-172. [Pg.259]

CHD = myocardial infarction (Ml), significant myocardial ischemia (angina), history of coronary artery bypass graft (CABG), history of coronary angioplasty, angiographic evidence of lesions, carotid endarterectomy, abdominal aortic aneurysm, peripharal vascular disease (claudication), thrombotic/embolic stroke, transient ischemic attack (TIA)... [Pg.441]

Atrial fibrillation is increasing in incidence in developed countries and, because of the risk of embolic stroke, most patients require continuous anticoagulation. A large number of patients with atrial fibrillation are currently treated with vitamin K antagonists. Results of clinical trials in patients with atrial fibrillation indicate that oral direct TIs may become potential drugs for the prevention of embolic stroke and may replace warfarin (62,78,79-81). [Pg.115]

Yenari MA, de Crespigny A, Palmer JT, Roberts S, Schrier SL, Albers GW, Moseley ME, Steinberg GK (1997) Improved perfusion with rt-PA and hirulog in a rabbit model of embolic stroke. J Cereb Blood Flow Metab 17 401-411... [Pg.40]

Animal models of embolic stroke enable us to study effects of fibrinolytic drugs like recombinant tissue... [Pg.59]

J, Oertel WH, Baethmann A (2002) Early versus delayed thrombolysis in embolic stroke effects on blood flow, DC potential and infarct morphology. In Krieglstein J, Klumpp S (eds) Pharmacology of cerebral ischemia. MedPharm Scientific Publishers, Stuttgart, pp 159-169... [Pg.67]

Back T, Otto D, Kittner D, Hemmen T, Oertel WH (2004) Failure to enhance thrombolytic therapy by neuroprotection with memantine in embolic stroke. Cerebrovasc Dis 17 59 Baird AE, Benfield A, Schlaug G, Siewert B, Lovblad K-O, Edel-man RR, Warach S (1997) Enlargement of human cerebral... [Pg.67]

Busch E, Kruger K, Allegrini PR, Kerskens CM, Gyngell ML, Hoehn-Berlage M, Hossmann KA (1998) Reperfusion after thrombolytic therapy of embolic stroke in the rat magnetic resonance and biochemical imaging. J Cereb Blood Flow Metab 18 407-418... [Pg.68]

In the second part we will describe the clinical MR features of embolic stroke, with emphasis on cardioembolic stroke. [Pg.210]

Meden P., Overgaard K., Pedersen H., and Boysen G. (1994) The influence of body temperature on infarct volume and thrombolytic therapy in a rat embolic stroke model. Brain Res. 647,131-138. [Pg.59]

The effect of hypothermia in combination with thrombolytics has also been evaluated in only a few experimental studies. Meden et al. (11) studied differences in thrombolytic effectiveness in a rat embolic stroke model. In this study, 2 h of intraischemic hypothermia was administered with or without thrombolytic therapy. Thrombolysis was initiated at 2 h after ischemia onset. The investigators found that both hypothermia and thrombolysis significantly reduced infarct volume, but they could not demonstrate any added benefit of thrombolysis over hypothermia alone. A recent study by Wang et al. (12) used a focal embolic brain ischemia model to study the effects of minocycline, an antiinflammatory agent, alone or in combination with mild hypothermia (34—35°C started 1 h after embolization, 2-h duration). The results showed that both minocycline and the hypothermia-minocycline combination reduced infarct volume significantly, but no additive effect was observed. [Pg.98]

Wang C. X., Yang T. and Shuaib A. (2003) Effects of minocycline alone and in combination with mild hypothermia in embolic stroke. Brain Res. 963, 327-329. [Pg.102]

Shimizu T., Naritomi H., OeH., et al. (1996) Mild hypothermia prevents the development of cerebral edema and hemorrhagic transformation in acute embolic stroke. Cerebrovasc. Dis. (Suppl 2), 32-178. [Pg.117]


See other pages where Stroke embolic is mentioned: [Pg.32]    [Pg.56]    [Pg.50]    [Pg.301]    [Pg.1]    [Pg.9]    [Pg.11]    [Pg.43]    [Pg.57]    [Pg.61]    [Pg.63]    [Pg.70]    [Pg.137]    [Pg.145]    [Pg.224]    [Pg.6]   
See also in sourсe #XX -- [ Pg.569 ]




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Embolic stroke hypothermia

Embolism

Embolism ischemic stroke

Embolism major stroke

Embolization

Paradoxical embolism, stroke

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