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Ischemic Attack clinical trials

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NCT ID: NCT03688815 Completed - Clinical trials for Ischemic Heart Disease

Dipyridamole Induced Ischemia and Biomarkers

Start date: January 1, 2009
Phase:
Study type: Observational

Analysis of certain biomarkers and transient myocardial perfusion deficit revealed by myocardial perfusion scintigraphy.

NCT ID: NCT03162588 Completed - Ischemic Stroke Clinical Trials

Multiple Burrhole Therapy With Erythropoietin for Unstable Moyamoya

Start date: May 1, 2010
Phase: Phase 1/Phase 2
Study type: Interventional

In this study, the investigators aim to evaluate the indirect revascularization outcomes of a new combination therapy of multiple burrhole procedure with promotion of arteriogenesis by intravenous (IV) erythropoietin (EPO) pretreatment on Moyamoya patients with acute neurological presentation, and outline the clinical and vascular factors associated with revascularization through the burrholes.

NCT ID: NCT02722720 Completed - Stroke Clinical Trials

Carotid Arteries Stenting Complications: Transradial Approach Versus Transfemoral

Start date: September 2015
Phase: N/A
Study type: Interventional

The aim is to compare the safety of using transfemoral and transradial approach in patient undergoing carotid arteries stenting.

NCT ID: NCT01955642 Completed - Brain Ischemia Clinical Trials

Evaluation of the Biological Response to Clopidogrel in Patients With Ischemic Stroke

AAPIX
Start date: September 2013
Phase: N/A
Study type: Observational

Ischemic stroke (AIC) is the leading cause of non-traumatic disability in adults, the second leading cause of dementia and the third leading cause of death in France. Clopidogrel is one of the recommended first line in the secondary prevention of AIC non cardioembolic origin. However recurrences occur in approximately 9% of patients receiving clopidogrel. Some studies in patients with coronary artery disease have made the connection between these treatment failures and non-biological response to clopidogrel. This non-biological response is found for approximately 30% to 50% of patients. Several mechanisms may explain this non-response. The most accepted mechanism is pharmacokinetic. Indeed, clopidogrel is a prodrug that requires intestinal absorption by P-glycoprotein (PGP) and a transformation by hepatic cytochrome into active metabolites. The genetic polymorphism of proteins involved in these two steps explain the low plasma concentration of active metabolites and thus the low efficacy of clopidogrel in some patients. A new pharmacodynamic hypothesis suggests the involvement of platelet alpha 2-adrenergic receptors. The activation of these receptors potentiates signaling pathway P2Y12 receptor (channel inhibited by clopidogrel) and helps reduce platelet aggregation inhibiting response to clopidogrel.

NCT ID: NCT01706133 Completed - Stroke Clinical Trials

An Intervention for Elderly in Emergency Services

Start date: June 2013
Phase: N/A
Study type: Interventional

-Can a scheme based on inter geriatricians visiting nurse consultants and reduce negative impacts on the health of elderly over 70 years ?