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Aspirin resistance coincide with clopidogrel non-response
Abstracts / Journal of the Neurological Sciences 357 (2015) e363–e423
Material and method: From August 2013 to Januar 2015 we treated 7 patients (2 women and 5 men aged 58-65 years, mean age 64 years), with occlusion of middle cereberal artery and simultaneously with significant stenosis (N90 %) or occlusion of internal carotid artery in carotid bifurcation at our department. All patients were admitted to hospital within 6 hours after onset of symptoms. Results: Acute carotid stenting was technically successful in all patients, 100 %. Intracranial recanalization with TICI 3 was achieved in 4 patients, TICI 2b in 3 patients. Symptomatic hemorrhage occurred in one patient. Good clinical outcomes (mRS ≤ 2 at 3 months) had 5 patients. Conclusion: Endovascular recanalization of tandem occlusion of extracranial internal carotid artery and middle cerebral artery is feasible with good technical and clinical results. doi:10.1016/j.jns.2015.08.1320
1257 WFN15-0594 Stroke Regulation of astrocyte networking by G-protein regulatory motif peptides of AGS3 protein K. Songa, M.S. Ockb, H.J. Chab. aPhysiology, Kosin University, Busan, Korea; bParasitology and Genetics, Kosin University, Busan, Korea Background: Inflammation characteristics in CNS disorder such as stroke, trauma, and autoimmunity have been essential for astrocyte. To investigate how inflammation signaling controls astrocyte functions, we texted effects of CXCR4 on cultured mouse primary cortical astrocyte. Objective: The aims of the present study were to examine the mechanisms by which CXCL12 affects cell death-specific signaling and modulation in astrocyte, which depend on activator of G-protein signaling (AGS) 3 and to identify specific molecules that suppress CXCL12-induced injury by acting on G-protein-coupled receptors. Methods: We used cytokine array to perform cytokine/chemokine secretion profiling, and measured its own signaling, which is involved to astrocyte functions. Results: Herein, AGS3 suppresses CXCL12-mediated upregulation of TNFα by regulating Gαi. We found that the G-protein regulatory (GPR) motif peptide in AGS3 binds to Gαi and downregulates TNFα expression and cell death; in contrast, this motif upregulates them. Mutated GPR peptide increased the expression of TGFβ but decreased the expression of TNFα, thus decreased astrocyte cell death. Moreover, CXCR4-induced dendritic extensions in 2D and 3D matrix cultures were inhibited by the mutant GPR peptide compared with a wild-type GPR peptide. Conclusion: These results suggest that inflammatory stimuli upregulate astrocyte molecular communications associated with cell death-related functions and significantly alter astrocyte signaling stimulated by CXCR4 GPCR.
doi:10.1016/j.jns.2015.08.1321
1260 WFN15-0259 Stroke Extensive cerebral venous sinus thrombosis originated from internal jugular vein catheter for chemoport J.E. Lee, K.S. Lee, Y.S. Oh, W. Kim, A. Cho. Neurology, Catholic University of Korea, Seoul, Korea
e369
Background and objective: Internal jugular vein catheterization for chemoport can be complicated by infection and thrombosis. Particularly in patients with malignancy, activated coagulation system is prone to the development of thrombosis. We aimed to report a case of cerebral venous thrombosis in a cancer patient with chemoport. Methods: We performed a chart review in a case of cerebral venous thrombosis developed from kinked internal jugular vein catheter chemoport. Results: A 58-year-old man with angioimmunoblastic T cell lymphoma presented with headache and left hemiparesis. Headache and left side weakness developed 8 days ago. The weakness was worsening for several days. Blood test showed increased level of D-dimer and fibrinogen degradation product. On initial diffusion weighted MRI, linear high signals on precentral gyrus were observed. On gradient-echo MRI, prominent linear branching dark signal intensities at both frontal, parietal, and temporal sulci, probable cortical vein congestion. MR venography revealed non visualization of both transverse sinus, partially visualized superior sagittal sinus. Engorgement of cortical veins, basal vein of Rosenthal, vein of Galen and straight sinus were also observed. On CT angiography, extensive venous sinus thrombosis along the superior sagittal vein, right transverse sinus due to the implanted chemoport with kinking catheter in the os of right internal jugular vein. With removal of the chemoport, the patient received anticoagulation. The patient’s symptom subsequently improved. Conclusion: This case warns the risk of cerebral venous thrombosis in a catheter imported patients in a highly thrombogenic condition such as malignancy. doi:10.1016/j.jns.2015.08.1322
1261 WFN15-0888 Stroke Aspirin resistance coincide with clopidogrel non-response I. Chooa, J.H. Kima, H.W. Kima, S.H. Ahna, J.Y. Jeonga, H.G. Kanga, M.Y. Kima, J.B. Bonga, K.H. Kima, H.G. Ob. aNeurology, Chosun University Hospital, Gwangju, Korea; bNeurology, Korea Veterans Hospital of Gwangju, Gwangju, Korea Background and Objective: Aspirin (ASA), the most commonly used antiplatelet agent, prevents stroke recurrence among patients with a recent stroke or transient ischemic attack (TIA). However, clinical and laboratory evidence demonstrates diminished or no response to ASA in some patients that is called ASA resistance. This situation has been reported to be independently associated with an increased risk of adverse cardiovascular events. Current evidence-based guidelines provide little or no recommendations on the proper management strategy for stroke patients who have ASA resistance. Also, clopidogrel non-responder by CYP2C19 polymorphism is reported about 20%, in particular in the case of East Asian 35-50% have been reported. The purpose of our study is that ASA resistance seen with clopidogrel non-response at the same time to analyze the frequency and the clinical difference. Methods and Results: 193 patients who admitted to ischemic stroke from February to May, 2014 in Chosun university hospital were assessed. For patients with cardioembolic stroke stroke and without resistance records were excluded. Resistance was checked after 5-7 days from ASA medication and analyzed using the PFA-100 aggregometer. CYP2C19 polymorphism was investigated. 44 patients (6.6%) showed ASA resistance. Clopidogrel intermediate or poor response were 18%. The 5 patients (11.3%) with ASA resistance were clopidogrel non-response. We found no correlation between dual resistance and vascular risk factors, type of stroke, severity or sex. However, patients with resistance to ASA presented a higher frequency of previous stroke (p = 0.01). doi:10.1016/j.jns.2015.08.1323
Material and method: From August 2013 to Januar 2015 we treated 7 patients (2 women and 5 men aged 58-65 years, mean age 64 years), with occlusion of middle cereberal artery and simultaneously with significant stenosis (N90 %) or occlusion of internal carotid artery in carotid bifurcation at our department. All patients were admitted to hospital within 6 hours after onset of symptoms. Results: Acute carotid stenting was technically successful in all patients, 100 %. Intracranial recanalization with TICI 3 was achieved in 4 patients, TICI 2b in 3 patients. Symptomatic hemorrhage occurred in one patient. Good clinical outcomes (mRS ≤ 2 at 3 months) had 5 patients. Conclusion: Endovascular recanalization of tandem occlusion of extracranial internal carotid artery and middle cerebral artery is feasible with good technical and clinical results. doi:10.1016/j.jns.2015.08.1320
1257 WFN15-0594 Stroke Regulation of astrocyte networking by G-protein regulatory motif peptides of AGS3 protein K. Songa, M.S. Ockb, H.J. Chab. aPhysiology, Kosin University, Busan, Korea; bParasitology and Genetics, Kosin University, Busan, Korea Background: Inflammation characteristics in CNS disorder such as stroke, trauma, and autoimmunity have been essential for astrocyte. To investigate how inflammation signaling controls astrocyte functions, we texted effects of CXCR4 on cultured mouse primary cortical astrocyte. Objective: The aims of the present study were to examine the mechanisms by which CXCL12 affects cell death-specific signaling and modulation in astrocyte, which depend on activator of G-protein signaling (AGS) 3 and to identify specific molecules that suppress CXCL12-induced injury by acting on G-protein-coupled receptors. Methods: We used cytokine array to perform cytokine/chemokine secretion profiling, and measured its own signaling, which is involved to astrocyte functions. Results: Herein, AGS3 suppresses CXCL12-mediated upregulation of TNFα by regulating Gαi. We found that the G-protein regulatory (GPR) motif peptide in AGS3 binds to Gαi and downregulates TNFα expression and cell death; in contrast, this motif upregulates them. Mutated GPR peptide increased the expression of TGFβ but decreased the expression of TNFα, thus decreased astrocyte cell death. Moreover, CXCR4-induced dendritic extensions in 2D and 3D matrix cultures were inhibited by the mutant GPR peptide compared with a wild-type GPR peptide. Conclusion: These results suggest that inflammatory stimuli upregulate astrocyte molecular communications associated with cell death-related functions and significantly alter astrocyte signaling stimulated by CXCR4 GPCR.
doi:10.1016/j.jns.2015.08.1321
1260 WFN15-0259 Stroke Extensive cerebral venous sinus thrombosis originated from internal jugular vein catheter for chemoport J.E. Lee, K.S. Lee, Y.S. Oh, W. Kim, A. Cho. Neurology, Catholic University of Korea, Seoul, Korea
e369
Background and objective: Internal jugular vein catheterization for chemoport can be complicated by infection and thrombosis. Particularly in patients with malignancy, activated coagulation system is prone to the development of thrombosis. We aimed to report a case of cerebral venous thrombosis in a cancer patient with chemoport. Methods: We performed a chart review in a case of cerebral venous thrombosis developed from kinked internal jugular vein catheter chemoport. Results: A 58-year-old man with angioimmunoblastic T cell lymphoma presented with headache and left hemiparesis. Headache and left side weakness developed 8 days ago. The weakness was worsening for several days. Blood test showed increased level of D-dimer and fibrinogen degradation product. On initial diffusion weighted MRI, linear high signals on precentral gyrus were observed. On gradient-echo MRI, prominent linear branching dark signal intensities at both frontal, parietal, and temporal sulci, probable cortical vein congestion. MR venography revealed non visualization of both transverse sinus, partially visualized superior sagittal sinus. Engorgement of cortical veins, basal vein of Rosenthal, vein of Galen and straight sinus were also observed. On CT angiography, extensive venous sinus thrombosis along the superior sagittal vein, right transverse sinus due to the implanted chemoport with kinking catheter in the os of right internal jugular vein. With removal of the chemoport, the patient received anticoagulation. The patient’s symptom subsequently improved. Conclusion: This case warns the risk of cerebral venous thrombosis in a catheter imported patients in a highly thrombogenic condition such as malignancy. doi:10.1016/j.jns.2015.08.1322
1261 WFN15-0888 Stroke Aspirin resistance coincide with clopidogrel non-response I. Chooa, J.H. Kima, H.W. Kima, S.H. Ahna, J.Y. Jeonga, H.G. Kanga, M.Y. Kima, J.B. Bonga, K.H. Kima, H.G. Ob. aNeurology, Chosun University Hospital, Gwangju, Korea; bNeurology, Korea Veterans Hospital of Gwangju, Gwangju, Korea Background and Objective: Aspirin (ASA), the most commonly used antiplatelet agent, prevents stroke recurrence among patients with a recent stroke or transient ischemic attack (TIA). However, clinical and laboratory evidence demonstrates diminished or no response to ASA in some patients that is called ASA resistance. This situation has been reported to be independently associated with an increased risk of adverse cardiovascular events. Current evidence-based guidelines provide little or no recommendations on the proper management strategy for stroke patients who have ASA resistance. Also, clopidogrel non-responder by CYP2C19 polymorphism is reported about 20%, in particular in the case of East Asian 35-50% have been reported. The purpose of our study is that ASA resistance seen with clopidogrel non-response at the same time to analyze the frequency and the clinical difference. Methods and Results: 193 patients who admitted to ischemic stroke from February to May, 2014 in Chosun university hospital were assessed. For patients with cardioembolic stroke stroke and without resistance records were excluded. Resistance was checked after 5-7 days from ASA medication and analyzed using the PFA-100 aggregometer. CYP2C19 polymorphism was investigated. 44 patients (6.6%) showed ASA resistance. Clopidogrel intermediate or poor response were 18%. The 5 patients (11.3%) with ASA resistance were clopidogrel non-response. We found no correlation between dual resistance and vascular risk factors, type of stroke, severity or sex. However, patients with resistance to ASA presented a higher frequency of previous stroke (p = 0.01). doi:10.1016/j.jns.2015.08.1323