Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
J Neurointerv Surg ; 6(5): 373-8, 2014 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-23794673

RESUMEN

OBJECTIVE: Limited data exist regarding the use of antiplatelet response assays during neuroendovascular intervention. We report outcomes after carotid artery stenting (CAS) based on aspirin and P2Y12 assays. METHODS: We retrospectively identified patients who had aspirin and P2Y12 assays at the time of stenting. Aspirin (325 mg) and clopidogrel (75 mg) were started 7-10 days pre-intervention. If not possible, aspirin (650 mg) and clopidogrel (600 mg) loading doses were given pre-intervention. Assays were checked on postoperative day 0/1. Outcomes included neurological ischemic sequela at 30 days, 1 and 2 years, as well as 30 day death/hemorrhage/myocardial infarction. RESULTS: 449 patients were included. Mean P2Y12 reaction unit (PRU) values were higher in patients with an ipsilateral ischemic event (stroke/transient ischemic attack (TIA)) or stroke (alone) at 1 and 2 years than in patients with no events: ischemic event versus no event at 1 year, 252 vs 202 (p=0.008); stroke versus no stroke at 1 year, 252 versus 203(p=0.029); ischemic event versus no event at 2 years, 244 vs 203 (p=0.047); stroke versus no stroke at 2 years, 243 versus 203 (p=0.082). Ischemic event free survival (stroke/TIA, p=0.0268) and overall survival (p=0.0291) post-CAS were longer in patients with PRU ≤198 compared with an initial threshold of PRU ≤237. Mean PRU values were higher in patients who died from all causes at 30 days than in survivors (p=0.031). No correlation was found between lower PRU values and hemorrhage. Aspirin reaction units did not correlate with outcome. CONCLUSIONS: PRU ≤198 may be associated with a lower incidence of ischemic neurological sequela and death post-CAS. Prospective studies are needed to validate the relationship between antiplatelet assays and outcomes post-CAS.


Asunto(s)
Aspirina/administración & dosificación , Estenosis Carotídea/tratamiento farmacológico , Estenosis Carotídea/cirugía , Revascularización Cerebral/métodos , Stents , Ticlopidina/análogos & derivados , Adulto , Anciano , Anciano de 80 o más Años , Isquemia Encefálica/mortalidad , Isquemia Encefálica/prevención & control , Estenosis Carotídea/mortalidad , Clopidogrel , Monitoreo de Drogas/métodos , Femenino , Estudios de Seguimiento , Humanos , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Inhibidores de Agregación Plaquetaria/administración & dosificación , Prevalencia , Receptores Purinérgicos P2Y12/metabolismo , Sistema de Registros/estadística & datos numéricos , Estudios Retrospectivos , Accidente Cerebrovascular/mortalidad , Accidente Cerebrovascular/prevención & control , Ticlopidina/administración & dosificación , Resultado del Tratamiento
2.
Clin Neurol Neurosurg ; 115(11): 2362-4, 2013 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-24034819

RESUMEN

OBJECTIVE: Intraventricular tissue plasminogen activator (alteplase) has been advocated for prevention of vasospasm in aneurysmal subarachnoid hemorrhage and treatment of traumatic or spontaneous intraventricular hemorrhage. External ventricular drain (EVD) insertion is often performed to manage increased intracranial pressure and hydrocephalus associated with these disease states. EVD-related ventriculitis is a serious infection with an up to 50% mortality rate. METHODS: We assessed the EVD infection rate in patients receiving intraventricular alteplase over a 12-month period. Patients were divided into intraventricular alteplase and non-intraventricular alteplase groups; ventriculitis rates were compared. RESULTS: EVDs were placed in 93 patients. Six of 7 (86%) patients who received intraventricular alteplase developed ventriculitis versus 4 of 86 (5%) patients in the non-intraventricular alteplase group (p<0.0001). CONCLUSION: Intraventricular alteplase use may increase ventriculitis risk. Currently, we reserve intraventricular alteplase for patients with EVDs obstructed by hematoma accompanied by increased intracranial pressure.


Asunto(s)
Infección de la Herida Quirúrgica/etiología , Activador de Tejido Plasminógeno/uso terapéutico , Ventriculostomía/efectos adversos , Hemorragia Cerebral/tratamiento farmacológico , Hemorragia Cerebral/cirugía , Femenino , Humanos , Hidrocefalia/tratamiento farmacológico , Hidrocefalia/cirugía , Masculino , Terapia Trombolítica/efectos adversos , Terapia Trombolítica/métodos , Resultado del Tratamiento , Ventriculostomía/métodos
3.
Ann Pharmacother ; 40(11): 2053-8, 2006 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-17062831

RESUMEN

OBJECTIVE: To describe the hypotheses that may explain a diminished hemostatic response in a patient receiving multiple doses of recombinant coagulation factor VIIa (rFVIIa) for off-label treatment of bleeding events. CASE SUMMARY: A 70-year-old female with a significant history of idiopathic thrombocytopenic purpura (ITP) was admitted for coronary artery bypass grafting surgery. The patient developed thrombocytopenia and persistent hemorrhage postoperatively that was refractory to conventional therapy for ITP. She experienced an initial hemostatic response to rFVIIa after receiving 3 doses. During her second trial of rFVIIa a few days later, the duration of hemostatic effect was approximately half that of the first. The patient then received rFVIIa almost daily over the following 9 days to which she remained unresponsive, ultimately resulting in death. All doses in this patient were 9.6 mg (101 microg/kg), except the last, which was 4.8 mg (50.5 microg/kg). DISCUSSION: Several hypotheses may explain this patient's resistance to rFVIIa therapy. Two involve depletion of platelets or coagulation factors essential for rFVIIa efficacy. Another involves development of an antibody to rFVIIa. The last involves acidemia, which may interfere with the pharmacologic effect of rFVIIa. CONCLUSIONS: The combination of persistent thrombocytopenia and exhaustion of coagulation factors is the likely cause leading to resistance to rFVIIa therapy in this patient.


Asunto(s)
Factor VII/uso terapéutico , Púrpura Trombocitopénica Idiopática/tratamiento farmacológico , Anciano , Resistencia a Medicamentos/efectos de los fármacos , Resistencia a Medicamentos/fisiología , Factor VIIa , Femenino , Humanos , Recuento de Plaquetas , Púrpura Trombocitopénica Idiopática/sangre , Púrpura Trombocitopénica Idiopática/complicaciones , Proteínas Recombinantes/uso terapéutico , Trombocitopenia/sangre , Trombocitopenia/complicaciones , Trombocitopenia/tratamiento farmacológico
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA