RESUMEN
BACKGROUND AND PURPOSE: Previous studies showed that insular strokes are associated with electrocardiographic (ECG) changes. However, they did not take into account the 1(st) ECG recorded at admission, but continuous ECG recorded up to 72 hours after onset. Whether these changes are the consequence of the infarct, or are associated with a cardiac source of cerebral ischemia, remains unsettled. If ECG changes are the consequence of insular infarcts, they should not have developed by the time of admission. The aim of this study was to test the hypothesis that ECG changes in patients with insular infarcts are not present at admission. METHODS: We recruited consecutive patients admitted within 48 hours (median 3 hours) after the onset of symptoms of acute hemispheric cerebral ischemia. We compared ECG variables between patients with and without insular infarcts, and with left and right insular infarcts. RESULTS: The study population consisted of 208 patients (94 men; median age: 69 years). Seventy patients had a recent insular infarct (right in 33). ECG variables did not significantly differ between patients with and without insular infarcts, and with left and right insular infarcts. These results were not explained by a lack of statistical power (1-beta >/= 0.90). CONCLUSION: The lack of statistical link between insular infarcts and ECG changes at admission, suggests that ECG changes are not associated with the cause of insular infarcts, but are their consequence.
Asunto(s)
Infarto Cerebral/fisiopatología , Electrocardiografía/métodos , Frecuencia Cardíaca/fisiología , Accidente Cerebrovascular/patología , Accidente Cerebrovascular/fisiopatología , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Progresión de la Enfermedad , Femenino , Escala de Coma de Glasgow/estadística & datos numéricos , Humanos , Masculino , Persona de Mediana Edad , Examen Neurológico , Factores de TiempoRESUMEN
In stroke, there is an imperative need to develop disease-modifying drugs able to (1) induce neuroprotection and vasculoprotection, (2) modulate recovery and brain plasticity, and (3) limit the short-term motor and cognitive consequences. We hypothesized that fenofibrate, a peroxisome proliferator-activated receptor-α (PPAR-α) agonist, could exert a beneficial effect on immediate and short-term poststroke consequences related to its pleiotropic mechanisms. Rats or mice were subjected to focal ischemia to determine the effects of acute treatment by fenofibrate on (i) motor and memory impairment, (2) both cerebral and vascular compartments, (3) inflammation, (4) neurogenesis, and (5) amyloid cascade. We show that fenofibrate administration results in both neuronal and vascular protection and prevents the short-term motor and cognitive poststroke consequences by interaction with several mechanisms. Modulation of PPAR-α generates beneficial effects in the immediate poststroke consequences by mechanisms involving the interactions between polynuclear neutrophils and the vessel wall, and microglial activation. Fenofibrate modulates mechanisms involved in neurorepair and amyloid cascade. Our results suggest that PPAR-α agonists could check the key points of a potential disease-modifying effect in stroke.
Asunto(s)
Isquemia Encefálica/tratamiento farmacológico , Fenofibrato/uso terapéutico , Fármacos Neuroprotectores/uso terapéutico , PPAR alfa/agonistas , Animales , Conducta Animal/efectos de los fármacos , Isquemia Encefálica/complicaciones , Isquemia Encefálica/metabolismo , Isquemia Encefálica/fisiopatología , Modelos Animales de Enfermedad , Relación Dosis-Respuesta a Droga , Esquema de Medicación , Fenofibrato/administración & dosificación , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Memoria/efectos de los fármacos , Ratones , Ratones Endogámicos C57BL , Actividad Motora/efectos de los fármacos , Neurogénesis/efectos de los fármacos , Fármacos Neuroprotectores/administración & dosificación , Ratas , Ratas Wistar , Factores de Tiempo , Vasodilatación/efectos de los fármacosRESUMEN
In the present subanalysis of a cross-sectional study showing the favorable effect of prior transient ischemia, leisure-time physical activity, and lipid-lowering drug therapy on stroke severity, we aimed to evaluate whether previous physical activity was dose dependently associated to minor stroke (NIHSS 0-3) and to identify possible underlying factors. Among 362 consecutive patients, less severe stroke was related to weekly exercise duration prior to stroke (no exercise: 36.1%; <2 hours: 49.3%; 2-5 hours: 58.8%; >5 hours: 64.0%; P = 0.003). Only weak and moderate exercise practices were protective (weak: 50.0%; moderate: 79.3%; heavy: 22.2%; P < 0.0001). Such a beneficial effect was observed independently of age and was associated with a trend to a lower frequency of arterial hypertension, alcohol abuse, and a better metabolic profile. Besides other therapeutic approaches, physical activity may be a simple way to decrease cerebral ischemia severity.