Risk of recurrent stroke, myocardial infarction, or death in hospitalized stroke patients.

OBJECTIVE: This study examines the risk of recurrent stroke, myocardial infarction (MI), vascular death, or all-cause death after hospitalized stroke in South Carolina. METHODS: Patients with a primary diagnosis of stroke discharged from the year 2002 were identified from the state hospital discharge database. Kaplan-Meier estimates of recurrent stroke, MI, vascular death, all-cause death, and composite events were calculated at 1 month, 6 months, 1 year, 2 years, 3 years, and 4 years. Prognostic factors were assessed with multivariate Cox proportional hazard models. RESULTS: The search strategy identified 10,399 patients in 2002. The Kaplan-Meier estimate of cumulative risk at 1 month, 6 months, 1 year, 2 years, 3 years, and 4 years for recurrent stroke is 1.8%, 5.0%, 8.0%, 12.1%, 15.2%, and 18.1%; MI, 0.3%, 1.0%, 2.1%, 3.7%, 5.0%, and 6.2%; all-cause death, 14.6%, 20.6%, 24.5%, 30.9%, 36.2%, and 41.3%; vascular death, 11.4%, 14.8%, 17.1%, 20.7%, 23.8%, and 26.7%; and composite events of recurrent stroke, MI, or vascular death 13.6%, 19.5%, 24.7%, 31.6%, 36.8%, and 41.3%. The hazard ratio for composite events (recurrent stroke, MI, or death) increases with age (1.38, 1.35-1.41), is 1.12 (1.05-1.19) for African Americans compared to Caucasians, is 1.67 (1.57-1.77) for patients with a higher comorbidity index (> or = 2 vs <2), and is 1.34 (1.28-1.39) for patients with subarachnoid hemorrhage or intracerebral hemorrhage compared with ischemic stroke. CONCLUSIONS: These findings suggest there is room for further improvement in secondary stroke prevention in South Carolina.

Tianeptine increases brain-derived neurotrophic factor expression in the rat amygdala.

Chronic restraint stress affects hippocampal and amygdalar synaptic plasticity as determined by electrophysiological, morphological and behavioral measures, changes that are inhibited by some but not all antidepressants. The efficacy of some classes of antidepressants is proposed to involve increased phosphorylation of cAMP response element binding protein (CREB), leading to increased expression of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF). Conversely, some studies suggest that acute and chronic stress downregulate BDNF expression and activity. Accordingly, the aim of the current study was to examine total and phosphorylated CREB (pCREB), as well as BDNF mRNA and protein levels in the hippocampus and amygdala of rats subjected to chronic restraint stress in the presence and absence of the antidepressant tianeptine. In the hippocampus, chronic restraint stress increased pCREB levels without affecting BDNF mRNA or protein expression. Tianeptine administration had no effect upon these measures in the hippocampus. In the amygdala, BDNF mRNA expression was not modulated in chronic restraint stress rats given saline in spite of increased pCREB levels. Conversely, BDNF mRNA levels were increased in the amygdala of chronic restraint stress/tianeptine rats in the absence of changes in pCREB levels when compared to non-stressed controls. Amygdalar BDNF protein increased while pCREB levels decreased in tianeptine-treated rats irrespective of stress conditions. Collectively, these results demonstrate that tianeptine concomitantly decreases pCREB while increasing BDNF expression in the rat amygdala, increases in neurotrophic factor expression that may participate in the enhancement of amygdalar synaptic plasticity mediated by tianeptine.