Depression but not anxiety predicts recurrent cerebrovascular events.

OBJECTIVES: Depression and anxiety after stroke occur frequently and have been suggested to have negative influence on functional outcomes. However, the effect of emotional symptoms on stroke recurrence is uncertain. The aim of this study was to define the effect of emotional symptoms on recurrent cerebrovascular events in patients with ischemic stroke. MATERIALS AND METHODS: This was a hospital-based cohort study including patients with ischemic stroke who participated in a Community Stroke Care Program that provided secondary stroke prevention strategies during 6 months transition period after discharge. We examined the association between depression and anxiety and the risk of recurrent cerebrovascular events using logistic regression model. Depression and anxiety were defined as a score of 7 or more in Hospital Anxiety and Depression Scale at 2 weeks after discharge. Recurrent cerebrovascular events comprised any recurrent stroke and transient ischemic attack (TIA) occurring during 6 months after discharge. RESULTS: Among 182 patients, 29 (15.9%) were depressed and 41 (22.5%) had anxiety symptoms. During the follow-up period, 9 patients experienced recurrent cerebrovascular events (5 of stroke and 4 of TIA). Depression was associated with recurrent cerebrovascular events at 6 months after adjustment for age, sex, and stroke severity (OR 5.22, 95% CI 1.08-25.12; P = 0.04), whereas anxiety was not (OR 0.98, 95% CI 0.2-4.92; P = 0.982). CONCLUSIONS: Depression occurring early after stroke was associated with the increased risk of recurrent cerebrovascular events in ischemic stroke survivors. Care plan to detect and manage depression should be implemented to prevent recurrent stroke.

Endostatin and physical exercise in young female and male athletes and controls.

It was suggested that endostatin, an angiogenic mediator, is influenced by physical exercise. We performed bicycle stress testing in 88 healthy non-smoking female and male individuals, divided into athlete and non-athlete groups. Serum endostatin and norepinephrine were measured at rest, after reaching maximum workload and after 20 min of recovery. At baseline, both female and male controls showed significant lower levels compared to female and male athletes (89.39±15.32 resp. 93.39±15.00 ng/ml; p<0.001 vs. 128.81±20.84 resp. 147.52±27.72; p<0.001). An increase in endostatin levels in both groups and sexes was associated with bicycle stress testing (p for all groups<0.001). The extent of endostatin increase was comparable in both groups and sexes and varied between 23-27%. Significance was obscured when the performance was entered as covariate. Acutely induced physical strain leads to an increase in endostatin levels in athletes and controls of both sexes, the extent of increase depending on the extent of workload. An athletic lifestyle with >3 h of endurance training/week seems to lead to higher long-term endostatin levels which might play a role in the connection between sports and cardiovascular prevention.