Background: and Purpose Although numerous measures for stroke exist, stroke remains one of the leading causes of death in Japan. In this study, we aimed to determine the long-term survival rate after first-ever stroke using data from a large-scale population-based stroke registry study in Japan. Methods: Part of the Shiga Stroke and Heart Attack Registry, the Shiga Stroke Registry is an ongoing population-based registry study of stroke, which covers approximately 1.4 million residents of Shiga Prefecture in Japan. A total 1,880 patients with non-fatal first-ever stroke (among 29-day survivors after stroke onset) registered in 2011 were followed up until December 2016. Five-year cumulative survival rates were estimated using the Kaplan-Meier method, according to subtype of the index stroke. Cox proportional hazards models were used to assess predictors of subsequent all-cause death. Results: During an average 4.3-year follow-up period, 677 patients died. The 5-year cumulative survival rate after non-fatal first-ever stroke was 65.9%. Heterogeneity was present in 5-year cumulative survival according to stroke subtype: lacunar infarction, 75.1%; large-artery infarction, 61.5%; cardioembolic infarction, 44.9%; intracerebral hemorrhage, 69.1%; and subarachnoid hemorrhage, 77.9%. Age, male sex, Japan Coma Scale score on admission, and modified Rankin Scale score before stroke onset were associated with increased mortality during the chronic phase of ischemic and hemorrhagic stroke. Conclusions In this study conducted in a real-world setting of Japan, the 5-year survival rate after non-fatal first-ever stroke remained low, particularly among patients with cardioembolic infarction and large-artery infarction in the present population-based stroke registry.

Objective To assess the effect of D-JNKI1, an inhibitor of c-Jun N-terminal kinase (JNK), on delayed neuronal death (DND) in a gerbil model of transient global cerebral ischemia, so as to further study the roles of JNK activation in mediating neuronal cell death in brain ischemia. Methods Fifty-five Mongolian gerbils were randomly divided into 11 groups. Animals (n=35) assigned into 7 groups (n=5 per group) were subjected to 5-min occlusion of bilateral common carotid arteries (BCCAO);among the 7 groups, different doses of D-JNKI1 (0.00012, 0.0012, 0.012, 0.12, 1.2 μmol/L in 2 μL PBS,n=5 each) were administered stereotaxically into right lateral ventricles 3 h after reperfusion; the control group (n=5) received 2 μL PBS; and another group (n=5) received 1.2 μmol/L of D-JNKI1 in 0.5 mL PBS intraperitoneally. Sham-operated animals (n=5) only received the exposure of bilateral common carotid arteries without occlusion. Three groups (n=5 in each) were pretreated with D-JNKI1 (0.00012,0.0012 μmol/L in 2 μL PBS) or only 2 μL PBS 30 min before 2-min BCCAO, and subjected to 5-min BCCAO 48 h after the first ischemic insult. All animals were sacrificed 4 d after 5-min BCCAO and prepared for frozen section and Nissl staining. Results The treatment with D-JNKI 3 h after 5-min ischemia was neuroprotective with a maximum effect at a dose of 0.0012 μmol/L. Pretreatment with D-JNKI augmented ischemic tolerance induced by 2-min ischemia. Conclusion D-JNKI1 has a potential neuroprotective effect on DND in CA1 of hippocampus in gerbils with global cerebral ischemia-reperfusion injury.