RESUMO
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.
RESUMO
Background: Cerebral saccular aneurysm is a major cause of subarachnoid hemorrhage, one of the cerebrovascular diseases with the highest mortality. The mechanisms underlying the development of aneurysm, however, still remain unclear. Objective: The authors have made a series of reports on an animal model of experimentally induced cerebral aneurysms that resemble human cerebral aneurysms in their location and morphology. The objective of this brief review is to introduce our evidence about the pathogenesis of cerebral aneurysms using the experimentally induced cerebral aneurysm model, particularly focused upon the role of nitric oxide (NO) and shear stress on degenerative changes of the arterial wall during aneurysm development. Methods: We first introduce methods of aneurysm-inducing surgery, and then refer to morphological analysis of aneurysmal induction. Next, we explain the association between aneurysmal development and shear stress and NO. Finally, we show several mechanisms of aneurysmal development using genetically modified animals. Results and conclusion: In our animal model, cerebral aneurysms are induced in rats, monkeys, and mice by ligation of the unilateral common carotid artery and renal hypertension, suggesting that an increase in hemodynamic stress is a key requirement for the aneurysm development. Our morphological and molecular studies suggest that increased wall shear stress, iNOS-derived NO, MMP-2 \& 9, cathepsin B, NF-κB, interleukin-1β, and endothelin B receptor are associated with the progression of cerebral aneurysms. Statin and Nifedipine may be possible drugs for the prevention of cerebral aneurysm development.