ARCADIA CSI (Cognition and Silent Infarcts)

项目摘要： 脑卒中后认知功能下降和痴呆是一个主要的公共卫生问题， 比中风后增加一倍，仅在美国就影响了200万人。然而， 没有有效的治疗方法来预防中风后的认知能力下降和痴呆。无症状性脑梗死 与认知能力下降有关，特别是在那些心脏栓塞的高危人群中。是 因此，降低高风险中风患者无症状性梗死发生率的治疗可能 心血管栓塞，也将降低认知能力下降和痴呆症的发病率。为了验证这一点，我们建议 对NINDS申办的ARCADIA试验进行辅助研究。ARCADIA将治疗与 阿哌沙班与阿司匹林预防隐源性卒中和左室肥厚患者临床卒中复发的比较 心房性心脏病我们正在利用母体试验来解决阿哌沙班可能 还可以降低无症状性梗死的发生率，并随着时间的推移与更好的认知功能相关 与阿司匹林相比。我们将从参加ARCADIA的1,100名患者中招募500名患者。患者 参与辅助研究（ARCADIA-CSI）的患者将在基线时接受认知评估， 此后每年使用基于电话的认知电池。我们将检验以下假设： 阿哌沙班治疗的患者认知功能的变化比阿司匹林治疗的患者要小。 我们还将收集合格卒中前后的初始MRI和当时的随访MRI 受试者完成ARCADIA母研究的参与。根据这两个MRI扫描， 将评估随访期间新发无症状性梗死的发生率，并检验以下假设： 阿哌沙班治疗导致无症状性梗死患者的百分比降低， 阿司匹林疗法探索性分析还将寻找新发无症状性梗死与 认知改变我们的项目将是第一个前瞻性地确定沉默的影响的项目之一。 对认知功能的影响而且，如果阿哌沙班可以改善认知能力下降，那么我们将有 建立了第一个预防中风后认知能力下降的治疗方法。

Project Summary: Cognitive decline and dementia after stroke is a major public health problem, with risk of dementia more than doubling after stroke and affecting more the 2 million people in the United States alone. Yet, there are no effective treatments to prevent cognitive decline and dementia after stroke. Silent brain infarction has been associated with cognitive decline, especially among those at high risk for cardio-embolism. It is therefore likely that treatments that reduce the incidence of silent infarcts in stroke patients at high risk for cardio-embolism, will also reduce the rate of cognitive decline and dementia. To test this, we propose to conduct an ancillary study to the NINDS-sponsored ARCADIA trial. ARCADIA compares treatment with apixaban versus aspirin to prevent a recurrent clinical stroke in patients with cryptogenic stroke and left atrial cardiopathy. We are taking advantage of the parent trial to address the possibility that apixaban might also reduce the incidence of silent infarction and be associated with better cognitive function over time compared to aspirin. We will enroll 500 patients from the 1,100 that will participate in ARCADIA. Patients who participate in the ancillary study (ARCADIA-CSI) will receive cognitive assessments at baseline and yearly thereafter using a telephone-based cognitive battery. We will test the hypothesis that the slope of change in cognitive function is less steep in patients on apixaban compared to patients on aspirin therapy. We will also collect an initial MRI around the time of the qualifying stroke and a follow-up MRI at the time that the subject completes participation in the ARCADIA parent study. Based on these two MRI scans we will assess the incidence of new silent infarcts during the follow-up period and test the hypothesis that apixaban treatment results in a reduction of the percentage of patients with silent infarcts compared to aspirin therapy. An explorative analysis will also look for the relationship between new silent infarcts and cognitive change. Our project will be among the first to determine prospectively the impact of silent infarction on cognitive function. And, if cognitive decline can be ameliorated by apixaban, then we will have established the first ever treatment for the prevention of post-stroke cognitive decline.