ARCADIA CSI (Cognition and Silent Infarcts)

项目总结： 中风后认知能力下降和痴呆症是一个主要的公共健康问题，患痴呆症的风险更大 比中风后增加一倍，仅在美国就影响了200多万人。然而，在那里 没有有效的治疗方法来预防中风后的认知衰退和痴呆症。无症状性脑梗塞 与认知能力下降有关，特别是在心脏栓塞的高危人群中。它是 因此，降低中风高危患者无症状性脑梗塞发生率的治疗可能 心脏栓塞，也会降低认知功能减退和痴呆症的发生率。为了测试这一点，我们建议 对NINDS赞助的阿卡迪亚试验进行一项辅助研究。阿卡迪亚将治疗与 阿皮沙班与阿司匹林预防隐源性卒中和左侧卒中患者临床复发的比较 房性心脏病。我们正在利用家长试验来解决阿皮沙班可能 还可以减少静止性脑梗塞的发生率，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。我们将从参加阿卡迪亚的1100名患者中招募500名患者。病人 参与辅助研究(Arcadia-CSI)的人将在基线和 此后每年使用基于电话的认知电池。我们将检验这一假设 与服用阿司匹林的患者相比，服用阿匹沙班的患者认知功能的变化不那么严重。 我们还将收集符合条件的中风前后的初始MRI和当时的后续MRI 受试者完成了阿卡迪亚父母研究的参与。基于这两次核磁共振扫描，我们 将评估在随访期内新的无症状性脑梗塞的发生率，并检验以下假设 阿匹沙班治疗可降低无症状心肌梗死患者的百分比 阿司匹林疗法。一项探索性分析也将寻找新的无症状脑梗塞和 认知变化。我们的项目将是第一批前瞻性地确定沉默的影响的项目之一 认知功能障碍。而且，如果APIXABAN可以改善认知能力下降，那么我们将有 建立了有史以来第一个预防中风后认知功能衰退的治疗方法。

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.