SILENT STROKE IN A POPULATION OF PATIENTS AT RISK FOR CEREBROVASCULAR DISEASE

有脑血管疾病风险的患者群体中的无症状中风

• 批准号: 7604686
• 负责人: Paul Alan Nyquist
• 金额: $ 0.09万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-01 至 2007-09-16
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604686
• 关键词: Biological Markers; Cerebrovascular Disorders; Computer Retrieval of Information on Scientific Projects Database; Coronary heart disease; Disease; Event; Family; Funding; Genes; Grant; Inflammation; Inflammatory; Institution; Lipids; Lipoproteins; Magnetic Resonance Imaging; Mediating; Patients; Pilot Projects; Platelet Function Tests; Population; Prevalence; Research; Research Personnel; Resources; Risk; Risk Factors; Smoking; Source; Stroke; United States National Institutes of Health; Vascular Diseases; Visit; gene environment interaction; genetic analysis; vascular bed

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The primary specific aim of this pilot study is to demonstrate the prevalence of silent stroke within a high risk population identified from families known to be an increased risk of premature coronary disease. A secondary aim is to determine the relationship of silent stroke to occult disease in other vascular beds, primarily coronary disease. The third aim is to determine the relationship of silent stroke to inflammatory biomarkers, platelet function tests and other procoagulation factors, lipids and lipoproteins, current smoking and other risk factors characterized in this population at their most recent visit. Ultimately, the longer-term aims for grant submissions will be to determine the contribution of genes and gene-environment interactions to different forms of vascular disease that appear to cluster in families with premature events and that appear to be mediated by inflammation. Demonstrating the ability to detect silent strokes on MRI in this population is the logical first step. Without determining the extent to which this exists, genetic analysis or examination of shared markers will not be possible or salient.

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