Heart-Brain Interactions In Human Acute Ischemic Stroke

人类急性缺血性中风的心脑相互作用

• 批准号: 8064699
• 负责人: Hakan Ay
• 金额: $ 38.5万
• 依托单位: MASSACHUSETTS GENERAL HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-15 至 2014-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8064699
• 关键词: Acute; Acute Brain Injuries; Address; Adopted; Adrenal Glands; Affect; Anatomy; Atrial Fibrillation; Blood Glucose; Brain; Brain Diseases; Brain region; Cardiac; Cerebral Ischemia; Cerebrum; Congenital Heart Defects; Coronary Arteriosclerosis; Data; Data Set; Development; Diagnosis; Educational process of instructing; Electrocardiogram; Enzymes; Event; Functional Magnetic Resonance Imaging; Goals; Health; Heart; Heart Diseases; Human; Hyperglycemia; Infarction; Injury; Insula of Reil; Ischemia; Ischemic Stroke; Knowledge; Lead; Link; Location; Magnetic Resonance Imaging; Maps; Mediating; Methodology; Methods; Modeling; Morbidity - disease rate; Multivariate Analysis; Myocardial; Nervous System Trauma; Neurological outcome; Outcome; Pathway interactions; Patients; Play; Population; Prevalence; Prevention strategy; Preventive; Research; Research Personnel; Risk; Serum; Site; Statistical Methods; Stroke; Subgroup; Sudden Death; Sympathetic Nervous System; Techniques; Testing; Textbooks; Tissues; Troponin; Troponin T; Work; acute stress; acute stroke; base; biological adaptation to stress; cohort; improved; mortality; patient population; prospective; relating to nervous system; response

DESCRIPTION (provided by applicant): Acute brain infarcts can lead to injury to the heart in the absence of primary cardiac causes, with serious outcomes ranging from myocardial damage to sudden death. Our research aims to investigate the neuroanatomic substrate of myocardial injury and acute stress response occurring after ischemic stroke and link this localization to tissue outcome in cerebral ischemia. Identification of a cerebral site for stroke-related myocardial injury and acute stress response could facilitate development of preventive strategies and improve neurological outcome and survival. However, there are unresolved issues in the study of heart-brain interactions due to inability to differentiate between neurogenic and cardiogenic mechanisms of myocardial injury and the bias caused by using a-priori anatomic assumptions in the study of cerebral localization. We have recently demonstrated that the permutation method originally developed for functional MRI analysis is a feasible approach in the study of heart-brain interactions. The method is free from the bias of an a-priori hypothesis as to any specific location and tests the null hypothesis at the voxel level in a statistically valid manner for correlation with an externally defined event. Using this methodology we have demonstrated that infarction in the right insula is associated with elevated serum troponin-T level indicating acute myocardial injury. Here we propose to first validate our findings in a prospective dataset, and then extend this work by developing an anatomical map for acute stress response defined by acute stress hyperglycemia in acute ischemic stroke. Specifically, we will: 1) Test the hypothesis that there are focal brain regions that when infarcted are associated with cardiac troponin-T elevation indicative of myocardial injury. 2) Test the hypothesis that there are focal brain regions that when infarcted are associated with acute stress response characterized by acute stress hyperglycemia. 3) Identify whether the neural substrate linked to cardiac and systemic alterations confers an independent risk for myocardial injury and acute stress response in acute ischemic stroke. If proven, the information gained from this research could be used to generate models that can accurately assess the risk for cardiac and systemic complications in a given stroke patient. PUBLIC HEALTH RELEVANCE: Acute brain injury can independently lead to injury to the heart in the absence of primary cardiac causes, often with serious outcomes ranging from myocardial damage to sudden death. The goal of our research is to investigate the brain anatomy of neurogenic myocardial injury in acute ischemic stroke. Identification of a cerebral site that is linked to stroke-related myocardial injury could facilitate development of preventive strategies and allow the timely management of cardiac complications and thus lead to improved neurological outcomes and survival in stroke patients.

描述（由申请人提供）：急性脑梗死可在无主要心脏原因的情况下导致心脏损伤，严重后果包括心肌损伤至猝死。我们的研究旨在探讨缺血性卒中后心肌损伤和急性应激反应的神经解剖学基础，并将这种定位与脑缺血的组织结局联系起来。识别中风相关心肌损伤和急性应激反应的大脑部位可以促进预防策略的制定并改善神经系统结局和生存率。然而，由于无法区分心肌损伤的神经源性和心源性机制，以及在脑定位研究中使用先验解剖假设造成的偏倚，因此在心脑相互作用的研究中存在未解决的问题。我们最近证明，最初为功能性MRI分析开发的排列方法是研究心脑相互作用的可行方法。该方法不受先验假设对任何特定位置的偏差的影响，并以统计有效的方式在体素水平上测试零假设，以与外部定义的事件相关。使用这种方法，我们已经证明，梗死在右心室是与血清肌钙蛋白T水平升高，表明急性心肌损伤。在这里，我们建议首先在前瞻性数据集中验证我们的发现，然后通过开发急性缺血性中风中急性应激性高血糖定义的急性应激反应的解剖图来扩展这项工作。具体而言，我们将：1）检验以下假设：存在局灶性脑区域，当梗塞时，其与指示心肌损伤的心肌肌钙蛋白-T升高相关。2)检验以下假设：脑中存在局灶性区域，当梗死时，这些区域与急性应激反应相关，其特征为急性应激性高血糖症。3)确定与心脏和全身改变相关的神经基质是否赋予急性缺血性卒中中心肌损伤和急性应激反应的独立风险。如果得到证实，从这项研究中获得的信息可以用来生成模型，可以准确评估特定中风患者的心脏和全身并发症的风险。公共卫生关系： 急性脑损伤可在没有主要心脏原因的情况下独立地导致心脏损伤，通常具有从心肌损伤到猝死的严重后果。本研究的目的是探讨急性缺血性脑卒中神经源性心肌损伤的脑解剖。识别与卒中相关心肌损伤相关的脑部位有助于制定预防策略，并允许及时管理心脏并发症，从而改善卒中患者的神经功能结局和生存率。