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: 8257955
• 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/8257955
• 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(申请人提供)：急性脑梗塞可在没有心脏原发病的情况下导致心脏损伤，严重后果从心肌损伤到猝死。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。确定卒中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发展，改善神经预后和存活率。然而，由于不能区分心肌损伤的神经源性和心源性机制，以及先验解剖学假设在脑定位研究中造成的偏差，心脑相互作用的研究仍存在一些悬而未决的问题。我们最近已经证明，最初为功能磁共振分析而开发的排列方法是研究心脏-大脑相互作用的一种可行的方法。该方法不受先验假设对任何特定位置的偏差，并且以统计上有效的方式在体素级别测试零假设，以便与外部定义的事件相关联。使用这种方法，我们已经证明了右脑岛梗塞与血清肌钙蛋白-T水平升高有关，这表明急性心肌损伤。在这里，我们建议首先在前瞻性数据集中验证我们的发现，然后通过开发急性应激性高血糖定义的急性缺血性卒中急性应激反应的解剖学地图来扩展这项工作。具体地说，我们将：1)测试这一假设，即当脑梗塞时，局部脑区与心肌肌钙蛋白-T升高有关，表明心肌损伤。2)测试假设，当脑梗塞时，大脑局部区域与以急性应激性高血糖为特征的急性应激反应有关。3)确定与心脏和全身改变有关的神经底物是否对急性缺血性卒中的心肌损伤和急性应激反应具有独立的风险。如果得到证实，从这项研究中获得的信息可以用来生成能够准确评估特定中风患者心脏和全身并发症风险的模型。公共卫生相关性： 在没有原发心脏原因的情况下，急性脑损伤可以独立地导致心脏损伤，通常会导致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卒中神经源性心肌损伤的脑解剖。确定与中风相关的心肌损伤相关的大脑部位可以促进预防策略的发展，并允许及时处理心脏并发症，从而改善中风患者的神经预后和存活率。