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.
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.
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