Abstract 162: Viscerotoxic Brain Infarcts: The Results of Heart-Brain Interactions Study

Introduction: Acute brain infarcts can provoke functional and morphologic changes in internal organs in the absence of primary visceral causes. We tested the hypothesis that infarcts in certain regions of the brain were much more likely to be associated with internal organ injury (IOI) than other regions using a method that was free from the bias of a-priori hypothesis as to any specific location. Methods: We generated neuroanatomic maps of brain infarcts for plasma troponin T elevation (structural cardiac marker), QTc prolongation on ECG (electrophysiological cardiac marker), pneumonia and urinary tract infection (marker for altered immune/pulmonary/urinary physiology), acute stress hyperglycemia (hepatic marker of glycogenolysis) in 1208 consecutive patients who were prospectively recruited into the NIH-funded HBI study. We utilized Threshold-Free Cluster Enhancement to examine the relationship between infarct location and IOI. We generated voxel-wise p-value maps using a permutation-based approach and identified clusters of contiguous voxels associated with IOI with a p-value <0.05. Results: We identified significant clusters of voxels for each form of IOI. The clusters for troponin elevation and QTc prolongation encompassed similar regions in the right insular cortex. The cluster for acute stress hyperglycemia involved the left insula. We found two large clusters for post-stroke infection, one for pneumonia in the left and one for urinary tract infection in the right hemisphere, both encompassing the insular cortex. The relationship between infarct location and IOI persisted after adjusting for infarct volume, vascular risk factors, and stroke etiology. Conclusion: Our results uncover the neuroanatomical substrate of post-stroke IOI. Localizing discrete regions of brain infarcts associated with IOI could be used to bootstrap towards new markers for better differentiation between neurogenic and non-neurogenic mechanisms of post-stroke IOI.