Key result
Right-hemisphere stroke lesions map specifically to troponin elevation and QTc prolongation.
Why the study?
Functional and morphologic extracranial organ changes occur after acute brain injury, but the neuroanatomic correlates of these cardiac and systemic abnormalities are not fully known.
Does brain infarct location independently associate with the development of cardiac and systemic abnormalities in patients with acute ischemic stroke?
Cohort (n=1,208)
Blinded outcome assessment
No
Does brain infarct location independently associate with the development of cardiac and systemic abnormalities in patients with acute ischemic stroke?
p-value: p=<0.05
Specific post-stroke complications, such as troponin elevation and QTc prolongation, localize to distinct brain infarct regions, highlighting the role of neurogenic mechanisms in acute stroke.
Right-hemisphere infarcts were associated with troponin elevation and QTc prolongation; hypothesis-generating for neurogenic effects, needs prospective validation.
OBJECTIVE: Functional and morphologic changes in extracranial organs can occur after acute brain injury. The neuroanatomic correlates of such changes are not fully known. Herein, we tested the hypothesis that brain infarcts are associated with cardiac and systemic abnormalities (CSAs) in a regionally specific manner. METHODS: We generated voxelwise p value maps of brain infarcts for poststroke plasma cardiac troponin T (cTnT) elevation, QTc prolongation, in-hospital infection, and acute stress hyperglycemia (ASH) in 1,208 acute ischemic stroke patients prospectively recruited into the Heart-Brain Interactions Study. We examined the relationship between infarct location and CSAs using a permutation-based approach and identified clusters of contiguous voxels associated with p < 0.05. RESULTS: cTnT elevation not attributable to a known cardiac reason was detected in 5.5%, QTc prolongation in the absence of a known provoker in 21.2%, ASH in 33.9%, and poststroke infection in 13.6%. We identified significant, spatially segregated voxel clusters for each CSA. The clusters for troponin elevation and QTc prolongation mapped to the right hemisphere. There were 3 clusters for ASH, the largest of which was in the left hemisphere. We found 2 clusters for poststroke infection, one associated with pneumonia in the left and one with urinary tract infection in the right hemisphere. The relationship between infarct location and CSAs persisted after adjusting for infarct volume. INTERPRETATION: Our results show that there are discrete regions of brain infarcts associated with CSAs. This information could be used to bootstrap toward new markers for better differentiation between neurogenic and non-neurogenic mechanisms of poststroke CSAs. ANN NEUROL 2023;94:1155-1163.
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Arsava et al. (2023) conducted a cohort in Acute ischemic stroke (n=1,208). Brain infarct location was evaluated on Significant clusters of contiguous brain voxels associated with cardiac and systemic abnormalities (p=<0.05). Brain infarct locations were significantly associated with specific cardiac and systemic abnormalities, with troponin elevation and QTc prolongation mapping to the right hemisphere.
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