Abstract
AimsAutonomic, cognitive, and neuropsychologic deficits appear in heart failure (HF) subjects, and these compromised functions depend on cerebral cortex integrity in addition to that of subcortical and brainstem sites. Impaired autoregulation, low cardiac output, sleep-disordered-breathing, hypertension, and diabetic conditions in HF offer considerable potential to affect cortical areas by loss of neurons and glia, which would be expressed as reduced cortical thicknesses. However, except for gross descriptions of cortical volume loss/injury, regional cortical thickness integrity in HF is unknown. Our goal was to assess regional cortical thicknesses across the brain in HF, compared to control subjects.Methods and ResultsWe examined localized cortical thicknesses in 35 HF and 61 control subjects with high-resolution T1-weighted images (3.0-Tesla MRI) using FreeSurfer software, and assessed group differences with analysis-of-covariance (covariates; age, gender; p<0.05; FDR). Significantly-reduced cortical thicknesses appeared in HF over controls in multiple areas, including the frontal, parietal, temporal, and occipital lobes, more markedly on the left side, within areas that control autonomic, cognitive, affective, language, and visual functions.ConclusionHeart failure subjects show reduced regional cortical thicknesses in sites that control autonomic, cognitive, affective, language, and visual functions that are deficient in the condition. The findings suggest chronic tissue alterations, with regional changes reflecting loss of neurons and glia, and presumably are related to earlier-described axonal changes. The pathological mechanisms contributing to reduced cortical thicknesses likely include hypoxia/ischemia, accompanying impaired cerebral perfusion from reduced cardiac output and sleep-disordered-breathing and other comorbidities in HF.
Highlights
Multiple autonomic, cognitive, and neuropsychologic deficits appear in heart failure (HF) subjects [1,2,3]
We examined localized cortical thicknesses in 35 HF and 61 control subjects with high-resolution T1-weighted images (3.0-Tesla magnetic resonance imaging (MRI)) using FreeSurfer software, and assessed group differences with analysis-of-covariance
Those injured sites were detected by magnetic resonance imaging (MRI) procedures, including high-resolution T1-weighted imaging, T2-weighted imaging, T2-relaxometry, and diffusion tensor imaging (DTI) [4,6,7,8], which were accompanied by aberrant functional MRI responses to the Valsalva maneuver and cold pressor autonomic challenges [2,3]
Summary
Cognitive, and neuropsychologic deficits appear in heart failure (HF) subjects [1,2,3]. The impairments stem from structural brain changes in several gray matter sites in the forebrain and brainstem, white matter hyper-intensities, as well as interconnecting axons [4,5] Those injured sites were detected by magnetic resonance imaging (MRI) procedures, including high-resolution T1-weighted imaging, T2-weighted imaging, T2-relaxometry, and diffusion tensor imaging (DTI) [4,6,7,8], which were accompanied by aberrant functional MRI responses to the Valsalva maneuver and cold pressor autonomic challenges [2,3]. Visual examination procedures are poor for cortical injury detection over quantitative methods Both regional gray matter volumes and tissue integrity, assessed with voxel-based gray matter volumetric, T2-relaxometry, and DTI-based procedures, may be influenced by analytical differences in extra-cortical cerebrospinal fluid and surface curvature/complexities. Since FreeSurfer tools target the white matter surface for registration, gray matter tissue is not influenced by registration accuracy, and the procedures may be useful to assess precisely regional cortical thicknesses in HF subjects
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