Abstract 18845: Visual Assessment of the Insular Cortices Using Routine Brain Magnetic Resonance Images in Heart Failure
INTRODUCTION: Heart failure (HF) patients show compromised autonomic control that contributes to increased mortality in the condition. The insular cortices contribute to regulation of the autonomic nervous system, and damage in those regions can contribute to cardiac death by exaggerating sympathetic responses characteristic of HF. Structural brain changes have been reported in the insular cortices using quantitative magnetic resonance imaging (MRI) procedures commonly used in research, but rarely applied in clinical practice. It is unclear whether insular injury can be determined by visual examination using routine MRI clinical procedures in HF. Our aim was to visually examine insular cortices in HF and control subjects to determine if appearance of damage appeared based on quantitative MRI procedures can be identified using routine MRI procedures.
METHODS: We visually assessed insular brain regions in 17 HF (mean age ± SD, 54.4 ± 8.1 years; BMI, 29.4 ± 5.7 kg/m2; 12 male; LVEF, 0.28 ± 0.07) and 50 control subjects (age, 50.6 ± 7.0 years; BMI, 24.9 ± 4.0 kg/m2; 29 male) using T2-weighted and proton density-weighted images acquired from a 3.0-Tesla MRI scanner. Standardized visual assessment scores of the insular cortices were compared between HF and control groups.
RESULTS: No significant differences in age or gender appeared between HF and control subjects. Body-mass-indices showed significant differences between HF and control subjects. Significant differences arose in the left insular cortex (HF vs. control; 2.53 ± 1.01 vs. 1.88 ± 0.87; P = 0.003) and right insular cortex (2.53 ± 0.87 vs. 1.76 ± 0.87; P = 0.001) in HF compared to control subjects.
CONCLUSIONS: Visual assessment of routine MR images can detect insular cortical atrophy in HF patients, and may allow for increased opportunity to evaluate the progression of injury accompanying the enhanced sympathetic drive characteristic of the syndrome.
- © 2013 by American Heart Association, Inc.