Brain injury in autonomic, emotional, and cognitive regulatory areas in patients with heart failure

Abstract

Background: Heart failure (HF) is accompanied by autonomic, emotional, and cognitive deficits, indicating brain alterations. Reduced gray matter volume and isolated white matter infarcts occur in HF, but the extent of damage is unclear. Using magnetic resonance T2 relaxometry, we evaluated the extent of injury across the entire brain in HF.

Methods and results: Proton-density and T2-weighted images were acquired from 13 HF (age 54.6 +/- 8.3 years; 69% male, left ventricular ejection fraction 0.28 +/- 0.07) and 49 controls (50.6 +/- 7.3 years, 59% male). Whole brain maps of T2 relaxation times were compared at each voxel between groups using analysis of covariance (covariates: age and gender). Higher T2 relaxation values, indicating injured brain areas (P < .005), emerged in sites that control autonomic, analgesic, emotional, and cognitive functions (hypothalamus, raphé magnus, cerebellar cortex, deep nuclei and vermis; temporal, parietal, prefrontal, occipital, insular, cingulate, and ventral frontal cortices; corpus callosum; anterior thalamus; caudate nuclei; anterior fornix and hippocampus). No brain areas showed higher T2 values in control vs. HF subjects.

Conclusions: Brain structural injury emerged in areas involved in autonomic, pain, mood, language, and cognitive function in HF patients. Comorbid conditions accompanying HF may result from neural injury associated with the syndrome.

Figure 1

Injury in the raphé magnus in sagittal (A, arrow) and axial (B, arrow) views. Injury also appears in the hypothalamus [arrows, C (coronal), D (sagittal), and E (axial) views]. Areas of injury are color-coded for level of significance (color scale t values). L= left, R= right side of brain; X, Y and Z values represent lateral distance in mm from midline, dorsal-ventral, and rostral-caudal from the anterior commissure, respectively. For all figures, the injury is presented as a group/averaged for HF vs. Control subjects.

Figure 2

Injury in cortical regions which influence hypothalamic outflow. The right anterior insula, left posterior insula (A), anterior cingulate, subgenu of anterior cingulate (bordering caudal corpus callosum), caudal ventral medial prefrontal cortex (B), and posterior cingulate (C), arrows, were affected. Figure conventions as in Figure 1.

Figure 3

Injury appeared in a region extending from the left and right caudate nuclei through the internal capsule (A), fornix (B, vertical solid arrow), and septum (A, C) to the anterior hypothalamus (A, B). Injury also appears in the anterior and mid-corpus callosum (B, dashed blue arrow). Figure conventions as in Figure 1.

Figure 4

Areas of injury in the left and right caudate (A, C), anterior thalamus (B), posterior hippocampus (D), and cerebellar cortex (E, F). Figure conventions as in Figure 1.