Journal of Cardiac Failure
Volume 15, Issue 3 , Pages 214-223, April 2009

Brain Injury in Autonomic, Emotional, and Cognitive Regulatory Areas in Patients With Heart Failure

  • Mary A. Woo, DNSc, RN

      Affiliations

    • School of Nursing, University of California at Los Angeles, Los Angeles, California
    • Corresponding Author InformationReprint requests: Mary A. Woo, DNSc, RN, UCLA School of Nursing, 700 Tiverton Avenue, Los Angeles, CA 90095-1702, Tel: (310) 206-2032, FAX: (310) 206-7433.
  • ,
  • Rajesh Kumar, PhD

      Affiliations

    • Departments of Neurobiology, University of California at Los Angeles, Los Angeles, California
  • ,
  • Paul M. Macey, PhD

      Affiliations

    • School of Nursing, University of California at Los Angeles, Los Angeles, California
    • Brain Research Institute, University of California at Los Angeles, Los Angeles, California
  • ,
  • Gregg C. Fonarow, MD

      Affiliations

    • Cardiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California
  • ,
  • Ronald M. Harper, PhD

      Affiliations

    • Brain Research Institute, University of California at Los Angeles, Los Angeles, California
    • Departments of Neurobiology, University of California at Los Angeles, Los Angeles, California

Received 7 May 2008; received in revised form 26 August 2008; accepted 14 October 2008. published online 24 December 2008.

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.

Key words: Depression, T2 relaxometry, dyspnea, pain

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 This research was supported by the National Institute of Nursing Research R01 NR-009116 and by NHLBI-60296.

 Conflict of interest: None.

PII: S1071-9164(08)01044-0

doi:10.1016/j.cardfail.2008.10.020

Journal of Cardiac Failure
Volume 15, Issue 3 , Pages 214-223, April 2009