Cardiac Vagal Activation by Adrenocorticotropic Hormone Treatment in Infants with West Syndrome

  • Hattori Ayako
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Hayano Junichiro
    Medical Education, Nagoya City University, Graduate School of Medical Sciences
  • Fujimoto Shinji
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Ando Naoki
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Mizuno Kumiko
    Department of Central Clinical Laboratory, Nagoya City University Hospital
  • Kamei Michi
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Kobayashi Satoru
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Ishikawa Tatsuya
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences
  • Togari Hajime
    Department of Pediatrics, Neonatology and Congenital Disorders, Nagoya City University Graduate School of Medical Sciences

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Abstract

West syndrome (WS) is a generalized epileptic syndrome of infancy and early childhood with various etiologies, and consists of a triad of infantile spasm, arrest or regress of psychomotor development and specific electroencephalogram (EEG) pattern of hypsarrhythmia. WS had been believed to be refractory, but recent evidence supports effectiveness of adrenocorticotropic hormone (ACTH) treatment. The ACTH treatment, however, has a problem that it is often accompanied by adverse autonomic symptoms. We therefore examined heart rate variability (HRV) for assessing cardiac autonomic functions in WS and prospectively observed the changes during ACTH treatment. We studied 15 patients with WS and 9 age-matched controls during sleep (EEG stage 2). Compared with controls, the patients with WS were greater in the low-frequency component (LF) of HRV, an index reflecting sympatho-vagal interaction (p = 0.02), but were comparable for high-frequency component (HF) and LF-to-HF ratio (LF/HF), indices reflecting cardiac vagal activity and sympathetic predominance, respectively. During ACTH treatment, heart rate decreased (p < 0.01), LF and HF increased (p < 0.01), and LF/HF did not differ significantly. These results indicate that WS might be accompanied by autonomic changes and that ACTH treatment enhances parasympathetic function and causes bradycardia.

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