title: Insular cortex atrophy as an independent determinant of disrupted diurnal rhythm of ambulatory blood pressure in elderly hypertension.
abstract: BACKGROUND
  Insular cortex (Ic) has been suggested to be a key site in limbic-autonomic integration. Association of Ic damage with disruption of diurnal blood pressure (BP) variation and higher serum level of noradrenaline has been reported. We examined the relationships of Ic volume with ambulatory BP measures and noradrenaline concentration.
  
  
  METHODS
  Ambulatory BP monitoring and brain magnetic resonance imaging (MRI) were performed in 55 elderly never-treated hypertensives. Ic volumes were measured using an intensity contour mapping algorithm. Serum adrenaline and noradrenaline concentrations were evaluated.
  
  
  RESULTS
  Subjects were classified into an Ic-atrophy group (n = 14) and non-Ic-atrophy group (n = 41) based on a total Ic volume (left and right side) of 12.6 cm(3) (lowest quartile). In the Ic-atrophy group, 24 h (145 mm Hg vs. 134 mm Hg, P < 0.05) and sleep (143 mm Hg vs. 127 mm Hg, P < 0.01) systolic BP (SBP) and nocturnal SBP dipping (1.30% vs. 8.54%, P < 0.05) were significantly different, and noradrenaline (373 pg/ml vs. 296 pg/ml, P = 0.08) was marginally different from those in the non-Ic-atrophy group. Left Ic volume was significantly correlated with 24 h (r = -0.277) and sleep (r = -0.499) SBP and nocturnal SBP dipping (r = 0.413), while right Ic volume was significantly correlated with 24 h (r = -0.261) and sleep (r = -0.430) SBP, nocturnal SBP dipping (r = 0.321) and noradrenaline (r = -0.335). In multiple linear regression analysis adjusted for age, gender and body mass index (BMI), left Ic volume was significantly negatively associated with sleep SBP (P < 0.01) and positively with nocturnal SBP dipping (P < 0.05).
  
  
  CONCLUSIONS
  Ic atrophy, specifically in the left side, may partly contribute to disruption of diurnal ambulatory BP rhythm via central autonomic nervous system (ANS) dysregulation.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medicine, Jichi Medical University School of Medicine, Tochigi, Japan.
authors.forename: Michiaki
authors.initials: M
authors.lastname: Nagai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hoshide
authors.forename: Joji
authors.initials: J
authors.lastname: Ishikawa
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shimada
authors.forename: Kazuomi
authors.initials: K
authors.lastname: Kario
mesh_terms: D000368:Aged; D001284:Atrophy; D001341:Autonomic Nervous System / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D018660:Blood Pressure Monitoring, Ambulatory; D001921:Brain / Q000503:physiopathology; D002540:Cerebral Cortex / Q000473:pathology* / Q000503:physiopathology; D002940:Circadian Rhythm / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D012044:Regression Analysis
chemical_list: D009638:Norepinephrine