title: Temporal changes in cardiovascular autonomic regulation in type II diabetic patients: association with coronary risk variables and progression of coronary artery disease.
abstract: OBJECTIVE
  This research was designed to study the temporal changes in cardiovascular autonomic regulation, assessed by 24-hour heart rate (HR) variability, and the possible relation of changes in HR variability to cardiovascular risk factors and progression of coronary artery disease (CAD) among type II diabetic subjects.
  
  
  METHODS
  In a single-center substudy of The Diabetes Atherosclerosis Intervention Study (DAIS), 53 patients assigned to fenofibrate (n = 26) or placebo (n = 27), underwent time and frequency domain and fractal analysis of HR variability, coronary risk variable analyses and quantitative coronary angiograms at baseline and after three years' follow-up.
  
  
  RESULTS
  Twenty-four hour standard deviation of sinus intervals (SDNN) decreased from 113 +/- 35 to 94 +/- 30 msec (P < 0.001) during the three year period. Low frequency power spectral component and short-term fractal scaling exponent also decreased (P < 0.001 and P < 0.05, respectively). The reduction of SDNN was weakly related to a change in the triglyceride level (r = -0.33, P < 0.05), glucose level (r = -0.28, P < 0.05) and total cholesterol concentration (r = -0.35, P < 0.01). Furthermore, the reduction of SDNN was related to a decrease in the minimum lumen and mean segment diameter of the coronary arteries (r = 0.36, P < 0.01, and r = 0.39, P < 0.01, respectively). This association was more marked in the placebo group (r = 0.50, P < 0.01 and r = 0.44, P < 0.05, respectively) than among the patients randomized to fenofibrate (not significant for both).
  
  
  CONCLUSIONS
  Cardiovascular autonomic regulation assessed by HR variability deteriorates rapidly in type II diabetic subjects with CAD during the time course. Impairment in HR variability is associated with changes in common coronary risk variables and with a progression of CAD.
authors.affiliation: Division of Cardiology, University of Oulu, Finland [corrected]
authors.forename: Vesa
authors.initials: V
authors.lastname: Jokinen
authors.forename: Olavi
authors.initials: O
authors.lastname: Ukkola
authors.forename: K E Juhani
authors.initials: KE
authors.lastname: Airaksinen
authors.forename: Juhani M
authors.initials: JM
authors.lastname: Koistinen
authors.forename: Markku J
authors.initials: MJ
authors.lastname: Ikäheimo
authors.forename: Y Antero
authors.initials: YA
authors.lastname: Kesäniemi
authors.forename: Heikki V
authors.initials: HV
authors.lastname: Huikuri
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy; D001341:Autonomic Nervous System / Q000503:physiopathology*; D017023:Coronary Angiography; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use; D005500:Follow-Up Studies; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013997:Time Factors
chemical_list: D000960:Hypolipidemic Agents; D011345:Fenofibrate