title: Location of arterial stiffening differs in those with impaired fasting glucose versus diabetes: implications for left ventricular hypertrophy from the Multi-Ethnic Study of Atherosclerosis.
abstract: OBJECTIVE
  To determine whether middle-aged and older individuals with impaired fasting glucose (IFG), but no clinical evidence of cardiovascular disease, exhibit abnormal changes in proximal thoracic aortic stiffness or left ventricular (LV) mass when compared with healthy counterparts.
  
  
  METHODS
  From the Multi-Ethnic Study of Atherosclerosis, 2,240 subjects with normal fasting glucose (NFG), 845 with IFG, and 414 with diabetes, all aged 45 to 85 years and without preexisting coronary artery disease, underwent MRI determinations of total arterial and proximal thoracic aortic stiffness and LV mass. The presence or absence of other factors known to influence arterial stiffness was assessed.
  
  
  RESULTS
  After adjustment for clinical factors known to modify arterial stiffness, proximal thoracic aortic stiffness was not increased in those with IFG compared with those with NFG (1.90 +/- 0.05 versus 1.91 +/- 0.04 10(-3) mmHg(-1), respectively, P = 0.83). After accounting for clinical factors known to influence LV mass, LV mass was increased in those with diabetes relative to those with NFG (150.6 +/- 1.4 versus 145.8 +/- 0.81 g, P < 0.0009) but not in those with IFG in comparison with NFG (145.2 +/- 1.03 versus 145.8 +/- 0.81 g, P = 0.56).
  
  
  CONCLUSIONS
  Middle-aged and older individuals with the pre-diabetes state of IFG do not exhibit abnormal proximal thoracic distensibility or LV hypertrophy relative to individuals with NFG. For this reason, an opportunity may exist in those with IFG to prevent LV hypertrophy and abnormal aortic stiffness that is observed in middle-aged and older individuals with diabetes.
authors.affiliation: Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
authors.forename: Pairoj
authors.initials: P
authors.lastname: Rerkpattanapipat
authors.forename: Ralph B
authors.initials: RB
authors.lastname: D'Agostino
authors.forename: Kerry M
authors.initials: KM
authors.lastname: Link
authors.forename: Eyal
authors.initials: E
authors.lastname: Shahar
authors.forename: Joao A
authors.initials: JA
authors.lastname: Lima
authors.forename: David A
authors.initials: DA
authors.lastname: Bluemke
authors.forename: Shantanu
authors.initials: S
authors.lastname: Sinha
authors.forename: David M
authors.initials: DM
authors.lastname: Herrington
authors.forename: W Gregory
authors.initials: WG
authors.lastname: Hundley
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001013:Aorta, Thoracic / Q000502:physiology / Q000503:physiopathology; D001158:Arteries / Q000503:physiopathology*; D050197:Atherosclerosis / Q000473:pathology / Q000503:physiopathology*; D001786:Blood Glucose / Q000032:analysis*; D005006:Ethnicity; D005260:Female; D018149:Glucose Intolerance / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011236:Prediabetic State / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D044469:Racial Groups; D012016:Reference Values
chemical_list: D001786:Blood Glucose