The 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

  1. Pairoj Rerkpattanapipat, MDe,
  2. Ralph B. D'Agostino, Jr, PhDe,
  3. Kerry M. Link, MDg,
  4. Eyal Shahar, MDa,
  5. Joao A. Lima, MDb,
  6. David A. Bluemke, MD, PhDc,
  7. Shantanu Sinha, PhDd,
  8. David M. Herrington, MD, MPHf,h and
  9. W.Gregory Hundley, MD (ghundley{at}wfubmc.edu)e,f
  1. From the Division of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, The University of Arizonaa
  2. D.W. Reynolds Cardiovascular Research Center, Johns Hopkins, Baltimoreb
  3. Russell H. Morgan Dept. of Radiology & Radiological Sciences, Johns Hopkins, Baltimorec
  4. Dept.of Radiology, The University of California at San Diegod
  5. Dept.of Public Health Sciences, Wake Forest Univ. School of Medicine, Winston-Saleme
  6. Dept.of Internal Medicine(Cardiology Section), Wake Forest Univ. School of Medicinef
  7. Depts. of Internal Medicine (Cardiology Section), Dept. of Radiology, Wake Forest Univ. School of Medicineg
  8. &Biomedical Engineering, Wake Forest Univ. School of Medicineh

    Abstract

    Objective: To determine if 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 mass when compared to healthy counterparts.

    Research Design and Methods: From the Multi-Ethnic Study of Atherosclerosis, 2240 subjects with normal fasting glucose (NFG), 845 with IFG, and 414 with diabetes mellitus (DM), all aged 45 to 85 years without pre-existing coronary artery disease, underwent magnetic resonance imaging (MRI) determinations of total arterial and proximal thoracic aortic stiffness, and left ventricular mass. The presence or absence of other factors known to influence arterial stiffness were assessed.

    Results: After adjustment for clinical factors known to modify arterial stiffness, proximal thoracic aortic stiffness was not increased in those with IFG compared to those with NFG (1.90±0.05 vs 1.91±0.04 10−3mmHg−1, respectively, p=0.83). After accounting for clinical factors known to influence LV mass, LV mass was increased in those with DM relative to those with NFG (150.6±1.4 vs 145.8±0.81 gms [p<0.0009]), but not in those with IFG in comparison with NFG (145.2±1.03 vs 145.8±0.81 gms [p=0.56]).

    Conclusions: Middle aged and older individuals with with the pre-diabetes state of impaired fasting glucose do not exhibit abnormal proximal thoracic distensibility nor left ventricular hypertrophy relative to individuals with normal fasting glucose. For this reason, an opportunity may exist in those with IFG to prevent LV hypertrophy and abnormal aortic stiffness that is observed in middle and older age individuals with diabetes.

    Footnotes

      • Received August 28, 2008.
      • Accepted January 3, 2009.