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2 OBESITY AND GLUCOSE INTOLERANCE ARE ASSOCIATED WITH DIASTOLIC DYSFUNCTION: EXPOSING THE ACHILLES HEEL OF EARLY DIABETIC CARDIOMYOPATHY.
  1. B. Molavi1,
  2. S. Bagwee1,
  3. F. Amani1,
  4. N. Rasouli1,
  5. J. L. Mehta1
  1. 1University of Arkansas for Medical Sciences, Little Rock, AR.

Abstract

Background The alarming rise in the incidence of obesity has paralleled the surge in the incidence of impaired glucose tolerance (prediabetes) and overt diabetes. The cardiovascular sequelae of insulin resistance are thought to occur later, along with the development of atherosclerotic coronary artery disease. Yet emerging evidence suggesting early organ dysfunction in insulin resistance (such as nonalcoholic steatohepatitis) points to an early visceral ectopic fat deposition referred to as lipotoxicity. We sought to evaluate the effects of insulin resistance and impaired glucose tolerance on cardiac function in otherwise healthy overweight volunteers.

Methods Twenty healthy obese and overweight volunteers (mean age 42 ± 6 years; 15 females) underwent glucose tolerance testing, direct insulin measurements, as well as dual x-ray absorptiometry (DXA, to assess subcutaneous and visceral fat mass). The cardiac evaluation included complete two-dimensional, Doppler, and tissue velocity imaging (TVI). The postprocessing of the TVI data was performed on an EchoPac work station (GE Health Systems) and the data were analyzed using Pearson correlation model and unpaired Student's t-test.

Results The mean weight of the subjects was 90 ± 12 kg, mean BMI of 32 ± 4 kg/m2, and mean systolic BP of 127 ± 15. The mean fasting blood glucose levels was 91 ± 13 with a mean HbA1C of 5.7 ± 0.4. The peak diastolic strain rate showed a significant inverse relationship with subcutaneous fat mass as well as fasting and 2-hour blood glucose levels (r = .54, p < .05). However neither myocardial systolic function nor the peak systolic strain rate changed significantly with increasing subcutaneous fat or glucose levels. In addition, the peak diastolic strain rate had a negative correlation with insulin sensitivity index as measured by the homeostasis model assessment (HOMA). Lastly, subjects with impaired glucose tolerance had a lower peak diastolic strain rate compared with those with normal glucose tolerance (0.8 vs 2.6 1/s; p = .01).

Conclusion Diastolic dysfunction occurs early in the course of obesity and glucose intolerance and may be a precursor of overt diabetic cardiomyopathy.

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