Abstract 40: Duration of Prediabetes is Associated with Subclinical Atherosclerosis and Cardiac Dysfunction in Middle-Age: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Background: A prolonged duration of diabetes has been shown to be independently associated with incident cardiovascular disease (CVD). Whether duration of prediabetes is similarly associated with CVD is unknown. We sought to determine whether the duration of prediabetes during young adulthood is associated with the presence of coronary artery calcified plaque (CAC) and cardiac structure/function in middle-age.
Methods: Participants were 3244 white and black adults aged 18-30 years without prediabetes or diabetes at baseline (1985-86) or diabetes during follow-up in the multicenter community-based CARDIA Study. Prediabetes was defined at follow-up examinations 7, 10, 15, 20, and 25 years after baseline as fasting glucose 100-125 mg/dL, 2-hour oral glucose tolerance 140-199 mg/dL or HbA1c 5.7-6.4%. Presence of CAC was measured by computed tomography at follow-up years 15, 20, and 25. Measures of cardiac structure and function were obtained from echocardiography performed at year 25.
Results: Of the 3244 individuals, 1561 (48.2%) developed prediabetes during follow-up. Among those who developed prediabetes, the median (IQR) duration was 10 (5-12) years. After adjustment for age, sex, race, education, study center, and CVD risk factors, the hazard ratio for the presence of CAC was 1.21 times higher for each 10-year increase in duration of prediabetes (95% CI: 1.06, 1.37). Duration of prediabetes was also associated with worse global longitudinal strain (per 10 years: 0.2%; 95% CI: 0.1, 0.4; P=.005), e′ (-0.2 cm/s; 95% CI: -0.3, -0.1; P < .001), and E/e′ ratio (0.113; 95% CI: -0.007, 0.233; P=.06) (Table). These results did not differ significantly by race or sex.
Conclusions: Exposure to a longer duration of prediabetes is associated with subclinical atherosclerosis and cardiac dysfunction in middle-age. Further research is needed to better understand the pathophysiology of these relationships.
Author Disclosures: J.P. Reis: None. N.B. Allen: None. M.P. Bancks: None. J. Carr: None. C.E. Lewis: None. J.A. Lima: None. J.S. Rana: None. P.J. Schreiner: None.
- © 2017 by American Heart Association, Inc.