OBJECTIVE Gestational diabetes mellitus (GDM) predicts incident cardiovascular disease (CVD). However, mechanisms linking GDM to CVD beyond intervening incident diabetes are not well understood. We examined the relation of GDM with echocardiographic parameters of left ventricular (LV) structure and function, which are important predictors of future CVD risk. RESEARCH DESIGN AND METHODS We studied 609 women (43% black) from the Coronary Artery Risk Development in Young Adults (CARDIA) study who delivered one or more births during followup and had echocardiograms in 1990-1991 (mean age 28.8 years) and 2010- 2011. RESULTS During the 20-year follow-up, 965 births were reported, with GDM developing in 64 women (10.5%). In linear regression models adjusted for sociodemographic factors, BMI, physical activity, parity, smoking, use of oral contraceptives, alcohol intake, family history of coronary heart disease, systolic blood pressure, and lipid levels, women with GDM had impaired longitudinal peak strain (215.0 vs. 215.7%, P = 0.025), circumferential peak strain (214.8 vs. 215.6%, P = 0.028), lateral e9 wave velocity (11.0 vs. 11.8 cm/s, P = 0.012), and septal e9 wave velocity (8.6 vs. 9.3 cm/s, P = 0.015) in 2010-2011 and a greater 20-year increase in LV mass indexed to body surface area (14.3 vs. 6.0 g/m 2, P = 0.006) compared with women with non-GDMpregnancies. Further adjustment for incident type 2 diabetes after pregnancy did not attenuate these associations. CONCLUSIONS Pregnancy complicated by GDM is independently associated with increased LV mass and impaired LV relaxation and systolic function. Implementation of postpartum cardiovascular health interventions in women with a history of GDMmay offer an additional opportunity to reduce future CVD risk.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Mar 2016|
Bibliographical noteFunding Information:
The CARDIA study is supported by contractsHHSN268201300025C, HHSN268201300026C, HHSN268201300027C, HHSN268201300028C, HHSN268201300029C, and HHSN268200900041C fromthe National Heart, Lung, and Blood Institute (NHLBI); the Intramural Research Program of the National Institute on Aging (NIA); and an intraagency agreement between the NIA and NHLBI (AG0005). The analyses were supported by grants K01-DK-059944 (E.P.G., Principal Investigator) and R01-DK-090047 (E.P.G., Principal Investigator) fromthe National Institute of Diabetes and Digestive and Kidney Diseases. D.A. was supported by NHLBI training grant T32-HL-007779.
© 2016 by the American Diabetes Association.