Abstract P321: Pregnancy Loss is Associated With Subclinical Cardiovascular Disease in Mexican Women
Introduction: Cardiovascular disease (CVD) in women often develops in the absence of conventional risk factors. Prenatal loss, a common pregnancy outcome, may result in physiologic changes that could affect future risk of myocardial infarction. Little is known about the impact of pregnancy loss on early markers of CVD risk.
Hypothesis: Pregnancy loss affects carotid artery intima-media thickness (CIMT).
Methods: We conducted a cross-sectional analysis among 1,769 disease-free women from the Mexican Teachers’ Cohort who had been pregnant to evaluate the relation between pregnancy loss and CIMT. In 2008 participants answered a baseline questionnaire on reproductive history, risk factors for chronic disease and medical conditions that was updated in 2011. We defined pregnancy loss as abortion and/or stillbirth. Between 2012 and 2016, CIMT was measured by trained neurologists using ultrasound in three clinical sites. We log-transformed CIMT and defined carotid atherosclerosis as CIMT ≥0.8mm or plaque. We used multivariable linear and logistic regression models to assess the relation between pregnancy loss, CIMT and carotid atherosclerosis.
Results: Mean age of participants was 49.8 (SD ± 5.1) years. The prevalence of pregnancy loss was 22% (394 of 1769) , while we observed carotid atherosclerosis in 23% (405 of 1769) of participants. Comparing participants who reported a pregnancy loss to those who did not, the multivariable-adjusted odds ratio for carotid atherosclerosis was 1.52 (95% CI 1.12, 2.06). Women who experienced a stillbirth had 2.32 higher odds (95% CI 1.03, 5.21) of carotid atherosclerosis than those who did not. Mean CIMT appeared to be higher in women who reported a pregnancy loss relative to those who did not, however, in multivariable analyses, pregnancy loss and stillbirth were not significantly associated with CIMT.
Conclusions: Abortion and stillbirth may be associated with a higher risk of CVD. Additional investigation on potential underlying mechanisms for this association is required.
Author Disclosures: S.A. Hartasanchez: None. M. Flores: None. A. Monge: None. E. Yunes: None. C. Cantu-Brito: None. L. Espinosa: None. R. Lopez-Ridaura: B. Research Grant; Modest; Astra Zeneca. M. Lajous: B. Research Grant; Modest; Astra Zeneca.
- © 2017 by American Heart Association, Inc.