Abstract

Introduction: Preterm birth (PTB, delivery <37 weeks) may be a marker of a chronic pro- inflammatory response associated with excess risk of coronary artery disease. Hypothesis: We hypothesized that women with PTB would have elevated blood pressure, markers of inflammation (C-reactive protein [CRP], Interleukin-6 [IL-6]) as well as higher intima medial thickness (IMT) in the years following pregnancy. Further, we considered that these differences would persist after removing PTB cases due to self-reported hypertensive disorders of pregnancy (primary reason for indicated PTB). Methods: We studied 916 women (46% Black) who delivered 1,181 live births between enrollment in the Coronary Artery Risk Development in Young Adults (CARDIA) study (age 18-30 years) and 20 years later (age 38-50 years). CRP was measured at years 7, 15 and 20; IL-6 and common carotid IMT (average of the maximum wall thickness of the respective carotid artery segment based on 4 ultrasonic measurements for the common carotid arteries) were measured at year 20. Blood pressure, lipids, and anthropometrics were measured at baseline and 6 follow-up visits. Median concentrations of inflammatory markers and mean IMT were compared in women with and without a history of PTB. Change in blood pressure, lipids, body size and CRP concentrations according to PTB status was also evaluated using generalized estimating equations (GEE). Results: A total of 226 women (24.7%) reported at least one PTB. Women with PTBs had modestly higher pre-pregnancy systolic blood pressure (SBP) compared to women who delivered term births (106.3 vs. 104.9 mmHg, p=0.02); SBP was higher across follow-up (p=0.03 for group differences) and increased more rapidly over 20 years compared to women with term births (p<0.01 for group*time interaction). These differences remained significant after removal of women with hypertension in pregnancy. Women with PTB had modestly higher mean body mass index (BMI) at baseline, and differences were more robust beginning in year 7 of follow up. Compared to women with term births, women with PTB had borderline higher mean IMT at year 20, adjusted for age and BMI (difference=0.016 mm, p=0.06). Adjustment for blood pressure change from baseline to year 20 did not affect the estimate. Adjustment for race attenuated this difference (p=0.33), and after excluding women with self-reported hypertension in pregnancy IMT no longer differed by PTB status. CRP, IL-6 and lipids did not differ according to PTB status. Conclusion: Women with PTBs, regardless of hypertension during pregnancy, had higher blood pressure before pregnancy and in the two decades after pregnancy compared to women with term births. They also higher mean IMTs, explained in part by race. Differences in IMT may be limited to women who reported hypertension in pregnancy, and were not related to inflammatory markers. PTB may mark women at excess risk of atherosclerosis.

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