Abstract

Background: Spontaneous abortion (SAB) is a common early pregnancy complication globally, impacting 15% of clinically recognized pregnancies. The biological pathways leading to SAB are not clearly understood, although early SAB is often attributed to chromosomal abnormalities. Elevated blood pressure (BP) in women of reproductive age predicts cardiovascular disease later in life, but less clear is whether elevated BP during preconception and/or early pregnancy BP elevations can affect prenatal outcomes. Hypothesis: Elevated BP during preconception and the first trimester will be positively associated with SAB. Methods: We conducted a secondary analysis of data collected from 577 primiparous women (15-35 years) who participated in the Longitudinal Indian Family hEalth (LIFE) prospective pregnancy cohort study in Telangana State, India. Resting blood pressure was measured by trained technicians using a standardized study protocol at a preconception registration visit and in the first trimester. Odds ratio (OR) and 95% confidence intervals (CI) of any SAB (<22 weeks of gestation, n=108), early SAB (<8 weeks of gestation, n=25), and late SAB (8 to <22 weeks of gestation n=83) were assessed with a log link binomial distribution. Results: Preconception measurements were assessed at the first study visit, conducted at registration and within a mean±SD of 11±12 months prior to pregnancy. Higher than optimal preconception BP (120/80 mmHg) was not associated with SAB (OR adj 0.82 (95% CI 0.51, 1.32)). In contrast, first trimester elevated BP was associated with a two-fold increased likelihood of SAB, although results were of borderline significance (OR adj 2.12 (95%CI 0.87, 5.14). In addition, we observed an association between elevated first trimester BP and late SAB (OR adj 2.32 (95%CI 0.95, 5.68)); there were no associations between elevated preconception or first trimester BP and early SAB. Conclusions: We found that elevated first trimester but not preconception BP was associated with an increased risk of pregnancy loss, suggesting that dysregulated adaption to pregnancy may impact pregnancy loss more than preconception BP status, especially SABs that occur after 8 weeks gestation. Our findings support the notion that clinical and environmental factors may have a greater impact on later SABs as opposed to earlier losses. The null relationship with early pregnancy loss in our study may be due to an expected genetic mutation etiology for those losses. Studies exploring the trajectory of preconception and prenatal blood pressure changes and impact on pregnancy outcomes are warranted.

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