Optimizing Prepregnancy Cardiovascular Health to Improve Outcomes in Pregnant and Postpartum Individuals and Offspring

Authors, Journal, Affiliations, Type, DOI

• Sadiya S. Khan (Chair), Holly Gooding (Vice Chair), LaPrincess C. Brewer, Mary M. Canobbio, Marilyn J. Cipolla, William A. Grobman, Jennifer Lewey, Erin D. Michos, Eliza C. Miller, Amanda M. Perak, Gina S. Wei
• On behalf of the AHA Council on Epidemiology and Prevention; Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension; Council on Lifestyle and Cardiometabolic Health; Council on Peripheral Vascular Disease; and Stroke Council
• Circulation. 2023;147:e76–e91
• AHA Scientific Statement
• DOI: 10.1161/CIR.0000000000001124

Overview

CVD is the leading cause of pregnancy-related death in the United States, accounting for 26.5% of pregnancy-related deaths, while approximately 1 in 5 births is complicated by adverse pregnancy outcomes (APOs: hypertensive disorders, preterm birth, SGA birth, gestational diabetes) — rates that have worsened over the past decade. This statement argues that prepregnancy cardiovascular health (CVH), measured via Life's Essential 8, is a critical and underutilized target because biological processes underlying APOs begin before conception. Epidemiological data demonstrate a graded, consistent association between prepregnancy CVH metrics and APO risk, with intergenerational effects on offspring CVD. No large RCTs yet validate comprehensive prepregnancy CVH interventions, and the statement calls for multilevel (individual, community, policy) approaches with an equity focus.

Keywords

AHA Scientific Statements, cardiovascular diseases, pregnancy, pregnancy complications, primary prevention, risk factors

Key Takeaways

Current Status of CVH in Birthing Individuals

• Approximately 64.5 million reproductive-age (15–44 years) females in the US; ~3.5–4 million live births/year; by age 40–44, ~86% of females have given birth at least once
• Fewer than 1% have ideal levels of all CVH metrics (Life's Simple 7 or Essential 8); mean CVH score (LE8) in women: 68.1/100 (SD 0.48)
• By age 20–39, only 31.6% have ideal levels in ≥5 of 7 CVH metrics; females slightly better than males (21.5% vs 18.4% have ≥5 ideal metrics in adults ≥20 years)
• Significant racial/ethnic disparities: non-Hispanic Black females have lower mean CVH scores and worse values across most metrics including sleep
• Prepregnancy CVH declined between 2011 and 2019 in all subgroups (race/ethnicity, geography, socioeconomic status)
• Fewer than half of birthing individuals have favorable prepregnancy CVH by abbreviated metrics (absence of obesity, hypertension, diabetes, smoking)
• Individual risk factor prevalence in reproductive-age females: ~25% smoke, ~40% obesity, 9.3% hypertension, 4.5% diabetes, up to 33% hyperlipidemia; ~17% with hypertension and ~30% with diabetes were unaware of their diagnoses

Associations Between Prepregnancy CVH and APOs

• Consistent graded association: adjusted RR for preterm birth with 1, 2, 3, or 4 poor prepregnancy CVH metrics (obesity/diabetes/hypertension/smoking): 1.15, 1.62, 2.85, and 3.89 vs those with no poor metrics
• Healthier prepregnancy dietary patterns associated with lower risk of GDM, preterm birth, SGA, and HDP; better fitness associated with lower GDM risk
• Obesity: estimated population attributable fraction for HDP 26.5–30.3% in 2018; per 1 kg/m² inter-pregnancy BMI increase → OR 1.31 for HDP (meta-analysis)
• Prepregnancy BP associated with HDP; CHAP trial showed that treating mild chronic hypertension early in pregnancy reduced risk of preterm birth, SGA, and preeclampsia
• Prepregnancy lipid levels (TG, HDL-C) associated with GDM and HDP; prepregnancy glycemia associated with LGA, preterm birth, HDP
• Poor sleep quality/duration associated with GDM and HDP; chronic kidney disease also an important APO risk factor

Associations with Offspring Outcomes

• Preterm birth → 53% higher adjusted hazards for premature ischemic heart disease by age 43 in offspring
• Prepregnancy T2DM → adjusted HR 1.39 (95% CI 1.23–1.57) for offspring premature CVD by age 40
• Prepregnancy BMI more strongly associated with APOs and offspring CV risk factors in adolescence compared with gestational weight gain
• Direct evidence linking prepregnancy CVH to offspring CVD events is emerging but no study has yet reported total maternal prepregnancy CVH score and offspring cardiovascular outcomes

Pathophysiological Mechanisms

• Periconceptional window: epigenetic reprogramming links maternal metabolic status to gene expression in developing embryo and placenta; oocyte lipid enrichment in obesity → endoplasmic reticulum stress, mitochondrial respiration, reactive oxygen species
• Clinical parallel: glycemic control must be achieved before pregnancy to reduce congenital anomalies (transfer experiments in diabetic mice demonstrate periconceptional exposure sufficient to program postnatal phenotype)
• Placental malperfusion secondary to inappropriate uterine spiral artery remodeling → begins long before clinical APOs manifest
• Markers of preexisting vascular dysfunction (↓arterial compliance, retinal microvascular constriction, diastolic dysfunction) in early pregnancy → higher APO risk
• APOs may reflect unmasking of preexisting CVD risk under the physiological stress of pregnancy

Evidence for Prepregnancy Interventions

• No large randomized trials with sufficient power to test whether improving prepregnancy CVH reduces APOs or improves maternal/offspring outcomes
• Available RCTs intervened on single factors (diet, smoking, weight loss) rather than comprehensive CVH
• Bariatric surgery before pregnancy: OR 0.21 (95% CI 0.12–0.36) for GDM and OR 0.38 (95% CI 0.27–0.53) for HDP, but OR 2.18 (95% CI 1.41–3.38) for SGA — overall benefit uncertain
• Postpartum lifestyle interventions (weight loss, lifestyle) modestly improve CVH but long-term offspring outcomes unknown
• Growing consensus that hydrophilic statins (e.g., pravastatin) may be safe in pregnancy and reduce APO risk, but no confirmed evidence

Trial Design Framework (PICOTS)

• Population: age 25–44, overweight/obesity + intermediate risk factors (BP >120/80, FBG >100, non-HDL >160) not yet at pharmacotherapy thresholds; oversample Black, Hispanic, and Asian American individuals and those with prior APOs
• Intervention: moderate-intensity lifestyle (diet, physical activity, sleep) + adjunctive pharmacotherapy safe during pregnancy
• Comparison: standard of care
• Outcomes: maternal composite (preeclampsia, gestational HT, GDM, severe maternal morbidity, pregnancy-related mortality) + offspring composite (fetal death, preterm birth, SGA)
• Timing: 5-year trial; 4 years enrollment + 1 year follow-up
• Setting: pragmatic trial in federally qualified health centers, Indian Health Service, HMOs, research networks

Community and Policy Interventions

• Black women: superwoman schema (cultural coping behavior) may negatively affect maternal outcomes; culturally responsive mindfulness-based interventions warranted
• Digital health: smartphone apps, conversational agents (e.g., Gabby) shown to engage high-risk Black women in prepregnancy health behavior change
• Community-engaged strategies: peer leaders (community health workers, promotoras), place-based interventions (hair salons, churches, public housing, college campuses)
• Policy: dismantling structural racism, fair housing, equitable employment, continuous health insurance (insurance "churn" before/after childbirth limits preconception and postpartum care access)
• ~50% of pregnancies are unintended (disproportionately in low-income and underrepresented racial/ethnic groups), limiting the reach of individual-level prepregnancy interventions

Limitations of the Document

• No large RCTs testing comprehensive prepregnancy CVH interventions on maternal or offspring hard endpoints
• Almost all mechanistic evidence from animal and in vitro models; causal relationship between CVH, APOs, and CVD unproven in humans
• Limited disaggregated data for Asian subgroups, Hispanic subgroups, and American Indian/Alaska Native individuals
• CVH construct not validated during pregnancy (physiological changes alter individual metrics)
• ~50% of pregnancies unintended, limiting individual-level prepregnancy intervention reach
• Observational evidence predominantly; residual confounding limits attribution of APOs to specific CVH metrics

Key Concepts Mentioned

• concepts/Prepregnancy-Cardiovascular-Health — central thesis: prepregnancy period as critical CVH optimization window
• concepts/Adverse-Pregnancy-Outcomes — HDP, preterm birth, SGA, GDM; all associated with prepregnancy CVH
• concepts/Lifes-Essential-8 — updated AHA CVH construct (diet, PA, sleep, smoking, BMI, BP, cholesterol, glucose)
• concepts/ASCVD-Risk-Assessment — life-course framework for primordial prevention

Key Entities Mentioned

• entities/Maternal-Health-Disparities — non-Hispanic Black females bear disproportionate burden of poor CVH and APOs; structural racism as root cause

Wiki Pages Updated

• wiki/sources/prepregnancy-aha-2023.md (created)
• wiki/concepts/Prepregnancy-Cardiovascular-Health.md (created)
• wiki/concepts/Adverse-Pregnancy-Outcomes.md (created)
• wiki/concepts/Lifes-Essential-8.md (created)
• wiki/entities/Maternal-Health-Disparities.md (created)
• wiki/wikiindex.md (updated)
• wiki/sourceindex.md (updated)
• wiki/log.md (updated)