STUDY DESIGN: In this retrospective cohort study, we included children aged 5-20 years who received regular outpatient care at a large academic medical center between January 1996 and April 2016. BMI was expressed as age- and sex-specific percentiles and BP as age-, sex-, and height-specific percentiles. Linear mixed models incorporating linear spline functions with 2 breakpoints at 9 and 12 years of age were used to estimate the changes in BMI and BP percentiles over time during age periods: <9, 9-<12, and >12 years of age.
RESULTS: Among 5703 children (24.8% black, 10.1% Hispanic), Hispanic females had an increased rate of change in BMI percentile per year relative to white females during ages 5-9 years (+2.94%; 95% CI, 0.24-5.64; P = .033). Black and Hispanic males also had an increased rate of change in BMI percentile per year relative to white males that occurred from ages 5-9 (+2.35% [95% CI, 0.76-3.94; P = .004]; +2.63% [95% CI, 0.31-4.95; P = .026], respectively). There were no significant racial differences in the rate of change of BP percentiles, although black females had higher hypertension rates compared with white females (10.0% vs 5.7%; P
METHODS: From 5115 participants enrolled in 1985-1986 in the Coronary Artery Risk Development in Young Adults Study, 2533 had serial measures of depressive symptoms and subsequent echocardiography to measure normal LV geometry, concentric remodeling, and LVH. The primary exposure variable was trajectories of the Center for Epidemiologic Studies Depression (CES-D) scale score from 1990-1991 to 2010-2011. Multivariable polytomous logistic regression was used to assess associations of trajectories with a composite LV geometry outcome created using echocardiogram data measured in 2010-2011 and 2015-2016. Sex-specific conflicting results led to exploratory models that examined potential importance of testosterone and sex hormone-binding globulin.
RESULTS: Overall CES-D and Somatic subscale trajectories had significant associations with LVH for female participants only. Odds ratios for the subthreshold (mean CES-D ≈ 14) and stable (mean CES-D ≈ 19) groups were 1.49 (95% confidence interval = 1.05-2.13) and 1.88 (95% confidence interval = 1.16-3.04), respectively. For female participants, sex hormone-binding globulin was inversely associated with LVH, and for male participants, bioavailable testosterone was positively associated with concentric geometry.
CONCLUSIONS: Findings from cross-sectional and longitudinal regression models for female participants, but not male ones, and particularly for Somatic subscale trajectories suggested a plausible link among depression, androgens, and LVH. The role of androgens to the depression-LVH relation requires additional investigation in future studies.
METHODS: We pooled individual-level data from 6 contemporary US-based cohorts from the Cardiovascular Lifetime Risk Pooling Project. Total LE8 score (0-100 points), LE8 score without sleep (0-100 points), and prior LS7 scores (0-14 points) were calculated separately. We used multivariable-adjusted Cox models to evaluate the association of LE8 with CVD, CVD subtypes, and all-cause mortality among younger, middle, and older adult participants. Net reclassification improvement analysis was used to measure the improvement in CVD risk classification with the addition of LS7 and LE8 recategorization based on score quartile rankings.
RESULTS: Our sample consisted of 32 896 US adults (7836 [23.8%] Black; 14 941 [45.4%] men) followed for 642 000 person-years, of whom 9391 developed CVD events. Each 10-point higher overall LE8 score was associated with lower risk by 22% to 40% for CVD, 24% to 43% for congenital heart disease, 17% to 34% for stroke, 23% to 38% for heart failure, and 17% to 21% for all causes of mortality events across age strata. LE8 score provided more granular differentiation of the related CVD risk than LS7. Overall, 19.5% and 15.5% of the study participants were recategorized upward and downward based on LE8 versus LS7 categories, respectively, and the recategorization was significantly associated with CVD risk in addition to LS7 score. The addition of recategorization between LE8 and LS7 categories improved CVD risk reclassification across age groups (clinical net reclassification improvement, 0.06-0.12; P<0.01).
CONCLUSIONS: These findings support the improved utility of the LE8 algorithm for assessing overall cardiovascular health and future CVD risk.
Methods: We conducted a serial, cross-sectional study of National Center for Health Statistics Natality Data representing all live births in the US from 2011 to 2019. We assigned 1 point for each of four ideal prepregnancy metrics (nonsmoking and ideal body mass index [18.5-24.9 kg/m2] provided by maternal self-report, and absence of hypertension and diabetes ascertained by the healthcare professional at delivery) to construct a prepregnancy clinical CVH score ranging from 0 to 4. We described the distribution of prepregnancy CVH, overall and stratified by self-reported race/ethnicity, age, insurance status, and receipt of the Women, Infants, and Children program (WIC) for supplemental nutrition. We examined trends by calculating average annual percent changes (AAPCs) in optimal prepregnancy CVH (score of 4).
Results: Of 31,643,982 live births analyzed between 2011 and 2019, 53.6% were to non-Hispanic White, 14.5% non-Hispanic Black, 23.3% Hispanic, and 6.6% non-Hispanic Asian women. The mean age (SD) was 28.5 (5.8) years. The prevalence (per 100 live births) of optimal prepregnancy CVH score of 4 declined from 42.1 to 37.7 from 2011 to 2019, with an AAPC (95% CI) of -1.4% per year (-1.3,-1.5). While the relative decline was observed across all race/ethnicity, insurance, and WIC subgroups, significant disparities persisted by race, insurance status, and receipt of WIC. In 2019, non-Hispanic Black women (28.7 per 100 live births), those on Medicaid (30.4), and those receiving WIC (29.1) had the lowest prevalence of optimal CVH.
Conclusions: Overall, less than half of pregnant women had optimal prepregnancy CVH, and optimal prepregnancy CVH declined in each race/ethnicity, age, insurance, and WIC subgroup between 2011-2019 in the US. However, there were persistent disparities by race/ethnicity and socioeconomic status.
OBJECTIVE: To analyze trends in levels of lipids and apolipoprotein B in US youths during 18 years from 1999 through 2016.
DESIGN, SETTING, AND PARTICIPANTS: Serial cross-sectional analysis of US population-weighted data for youths aged 6 to 19 years from the National Health and Nutrition Examination Surveys for 1999 through 2016. Linear temporal trends were analyzed using multivariable regression models with regression coefficients (β) reported as change per 1 year.
EXPOSURES: Survey year; examined periods spanned 10 to 18 years based on data availability.
MAIN OUTCOMES AND MEASURES: Age- and race/ethnicity-adjusted mean levels of high-density lipoprotein (HDL), non-HDL, and total cholesterol. Among fasting adolescents (aged 12-19 years), mean levels of low-density lipoprotein cholesterol, geometric mean levels of triglycerides, and mean levels of apolipoprotein B. Prevalence of ideal and adverse (vs borderline) levels of lipids and apolipoprotein B per pediatric lipid guidelines.
RESULTS: In total, 26 047 youths were included (weighted mean age, 12.4 years; female, 51%). Among all youths, the adjusted mean total cholesterol level declined from 164 mg/dL (95% CI, 161 to 167 mg/dL) in 1999-2000 to 155 mg/dL (95% CI, 154 to 157 mg/dL) in 2015-2016 (β for linear trend, -0.6 mg/dL [95% CI, -0.7 to -0.4 mg/dL] per year). Adjusted mean HDL cholesterol level increased from 52.5 mg/dL (95% CI, 51.7 to 53.3 mg/dL) in 2007-2008 to 55.0 mg/dL (95% CI, 53.8 to 56.3 mg/dL) in 2015-2016 (β, 0.2 mg/dL [95% CI, 0.1 to 0.4 mg/dL] per year) and non-HDL cholesterol decreased from 108 mg/dL (95% CI, 106 to 110 mg/dL) to 100 mg/dL (95% CI, 99 to 102 mg/dL) during the same years (β, -0.9 mg/dL [95% CI, -1.2 to -0.6 mg/dL] per year). Among fasting adolescents, geometric mean levels of triglycerides declined from 78 mg/dL (95% CI, 74 to 82 mg/dL) in 1999-2000 to 63 mg/dL (95% CI, 58 to 68 mg/dL) in 2013-2014 (log-transformed β, -0.015 [95% CI, -0.020 to -0.010] per year), mean levels of low-density lipoprotein cholesterol declined from 92 mg/dL (95% CI, 89 to 95 mg/dL) to 86 mg/dL (95% CI, 83 to 90 mg/dL) during the same years (β, -0.4 mg/dL [95% CI, -0.7 to -0.2 mg/dL] per year), and mean levels of apolipoprotein B declined from 70 mg/dL (95% CI, 68 to 72 mg/dL) in 2005-2006 to 67 mg/dL (95% CI, 65 to 70 mg/dL) in 2013-2014 (β, -0.4 mg/dL [95% CI, -0.7 to -0.04 mg/dL] per year). Favorable trends were generally also observed in the prevalence of ideal and adverse levels. By the end of the study period, 51.4% (95% CI, 48.5% to 54.2%) of all youths had ideal levels for HDL, non-HDL, and total cholesterol; among adolescents, 46.8% (95% CI, 40.9% to 52.6%) had ideal levels for all lipids and apolipoprotein B, whereas 15.2% (95% CI, 13.1% to 17.3%) of children aged 6 to 11 years and 25.2% (95% CI, 22.2% to 28.2%) of adolescents aged 12 to 19 years had at least 1 adverse level.
CONCLUSIONS AND RELEVANCE: Between 1999 and 2016, favorable trends were observed in levels of lipids and apolipoprotein B in US youths aged 6 to 19 years.
OBJECTIVE: To determine if there is an association between maternal nativity and preterm birth rates among nulliparous individuals, and whether that association differs by self-reported race and ethnicity of the pregnant individual.
DESIGN, SETTING, AND PARTICIPANTS: This was a nationwide, cross-sectional study conducted using National Center for Health Statistics birth registration records for 8 590 988 nulliparous individuals aged 15 to 44 years with singleton live births in the US from 2014 to 2019. Data were analyzed from March to May 2022.
EXPOSURES: Maternal nativity (non-US-born compared with US-born individuals as the reference, wherein US-born was defined as born within 1 of the 50 US states or Washington, DC) in the overall sample and stratified by self-reported ethnicity and race, including non-Hispanic Asian and disaggregated Asian subgroups (Asian Indian, Chinese, Filipino, Japanese, Korean, Pacific Islander, Vietnamese, and other Asian), non-Hispanic Black, Hispanic and disaggregated Hispanic subgroups (Cuban, Mexican, Puerto Rican, and other Hispanic), and non-Hispanic White.
MAIN OUTCOMES AND MEASURES: The primary outcome was preterm birth (<37 weeks of gestation) and the secondary outcome was very preterm birth (<32 weeks of gestation).
RESULTS: Of 8 590 988 pregnant individuals included (mean [SD] age at delivery, 28.3 [5.8] years in non-US-born individuals and 26.2 [5.7] years in US-born individuals; 159 497 [2.3%] US-born and 552 938 [31.2%] non-US-born individuals self-identified as Asian or Pacific Islander, 1 050 367 [15.4%] US-born and 178 898 [10.1%] non-US-born individuals were non-Hispanic Black, 1 100 337 [16.1%] US-born and 711 699 [40.2%] non-US-born individuals were of Hispanic origin, and 4 512 294 [66.1%] US-born and 328 205 [18.5%] non-US-born individuals were non-Hispanic White), age-standardized rates of preterm birth were lower among non-US-born individuals compared with US-born individuals (10.2%; 95% CI, 10.2-10.3 vs 10.9%; 95% CI, 10.9-11.0) with an adjusted odds ratio (aOR) of 0.90 (95% CI, 0.89-0.90). The greatest relative difference was observed among Japanese individuals (aOR, 0.69; 95% CI, 0.60-0.79) and non-Hispanic Black individuals (aOR, 0.74; 0.73-0.76) individuals. Non-US-born Pacific Islander individuals experienced higher preterm birth rates compared with US-born Pacific Islander individuals (aOR, 1.15; 95% CI, 1.04-1.27). Puerto Rican individuals born in Puerto Rico compared with those born in US states or Washington, DC, also had higher preterm birth rates (aOR, 1.07; 95% CI, 1.03-1.12).
CONCLUSIONS AND RELEVANCE: Overall preterm birth rates were lower among non-US-born individuals compared with US-born individuals. However, there was substantial heterogeneity in preterm birth rates across maternal racial and ethnic groups, particularly among disaggregated Asian and Hispanic subgroups.
OBJECTIVES: The purpose of this study was to describe trends in maternal pre-pregnancy hypertension among women in rural and urban areas in 2007 to 2018 in order to inform community-engaged prevention and policy strategies.
METHODS: We performed a nationwide, serial cross-sectional study using maternal data from all live births in women age 15 to 44 years between 2007 and 2018 (CDC Natality Database). Rates of pre-pregnancy hypertension were calculated per 1,000 live births overall and by urbanization status. Subgroup analysis in standard 5-year age categories was performed. We quantified average annual percentage change using Joinpoint Regression and rate ratios (95% confidence intervals [CIs]) to compare yearly rates between rural and urban areas.
RESULTS: Among 47,949,381 live births to women between 2007 and 2018, rates of pre-pregnancy hypertension per 1,000 live births increased among both rural (13.7 to 23.7) and urban women (10.5 to 20.0). Two significant inflection points were identified in 2010 and 2016, with highest annual percentage changes between 2016 and 2018 in rural and urban areas. Although absolute rates were lower in younger compared with older women in both rural and urban areas, all age groups experienced similar increases. The rate ratios of pre-pregnancy hypertension in rural compared with urban women ranged from 1.18 (95% CI: 1.04 to 1.35) for ages 15 to 19 years to 1.51 (95% CI: 1.39 to 1.64) for ages 40 to 44 years in 2018.
CONCLUSIONS: Maternal burden of pre-pregnancy hypertension has nearly doubled in the past decade and the rural-urban gap has persisted.
STUDY DESIGN: A systematic search was performed using the MEDLINE, EMBASE, PsycINFO, CINAHL, and Web of Science databases to identify English-language articles published through June 2018. Articles were included if they were longitudinal studies in community-based populations, the primary exposure occurred during childhood, and the primary outcome was either a measure of subclinical CVD or a clinical CVD event occurring in adulthood. Two independent reviewers screened determined whether eligibility criteria were met.
RESULTS: There were 210 articles that met the predefined criteria. The greatest number of publications examined associations of clinical risk factors, including childhood adiposity, blood pressure, and cholesterol, with the development of adult CVD. Few studies examined childhood lifestyle factors including diet quality, physical activity, and tobacco exposure. Domains of risk beyond "traditional" cardiovascular risk factors, such as childhood psychosocial adversity, seemed to have strong published associations with the development of CVD.
CONCLUSIONS: Although the evidence was fairly consistent in direction and magnitude for exposures such as childhood adiposity, hypertension, and hyperlipidemia, significant gaps remain in the understanding of how childhood health and behaviors translate to the risk of adulthood CVD, particularly in lesser studied exposures like glycemic indicators, physical activity, diet quality, very early life course exposure, and population subgroups.
METHODS: Data from the Coronary Artery Risk Development in Young Adults study were analyzed. Participants (n = 2,833) had a mean baseline age of 30.1 years; 45% were black, and 56% were women. Generalized estimating equation logistic regression was used to estimate age-related probabilities of stage B LV abnormalities (remodeling, hypertrophy, or dysfunction) and logistic regression to examine risk factor-adjusted associations between baseline LV parameters and incident abnormalities. Cox regression was used to assess whether baseline LV parameters associated with incident stage B LV abnormalities were also associated with incident clinical (stage C/D) HF events over >25 years' follow-up.
RESULTS: Probabilities of stage B LV abnormalities at ages 25 and 60 years were 10.5% (95% CI, 9.4%-11.8%) and 45.0% (95% CI, 42.0%-48.1%), with significant race-sex disparities (e.g., at age 60, black men 52.7% [95% CI, 44.9%-60.3%], black women 59.4% [95% CI, 53.6%-65.0%], white men 39.1% [95% CI, 33.4%-45.0%], and white women 39.1% [95% CI, 33.9%-44.6%]). Over 25 years, baseline LV end-systolic dimension indexed to height was associated with incident systolic dysfunction (adjusted odds ratio per 1 SD higher, 2.56; 95% CI, 1.87-3.52), eccentric hypertrophy (1.34; 95% CI, 1.02-1.75), concentric hypertrophy (0.69; 95% CI, 0.51-0.91), and concentric remodeling (0.68; 95% CI, 0.58-0.79); baseline LV mass indexed to height2.7 was associated with incident eccentric hypertrophy (1.70; 95% CI, 1.25-2.32]), concentric hypertrophy (1.63; 95% CI, 1.19-2.24), and diastolic dysfunction (1.24; 95% CI, 1.01-1.52). Among the entire cohort with baseline echocardiographic data available (n = 4,097; 72 HF events), LV end-systolic dimension indexed to height and LV mass indexed to height2.7 were significantly associated with incident clinical HF (adjusted hazard ratios per 1 SD higher, 1.56 [95% CI, 1.26-1.93] and 1.42 [95% CI, 1.14-1.75], respectively).
CONCLUSIONS: Stage B LV abnormalities and related racial disparities were present in young adulthood, increased with age, and were associated with baseline variation in indexed LV end-systolic dimension and mass. Baseline indexed LV end-systolic dimension and mass were also associated with incident clinical HF. Efforts to prevent the LV abnormalities underlying clinical HF should start from a young age.
Objective: To examine associations between maternal gestational CVH and offspring CVH.
Design, Setting, and Participants: This cohort study used data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study (examinations: July 2000-April 2006) and HAPO Follow-Up Study (examinations: February 2013-December 2016). The analyses included 2302 mother-child dyads, comprising 48% of HAPO Follow-Up Study participants, in an ancillary CVH study. Participants were from 9 field centers across the United States, Barbados, United Kingdom, China, Thailand, and Canada.
Exposures: Maternal gestational CVH at a target of 28 weeks' gestation, based on 5 metrics: body mass index, blood pressure, total cholesterol level, glucose level, and smoking. Each metric was categorized as ideal, intermediate, or poor using pregnancy guidelines. Total CVH was categorized as follows: all ideal metrics, 1 or more intermediate (but 0 poor) metrics, 1 poor metric, or 2 or more poor metrics.
Main Outcomes and Measures: Offspring CVH at ages 10 to 14 years, based on 4 metrics: body mass index, blood pressure, total cholesterol level, and glucose level. Total CVH was categorized as for mothers.
Results: Among 2302 dyads, the mean (SD) ages were 29.6 (2.7) years for pregnant mothers and 11.3 (1.1) years for children. During pregnancy, the mean (SD) maternal CVH score was 8.6 (1.4) out of 10. Among pregnant mothers, the prevalence of all ideal metrics was 32.8% (95% CI, 30.6%-35.1%), 31.7% (95% CI, 29.4%-34.0%) for 1 or more intermediate metrics, 29.5% (95% CI, 27.2%-31.7%) for 1 poor metric, and 6.0% (95% CI, 3.8%-8.3%) for 2 or more poor metrics. Among children of mothers with all ideal metrics, the prevalence of all ideal metrics was 42.2% (95% CI, 38.4%-46.2%), 36.7% (95% CI, 32.9%-40.7%) for 1 or more intermediate metrics, 18.4% (95% CI, 14.6%-22.4%) for 1 poor metric, and 2.6% (95% CI, 0%-6.6%) for 2 or more poor metrics. Among children of mothers with 2 or more poor metrics, the prevalence of all ideal metrics was 30.7% (95% CI, 22.0%-40.4%), 28.3% (95% CI, 19.7%-38.1%) for 1 or more intermediate metrics, 30.7% (95% CI, 22.0%-40.4%) for 1 poor metric, and 10.2% (95% CI, 1.6%-20.0%) for 2 or more poor metrics. The adjusted relative risks associated with 1 or more intermediate, 1 poor, and 2 or more poor (vs all ideal) metrics, respectively, in mothers during pregnancy were 1.17 (95% CI, 0.96-1.42), 1.66 (95% CI, 1.39-1.99), and 2.02 (95% CI, 1.55-2.64) for offspring to have 1 poor (vs all ideal) metrics, and the relative risks were 2.15 (95% CI, 1.23-3.75), 3.32 (95% CI,1.96-5.62), and 7.82 (95% CI, 4.12-14.85) for offspring to have 2 or more poor (vs all ideal) metrics. Additional adjustment for categorical birth factors (eg, preeclampsia) did not fully explain these significant associations (eg, relative risk for association between 2 or more poor metrics among mothers during pregnancy and 2 or more poor metrics among offspring after adjustment for an extended set of birth factors, 6.23 [95% CI, 3.03-12.82]).
Conclusions and Relevance: In this multinational cohort, better maternal CVH at 28 weeks' gestation was significantly associated with better offspring CVH at ages 10 to 14 years.
Objective: To determine whether rates of gestational diabetes among individuals at first live birth changed from 2011 to 2019 and how these rates differ by race and ethnicity in the US.
Design, Setting, and Participants: Serial cross-sectional analysis using National Center for Health Statistics data for 12 610 235 individuals aged 15 to 44 years with singleton first live births from 2011 to 2019 in the US.
Exposures: Gestational diabetes data stratified by the following race and ethnicity groups: Hispanic/Latina (including Central and South American, Cuban, Mexican, and Puerto Rican); non-Hispanic Asian/Pacific Islander (including Asian Indian, Chinese, Filipina, Japanese, Korean, and Vietnamese); non-Hispanic Black; and non-Hispanic White.
Main Outcomes and Measures: The primary outcomes were age-standardized rates of gestational diabetes (per 1000 live births) and respective mean annual percent change and rate ratios (RRs) of gestational diabetes in non-Hispanic Asian/Pacific Islander (overall and in subgroups), non-Hispanic Black, and Hispanic/Latina (overall and in subgroups) individuals relative to non-Hispanic White individuals (referent group).
Results: Among the 12 610 235 included individuals (mean [SD] age, 26.3 [5.8] years), the overall age-standardized gestational diabetes rate significantly increased from 47.6 (95% CI, 47.1-48.0) to 63.5 (95% CI, 63.1-64.0) per 1000 live births from 2011 to 2019, a mean annual percent change of 3.7% (95% CI, 2.8%-4.6%) per year. Of the 12 610 235 participants, 21% were Hispanic/Latina (2019 gestational diabetes rate, 66.6 [95% CI, 65.6-67.7]; RR, 1.15 [95% CI, 1.13-1.18]), 8% were non-Hispanic Asian/Pacific Islander (2019 gestational diabetes rate, 102.7 [95% CI, 100.7-104.7]; RR, 1.78 [95% CI, 1.74-1.82]), 14% were non-Hispanic Black (2019 gestational diabetes rate, 55.7 [95% CI, 54.5-57.0]; RR, 0.97 [95% CI, 0.94-0.99]), and 56% were non-Hispanic White (2019 gestational diabetes rate, 57.7 [95% CI, 57.2-58.3]; referent group). Gestational diabetes rates were highest in Asian Indian participants (2019 gestational diabetes rate, 129.1 [95% CI, 100.7-104.7]; RR, 2.24 [95% CI, 2.15-2.33]). Among Hispanic/Latina participants, gestational diabetes rates were highest among Puerto Rican individuals (2019 gestational diabetes rate, 75.8 [95% CI, 71.8-79.9]; RR, 1.31 [95% CI, 1.24-1.39]). Gestational diabetes rates increased among all race and ethnicity subgroups and across all age groups.
Conclusions and Relevance: Among individuals with a singleton first live birth in the US from 2011 to 2019, rates of gestational diabetes increased across all racial and ethnic subgroups. Differences in absolute gestational diabetes rates were observed across race and ethnicity subgroups.
OBJECTIVE: The purpose of this study was to examine the association of gestational cardiovascular health-formally characterized by a combination of 5 metrics-with adverse maternal and newborn outcomes.
STUDY DESIGN: We analyzed data from the Hyperglycemia and Adverse Pregnancy Outcome study, including 2304 mother-newborn dyads from 6 countries. Maternal cardiovascular health was defined by the combination of the following 5 metrics measured at a mean of 28 (24-32) weeks' gestation: body mass index, blood pressure, lipids, glucose, and smoking. Levels of each metric were categorized using pregnancy guidelines, and the total cardiovascular health was scored (0-10 points, where 10 was the most favorable). Cord blood was collected at delivery, newborn anthropometrics were measured within 72 hours, and medical records were abstracted for obstetrical outcomes. Modified Poisson and multinomial logistic regression were used to test the associations of gestational cardiovascular health with pregnancy outcomes, adjusted for center and maternal and newborn characteristics.
RESULTS: The average age of women at study exam was 29.6 years old, and they delivered at a mean gestational age of 39.8 weeks. The mean total gestational cardiovascular health score was 8.6 (of 10); 36.3% had all ideal metrics and 7.5% had 2+ poor metrics. In fully adjusted models, each 1 point higher (more favorable) cardiovascular health score was associated with lower risks for preeclampsia (relative risk, 0.67 [95% confidence interval, 0.61-0.73]), unplanned primary cesarean delivery (0.88 [0.82-0.95]), newborn birthweight >90th percentile (0.81 [0.75-0.87]), sum of skinfolds >90th percentile (0.84 [0.77-0.92]), and insulin sensitivity <10th percentile (0.83 [0.77-0.90]). Cardiovascular health categories demonstrated graded associations with outcomes; for example, relative risks (95% confidence intervals) for preeclampsia were 3.13 (1.39-7.06), 5.34 (2.44-11.70), and 9.30 (3.95-21.86) for women with ≥1 intermediate, 1 poor, or ≥2 poor (vs all ideal) metrics, respectively.
CONCLUSION: More favorable cardiovascular health at 24 to 32 weeks' gestation was associated with lower risks for several adverse pregnancy outcomes in a multinational cohort.