tbuckley/cabot-search huggingface dataset:
Abstract 30: Early-Life Tobacco Exposure, Genetic Risk, and Incident Type 2 Diabetes
Authors: Xuanwei Jiang, Victor W Zhong
Journal: Circulation (2024)

Introduction: Tobacco exposure in adulthood is a well-established risk factor for type 2 diabetes (T2D), but how early-life tobacco exposure implicates in the development of T2D as well as whether this association varies by different genetic predisposition to T2D are unclear. Addressing these gaps may provide novel insights into early interventions of T2D. Hypothesis We hypothesized that tobacco exposure in utero and childhood/adolescence stages was significantly associated with incident T2D in adulthood and there were significant interactions and joint effects between early-life tobacco exposure and genetic risk for T2D in relation to risk of T2D. Methods: This prospective cohort study used data from the UK Biobank. In utero tobacco exposure and age of smoking initiation [never smoking, childhood (5-14 years), adolescence (15-17 years), and adulthood (≥18 years)] were assessed through self-reported questionnaires. Multivariable Cox proportional hazard models, adjusted for demographics and early-life factors, were used to estimate the associations of tobacco exposure in utero and childhood/adolescence stages with incident T2D. A polygenic risk score (PRS) for T2D divided into tertiles was used to assess the interactions and joint effects between early-life tobacco exposure and genetic susceptibility on the development of T2D. Results: A total of 475,957 participants without T2D at baseline were included. During a median follow-up time of 14.6 years (IQR, 13.7-15.3), 23,480 incident T2D events occurred. Tobacco exposure in utero vs no exposure was significantly associated with incident T2D (hazard ratio [HR], 1.22 [95% CI, 1.18-1.26]). Compared with never smoking, smoking initiation in childhood (HR, 2.19 [95% CI, 2.08-2.29]), adolescence (HR, 1.57 [95% CI, 1.51-1.62]), and adulthood (HR, 1.33 [95% CI, 1.28-1.38]) were significantly associated with incident T2D ( P for trend &lt;0.001). Additive interactions were observed between tobacco exposure in utero or childhood/adolescence stages and PRS for T2D (relative excess risk due to interaction &gt;0, P interaction &lt;0.001). Compared with participants having no early-life tobacco exposure and a low PRS, those with a high PRS had a 330% higher risk of developing T2D when exposed to tobacco in utero (HR, 4.30 [95% CI, 4.07-4.54]), a 639% higher risk of developing T2D when starting smoking in childhood (HR, 7.39 [95% CI, 6.84-7.99]), and a 427% higher risk when starting smoking in adolescence (HR, 5.27 [95% CI, 4.95-5.62]). Conclusions: In utero tobacco exposure was significantly associated with incident T2D. Earlier smoking initiation was more strongly associated with incident T2D than later initiation. Early-life tobacco exposure and genetic predisposition to T2D interacted and jointly determined risk of T2D.
Abstract 10: Trends in Blood Pressure Control With the Covid-19 Pandemic, 2017 to 2022: A Study of 17 US Health Systems in the PCORnet <sup>®</sup> Blood Pressure Control Laboratory
Authors: Alanna M Chamberlain, Rhonda M Cooper-Dehoff, Feng Lin, Valy Fontil, Kathryn M Shaw, Myra Smith, Thomas Carton, Emily C O'Brien, Madelaine Faulkner Modrow, Gregory Wozniak, Michael Rakotz, Steven M Smith, Mark J Pletcher
Journal: Circulation (2024)

Background: The COVID-19 pandemic resulted in reduced in-person clinic visits and declines in blood pressure (BP) control among patients with hypertension. The purpose of this study was to report on pre- to post-pandemic trends in BP control and related BP metrics through 2022. Methods: We utilized data from 17 US health systems with electronic health record data standardized to the PCORnet ® Common Data Model. Multiple BP control metrics were calculated as a series of quarterly, 12-month rolling measurement periods from 2017 to 2022 (i.e., 1/1/2017-12/31/2017, 4/1/2017-3/31/2018, …, 1/1/2022-12/31/2022). BP control was defined as the percentage of patients with hypertension whose most recent BP measurement at an ambulatory visit was &lt;140/&lt;90 mmHg. Improvement in BP was defined as the percentage of patients with a reduction of 10 mmHg in systolic BP or achievement of systolic BP &lt;140 mmHg during the last 3 months of the measurement period in patients with previously uncontrolled hypertension. Results: In 2022, 1,499,418 persons with hypertension were included (50% 65-85 years old; 47% men; 11% Hispanic, 3% non-Hispanic Asian, 20% non-Hispanic Black, 63% non-Hispanic White). BP control was relatively stable within health systems prior to the COVID-19 pandemic. Worsening of BP control was seen for most health systems in the second quarter of 2020 coinciding with onset of the COVID-19 pandemic (Figure, left panel). The weighted average BP control was 65.3% in 2019, dropped to 61.8% in 2020, and increased to 62.9% in 2021 and 62.6% in 2022. Similar patterns were observed for the improvement in BP metric (Figure, right panel): weighted average 31.4% in 2019, 25.7% in 2020, 29.1% in 2021 and 28.6% in 2022. Conclusion: BP control and improvement in BP decreased substantially during the COVID-19 pandemic. While both metrics improved after 2020, they were still below pre-pandemic levels through 2022. These findings underscore the importance of continued surveillance of BP control and other health impacts of the COVID-19 pandemic.
Abstract 40: Causal Aspects of Preeclampsia and Gestational Hypertension for Risk of Future Cardiovascular Diseases
Authors: Sofie Taageby Nielsen, Jiao Luo, Jesper Qvist Thomassen, Ruth Frikke-Schmidt
Journal: Circulation (2024)

Introduction: Preeclampsia is a multifactorial disease and a cause of maternal and neonatal morbidity and mortality. Observational studies show that women with preeclampsia have increased risk of cardiovascular diseases later in life. Whether this association is causal is however uncertain. Hypothesis: We assessed the hypothesis that preeclampsia and gestational hypertension are causal risk factors for future cardiovascular diseases, including ischemic heart disease, myocardial infarction, stroke, ischemic stroke, atrial fibrillation, and heart failure. Methods: For this purpose, we performed one-sample Mendelian randomization (MR) analyses using individual level data from 202,876 white British women from the UK Biobank. Subsequently, two-sample MR analyses were performed using summary level data from FinnGen and from the to date largest consortia for each endpoint individually and then pooled in fixed-effects meta-analyses. Genetic instruments for preeclampsia and gestational hypertension were from the most updated genome-wide association study (n=20,064 preeclampsia cases; n=703,117 controls; n=11,027 gestational hypertension cases; n=412,788 controls). Results: In one-sample MR analyses, the odds ratios (95% CI) for preeclampsia were 1.26 (1.11-1.43) for ischemic heart disease, 1.26 (0.99-1.60) for myocardial infarction, 1.28 (1.04-1.57) for stroke, and 1.37 (1.08-1.74) for ischemic stroke; for gestational hypertension the odds ratios (95% CI) were 1.17 (1.07-1.28) for ischemic heart disease, 1.16 (0.98-1.36) for myocardial infarction, 1.35 (1.17-1.56) for stroke, 1.36 (1.15-1.60) for ischemic stroke, 1.16 (1.04-1.29) for atrial fibrillation, and 1.22 (1.04-1.43) for heart failure. The two-sample MR analyses confirmed all associations from one-sample MR analyses with similar results from multiple sensitivity analyses. The MR-Egger results did not suggest pleiotropy. Conclusion: Genetic predisposition to preeclampsia or gestational hypertension was associated with increased risk of cardiovascular diseases later in life, suggesting preeclampsia as a likely causal factor.
Abstract 42: Metabolite Risk Scores of Lifestyle Measures Improve Incident Hypertension Prediction
Authors: Tamar Sofer, Yu Zhang, Tariq Faquih, Ying Zhang, Heming Wang, Qibin Qi, Eric Boerwinkle, Robert Kaplan, Carmen R Isasi, Bing Yu
Journal: Circulation (2024)

Introduction: Metabolites capture the metabolic environment associated with exposures. Objective: To develop and assess the usefulness of metabolite risk scores (MRSs) as biomarkers representing exposure measures. Methods: We used two separate sets of individuals sampled from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Both sets of individuals had metabolite data measures on the Metabolon HD4 platform. We applied the least absolute selection and shrinkage operator (LASSO) to develop MRSs for current smoking, physical activity, Mediterranean diet, and anxiety in set 1 (n=2,178), cross-sectionally, and evaluated them for replication in set 2 individuals (n=4,002). We defined hypertension as SBP140, DBP90, or hypertension medication use, and estimated MRS associations with incident hypertension longitudinally (6 years after the baseline exam, on average) in set 2 individuals free of hypertension at baseline (426 cases and 1,556 controls). The association models were adjusted for age, sex, and BMI. We compared the estimated association with those of self-reported phenotypes. Results: All MRSs were developed in set 1 individuals have replicated associations in set 2 individuals. The figure provides the estimated association of MRSs for diet, smoking, physical activity, and anxiety with incident hypertension and compares them to the associations of self-reported Mediterranean diet, anxiety measured using the Spielberger trait anxiety scale, pack-years of smoking, and self-reported physical activity in MET-min/day. All associations are per 1 SD increase in the exposure measure. The figure shows that the MRS associations are often stronger than those of the self-reported measure. Conclusions: MRSs have the potential to serve as accurate biomarkers of self-reported exposures.
Abstract 36: Clinical Guidelines May Help Mitigate the Impact of Physician Implicit Bias on Patient Care and Treatment
Authors: Erika T Beidelman, Corey A Kalbaugh
Journal: Circulation (2024)

Introduction: We previously found that physician pro-White implicit bias was associated with the performance of low-value revascularization procedures for Black patients with claudication. These treatments are commonly considered risk greater than benefit but are not expressly discouraged by guidelines. We sought to investigate whether implicit bias is less likely to impact care in settings with well-defined Class Ia-supported guidelines. Hypothesis: We hypothesized that a physician’s implicit bias would not be associated with the performance of clinical practices as outlined in the 2016 AHA/ACC Guidelines on the Management of Patients with Lower Extremity Peripheral Artery Disease. Methods: We measured implicit bias via the race Implicit Association Test (IAT) using a sample of physicians from the Society for Vascular Surgery’s Vascular Quality Initiative (VQI). The IAT asks participants to classify sequential images of Black and White faces to positive and negative attributes. Based on reaction times and responses on the IAT, physicians were categorized as having no bias, pro-Black bias, or pro-White bias. IAT results were then weighted to reflect the overall VQI demographics and linked to peripheral revascularization data. We used mixed effects logistic regression models to assess the association of physician implicit bias category with pre-operative prescriptions of antiplatelets (ASA, P2Y12) and statins, as well as current smoking status (reported as aORs). All models included a random intercept for the physician and were adjusted for year, physician race/ethnicity, and patient factors of race/ethnicity, diabetes, and hypertension. We examined effect modification by patient race/ethnicity through the inclusion of an interaction term with physician implicit bias category. Finally, we calculated a summary index across the four primary clinical practices and assessed the association with physician implicit bias category via a mixed effects Poisson model (reported as IRRs). Results: A total of 218 physicians successfully completed the IAT and were linked to 6,588 peripheral revascularizations they completed for claudication. We found no significant associations between the physician’s implicit bias category and the performance of any of the assessed guideline metrics for their Black or White patients (Summary Index - IRR: 1.02, 95% CI: 0.98-1.06). Additionally, we found no evidence of effect modification by patient race/ethnicity (ASA - aOR: 0.91, 95% CI: 0.61-1.34; P2Y12 - aOR: 1.22, 95% CI: 0.88-1.69; Statin - aOR: 1.12, 95% CI: 0.76-1.67). Conclusions: The performance of guideline-driven practices were not associated with a physician’s measured racial implicit bias. We provide preliminary evidence that appropriately designed guidelines could be successful in combatting Black-White health inequities stemming from the implicit bias of physicians.
Abstract 29: Effects of a Novel Structural Variant in Hemoglobin on Racial Differences in Hemoglobin A1c
Authors: Amelia S Wallace, Goo Jun, Eric Boerwinkle, Mary R Rooney, Dan E Arking, Joe Coresh, Elizabeth Selvin
Journal: Circulation (2024)

Background: Studies have found higher hemoglobin A1c (HbA1c) at similar levels of glucose for adults who self-identify as Black vs. White, but the mechanism for this difference is poorly understood. Genetic variants that are more common in persons of African descent that affect hemoglobin (Hb) or red cell turnover may explain some of this difference. A recently discovered deletion in a non-coding region of the HBA2 gene is common in persons of African descent and may contribute to differences in Hb and HbA1c. Methods: We evaluated 5178 participants (mean age 56 years, 18% Black, 55% female) who attended Visit 2 (1990-1992) of the Atherosclerosis Risk in Communities Study without diagnosed diabetes and BMI &lt;30 kg/m 2 . We compared the distributions of Hb and HbA1c in Black and White participants by the number of deletions in the HBA2 region (zero, one, or two). We used linear regression to evaluate the extent to which this genetic variant explained glucose-independent Black-White differences in HbA1c and Hb. Results: Deletions in the HBA2 region were common in Black participants (30% one, 4% two) but rare in White participants (1%: one, 0%: two). Mean Hb was lower in Black participants with one (-0.38 g/dL, p&lt;0.001) and two deletions (-0.76 g/dL, p=0.002) and HbA1c was higher (one: +0.11%, p&lt;0.001; two deletions: +0.13%, p=0.11) ( Figure ). Results were similar in White participants with one deletion (N=38), but non-significant. In a regression model adjusted for age, sex, fasting glucose, and BMI, the differences in HbA1c and Hb comparing Blacks vs White adults were +0.2% and -0.6 g/dL, respectively. Additional adjustment for HBA2 deletions explained 16% of the difference in HbA1c and 19% of the difference in Hb. Conclusions: A variation in the non-coding region of the HBA2 gene common in those with African ancestry results in significantly lower Hb and significantly higher HbA1c, partially explaining the small observed racial differences in HbA1c. Other undiscovered variants could more fully explain observed racial differences in HbA1c.
Abstract 26: Types of Adverse Childhood Experiences and Association With Sleep Duration in Children: Analysis of 2020-2021 National Survey of Children’s Health
Authors: Minkyoung Song, Andrew W McHill, Nathan F Dieckmann, Carol M Musil, Laura L Hayman
Journal: Circulation (2024)

Background: The number of adverse childhood experiences (ACEs) is associated with suboptimal sleep duration in children; however, the differential association of types of ACEs with sleep duration in youth is unknown. Given the known associations of both ACEs and sleep duration with cardiovascular health, such an investigation will provide insights for targeted clinical intervention. Objective: We investigated the most frequently reported ACE types and the association between each type of ACE and sleep duration among U.S. children aged 6-17 years. Methods: We used data from the 2020-2021 National Survey of Children’s Health, the most recent publicly available dataset. Parents or guardians were asked whether their child had ever experienced ten different types of ACEs. Multinomial logistic regression was used to assess the association of sleep duration with each of ACEs. We used the American Heart Association (AHA) Life Essential 8 scoring algorithm to calculate scores for sleep duration (range 0 [lowest] to 100 [highest]). Participants were categorized into three subgroups: (1) meeting age-appropriate optimal sleep duration; (2) ≥1-&lt;2 hour below or ≥ 1 hour above optimal sleep duration; and (3) ≥ 2 hours below optimal sleep duration. Analyses controlled for child’s sex, age, race/ethnicity, household poverty level, regular bedtime, physical activity, and caregiver’s level of education. Results: Parental divorce was the most frequently reported ACE (28.1%) followed by financial hardship (12.9%) and drug abuse (10.1%) among U.S. children aged 6 to 17 years. Adjusting for covariates, 5 of 10 ACEs (parental divorce, parental imprisonment, domestic violence, living with someone who had a problem with alcohol or drugs, unfair treatment because of their sexual orientation or gender identity) were significantly associated with suboptimal sleep category 2. All 10 ACEs were significantly associated with suboptimal sleep category 3. Conclusions: These findings support that ACE type is differentially associated with suboptimal childhood sleep duration and suggests that certain traumatic events experienced during childhood could amplify the adverse effects of poor sleep on cardiovascular health. Healthcare providers should consider screening for ACE type concurrent with sleep duration to better understand aspects contributing to cardiovascular health in childhood.
Abstract 05: Association Between Cumulative Social Risks and Life’s Essential 8 in US Adults: NHANES 2013-2020
Authors: Faith E Metlock, Oluwabunmi V Ogungbe, Biruk Teshome, THOMAS HINNEH, Garima Sharma, Cheryl R Dennison Himmelfarb, Yvonne Commodore-Mensah
Journal: Circulation (2024)

Introduction: Cardiovascular disease remains a leading cause of death in the U.S. Although social risks have been linked to cardiovascular health, our understanding of how co-occurring social risk factors collectively influence cardiovascular health remains limited. We sought to evaluate the contributions of cumulative social risks (SR) to cardiovascular health in US adults. Methods: We analyzed cross-sectional data from the National Health and Nutrition Examination Survey (2013-2020). Social risks (low family income, low education level, minority race/ethnic group, single-living status, uninsured, unemployed) were examined via self-report questionnaires. Cardiovascular health was modeled as quartiles of Life’s Essential 8 (LE8) scores. Cumulative SR was modeled as number of SR (0,1,2,3, and ≥ 4). Multinomial logistic regression models were used to assess the association between cumulative SR and LE8 scores, adjusting for age and gender. Results: Among 13,982 US adults (mean age 32 ± 25; 51% female), the prevalence of 0 SR, 1 SR, 2 SR, 3 SR, and ≥ 4 SR, were 16%, 36%, 29%, 13%, and 6%, respectively. Adults with one or more social risks had significantly higher odds of having worse LE8 scores across multiple quartiles. Compared to adults with the lowest SR (0), those with the highest SR (≥ 4) had significantly higher odds of worse LE8 scores (Quartile 1 adjusted odds ratio (aOR) 7.11; 95% CI 5.32-9.50; Quartile 2 aOR 5.22; 95% CI 3.88-7.04; Quartile 3 aOR 3.39; 95% CI 2.52-4.54). Conclusion: US adults with an increasing number of social risks were more likely to have worse cardiovascular health scores. Social and economic policies are necessary to address adverse social determinants to improve cardiovascular health.
Abstract 25: Association Between Household Sleep Environment and Sleep Health Characteristics: The Coronary Artery Risk Development in Young Adults (CARDIA)—Sleep Study
Authors: Swaty Chapagai, Thanh-Huyen T Vu, Shaina J Alexandria, Kathryn Reid, Sabra Abbott, Katharine Harrington, S. Thomas, Cora E Lewis, Pamela Schreiner, Mercedes R Carnethon, Kristen Knutson
Journal: Circulation (2024)

Introduction: Household environmental factors and sleep behaviors may contribute to poor sleep health. We identified associations between household sleep environment (HHSE) and sleep health characteristics. Hypothesis: Individuals with adverse HHSE will have poorer sleep health. Methods: We used cross-sectional data from the CARDIA sleep ancillary study at Year 35. HHSE (i.e., sleep disruptors and sleep behaviors) scores were derived from responses to questions in the questionnaire (see Table footnote), where a higher score indicated higher sleep disruptors or more detrimental sleep behaviors. Sleep outcomes were: 1) sleep quality assessed with the Pittsburgh Sleep Quality Index (PSQI) and daytime sleepiness assessed with the Epworth Sleepiness Scale (ESS) (N=699) and 2) sleep duration (minutes) and efficiency (%) measured by 7-day wrist actigraphy (N=574). Robust regression estimated differences in sleep outcomes corresponding to each 1-score increment in HHSE. We adjusted for age, sex, race, education, smoking status, body mass index, depressive symptoms, and comorbidities. Racial differences in associations of interest were examined by testing for interaction. Results: Participants mean age was 61.5 years, 63.1% were female and 35.9% were Black. Means (SD) of PSQI, ESS scores, sleep duration, and sleep efficiency were 6.2 (3.7), 5.5 (3.7), 414.6 minutes (SD=60.4), and 84.4% (SD= 6.7), respectively. After multivariable adjustment, both higher sleep disruptors and more detrimental sleep behaviors were associated with poorer sleep quality and greater daytime sleepiness. HHSE showed no association with sleep duration and efficiency (Table 1). Sleep disruptors were only significantly associated with daytime sleepiness among Black participants (p-interaction= 0.01). Conclusions: Adverse household sleep environment was related to poorer subjective sleep quality and daytime sleepiness. Future studies should investigate reasons why Black adults appear more susceptible to household sleep disruptors.