Journal of the American Heart Association

IntroductionBlack Americans have greater coronary heart disease (CHD) burden than White Americans, disparities that are largely socially determined. Discriminatory societal practices that systematically disadvantage Black Americans are forms of structural racism but few studies have examined structural racism and incident CHD. We sought to determine associations between three validated measures of structural racism and incident CHD, hypothesizing that greater state-level structural racism is associated with incident CHD for Black but not White individuals. MethodsWe used data from the national REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort, which enrolled 30,239 Black and White community dwelling adults between 2003-7 who were contacted every 6 months with retrieval of medical records and expert adjudication of myocardial infarction and cause of death. Incident CHD was defined as myocardial infarction or death due to CHD. Structural racism variables included Black:White % living below the Federal poverty line, Black:White % uninsured, and the Dissimilarity Index (DI), a measure of residential racial segregation. Structural racism variables were dichotomized at the median. Separate race-stratified Cox proportional hazards models examined associations between each measure of structural racism and incident CHD. ResultsThe 24,099 participants free of CHD at baseline included 10,286 Black and 13,813 White participants. Mean age at baseline was 64 years, 58% were women, and 47% had annual household income <$35,000. Greater structural racism was significantly associated with incident CHD for Black but not White participants. For high Black:White poverty, Black HR=1.17 (95% CI 1.01-1.35), White HR=0.93 (0.83-1.06); for high Black:White uninsurance, Black=HR 1.34 (1.06-1.70), White HR=1.20 (0.98-1.47); for high DI, Black HR=1.17 (1.01-1.35), White HR=0.99 (0.88-1.12). Findings suggest that structural racism variables indirectly influence CHD via individual-level income and education. Results were similar for men and women and for older and younger individuals. Significant associations were observed for fatal but not nonfatal CHD events. ConclusionsStructural racism was associated with higher incidence of CHD for Black but not White individuals. If these associations are causal, changing state level laws to combat poverty in Black communities, expand Medicaid, and reduce segregation could potentially lessen Black:White disparities in CHD.

BACKGROUNDSocioeconomic factors may lead to a disproportionate impact on healthcare utilization and mortality among individuals with congenital heart defects (CHD) by race, ethnicity, and socio-economic factors. How neighborhood poverty affects racial and ethnic disparities in healthcare utilization and mortality among individuals with CHD across the lifespan is not well described. METHODSIndividuals, 1-64 years, with at least one CHD-related ICD-9-CM code were identified from healthcare encounters between 01/01/2011-12/31/2013 from four U.S. sites. Residence was classified into lower or higher poverty neighborhoods based on ZCTA from the 2014 American Community Survey 5-Year Estimates. Multivariable logistic regression models, adjusting for site, sex, CHD anatomic severity, and insurance evaluated associations between race and ethnicity, and healthcare utilization and mortality, stratified by neighborhood poverty. RESULTSOf 31,542 individuals, 22.2% were non-Hispanic Black (nHB) and 17.0% Hispanic. In high poverty neighborhoods, nHB (44.4%) and Hispanic (47.7%) individuals, respectively, were more likely to be hospitalized (aOR)=1.2 [95%CI=1.0-1.3] and aOR=1.3 [95%CI=1.2-1.5]) and have ED visits (aOR=1.3 [95%CI=1.2-1.5] and aOR=1.7 [95%CI=1.5-2.0]) compared to non-Hispanic White (nHW) individuals. In high poverty neighborhoods, nHB individuals with CHD had 1.7 times the odds of mortality compared to nHW individuals in high poverty neighborhoods (95%CI=1.1-2.7). Racial and ethnic disparities in healthcare utilization were similar in low poverty neighborhoods, but disparities in mortality were attenuated (aOR for nHB=1.2 [95%CI=0.9-1.7]). CONCLUSIONSRacial and ethnic disparities in healthcare utilization were found among individuals with CHD in low and high poverty neighborhoods, but mortality disparities were larger in high poverty neighborhoods. Understanding individual- and community-level social determinants of health, including access to healthcare, may help address racial and ethnic inequities in healthcare utilization and mortality among individuals with CHD.

In this prospective cohort study, we included 196 patients presenting with dyspnea and suspected pulmonary embolism (PE) at the emergency department of Uppsala University Hospital, Sweden, between June 2019 and July 2022. All patients underwent CT for PE confirmation. Blood samples were collected and stored in a biobank, allowing for comprehensive biomarker analysis. Of the 196 patients, 89 (45.4%) were diagnosed with PE. Patients with confirmed PE showed significantly elevated levels of D-dimer (median 5.7 mg/L [IQR 2.3-14) vs. 1.0 mg/L [0.4-1.8], p=1.2E-14) and CRP (41 mg/L [16-139] vs.7.2 mg/L [1.5-47], p=1.6E-7), indicating thrombotic and inflammatory activity. Cardiac biomarkers, including Troponin I and NT-pro-BNP, were also significantly higher in the PE group, reflecting cardiac strain. Interestingly, emergency room vital parameters and comorbidities were largely similar. On the other hand, there were notable differences in management, with PE patients more likely to be hospitalized and received thrombolysis more often. Patients were risk assessed using the PE Severity Index (PESI) and according to the European Society of Cardiology 2019 guidelines for PE. Patients with PE had a substantially increased mortality that remained after adjustment for comorbidities (OR: 6.0 (95% CI 2.3-15.3). The results highlight inflammation as a central component of PE pathophysiology, which may serve as both a precipitant and a response to embolic events. Biomarkers including D-dimer, CRP, and cardiac markers enhance diagnostic accuracy and can guide management in patients with suspected PE, aligning with clinical needs in emergency care settings. Further investigation into the interaction between inflammation and coagulation in PE is important to improve risk stratification and targeted treatment approaches as mortality remains high even after diagnosis.

BackgroundRecent studies in selected populations suggest that impaired venous return may affect brain health. We examined associations of right heart structure and function with cognition and MRI markers of brain health in a community-based cohort. MethodsThe Multi-Ethnic Study of Atherosclerosis (MESA) is a longitudinal cohort study of individuals 45 to 84 years of age who were free of clinically apparent cerebrovascular or cardiovascular disease at baseline in 2000-2002. From echocardiograms performed at Exam 6 during 2016-2018, we measured: right atrial pressure and end-systolic area; pulmonary artery systolic pressure; and right ventricular free wall strain, fractional area change, and end-diastolic area. Outcome variables were the Cognitive Assessment Screening Instrument, Digit Span, and Digit Symbol Coding tests and MRI-determined volumes of total white matter, total gray matter, and white matter hyperintensity -- as well as fractional anisotropy. Cognitive measures were obtained at Exam 6, and MRI measures, within a median of 18 months of echocardiograms. Covariates were demographics, APOE-{varepsilon}4 allele status, vascular risk factors, and echocardiographic markers of left heart function. We used general linear models to examine associations between each exposure and outcome variable. ResultsIn 1,913 participants with cognitive testing and echocardiography data, we found no associations between any of the echocardiographic exposure variables and worse scores on any of the cognitive tests. Similarly, in 1,035 participants with echocardiography and MRI data, we found no associations between any of the echocardiographic exposure variables and any of the MRI variables. DiscussionWe found no associations in this cohort of right heart structure and function with cognition or brain MRI measures. These findings do not support the hypothesis that right heart dysfunction impedes venous return sufficiently to adversely affect brain health among people without clinically apparent heart failure.

BackgroundCurrent cardiopulmonary resuscitation (CPR) guidelines recommend that chest compressions should be applied at "the center of the chest." However, in approximately 50% of patients experiencing out-of-hospital cardiac arrest (OHCA) the aortic valve (AV) is reportedly compressed, potentially obstructing blood flow and worsening prognosis. We aimed to use resuscitative transesophageal echocardiography (TEE) to elucidate the impact of compressed vs. uncompressed AV on outcomes of adult patients experiencing OHCA. MethodsThis prospective single-center observational cohort study included patients experiencing OHCA who underwent resuscitative TEE in the emergency department (ED). Exclusion criteria were early return of spontaneous circulation (ROSC) before TEE, resuscitative endovascular balloon occlusion of the aorta (REBOA) or extracorporeal membrane oxygenation (ECMO) initiation before ROSC, unidentifiable compression site, or poor quality/missing TEE images. Patients were divided into AV-compressed or uncompressed groups based on initial TEE findings. Documented patient characteristics, TEE recordings, resuscitation data, and critical time points were analyzed. Primary outcome was sustained ROSC. Secondary outcomes included end-tidal carbon dioxide (EtCO2) level at the 10th-minute post-ED arrival, any ROSC, survival to admission and discharge, active withdrawal post-resuscitation, and favorable neurological outcomes at discharge. Sample size was pre-estimated at 37 patients/group. ResultsFrom October 2020 to January 2023, 76 patients were enrolled (39 and 37 patients in the AV-uncompressed and compressed groups, respectively). Intergroup baseline characteristics were similar. The AV-uncompressed group had better probability of sustained ROSC (53.8% vs. 24.3%, odds ratio [OR] 3.63, adjusted OR [aOR] 4.72, P=0.010), any ROSC (56.4% vs. 32.4%, OR 2.70, aOR 3.30, P=0.033), and survival to admission (33.3% vs. 8.1%, OR 5.67, aOR 6.74, P=0.010) than the AV-compressed group. The 10th-minute EtCO2 levels (16.0 vs. 14.0 mmHg), active withdrawal post-resuscitation (7.7% vs. 5.4%), and survival to discharge (5.1% vs. 0%) revealed no significant intergroup differences. No patient was discharged with favorable neurological outcomes. An uncompressed AV remained an essential factor for sustained ROSC across all predefined subgroups. ConclusionsUncompressed AV during CPR increases the chances of ROSC and survival to admission among patients experiencing OHCA. However, its potential impact on long-term survival and neurological outcomes remains unclear. Clinical Trial RegistrationThis trial was registered at ClinicalTrials.gov, identifier NCT05932784. URL: https://clinicaltrials.gov/study/NCT05932784. Clinical Perspective1) What is new? O_LIWhen performing cardiopulmonary resuscitation according to the current guideline-recommended site, chest compressions may lead to accidental compression of the aortic valve (AV), which obstructs blood flow and worsens prognosis for patients experiencing out-of-hospital cardiac arrest. C_LIO_LIWe have used resuscitative transesophageal echocardiography to elucidate the impact of compressed vs. uncompressed AV on outcomes of these patients, a hitherto unexplored aspect. C_LIO_LIPrimary outcome was sustained return of spontaneous circulation (ROSC) and secondary outcomes included end-tidal carbon dioxide level at the 10th-minute post-emergency department arrival, any ROSC, survival to admission and discharge, active withdrawal post-resuscitation, and favorable neurological outcomes at discharge. C_LI 2) What are the clinical implications? O_LIThe AV-uncompressed group had a better chance of sustained ROSC, any ROSC, and survival to admission than the AV-compressed group. C_LIO_LIHowever, its potential impact on long-term survival and neurological outcomes remains unclear; if resuscitative transesophageal echocardiography can be successfully used or if more convenient and lightweight tools can detect AV compression, both in prehospital situations, stronger evidence may be obtained. C_LIO_LICurrent cardiopulmonary resuscitation guidelines may need to be revised for a more individualized approach, which can help rescuers avoid accidental AV compression and improve patient outcomes and prognosis. C_LI

BackgroundData remain sparse regarding the impact of chronic stress on cardiovascular disease (CVD) risk factors and outcomes. Prior work has been limited by incomplete assessments of perceived stress and focus on single stress domains. We evaluated the association between a composite measure of perceived stress and CVD risk factors and outcomes. MethodsParticipants from the Dallas Heart Study phase 2 (2007-2009) without prevalent CVD who completed questionnaire assessments of perceived stress were included (n=2685). Individual perceived stress subcomponents (generalized stress, psychosocial, financial, and neighborhood stress) were standardized and integrated into a single cumulative stress score (CSS) with equal weighting for each component. Associations between CSS and demographics, psychosocial variables and cardiac risk factors were assessed in univariable and multivariable analyses. Cox proportional hazards models were used to determine associations of the CSS with atherosclerotic CVD (ASCVD) and Global CVD (ASCVD, heart failure, and atrial fibrillation) after adjustment for demographics and traditional risk factors. ResultsMedian age of the study population was 48 years, 55% were female, 49% Black and 15% Hispanic/Latinx. CSS was higher among participants who were younger, female, Black or Hispanic, and those with lower income and educational attainment (p<.0001 for each). Higher CSS was associated with self-report of racial/ethnic discrimination, lack of health insurance and last medical contact > one year previously (p<.0001 for each). In multivariable regression models adjusting for age, gender, race/ethnicity, income and education, higher CSS associated with hypertension, smoking, and higher body mass index, waist circumference Hemoglobin A1C, hs-CRP and sedentary time (p< 0.01 for each). Over a median follow-up of 12.4 years, higher CSS associated with ASCVD (adjusted HR 1.22 per SD, 95% CI 1.01-1.47) and Global CVD (HR 1.20, 95% CI 1.03-1.40). No interactions were seen between CSS, demographic factors, and outcomes. ConclusionComposite multidimensional assessments of perceived stress may help to identify individuals at risk for CVD who may be targeted for stress mitigation or enhanced prevention strategies. These approaches may be best focused on vulnerable populations, given the higher burden of stress in women, Black and Hispanic individuals, and those with lower income and education. WHAT IS NEW?O_LIA novel measure of cumulative stress was created that integrates generalized, psychosocial, financial, and neighborhood perceived stress. C_LIO_LICumulative stress was higher among women, Black and Hispanic participants, younger individuals and persons with lower income and educational attainment and was associated with adverse health behaviors and increased burden of cardiovascular disease (CVD) risk factors. C_LIO_LIIn a diverse cohort, higher cumulative stress associated with incident CVD after adjustment for demographics and traditional risk factors. No interactions were seen based on demographic factors. C_LI CLINICAL IMPLICATIONSO_LIAlthough associations of chronic stress with CVD were similar across demographic subgroups, the higher burden of stress among younger individuals, women, Black and Hispanic participants, and those with lower SES suggests that CVD risk associated with higher stress affects marginalized groups disproportionately. C_LIO_LICumulative Stress is associated with modifiable risk factors and health behaviors. Future studies should explore targeting behavioral modification and risk factor reduction programs, as well as stress reduction strategies, to individuals with high cumulative stress. C_LIO_LIAdditional research is needed to uncover mechanisms that underly the association between chronic stress and cardiovascular disease. C_LI

Background: Placental function is associated with congenital heart defects (CHD), frequently presenting with malperfusion lesions and small-for-gestational-age size. However, placental villous vasculature in the setting of CHD is understudied. This study evaluated differences in placental, neonatal, and maternal outcomes among maternal/infant dyads with versus without CHD. Methods: We conducted a gestational age- and fetal sex-matched retrospective case control study using specimens prospectively collected by a local biobank. Neonatal outcomes included birthweight, placental weight, and their ratio (placental efficiency). We estimated the proportion of placental villous tissue comprised of fetal vascular endothelial cells (%FVE) using anti-CD34 immunohistochemistry and a pixel count algorithm. Placental weight multiplied by %FVE estimated the grams of placental tissue comprised of villous vasculature (placental vascular index). Maternal outcomes included hypertensive disorders of pregnancy and gestational diabetes. We compared cases and controls using linear and logistic regression adjusted for maternal smoking and cold ischemia time. Stratified analyses examined associations by preterm birth status. Results: Dyads (n=34 with CHD, n=34 without CHD) had maternal age of 29.4 +/- 4.9 years and were 35.6 +/- 4.0 gestational weeks at delivery. Groups had similar placental, neonatal, and maternal parameters. Among preterm neonates, we observed small-to-moderate effect sizes indicating lower placental weight, %FVE, and placental vascular index, and higher placental efficiency, in CHD cases. Among term neonates, moderate effect sizes suggested lower birthweight, placental weight, and placental vascular index in CHD cases. Conclusions: Though differences between groups were not significant, moderate effect sizes suggested that placental vascularization was lower among preterm neonates with CHD.

BackgroundCardiovascular disease (CVD) is the leading cause of mortality in the United States, with substantial economic and health impacts. While traditional risk factors are well studied, non-traditional factors like telomere length (TL), have garnered interest due to mixed findings on their association with CVD-specific mortality. This study investigates the association between TL and CVD-specific mortality, accounting for non-CVD-specific mortality as a competing risk, using a multistate framework. MethodsWe conducted a retrospective cohort study using data from the National Health and Nutrition Examination Survey 1999-2002 and 2019 Linked Mortality Files. This study included 6,516 non-institutionalized adults aged 25 years or older. TL was measured using quantitative PCR and analyzed continuously and categorically. We employed a multistate model to evaluate transitions from an event-free state to CVD-specific and non-CVD-specific mortality, estimating cause-specific hazard ratios (HRs) adjusted for sociodemographic and health risk factors. ResultsThe cumulative incidence function for CVD-specific mortality was significantly higher in the lowest TL quartile than in the highest quartile (Gray test, p < 0.01). Grays test was used to compare CIFs across quartiles without applying a Fine and Gray model. We found that a shorter TL was associated with a higher risk of CVD-specific mortality. In the adjusted model, each unit decrease in TL was associated with a 57% higher rate of CVD-specific mortality (HR: 1.57, 95% CI: 1.24-1.98). Adults in the shortest TL quartile had an 88% higher rate of CVD-specific mortality compared with those in the longest TL quartile (HR: 1.88, 95% CI: 1.29-2.72). ConclusionOur findings suggest a significant inverse association between TL and CVD-specific mortality, highlighting TL as a potential biomarker for CVD risk. The use of a multistate framework provides a comprehensive understanding of competing risks and enhances the robustness of our results. Further studies are needed to validate these findings and explore the underlying mechanisms.

BackgroundSudden cardiac arrest (SCA) disproportionately affects youths from lower socioeconomic neighborhoods. The underlying mechanisms for this disparity, particularly in youth athletes, remain unclear. While exercise-related cardiac symptoms serve as vital warning signs for identifying at-risk athletes, no studies have examined the prevalence of these symptoms across different socioeconomic strata. We hypothesized that social determinants of health, quantified by the Child Opportunity Index (COI), a validated multidimensional measure of neighborhood conditions, would be associated with cardiac symptoms identified during preparticipation screening. MethodsThis retrospective cross-sectional study analyzed data from the Simons Heart HeartBytes National Youth Cardiac Registry, a large preparticipation cardiac screening database. Youth athletes aged [&le;]17 years who completed standardized cardiovascular screening questionnaires were stratified by neighborhood opportunity level using the COI, a validated multidimensional measure of neighborhood conditions affecting child development. Multivariable logistic regression examined associations between COI quintiles and exercise-related cardiac symptoms, adjusting for demographics and comorbidities. ResultsAmong 10,000 youth athletes analyzed (median age 14.0 years; 38.8% female; 80.3% White), distribution across COI quintiles was 9.8% very low, 5.7% low, 7.7% moderate, 15.9% high, and 61.0% very high. Exercise-related chest pain and exercise-related fatigue demonstrated a higher prevalence in the lowest COI quintile (p<0.001). After adjustment for age, sex, race, physical activity, and comorbidities, participants from the very high COI quintile had significantly lower odds of exercise-related chest pain (p<0.001) and exercise-related fatigue (p=0.004) compared with the very low COI quintile. ConclusionsYouths from lower-opportunity neighborhoods were underrepresented in screening yet showed higher prevalence of exercise-related symptoms. Whether cardiac or noncardiac in origin, these disparities burden under-resourced communities with increased evaluations. Addressing screening inequities and understanding symptom patterns across socioeconomic strata are critical for equitable cardiovascular care. Prospective studies are needed to determine the clinical significance of these symptom patterns and develop equitable screening strategies.

IntroductionPregnancy is a critical test of womens cardiovascular risk. Structural factors may influence long-term cardiovascular health beyond individual, social experiences. We examined associations of neighborhood-level deprivation and individual-level social vulnerability (SV) during pregnancy with postpartum blood pressure (BP). MethodsThis secondary analysis of a prospective cohort study used data from 3,728 nulliparous women in the nuMoM2b-HHS cohort followed from early pregnancy to 2-7 years post-delivery (Mage: 30.8 years, 65% non-Hispanic White, 14% with adverse pregnancy outcomes [APOs]). Multivariable linear and logistic regression models tested relations of the Area Deprivation Index (ADI) and SV (a composite of perceived stress, discrimination, pregnancy experiences, social support, health literacy, depression, and anxiety) with systolic BP (SBP), diastolic BP (DBP), and incident hypertension, adjusting for demographic and behavioral covariates. Effect modification by APO history was assessed. ResultsIn unadjusted models, both ADI and greater SV were positively associated with SBP and DBP (all ps<0.001). After adjustment, ADI remained positively associated with BP: each 10-unit increase in ADI was associated with 1.0 mmHg higher SBP (p=0.008) and 0.6 mmHg higher DBP (p=0.013). However, SV was no longer associated with BP after adjustment. ADI and SV were not associated with incident hypertension. No evidence of effect modification by APO history was observed (interactions p>0.20). ConclusionsNeighborhood deprivation during pregnancy was associated with higher BP up to seven years later, independent of individual social vulnerability. Structural context during pregnancy may contribute to early maternal cardiovascular risk.

BackgroundPregnant patients with cardiovascular disease (CVD) face increased risk of preeclampsia and preterm delivery, yet data is limited data regarding degree of risk and impact of hypertensive disorders of pregnancy (HDP) on gestational age at delivery. ObjectivesTo examine HDP risk and impact on delivery timing in patients with CVD. MethodsThis retrospective cohort study included patients >18 years old who delivered between 10/1/2015 and 12/31/2020 using the Premier Healthcare Database. Patients with CVD were divided into six categories: congenital, ischemic, aortic pathology, pulmonary hypertension, cardiomyopathy, and valvular disease. The primary outcome was risk of HDP (gestational hypertension/ preeclampsia). The secondary outcome was gestational age at delivery. Multivariable mixed effects regression models were used to estimate adjusted outcomes, adjusting for CVD subtype, >1 CVD subtype present, demographics, hospital characteristics, and comorbidities. ResultsAmong 4,606,247 obstetric patients, 20,021 had CVD. The risk of HDP among people with CVD varied by CVD subtype, lowest in those with congenital heart disease (aOR,0.9; 95% CI [0.8, 1.0]) and highest in those with pulmonary hypertension (aOR, 1.5; 95% CI [1.3, 1.8]) and cardiomyopathy (aOR,1.5; 95% CI [1.4,1.6]). Patients with CVD delivered earlier than those without CVD, even in the absence of HDP(36.4-38.0 weeks versus 38.4 weeks). Among those with HDP, patients with severe pre-eclampsia with CVD, delivered earlier than those without CVD (33.1-34.6 weeks versus 35.5 weeks). ConclusionRisk of HDP and preterm delivery is higher those with CVD, particularly in pulmonary hypertension and cardiomyopathy. Patients with CVD should be advised of their increased risk.

BackgroundHypertensive disorders of pregnancy (HDP) are associated with significant cardiac remodeling during pregnancy and are important contributors to maternal morbidity and mortality. Whether acute adverse outcomes during HDP are associated with additional clinically relevant cardiac impairment has not been widely studied. MethodsA prospective observational study was conducted on 255 women with HDP who underwent transthoracic echocardiography during the peripartum period. Maternal echocardiographic parameters, including left ventricular morphology and function, were analyzed to determine their association with adverse maternal outcomes by univariate and multivariate analyses. The composite adverse maternal outcome was defined as at least one of the following: admission to a high dependence unit, acute renal injury, adverse cardio-pulmonary events, stroke and disseminated intravascular coagulation. ResultsAdverse maternal outcomes occurred in 68 (26.7%) participants. Women with adverse outcomes had significantly higher left atrial volume index (LAVI) (28.8 [23.4-32.3] ml/m2 vs 26.6 [22.2-30.9] ml/m2, p=0.045) and E/e' ratio (7.8 [6.6-9.2] vs 7.0 [5.9-8.1], p=0.002) compared to those without complications. In multivariable analysis, both LAVI (adjusted OR 1.09 [1.02-1.16], p=0.009) and E/e' ratio (adjusted OR 1.25 [1.04-1.49], p=0.018) remained independently associated with adverse maternal outcomes after adjusting for maternal factors and clinical variables. ConclusionsCardiac abnormalities, particularly in diastolic function, are more common in women with adverse maternal outcomes in HDP. Whether enhanced cardiovascular monitoring and management of these women in the peripartum period could have immediate and long-term health benefits requires further evaluation. GRAPHIC ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=125 SRC="FIGDIR/small/25319925v1_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@19c7684org.highwire.dtl.DTLVardef@128d803org.highwire.dtl.DTLVardef@7dc62borg.highwire.dtl.DTLVardef@15d6abf_HPS_FORMAT_FIGEXP M_FIG C_FIG

Early carotid revascularization (i.e. during the index hospitalization) may help reduce the risk of additional neurologic events without excess perioperative morbidity. We evaluated the relationship between rates of early carotid endarterectomy (CEA) or stenting (CAS) and hospital density/distribution within metropolitan areas of Texas. Patients with extracranial carotid artery stenosis and either stroke, transient ischemic attacks, or amaurosis were identified among all patients admitted from 2009 to 2013 to non-federal Texas hospitals within all 24 Texas metropolitan statistical areas (MSAs). Early CEA/CAS was defined as occurring during the index hospitalization. A Gini coefficient with bias correction factor was calculated to quantify the distribution of carotid procedures within an MSA. In total, 3,330 (15.4%) of the 21,665 metropolitan patients admitted to Texas hospitals with symptomatic carotid stenosis received early CEA/CAS. Only 263 (44%) of the 600 total hospitals where patients were admitted performed early CEA/CAS. An increasing proportion receiving early carotid CEA/CAS was inversely correlated with the procedural Gini coefficient (p=0.002) and directly correlated with the number of hospitals per 100K population (p=0.01). These two factors accounted for 51% of the variability among MSAs. Early CEA/CAS rates did not correlate with hospital volume or with level 1or 2 stroke centers within an MSA. Increasing the number of hospitals performing early carotid revascularization procedures (i.e. avoiding regionalization/concentration) may help increase the number of patients receiving early carotid revascularization for symptomatic carotid artery disease.

BackgroundImproved survival in children with congenital heart disease (CHD) has unveiled associated long-term neurocognitive impairments. However, the long-term effects on academic performance and the influence of sex, family, socioeconomic factors, and surgical era remain understudied, limited by small and incomplete cohorts. MethodsThis total-population cohort study, with nested sibling analysis, included 1 800 477 singletons born in Sweden between January 1, 1987, and December 31, 2005. Academic achievements at age 16 were assessed by upper secondary school eligibility, total grade sum, and subject-specific grades. Poisson and logistic regression were used to estimate adjusted prevalences, risk ratios (RR), and risk differences (RD). Adjustments were made for year of birth and socioeconomic status. Stratification by noncardiac congenital anomalies, sex, and surgical era was performed. ResultsAmong 1 800 477 Swedish-born singletons with complete socioeconomic data and residing in Sweden at 16 years of age, 16 075 (0.9%) individuals were identified with CHD and classified hierarchically as univentricular heart (UVH, n=349), severe (n=1 939), moderate (n=1 764), or mild CHD (n=12 023). After excluding major noncardiac congenital anomalies, the adjusted RD for failing to meet upper secondary school eligibility compared to children without CHD was 11 (95% confidence interval 5 to 17), 7 (4 to 9), 6 (3 to 8), and 2 (2 to 3) additional children per 100 for UVH, severe, moderate, and mild CHD, respectively. Children with both CHD and noncardiac anomalies had poorer academic outcomes than those with CHD alone. Additional risk factors were small for gestational age RR 2.34 (95% confidence interval 2.04-2.69) and prematurity RR 1.81 (95% confidence interval 1.64-1.99). Findings were consistent across core subjects, total grade sum, in sibling analyses, and over time. ConclusionAdolescents with CHD inherently face poorer academic performance, worsening with disease severity and persisting over time. This highlights ongoing educational disparities, especially among children with complex and univentricular heart disease. What Is New?O_LIThis nationwide cohort study demonstrates that academic achievement declines with increasing congenital heart disease (CHD) complexity, with disparities persisting after adjustment for socioeconomic and familial factors. C_LIO_LISmall for gestational age is identified as an independent risk factor for reduced academic outcomes in children with CHD, a previously unrecognized association. C_LIO_LIDespite the advancements in surgical survival rates over recent decades, academic outcomes did not demonstrate similar improvements. C_LI What Are the Clinical Implications?O_LIMultidisciplinary follow-up should extend beyond cardiac care in children with CHD, to include cognitive and educational support. C_LIO_LISmall for gestational age status represents an additional risk factor and should be incorporated into risk stratification. C_LIO_LIGenetic abnormalities associated with CHD significantly affect academic outcomes; routine genetic testing should be considered to guide individualized care. C_LI

Background: Resting electrocardiogram (ECG) is not currently recommended as part of cardiovascular disease (CVD) risk assessment, although accumulating evidence suggests a potential role. Objective: To examine the association between ECG abnormalities and incident CVD events as assessed by the 2023 Predicting Risk of Cardiovascular Disease Events (PREVENT) equations. Design: Secondary data analysis from the REasons for Geographic And Racial Differences in Stroke (REGARDS) prospective cohort, including study participants without a baseline CVD. Exposure: ECG abnormalities were classified by Minnesota Code (MC) as normal, any minor, or major abnormality at baseline (2003-2007). Outcome: Participants were followed for expert adjudicated incident CVD events through December 31, 2021. Results: Among 19,173 participants (mean age at baseline of 63.7 years; 57.8% were female). According to the PREVENT risk equations, 39.4% were classified as <7.5% 10-year risk CVD risk, 44.6% as 7.5-20% risk, and 16.0% as >20% risk. Overall, 47.0% had normal ECG, 44.0% had any minor abnormality, and 9.0% had any major abnormality. During follow-up, CVD events occurred in 12.4% of participants with normal ECG, 17.0% of those with any minor abnormality, and 25.4% of those with any major abnormality. Compared to those without ECG abnormality, the adjusted HR for incident CVD were 1.19 (95% CI 1.10-1.29) for any minor abnormality, and 1.53 (1.36-1.72) for any major ECG abnormality. In the <7.5% risk group, 43.6% had at least one ECG abnormality; in this risk group compared to those without ECG abnormality, the HR for incident CVD associated with any major ECG abnormality, present in 5.0% of the <7.5% risk group, was 1.87 (95% CI 1.34-2.62), The HR for any minor ECG abnormalities, present in 38.6% was 1.13 ( 95% CI 0.93 - 1.37). Conclusion: ECG abnormalities were associated with risk of CVD events across PREVENT risk groups. A substantial proportion of low-risk participants (according to the PREVENT equation) had ECG abnormalities and associated elevated risk. This supports the potential for using ECG to identify a subgroup of low-risk patients who may benefit from more aggressive primary prevention especially with major ECG abnormalities. Addition of electrocardiographic evaluation to the PREVENT risk equations may improves cardiovascular risk discrimination.

BACKGROUNDOver the past thirty years in the United States, hospitals have increasingly become incorporated into hospital systems, leading to organized care with more complex cases being managed at large urban-teaching hospitals. Over a similar period, changes in intervention guidelines for Aortic Dissection have occurred, with continually growing options for endovascular, minimally-invasive treatment. Given these dynamic changes, we examined trends in Aortic Dissection hospitalizations, intervention approaches, and hospital characteristics over past twenty-years to elucidate the effect of centralized care on outcomes. METHODSWe identified all patients presenting with aortic dissection, both ascending and descending, (ICD-9-CM: 441.0; ICD-10-CM: I71.0) in the NIS between 2000-2021. We then examined the utilization of open repair, endovascular and complex-endovascular repair, as well as nonoperative/medical management. Stratified by hospital setting (urban-teaching, urban-nonteaching, and rural), we analyzed trends of interventions and in-hospital mortality over time. If an operation was performed, we were able to discern between ascending/arch or descending aorta after the 2017 ICD revision. RESULTS553,030 patients with aortic dissection were identified. The number of inpatients in the US with aortic dissections has increased, with an incidence of 26.7 cases/100k in 2000 to 47.2 cases/100k in 2020 (p<0.01). Overall, including all hospital settings, aortic dissections were less frequently managed nonoperatively (2000-2021: 83%-71%) and more frequently managed endovascularly (Figure), with 85% of all descending and 16% of all ascending/arch aortic dissections undergoing TEVAR in 2021. Over time, aortic dissections have increasingly been managed at urban-teaching hospitals (2000-2021: 72%-92%;p<0.01). Since 2016, urban-teaching hospitals more frequently intervened on aortic dissections compared to their rural counterparts (21% vs. 6%;p<0.01), despite having similar rates of failed medical management (9.8% vs. 8.2%;p=0.30). Finally, comparing the last 5-years, urban-teaching hospitals have lower mortality rates when managing aortic dissection versus their rural counterparts (10.9% vs 11.7%, OR=1.10;p=0.02) and if managed operatively, there was a lower associated risk of mortality at urban-teaching hospitals compared to urban-nonteaching hospitals (12.5% vs. 17.3%, OR=1.46;p<0.01). CONCLUSIONBoth aortic dissection hospitalizations and interventions have significantly increased over the past two decades in the US. The growth of large hospital systems and their absorption of smaller hospitals into integrated primary through quaternary care centers has resulted in an increase in "regionalization" of care, in which complex cases are transferred to larger urban teaching centers. Our analysis suggests there is a mortality benefit from the centralization of aortic care to tertiary/urban-teaching centers, though further research into this question is required.

ObjectivesWe assessed stroke incidence in hypertensive patients according to cardiorespiratory fitness (CRF) and changes in CRF. MethodsA prospective cohort study of 483,379 US Veterans. Participants completed a maximal standardized Exercise Treadmill test (ETT) performed within the Veterans Affairs medical centers across the United States between 1999 and 2020. None exhibited evidence of unstable cardiovascular disease during the ETT. Participants were stratified into 5 age-and-gender specific CRF categories based on the peak metabolic equivalents (METs) achieved. A subgroup of participants with two ETT evaluations (n=110, 576) were also assigned to 4 categories based on MET changes from the initial ETT to the final ETT. Multivariable Cox models, adjusted for age, and co-morbidities were used to estimate HRs and 95% CIs for stroke risk. ResultsThe mean age {+/-} standard deviation (SD) was 59.4{+/-}9.0 years. During the median follow-up time of 10.6 years (5,182,179 person-years), there were 15,925 stroke events with an average annual rate of 3.1 events per 1,000 person-years. In a final adjusted model, relatively poor CRF was the strongest predictor of stroke risk than any other comorbidity (HR: 2.24; 95% CI: 2.10-2.40; P< 0.001). For each 1-MET higher exercise capacity, the risk was 10% lower (0.90, 95% CI 0.90-0.91, p<0.001). Compared to the Least-fit, stroke risk was 23% lower for Low-fit individuals (HR 0.77; 95% CI, 0.73-0.80; p<0.001); and declined progressively to 55% for those in the highest CRF category (HR 0.45; 95% CI 0.42-0.48; p<0.001). We also assessed stroke incidence according to change in CRF. Compared to fit individuals during both evaluations, the risk was 27% higher for those who became unfit (HR 1.27, 95% CI 1.15-1.41, p<0.001), and not significantly different for unfit who became fit (HR 1.10, 95% CI 0.97-1.25, p=0.13). ConclusionsPoor CRF was the strongest predictor of stroke incidence in hypertensive patients, regardless of age race, or gender. The association was independent, inverse, and graded for all stroke types. Changes in CRF over time reflected inverse changes in stroke risk, suggesting that risk of stroke can be modulated by improved CRF.

BackgroundPulmonary arterial hypertension (PAH) is a devastating disease that affects women more often than men; recent U.S. cohorts demonstrate a female:male ratio of 3 to 4:1. Paradoxically, males have worse survival. The differential effects of sex hormones, particularly estrogen, on the pulmonary vasculature and right ventricle likely account for some of these differences. The role of female-specific risk factors, such as reproductive exposures, are poorly understood in the pathophysiology of PAH. Research QuestionTo investigate the role of reproductive factors and exogenous estrogen exposures in PAH onset and severity in women enrolled in the United States Pulmonary Hypertension Scientific Registry (USPHSR). Study Design and MethodsUsing questionnaires from 390 women with PAH, enrolled in both the PAH Biobank and USPHSR, we conducted linear regression analyses to assess the association between patient reported reproductive variables and PAH disease severity variables, as well as REVEAL Lite 2.0 scores. We adjusted for potential confounders including age, race, BMI, and PAH sub-group (idiopathic, heritable, associated). ResultsYounger menopause age (< 40 years) associates with a lower cardiac index (CI) at diagnosis, even when controlling for use of hormone replacement therapy (HRT). There was a trend toward lower CI in women with menopause age of 41-50 years. Women who had ever used HRT were diagnosed with PAH an average of 13.4 years later and "ever use" of HRT associates with higher pulmonary vascular resistance and lower CI at diagnosis. InterpretationPremature menopause (age < 40 years) and ever use of HRT associate with worse hemodynamics, including lower CI, at diagnosis in women with PAH. Further investigations into reproductive history and estrogen exposures may offer an opportunity for more comprehensive risk factor screening and modification by physicians treating patients with PAH.

BackgroundYounger women have higher recurrent hospitalization rates and worse health status than men after their index episode of acute myocardial infarction (AMI). However, whether women have a higher risk of cardiovascular events in the year after discharge is unknown. MethodsWe used data from the VIRGO (Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients) study, which enrolled young AMI patients aged 18 to 55 years across 103 US hospitals. Sex differences in all-cause and cause-specific hospitalizations were compared by calculating incidence rates (IR, per 1,000 person-years) and incidence rate ratios (IRRs) with 95% confidence intervals (CIs). We then performed sequential modeling to evaluate the sex difference by calculating sub-distribution hazard ratios (SHR) accounting for deaths. ResultsAmong 2,007 women and 972 men, at least one all-cause hospitalization occurred among 905 (30.4%) participants in the year after discharge. The leading causes of hospitalization were MI-related (IR 171.8, 95% CI, 153.6-192.2 among women vs. IR 117.8, 95% CI, 97.3-142.6 among men), followed by non-cardiac (IR 145.8, 95% CI, 129.2-164.5 among women vs. IR 69.6, 95% CI, 54.5-88.9 among men) and other cardiac or stroke hospitalizations (IR 58.8, 95% CI, 48.8-70.7 among women vs. IR 53.8, 95% CI, 40.8-71.0 among men). Competing risk analysis showed that the sex difference was present for MI-related hospitalizations (SHR 1.33, 95%CI 1.04-1.70; P=0.02) and non-cardiac hospitalizations (SHR 1.51, 95%CI 1.13-2.07; P=0.01). ConclusionsYoung women with AMI have more adverse outcomes compared with men in the year after discharge. MI-related hospitalizations were the most common cause of hospitalizations, but non-cardiac hospitalizations showed the most significant sex disparity. Further studies to better understand the underlying mechanisms of non-cardiac hospitalizations are warranted.

ObjectiveTo examine the association between mood disorders in pregnancy and postpartum and peripartum cardiomyopathy (PPCM). MethodsRetrospective cohort study utilizing the National Inpatient Sample from the Healthcare Cost and Utilization Project, Agency for Healthcare Research and Quality of pregnant and postpartum patients from 2017-2019. Patients were separated into two groups based on ICD-10 coding for presence or absence of mood disorder (depression, bipolar depression, anxiety, or other mood diagnosis). The primary outcome was diagnosis of PPCM. Secondary outcomes included a composite of adverse cardiac events and maternal death. Groups were compared via t-tests, chi-squared analysis, and logistic regression that included all variables that differed between groups with p<0.05. ResultsOver 2.2 million subjects were analyzed and approximately 168,000 (7.4%) had an ICD-10 diagnosis of mood disorder. Those with mood disorders were more likely to be non-Hispanic white, obese, tobacco users, publicly insured, have comorbidities, and deliver at a large, private, non-profit hospital (all p<0.05). They were delivered at an earlier gestational age and were also more likely to undergo cesarean (37.0{+/-}4.6 vs 37.8{+/-}3.7 weeks and 35.8% vs 31.8%, respectively)., p<0.001). The primary outcome of PPCM was identified more than twice as often in those with mood disorder (0.12% vs 0.05%, p<0.001). Composite cardiac events, consisting of incidence of acute myocardial infarction, cardiac arrest, cardioversion, cardiac failure, and pulmonary edema were more frequent among patients with mood disorders (0.36% vs 0.14%, p<0.001). After controlling for confounders, PPCM remained independently associated with diagnosis of mood disorders (aOR 1.36, 95%CI 1.03-1.80) as did the composite of adverse cardiac events (aOR 1.57, 95% CI 1.37-1.81). ConclusionMood disorders in pregnancy and postpartum are associated with increased rates of PPCM and other cardiac events.